GHENT UNIVERSITY
Faculty of Medicine
Department of Psychiatry
and Medical Psychology
Traits and Eating Disorders:
associations with cognitive and behavioural characteristics
Thesis submitted in fulfilment of the requirements for the degree of Doctor in Medical Sciences
Myriam Vervaet
Ghent, 2005-07-08
Promotor: Prof. Dr. K. Audenaert
CONTENT
Introduction
Part I : ‘Dieting’ and ‘weight concerns’ as risk factors in the development
of eating disorders ...................................................................................................................................................... 8
1. Introduction ………………………………………………………………………………………………………....8
2. Binge eating in obese patients five years after treatment
.................................................................................................. 10
3. Weight concerns and eating patterns in schoolboys and schoolgirls
4. Eating-style and weight-concerns in young females
................................................................................ 20
.......................................................................................................... 34
Part II : The cognitive psychology of eating disorders: personality,
................................................................................................................................ 45
cognitions and behaviour
Chapter 1: Theoretical background
1. Definition and epidemiology
............................................................................................................................45
.............................................................................................................................................. 45
2. The complexity of the ED diagnosis
2.1. Categorical classification
.................................................................................................................................. 48
..................................................................................................................................... 48
2.2. Dimensional classification and co-morbidity
.................................................................................................... 50
3. Aetiology as a dynamic process: from trait- (vulnerability) to state- (eating disorder category) dependent characteristics
..................................................................................................................................................................................................... 53
3.1. Introduction
......................................................................................................................................................... 53
3.2. The relationship of low self-esteem and body-dissatisfaction
3.3. Perfectionism as a core trait
....................................................................... 55
.............................................................................................................................. 59
3.4. Perception of life events and the coping with life-events by individuals, characterized by low
self-esteem and clinical perfectionism .............................................................................................................. 63
4. Information processing in eating-disordered patients ............................................................................................................. 66
4.1. Neuropsychological processes ................................................................................................................................ 66
4.2. Cognitive processes…………………………………………………………………………………… 69
4.3. Information processing and emotional arousal………………………………………………………… 72
4.4. From schemata to behaviour…………………………………………………………………………… 75
5. A hypothetical model for the prediction of eating-disordered behaviour ............................................................................ 80
Chapter 2: Personality characteristics as trait-dependent vulnerability:
study results
........................................................................................................................................................................101
1. Binge eating disorder and non-purging bulimia: more similar than different?
............................................................101
2. Is ‘drive for thinness’ in anorectic patients associated with personality characteristics?
.............................................122
3. Cognitive and behavioural characteristics are associated with personality dimensions in
patients with eating disorders
...........................................................................................................................................138
4. Personality-related characteristics in restricting versus binging and purging eating
disordered patients
..............................................................................................................................................................166
5. Attempted suicide and personality in eating disorders. .........................................................................................................174
Chapter 3: Integration of personality characteristics in a psychobiological model
of eating disorders
......................................................................................................................................................... 195
Part III : Further study of the psychobiological model of eating
..........................................................................................................................................................................228
disorders
1. Introduction………………………………………………………………………………………………………228
2. Decreased 5-HT2a receptor binding in patients with anorexia nervosa
.......................................................................229
3. Binding potential of cortical 5-HT2A receptors is not different in bulimia nervosa patients and healthy
volunteers
.............................................................................................................................................................................236
General Conclusions
...........................................................................................................................................239
Nederlandse samenvatting
..........................................................................................247
BIJLAGE: GEBRUIKTE AFKORTINGEN
Ingesloten publicaties:
1. Vervaet M & van Heeringen C (1995). Binge Eating in Obese Patients Five Years after Treatment.
Eating Disorders: The Journal of Treatment and Prevention. Vol. 3 : 3, pp. 229-236.
2. Vervaet M, van Heeringen C, & Jannes C (1998). Weight Concerns and Eating Patterns in Schoolboys
and -Girls. Eating Disorders: The Journal of Treatment and Prevention, 6, 41-51.
3. Vervaet M & van Heeringen C (2000). Eating-style and weight concerns in young females. Eating
Disorders: The Journal of Treatment and Prevention. Vol. 8 : 233-240.
4. Vervaet M, van Heeringen C, & Audenaert K (2004). Psychological differences in Binge Eating
Disorder and Bulimia Non-Purging patients. European Eating Disorders Review, 12 (1), 27-33.
5. Vervaet M, van Heeringen C, & Audenaert K (2004). Is Drive for Thinness in Anorectic Patients
Associated with Personality Characteristics. European Eating Disorders Review, 12, 6, 375-379.
6. Vervaet M, Audenaert K, & van Heeringen C (2003). Cognitive and behavioural characteristics are
associated with personality dimensions in patients with eating disorders. European Eating Disorders
Review, 11 (5), 363-379.
7. Vervaet M, van Heeringen C, & Audenaert K (2004). Personality-related characteristics in restricting
versus binging and purging eating disordered patients. Comprehensive Psychiatry, 45 (1), 37-43.
8. Vervaet M, van Heeringen C, & Audenaert K (Submitted). Attempted suicide and personality in
eating disorders. Journal of Affective Disorders.
9. Audenaert K, Van Laere K, Dumont F, Vervaet M, Goethals I, Slegers G, Mertens J, van Heeringen
C, Dierckx R (2003). Decreased 5-HT2a receptor binding in patients with anorexia nervosa. European
Journal of Nuclear Medicine, 44, 163-169.
10. Goethals I, Vervaet M, Van De Wiele C, Audenaert K, Slegers G, van Heeringen C, Dierckx R
(2004). Binding potential of cortical 5-HT2A receptors is not different in bulimia nervosa patients and
healthy volunteers. American Journal of Psychiatry. 161:10, 1916-1918.
Voorwoord
Dit wetenschappelijk werk kwam tot stand onder leiding van Prof. van Heeringen wiens professionele
onuitputtelijkheid bijzonder stimulerend werkt, niet alleen bij de realisatie van dit werk. Aansluitend
wens ik Prof. Audenaert te bedanken voor zijn bereidwilligheid om het promotorschap op zich te
nemen. Beiden zijn voor mij meer dan waardevolle collega’s. Bovendien getuigen hun persoonlijkheden
van de realiteit dat dwang en impulsiviteit ook heel gezonde kenmerken kunnen zijn en vruchtbare
interacties kunnen opleveren.
Tevens wil ik alle leden van mijn begeleidings- en examencommissie bedanken voor hun waardevolle
vragen en opmerkingen. Speciale dank gaat uit naar Prof. Jansen, die als hoogleraar eetstoornissen mij
niet alleen reeds vele jaren boeide maar ook telkens weer verraste met haar originele onderzoeksvragen.
Dat uitzonderlijke psychologen ook snel carrière kunnen maken wordt ontegensprekelijk door Prof. De
Soete bewezen. Hij was nog student toen hij mij al leerde hoe ik een doctoraat moest schrijven.
Blijkbaar met succes, gezien het voor herhaling vatbaar was. Een gezamenlijke schrijfopdracht vijftien
jaar geleden en gezamenlijke pogingen om te stoppen met roken eindigden steevast in bijzonder gezellige
etentjes met Prof. Kaufman. Met Prof. Thiery ontwikkelde ik in al die jaren een zeer dierbare band, als
hoogleraar Medische Psychologie, als excellente deskundige in de Neuropsychologie, als toegewijd en
competent behandelaar en tenslotte (hopelijk) ook als vriend. Dat Prof. Colardyn bovenop zijn
uitgebreide professionele opdracht deze psychologische brok onderzoekswerk te verwerken kreeg, was
het gevolg van zijn, door ons zeer gewaardeerd, voormalig diensthoofdschap. Bovendien was hij als
hoofdarts steeds bereid tot luisteren en helpen als wij met onze patiënten weer diep in de moeilijkheden
zaten, met de snelheid en de flexibiliteit die hem zo kenmerkt. Ook Prof. Van Cauwenberge heeft
vaderlijk de verantwoordelijkheid als onze vakgroepvoorzitter opgenomen in tijden van hoge nood (en
die was er meermaals). Van bij mijn start in deze faculteit tot nu heeft hij meermaals zijn psychologische
kwaliteiten getoond bij de verzuchtingen van een vreemde eend tussen al die artsen-specialisten. Dat
Prof. Kips momenteel mee beleidslijnen uittekent ligt in het verlengde van zijn capaciteiten om zowel
structureel als inhoudelijk de puntjes op de i te zetten. Ook hem wil ik bedanken voor de vele
gesprekken, de doorverwijzingen van patiënten en zijn toestemming om in de examencommissie te
zetelen. En tenslotte mijn dank aan Prof. Debacquer die meermaals mijn obese databank bekeek en
probeerde via SPSS het juiste dieet te vinden.
In de voorgeschiedenis van dit proefschrift waren Prof. Evrard en Prof. Van Oost de sleutelfiguren bij
mijn eerste doctoraat over eetstoornissen. Daarnaast werd ik positief geconditioneerd door Prof.
Vandereycken, dé pionier in het onderzoek en behandeling van eetstoornissen in Vlaanderen. Ook hen
wil ik nu bedanken. Hun degelijke wetenschappelijke basis gaven mij het vertrouwen om in de faculteit
Geneeskunde een plaats te zoeken en te krijgen dank zij Prof. Jannes.
Als geboeid wetenschapper kon ik echter niet zonder de kliniek. Het behandelen van eetstoornissen kan
enkel door en met een multidisciplinair team dat via een duurzaam en intensief engagement de wondere
wereld van deze patiëntengroep probeert te begrijpen. De bouwstenen voor een gespecialiseerde
afdeling werden op de dienst Endocrinologie gelegd. Bij deze wens ik Dr. Deslypere en het
verpleegkundig team onder leiding van Bea van harte te bedanken voor de vele uren die zij extra
spendeerden aan onze probleemmeisjes. Het was de bakermat voor onze huidige 21-bedden tellende
eetkliniek. In 1998 verhuisden we naar de afdeling Psychiatrie. Van in het begin was daar een
bijzondere grote inzet en zonder deze kon dit werk nooit gemaakt worden. Siska, Tina, Bart, Katrien,
Nele, Rita en alle verpleegkundigen ben ik bijzonder dankbaar en ik geef met gerust gemoed het roer
door aan Dr. Katrien Bernagie die de hospitalisatie-eenheid in de toekomst zal leiden.
Bijzondere dank gaat uit naar Lieve Rousseau, die haar logistieke, esthetische en psychologische
kwaliteiten weet te combineren in een relativerende stijl die mij altijd opfleurt. Ook Betty die ons allen
buffert tegen de vaak overspoelende telefoons en afspraken. Samen met Brigitte vormden zij met zijn
drieën bovendien de trouwe achterhoede in moeilijke jaren.
Tot slot gaat mijn dank naar mijn familie. Ik ben de laatste jaren te veel en zeer belangrijke mensen
verloren, waardoor mijn werk vaak mijn troost werd. Mijn moeder wil ik bedanken omdat ze ondanks
haar gevleugelde uitspraak “dat ze niet begrijpt waarom ze haar kinderen zo lang heeft laten studeren om
daarna zo hard te moeten werken” toch accepteert dat zij ons daardoor minder ziet. Mijn zus No die mij
al 40 jaar probeert ‘in balans’ te krijgen: “meer sport, meer natuur, meer buiten”, en Isidoor die steeds
geboeid informeert naar de fenomenologie van onze patiënten en ondertussen zelf ‘mindful’ probeert te
worden. Ook mijn ongelooflijke kranige en mature nichten Ruth en Karlien, die het wetenschappelijke
niveau in de toekomst zullen ondersteunen, wil ik hierbij extra bedanken. En tenslotte Elise: bij de
finalisering van mijn eerste doctoraat zat zij op mijn schoot als baby en nu zat zij achter haar computer
Spaans te leren of Italiaans te sms-en. Haar doorzettingsvermogen in combinatie met haar grote
tolerantie zorgden ervoor dat ik mij als moeder nooit schuldig hoefde te voelen.
Gent, 20 juni 2005
Introduction
Recent models in psychiatry explain psychopathology as the consequence of an interaction between
stressors (eliciting factors) and a predisposition or vulnerability (predisposing factors), which is expressed
through (problem) behaviour. Due to its reinforcing properties, such behaviour may act as a maintaining
factor and may become a symptom. A disorder may thus be constituted of maintaining factors. The
vulnerability can be caused by genetic or developmental influences, and modified by environmental and
psychosocial variables.
Vulnarability is caused by neurobiological mechanisms, in particular by
neuroanatomical brain circuits with their neurophysiological and neuropsychological characteristics.
This vulnerability, however, becomes not necessarily manifest during all periods of life. Eating
disorders occur predominantly during adolescence or early adulthood, probably because this transition
period is characterised by biological, psychological and social changes. The experience and necessity of
change can be very stressful for an individual, especially for an anxious individual. In addition,
‘differentiating’, in terms of individuality/personality, becomes a very important process during
adolescence. Indeed, conformity through following the rules of caregivers, i.e. parents, is predominantly
the adaptive behavioural pattern during childhood. However, during adulthood, individuals are expected
to formulate their own goals and to direct their own behaviour in relation to chosen values and norms.
This demand can elicit dysfunctional coping behaviour, such as ‘creating a perfect body’ with divergent
meanings and motives. Thus, an extreme need for control can sustain the self-starvation in anorectic
patients, or the fear of rejection can motivate a bulimic girl to strive for ideal body shapes.
Over the past few decades, eating disorders have emerged as clinical problems of growing relevance,
due to their increasing prevalence, the substantial somatic and psychiatric co-morbidity, increased
mortality, frequent relapse, and common failure of treatment. With regard to treatment, and from a
cognitive-behavioural point of view, maintaining factors were the first target. The over-evaluation of
body shape and weight has been described as the ‘core psychopathology’ of clinical eating disorders
(Fairburn, Cooper, & Shafran, 2003). Dietary restraint is the most obvious behavioural expression of
this over-evaluation. In the nineties, the cultural standard of beauty ideals was assumed to be associated
with thinness in Western-societies, thus triggering weight concerns and behaviours such as dieting,
particularly among young women and girls. The terms ‘dietary restraint’ and ‘restrained eating’ refer to a
tendency to consciously restrict food intake in an effort to maintain weight or produce weight-loss
(Herman and Polivy, 1975). Dieters display the tendency to overeat when anxious or stressed, whereas
normal, unrestrained individuals tend to eat less when anxious (Rutledge and Linden, 1998).
Among
dieters, overeating can be induced by a dysphoric mood, alcohol consumption, and conditions, in which
restrained eaters believe that they have broken their diet-rules by consuming a preload of food. This
phenomenon is called ‘disinhibition’ or ‘counterregulation’. Explanations for this effect range from
physiological mechanisms, i.e. via a dissociation from conditioned satiety signals, to distraction from
distress and learned helplessness (Polivy and Herman, 1999).
Additional psychological features associated with restrained eating include exaggerated
responsiveness to nutritional or food-related cues (Tuschl, 1990), increased distractibility and
emotionality (Herman and Polivy, 1975; Polivy et al., 1978), and depression and anxiety (French and
Jeffery, 1994). Physiological consequences of dieting have also been noted, such as elevated triglyceride
levels (Laessle et al., 1989) and weight cycling, which in itself has been associated with a higher risk of
morbidity (Lissner et al., 1991). Unsuccessful dieters show poorer impulse regulation and more weight
fluctuation, and have higher levels of perfectionism and drive for thinness when compared to successful
dieters (Van Strien, 1997). They also are more prone to use dietary practices such as counting calories,
eating low-calorie foods, and avoiding certain foods. In contrast, dieters who exert more enduring
restraint tend to take smaller portions, and eat more slowly (Westenhoefer, 1991).
The relationship between body dissatisfaction and self-esteem on the one hand and unsuccessful
dieting on the other hand is less clear. Appearance-motivated dieters are at particular risk of eating
pathology. These dieters mainly are younger women, who are characterized by a low self-esteem, body
dissatisfaction, and a strong desire to change their bodies despite their normal weight. However, it
remains to be demonstrated whether it is the perception that one is “dieting” (the cognitive aspect), or
the actual decrease in caloric consumption and resulting physiological changes that disrupts normal
eating (Putterman & Linden, 2004).
The first three papers in Part 1 of this thesis describe aspects of the association between the risk
factors ‘weight concerns’ and ‘dieting’ and the development of eating disorders.
Without denying the importance of these eliciting and maintaining factors, the main goal of this
thesis was to explore the vulnerability for eating disorders, i.e. to study predisposing factors. Therefore, a
major research question for the studies as described in this thesis addressed, first the extent to which a
predisposition to eating disorders can be described in terms of personality dimensions, and secondly, the
expression of such a predisposition through cognitive and behavioural characteristics and their
interactions, which are of particular interest for eating disorders (see figure 1).
PREDISPOSING
FACTORS
Psychobiological dimensions
PERSONALITY
ELICITING
ENVIRONMENT
FACTORS
MAINTAINING
FACTORS
COGNITIVE
PROBLEM
SCHEMATA
BEHAVIOUR
- feelings o f uselessness
- feelings of loneliness and
emptiness
STATE
- BMI
- eating behaviour
~ CLINICAL-PHENOMENOLOGICAL
type of eating disorder (DSM-IV)
Figure 1: Model of the development of disturbed eating behaviour
Personality is commonly described as a stable organisation of psychobiological structures
reflecting temperamental and character dimensions. Rutter (1987) has defined temperament as “simple,
non-motivational, non-cognitive stylistic approaches that are heritable and likely rooted in underlying
neurobiological processes”.
Although biologically driven temperamental constructs motivate and
restrain behaviour, the expression of the same temperamental constructs is modified by experiences
(Kagan, Arcus, & Snidman, 1993). Temperament refers to automatic emotional responses to experience
that are moderately heritable and stable throughout life. In contrast, character refers to self-concepts
and individual differences in goals and values, which influence voluntary choices, intentions, and the
meaning of what is experienced in life. Dimensions of character are influenced by sociocultural learning,
and mature in progressive steps throughout life. Behavioural genetic research has indicated that nonshared environmental effects, i.e. experiences that are not shared by siblings in the same family, have the
greatest non-genetic effect on the development of psychopathology (Kendler, Neale, Kessler, Heath, &
Eaves, 1992).
These dimensions of personality interact with each other in order to motivate adaptation to life
experiences and to influence susceptibility to emotional and behavioural disorders.
Information
processing characteristics are determined by these temperamental and character structures, and result in
schemata. A schema is defined as a mental structure that consists of a stored domain of knowledge,
which interacts with the processing of new information (Williams, Watts, MacLeod, & Mathews, 1997).
It is a mental ‘filter’, which is shaped by previous experiences and which colours subsequent
interpretations. A schema is rich in meaning, and represents much more than a single belief. Schemata
comprise ‘meaning’, with its physical, emotional, verbal, visual, acoustic, kinetic, olfactory, tactile and
kinaesthetic features. A schema contains information about the self, the others and the surrounding
world, and directs our perception, interpretation and memory. Daily experiences activate schemata,
which elicit corresponding feelings and behaviours. While a behaviour is observable, cognition is the
quality of knowing which includes perceiving, judging, sensing, reasoning, and imaging” (Weisenberg,
1994). It should be mentioned that this “knowing” can take place inside or outside the realm of
attention.
Research findings regarding the application of this theoretical model to eating disorders are
described in Part 2, followed by an elaboration of the research hypothesis.
Data on 800 eating
disordered patients are reported and compared with previous research findings. Furthermore, particular
attention is given to the correlation between personality dimensions and three cognitive characteristics,
which are defined as core characteristics in the main trans-diagnostic models of eating disorders
(Fairburn, Cooper, & Shafran, 2003; Serpell & Troop, 2003).
These cognitive factors, i.e. body
dissatisfaction, perfectionism and interpersonal distrust, were measured using the Eating Disorder
Inventory (EDI; Garner, Olmstead, & Polivy, 1983).
The personality model as used in the studies, which constitute this thesis, is psychobiological in
nature, and serves as a basis for the study of the neurobiological correlates of these psychological
characteristics. Part 3 describes two such studies.
Conclusions and suggestions for further research are provided in the final chapter.
References
Fairburn CG, Cooper Z, & Shafran R (2003). Cognitive behaviour therapy for eating disorders: A ‘transdiagnostic’ theory
and treatment. Behaviour Research and Therapy, 41, 509-528.
French SA, & Jeffery RW (1994). Consequences of dieting to lose weight: Effects on physical and mental health. Health
Psychology, 13: 195-212.
Garner DM, Olmstead MP, & Polivy J (1983). Development and validation of a multidimensional Eating Disorder Inventory
for anorexia nervosa and bulimia nervosa. International Journal of Eating Disorders, 2, 15-24.
Herman CP, & Polivy J.(1975). Anxiety, restraint and eating behaviour. Journal of Abnormal Psychology, 84, 666-672.
Kagan J, Arcus D, & Snidman N (1993). The idea of temperament: Where do we go from here? In R.Plomin & G.E.
McClearn (Eds.), Nature, nurture and psychology. Washington, DC: American Psychological Association.
Kendler KS, Neale MC, Kessler RC, Heath AC, & Eaves LJ (1992). The genetic epidemiology of phobias in women: The
interrelationship of agoraphobia, social phobia, situational phobia, and simple phobia. Archives of General Psychiatry, 49,
273-281.
Laessle RG, Tushel RJ, Kotthaus BC, & Pirke KM (1989). Behavioral and biological correlated of dietary restraint in normal
life. Appetite 12: 83-94.
Lissner L, Odell PM, D’Agostino RB, Stokes J, Kreger BE. Belanger AJ & Brownell KD (1991). Variability of body weight
and health outcomes in the Framingham population. N. Eng. J. Med. 324-: 1839-1844.
Polivy J, & Herman CP (1999). Distress and eating: why do dieters overeat? International Journal of Eating Disorders, 26,
153-164.
Polivy J, Herman CP, & Warsh S (1978). Internal and external components of emotionality in restrained and unrestrained
eaters. J. Abnorm. Psychol. 87: 497-504.
Putterman E, & Linden W (2004). Appearance versus Health: Does the reason for dieting affect dieting behavior? Journal of
Behavioral Medicine, Vol. 27, 2, 185-204.
Rutledge T, & Linden W (1998). To eat or not to eat: Affective and physiological mechanisms in the stress-eating
relationship. J. Behav. Med. 21: 221-240.
Rutter M (1987). Temperament, personality, and personality disorder. British Journal of Psychiatry, 150, 443-458.
Serpell L, & Troop N (2003). Psychological factors. In : J. Treasure, U. Schmidt & E. van Furth (Eds), Handbook of Eating
Disorders. Second Edition, Wiley & Sons, Chichester.
Tuschl RJ, Laessle RG, Platte P, & Pirke KM (1990). Differences in food-choice frequencies between restrained and
unrestrained eaters. Appetite 14: 9-13.
Van Strien T (1997). The concurrent validity of a classification of dieters with low versus high susceptibility toward failure of
restraint. Addictive Behaviors, 22, 587-597.
Weisenberg M (1994). Cognitive aspects of pain. In P.D. Wall, & R. Melzack (Eds.), Textbook of pain (pp. 275-289). New
York: Churchill Livingstone.
Williams JMG, Watts FN, Mac Leod C, & Mathews A (1997). Cognitive psychology and emotional disorders (2nd ed.).
Chichester: Wiley.
PART I
‘Dieting’ and ‘weight concerns’ as risk factors in the development of eating
disorders
1. Introduction
The core psychopathological feature of eating disordered patients is their over-evaluation of
shape and weight. In contrast with the probably complex and badly understood cause of the disease, the
symptoms are clear forward, measurable and uniting all patients.
Moreover, the physical abnormalities
in these patients appear to be largely secondary to their disturbed eating habits, and the majority of the
somatic symptoms are reversed by restoration of healthy eating habits. Consequently, the somatic
treatment seems to be easy, and merely a question of willpower and clear indications. At the same time
young adolescents grow up, while living in a society with television soaps, commercials and computergames in which thin female bodies are idealized. The consequent pressure of ‘looking good’ often leads
to a ‘normative discontent’ (Rodin, Silberstein, & Striegel-Moore, 1985), due to which many girls worry
about their body shape and try to induce a negative energy balance. A dramatic consequence is the
prevailing view, even among medical professionals, that eating disorders are self-inflicted and that they
are an expression of temporary immaturity. Disturbed eating patterns can indeed be placed on a
continuum from harmless to pathological, but this unscientific opinion ignores the fact that typical
eating disorders are severe and often chronic disorders associated with high levels of physical and
psychological co-morbidity and poor quality of life.
For example, the mortality rate in anorectic
inpatients is indeed twice as high as the rate in other psychiatric inpatients. Equally important is the
question whether restricting behaviour can induce a psychiatric syndrome.
Bearing in mind the study
of Keys (1946), it was hypothesized that too strict dieting may have iatrogenic effects, such as inducing
binge eating and other eating-related pathology.
Following this line of reasoning, the first part of this thesis includes three studies describing the
presence of disturbed eating patterns among risk groups such as obese patients (after treatment with
strict diets), fashion models and young adolescents. These articles were published between 1995 and
2000 and formed the start for the search to distinguish between dieting as symptom of psychopathology
and dieting as a means of reaching a healthy weight.
2. Binge eating in obese patients five years after treatment.1
Abstract
Five years after treatment for obesity, combining cognitive-behavioral treatment with a very low calorie diet
(VLCD) or a low calorie diet (LCD), the eating behavior of 112 female patients was studied. At the time of
reassessment most of the women showed a restrained eating style combined with bingeing. Significantly more
patients in the VLCD-group than in the LCD-group reported bingeing. More than half of the successfully treated
women (BMI ≤ 30) reported binge eating. No association between treatment success and a restrained eating style
was found.
Habitual dieters show marked overcompensation in eating behavior in a way that is similar to the
bingeing in eating disorders (Polivy & Herman, 1985; Wardle, 1987). But binge eating does not occur in
all dieters (Tuschl, 1990). More-over, in some people binge eating is a transitory phenomenon, while for
others it progresses to a chronic condition. Nevertheless there is a close connection between dietary
restraint and binge eating. Hence it is no surprise that binge eating is a common problem among the
obese (Hudson et al., 1988; Kolotkin et al., 1987; Marcus & Wing, 1987).
Binge eating may also be a serious complication of treatment.
Marcus and Wing (1987) found
that between 20% and 46% of obese individuals participating in a behavioral weight control program
reported binge eating. The quantity of food consumed and the duration of episodes were similar to
those in patients with bulimia nervosa. Garner and Wooley (1991) suggest that excessive dieting
associated with overweight may induce binge eating, which in turn leads to increased caloric intake and
greater adiposity.
Since treatment of the obese according to the addiction model includes intensifying restraint
rather than just normalizing food intake (Bemis, 1985; Vandereycken, 1990; Wardle, 1987), it may have
iatrogenic effects. Of further interest is the finding that both obese and lean dieters eat more when
depressed, a pattern which is reversed in non-dieters (Baucom & Aiken, 1981; Polivy & Herman, 1985).
Therefore, dieting may cause depression which in turn makes the individual more vulnerable to bouts of
overeating.
1
Vervaet, M. & van Heeringen, C. (1995). Binge eating in obese patients five years after treatment. Eating
Disorders The Journal of Treatment and Prevention, 3, pp.229-236.
Telch, Agras, and Rossiter (1988) found that binge eating becomes significantly more common
when the degree of overweight increases. A significant positive relationship between the degree of
overweight and binge severity has also been demonstrated by other researchers (Kolotkin et al. 1987;
Marcus et al., 1985). These findings suggests that individuals who binge eat may be at greater risk for
overweight. Other studies have indicated that obese binge eaters may have a poorer treatment response
in standard behavioral weight loss programs than obese nonbinge eaters (Keefe et al., 1984) because of a
higher rate of dropout and a more rapid regain of weight (Marcus, Wing, & Hopkins, 1988).
The current study aimed at the assessment of differences in the prevalence of binge eating
between obese patients who followed a cognitive-behavioral treatment combined with a low calorie diet
and those with a very low calorie diet. The association between binge eating and treatment outcome was
also investigated.
Methods
We studied 260 obese women (definition: Body Mass Index of 30 or more) who followed a
multidisciplinary treatment according to two different programs. In the first group, treatment included
both a very low calorie diet (VLCD, 400-600 Kcal) and cognitive behavior group therapy for weight loss
during one year.
Treatment began with a six-week VLCD fasting program, followed by gradual
refeeding. The second group started with a low calorie diet (LCD, 800-1,200 Kcal) during several
months before refeeding, on an individually basis. During the initial three months, sessions occurred
weekly, then biweekly for the next six months, and monthly for the final three months of treatment.
Group sessions lasted for 60 minutes and individual sessions for 30 minutes. Both kinds of treatment
were supplied by a female behavior therapist.
The treatment included three basic elements. First, information about medical topics (e.g. the
risks of obesity, influence of different diets) was presented by an endocrinologist who also followed the
medical evolution of the patients. Fenfluramine was given in case of great carbohydrate cravings.
Second, patients were engaged in an exercise program included swimming, jogging, and fitness training
on a regular basis (minimally three times a week for one hour). As to the specific diet, patients learned
how to purchase, compose, and prepare meals that were different from fat- and carbohydrate-rich ones.
Third, we applied a form of cognitive-behavior therapy based on self-monitoring, stimulus control,
stress management, cognitive restructuring, relapse prevention training, enlargement of social support
and self-esteem, and amelioration of body image. The final aim of the program was to reach a sense of
self-control, especially in eating situations.
The patient group consisted of 78 females treated in an outpatient clinic in Antwerp and 182
female patients who were consecutively admitted to the Unit for Eating Disorders of the Department of
Endocrinology, University Hospital, Gent.
Five years after treatment, a questionnaire was sent to all 110 obese women who had participated
in the VLCD treatment and to the 150 in the LCD group.
The following characteristics were
monitored: age, situation of living, activity, weight before treatment and after 1 year and 5 years, body
mass index (BMI), highest weight ever, desired weight, use of laxatives and/or anorectic drugs, vomiting,
and eating-behavior. Subjects were also asked to fill out the Dutch eating questionnaire (Van Strien et
al., 1986). For this questionnaire the results were compared to the norm tables of obese women (Van
Strien et al., 1986) and divided in three groups: low (L), mean (M) and high (H) correspondence group,
using the cut-off-scores shown in Table 1.
Table 1: Cut-off Scores from the Dutch Eating Questionnaire
Restrained eating
External eating
Eating with clear emotions
Eating with diffuse emotions
Totally emotional eating
Low
Mean
High
<2.7
<2.4
<1.1
<1.7
<1.1
2.7-3.4
2.4-3.1
1.1-2.9
1.7-3.3
1.1-2.9
>3.4
>3.1
>2.9
>3.7
>2.9
Results
Of the total of 260 women, data on 112 patients (43 %) were available for analysis, including 56
patients of the VLCD group (group 1) and 56 females of the LCD group (group 2). To investigate the
relationship between frequency of binge eating and treatment outcome, the latter was dichotomized as
successful (BMI ≤ 30) or not successful (BMI > 30).
The following picture of the eating behavior emerged from questionnaires: 74 % ate between the
meals, including 49 % in the evening; 14 % skipped breakfast, 5 % lunch, and another 5 % dinner; 11 %
ate a lot of sweets, 28 % regularly and 56 % sometimes; most of the women (71 %) preferred sweet to
salt; 37 % ate alone regularly, 47 % thought a lot about food during the day, and 26 % counted calories.
Loss of control while eating was reported by 74 women (66%), including 12 women (11 %) who binged
daily. In order to get information about the difference of 'objective' and 'subjective' binges, patients
were asked to quantify their binges: 21 women (19%) reported binges involving the intake of more than
2,000 Kcal, while 31 (28 %) reported the intake of about 1,000 Kcal; 17 (15%) reported binges of less
than 500 Kcal, which can therefore be called ‘subjective’ binges.
Table 2: Bingeing in VLCD and LCD
Bingeing
Occurrence
VLCD
n
%
45
80.4
(n = 56)
n
30
%
53.6
Frequency
LCD (n = 56)
p*
.0026
.0200
*never
11
19.6
26
46.4
*daily
7
12.5
5
8.9
*regularly
24
42.9
15
26.8
*sometimes
14
25
10
17.9
Quantity
.1619
*0 Kcal
16
28.6
27
48.2
*< 500 Kcal
11
19.6
6
10.7
*> 1000 Kcal
18
32.1
13
23.2
*> 2000 Kcal
11
19.6
10
17.9
*Chi-square tests
A significant difference in the frequency of bingeing between the VLCD and the LCD group was
found. Of the VLCD women, 45 women (80.4%) reported bingeing versus 30 (53.6 %) LCD-women,
as shown in Table 2. No significant difference between the treatment groups could be found for the
quantity of binges.
No indications for an association between the occurrence or frequency of bingeing and treatment
outcome could be found (see Table 3).
Table 3: Bingeing in Successful and Unsuccessful Treatment Outcome.
Bingeing
Occurrence
BMI≤30 (n = 44)
BMI>30 (n = 68)
n
%
n
%
p*
25
56.8
50
73.5
.0663
frequency
never
.2729
19
43.2
18
26.5
daily
3
6.8
9
13.2
regularly
13
29.5
26
38.2
sometimes
9
20.4
15
22.1
Quantity
.0242
0 Kcal
19
43.2
18
26.5
< 500 Kcal
7
15.9
10
14.7
> 1000 Kcal
8
18.2
23
33.8
> 2000 Kcal
5
11.4
16
23.5
* Chi-square tests
However, a significant difference between successfully and unsuccessfully treated patients emerged for
the kind of binges : objective binges (involving the intake of at least 1,000 Kcal) were reported more
often by women in the non-successful group. No significant differences between the successfully and
unsuccessfully treated groups could be found for the use of other methods to influence the body weight:
34 patients (30 %) of the total group used appetite suppressing drugs, 9 patients (8 %) reported
vomiting, and 35 patients (31 %) used laxatives.
Table 4: High scores on the Dutch Eating Questionnaire in VLCD and LCD.
H-score
VLCD
(n = 56)
LCD
(n = 56)
n
%
n
%
p*
Restrained eating
28
52.8
27
50.0
.950
External eating
18
32.1
10
17.9
.120
Clear emotional eating
29
51.8
15
26.8
.004
Diffuse emotional eating
23
41.1
17
30.9
.037
Total emotional eating
32
57.1
17
30.4
.005
* Chi-square tests
Of particular interest is the finding of a significant difference between the VLCD and the LCD groups
on the indices for Emotional Eating of the Dutch Eating Questionnaire (df = 2; X2 = 10.277; p =
0.005). As shown in Table 4, 32 patients in the VLCD-group (57.1 %) had a high score versus 17 in the
LCD-group (30.4 %). Only two VLCD-patients (3.6 %) had a low score on this item, versus nine LCDpatients (16.1 %).
No significant differences between the treatment groups were found for the
proportion of high scores on Restrained Eating, and External Eating. However, high scores on Eating
by Clear Emotions and Eating by Diffuse Emotions were found more often in the VLCD group than in
the LCD group.
With respect to the association between high scores on the questionnaire and treatment outcome, it
appeared that high scores on External Eating and Eating by Clear Emotions were more common among
unsuccessfully treated patients (see Table 5).
Table 5: High scores on the Dutch Eating Questionnaire in Successful and Unsuccessful
Treatment Outcome.
H-score
BMI≤30
BMI>30
n
%
n
%
p*
Restrained eating
27
65.8
28
42.4
.060
External eating
8
18.9
20
29.4
.001
Clear Emotional eating
11
25.0
33
48.5
.035
Diffuse emotional eating
11
25.6
29
42.6
.170
Total emotional eating
15
34.1
34
50.0
.252
*Chi-square tests
Discussion
Preceding a discussion of the results of this study, some methodological shortcomings should be
addressed. First, the results are likely to be biased because follow-up data are known for only 43% of
the patients. Second, because of the retrospective nature of the study no base line data on the
occurrence and characteristics of bingeing before treatment were available. Thus, it cannot be concluded
that bingeing has been induced by the treatment.
Nevertheless, the differences between VLCD and LCD outcome seem to support the hypothesis
that the degree of dieting determines the degree of loss of control over eating: loss of control was
present in 80 % of the VLCD-patients and in 53 % of the LCD-group. Our results also suggest a link
between emotional eating and bingeing. VLCD-patients more often reported bingeing, and also more
commonly had high scores on items related to eating, because of clear or diffuse emotions.
With respect to the association between treatment outcome and binge eating, we found that
more than half of the successfully treated subjects reported bingeing, but objective binges occurred
significantly less often. Although restrained eating was as common as in unsuccessfully treated women,
the results suggest that successfully treated women lose less control in situations where they are
externally or emotionally stimulated to eat.
Anyway, the results from this study indicate that bingeing is a serious problem even several years
after treatment for obesity. Many women in this study used laxatives and anorectic drugs, vomited, and
dieted, without losing weight. One explanation for this failure can be found in their disturbed eating
pattern: they skip meals, prefer sweets, eat alone regularly, and think a lot about food, but most of all
they regularly lose control over their eating in emotional situations.
In view of the finding that better treatment outcome is associated with less external and
emotional eating, and with a smaller quantity of food intake in case of bingeing, the results of the current
study indicate that the focus of treatment for obesity should be shifted from stimulating dieting to
improving self-control. Finally, our follow-up data make the use of very low calorie diets - still very
popular in Europe - indicate a rather questionable practice.
References
Baucom, D. H., & Aiken, P.A.(1981). Effect of depressed mood on eating among obese and nonobese dieting and nondieting
persons. Journal of Personality and Social Psychology, 41, 577-585.
Bemis, K.(1985). "Abstinence" and "nonabstinence" models for the treatment of bulimia. International Journal of Eating
Disorders, 4, 389-406.
Garner, D.W., & Wooley S.C.(1991). Confronting the failure of behavioral and dietary treatments for obesity. Clinical
Psychology Review, Vol. 11, PP. 729-780.
Hudson, J.I., Pope, H.G., Wurtman, J., Yurgelun-Todd, D., Mark, S., & Rosenthal, N.E.(1988). Bulimia in obese individuals:
Relationship to normal-weight bulimia. Journal of Nervous and Mental Disease, 176, 144-152.
Keefe, P.H., Wyshogrod, D., Weinberger, E., & Agras, W.S. (1984). Binge eating and outcome of behavioral treatment of
obesity: A preliminary report, Behaviour Research and Therapy, 22, 319-321.
Kolotkin, R.L., Revis, E.S., Kirkley, B.G., & Janick, L. (1987). Binge eating in obesity: Associated MMPI characteristics.
Journal of Consulting and Clinical Psychology, 55, 872-876.
Marcus, M.D., & Wing, R.R.(1987). Binge eating among the obese. Annals of Behavioral Medicine, 9, 23-27.
Marcus, M.D., Wing, R.R., & Hopkins, J.(1988). Obese binge eaters: Affect, cognitions, and response to behavioral weight
control. Journal of Consulting and Clinical Psychology, 56, 433-439.
Marcus, M.D., Wing, R.R., & Lamparski, D.M.(1985). Binge eating and dietary restraint in obese patients. Addictive Behaviors,
10, 163-168.
Polivy, J., & Herman, C.P.(1985). Dieting and bingeing: A causal analysis. American Psychologist, 40, 193-201.
Telch, C.F., Agras, W.S., & Rossiter, E.M.(1988). Binge eating increases with increasing adiposity. International Journal of Eating
Disorders, 7, 115-119.
Telch, C.F., & Agras, W.S.(1993). The effects of a Very Low Calorie Diet on binge eating. Behavior Therapy, 34, 177-193.
Tuschl, R.J.(1990). From dietary restraint to binge eating: Some theoretical considerations. Appetite, 14, 105-109.
Van Strien, T., Frijters, J., Roosen, R., Knuiman-Mijl, D., & Defares, P.(1986). Eating behavior, personality traits and body mass in
women. Agricultural University, Wageningen, The Netherlands.
Vandereycken, W.(1990). The addiction model in eating disorders: Some critical remarks and a selected bibliography.
International Journal of Eating Disorders, 9, 95-101.
Wardle, J.(1987). Compulsive eating and dietary restraint. British Journal of Clinical Psychology, 26, 47-55.
3. Weight Concerns and Eating Patterns in Schoolboys and -Girls2
In this study, weight concerns and eating patterns were assessed in a large group of school-aged adolescents by
means of questionnaires. Girls far more commonly reported problems related to eating and body weight, restrained
eating with counting of calories, and abuse of laxatives. Loss of control over eating was reported by more than half
of the girls. The occurrence of eating problems and associated behavioral characteristics among girls clearly increased
with age, even though young girls reported problems related to body weight and eating patterns to such an extent
that the introduction of prevention programs should be considered in the first years of secondary school.
Outcome studies indicate a substantially increased risk of medical and psychiatric disorders
(Fombonne, 1995), and of premature death (Sullivan, 1995), among eating disordered patients. These
findings underline the need for more effective preventive measures that should be based on the
knowledge of factors that facilitate or predict the development of eating disorders.
Longitudinal studies have shown that dissatisfaction with body shape is a major factor
contributing to the development of eating disorders (Attie & Brooks-Gunn, 1989; Striegel-Moore,
Silberstein, & Rodin, 1989). Therefore, it is alarming that recent surveys consistently demonstrate high
levels of body dissatisfaction among adolescent girls despite normal actual weights (Attie & BrooksGunn, 1989; Huenemann, Shapiro, Hampton, & Mitchell, 1966; Paxton et al., 1991; Richards, Boxer,
Petersen, & Albrecht, 1990). Consequently, it is not surprising that adolescent girls commonly engage in
weight reducing behavior, most often by means of dieting. Weight reduction behavior was already
reported to be common by the 1960s (Dwyer, Feldman, Seltzer, & Mayer, 1969; Huenemann et al., 1966;
Nylander, 1971). However, the average weight of young women has tended to increase over the last 30
years (Gulliford, Rona, & Chinn, 1992; Shah, Hannan, & Jeffery, 1991), while the ideal body weight has
decreased 15 kg over the same period (Kinoy, 1994).
The relationship of dieting and development of eating disorders is not clear. Many studies have
shown only a limited association between dieting and being overweight. For example, only half of the
2
Vervaet, M., van Heeringen, C., & Jannes, C. (1998). Eating Disorders. The Journal of Treatment and
Prevention, 6,41-51.
girls studied by Dwyer et al. (1969) were actually overweight. Individuals such as ballet dancers, student
fashion models, and young athletes had higher scores on self-report measures of eating disturbances
than individuals in the general population, and they developed clinically defined eating disorders at much
higher frequencies (Attie & Brooks-Gunn, 1989; Garner, Garfinkel, Schwartz, & Thompson, 1980;
Garner, Garfinkel, Rockert, & Olmstead, 1987; Hamilton, Brooks-Gunn, & Warren, 1985; Szmukler,
Eisloer, Gillies, & Hayward, 1985). However, none of the authors mentioned in the studies cited above
have said that dieting per se is a risk factor for eating disorders in these populations.
Longitudinal studies of general population samples of school-aged girls also have demonstrated that
dieters at the time of the first interview were seven times as likely as nondieters to develop an eating
disorder by the time of the second interview 1 year later (Johnson-Sabine, Wood, Patton, Mann, &
Wakeling, 1988; Patton, Johnson-Sabine, Wood, Mann, & Wakeling, 1990) .
Recent studies indicate a difference in eating styles between men and women (Van Strien, 1994).
"Restrained eating" and "emotional eating" are more commonly reported by women. However, in
Western societies more men are overweight, and the typical male abdominal fat distribution is associated
with a higher risk of coronary diseases than the typical female fat distribution (Van Gaal, Rillaerts,
Creten, & De Leeuw, 1988). Therefore, the reported differences in eating styles and weight concerns
according to gender appear not to be due to medical reasons.
Next to an effect of gender, a limited number of studies have indicated a substantial effect of age
on body dissatisfaction and weight concern. At the onset of puberty, girls experience a weight spurt as
their body weight increases by 10 kg because of a substantial increase in body fat (Fombonne, 1995).
This increase is accompanied by negative psychological states, particularly among early maturers
(Dornbusch et al., 1984). On the contrary, during puberty boys experience an increase in weight and
muscularity that may enhance their self-esteem. Boys perceive thinness rather negatively, as they
generally prefer to be tall and muscular (Paxton et al., 1991).
Thus, the currently available data indicate that weight concerns and disturbed eating patterns are
common among adolescents and may provide clues to the prevention of eating disorders. However,
when the results of distinct studies are combined it appears that gender and age also have to be taken
into account to delineate specific subgroups with particularly increased risks of developing eating
disorders. Therefore, this study aimed at the assessment of (a) weight concerns and eating patterns and
(b) the effects of age and gender on these characteristics in a large sample of school-aged adolescents.
Subjects and methods
The study population consisted of students between 13 and 18 years of age who were attending
four secondary schools in Gent, Belgium.
Data were collected by means of two anonymous self-report questionnaires. Questionnaires were
filled in by the students collectively at the same moment in each class, under the supervision of the first
author. Items on the first questionnaire inquired about age, weight, gender, desired weight, use of
anorectic drugs and laxatives, weight and eating problems (defined as self-criticism on weight and eating
patterns: weight is perceived to be too high or too low and a feeling of lack of control over eating),
vomiting, eating patterns, thinking about eating (degree of preoccupation), eating alone (eating in secret),
counting calories, preference for sweet or salt, loss of control over eating, and the frequency and severity
of this loss.
We calculated body mass indexes (BMI = G/LXL) by using reported weights and heights. The
ideal BMI was defined as a current BMI between 20 and 25, and we calculated the desired BMI (DBMI)
by means of reported desired weights and heights.
Subjects were also asked to fill out the Dutch Eating Questionnaire (Van Strien, Frijters, Roosen,
Knuiman-i\tlijl, & Defares, 1986), which is based on the Eating Pattern Questionnaire (Wollersheim,
1970), the Questionnaire for Latent Obesity (Pudel, Metzdorff, & Oeting, 1975), and the Eating
Behavior Inventory (O'Neil et al., 1979). The following subscales can be identified: Emotional Eating,
Restrained Eating, and External Eating. We compared the scores on the questionnaire and on the
subscales with those of nonobese controls after dividing the subjects into three subgroups-low (L), mean
(M), and high (H)-using the cutoff scores (Van Strien et al., 1986) .
Table 1 Occurrence of assessed characteristics
Variable (total n = 745)
BMI < 20
20 <BMI <= 25
BMI > 25
DBMI < 20
20 < DBMI <= 25
DBMI > 25
Weight problems
Eating problems
Vomiting
Laxative abuse
Skipping breakfast
Skipping lunch
Skipping dinner
Eating between meals
Eating alone
Thinking about food during the day
Counting calories
Preference for sweet
Perception of loss of control
Restrained Eating scores > 2.38
Emotional Eating scores > 2.1
External Eating scores > 3.04
N
454
293
11
423
167
1
130
103
32
68
95
17
12
692
173
250
55
595
390
335
475
285
%
61
39
1
57
22
0.1
17
14
4
9
13
2
2
93
23
33
7
80
52
45
64
38
Note: BMI = body mass index; DBMI = desired body mass index
We examined the effect of age by comparing two subject age groups: 13-15 years versus 16-18 years.
We performed statistical analyses using Statistica (Statsoft, 1994). Differences between groups
were tested by means of the Mann-Whitney U test for continuous variables and the chi-square test for
the comparison of proportions.
Results
The questionnaires were filled in by 745 adolescents attending four secondary schools. Two
schools were exclusively attended by girls (n = 370), one school was attended exclusively by boys (n =
161), and the fourth school was attended by students of both sexes (n = 214).
The frequency distribution of the measured variables is shown in Table 1. Although 16% of the
participants indicated weight problems and 13% eating problems, 39% had a current BMI between 20
and 25. In 60% of the participants the BMI was even lower than 20. As indicated by the reported desired
BMI, 71 % wanted a BMI under the ideal BMI. Noteworthy was the common occurrence of "eating
between meals" (87%), perception of loss of control (49%), restrained eating (42%), and emotional
eating (60%). Loss of control was reported as occurring "sometimes" in 61 % of the subjects,
"regularly" in 30%, and "frequently" in 8%.
Table 2 shows the means of the current and desired BMIs for girls and boys and the scores for
restrained, emotional, and external eating as measured by the Dutch Eating Questionnaire.
Table 2 COMPARISON BETWEEN GIRLS AND BOYS
Characteristic
BMI
DBMI
Restrained Eating score
External Eating score
Emotional Eating score
Girls
(n=496)
Boys
(n=249)
19,5
18,7
2,5
2,8
2,6
19,2
19,7
1,6
2,9
1,7
Girls
Eating problems
Weight problems
Loss of cntrol
Use of laxatives
Thinking a lot about food
Counting calories
Eating alone
Vomiting
p
.105
.000
.000
.177
.000
Boys
n
%
n
%
87
107
275
59
168
50
97
25
17
21
54
8
22
6
19
5
16
20
109
9
78
5
73
7
6
7
41
1
10
1
27
3
.000
.000
.000
.000
.260
.000
.015
.085
Although no significant difference between girls and boys was found for the current BMI, the
desired BMI among girls was significantly lower than among boys and was clearly lower than the ideal
BMI. Furthermore, significant differences between boys and girls were found for restrained and
emotional eating.
Girls reported significantly more eating problems, weight problems, and loss of control over
eating. They abused laxatives and counted calories significantly more than boys did; however, boys
reported eating alone more than girls. Finally, no significant difference regarding thinking about eating
between both groups could be demonstrated.
Table 3 shows the mean scores and frequency distributions on the same characteristics for the two
age groups among the girls. Older girls restrained significant more commonly and ate more commonly in
emotional situations. No difference was found in regard to scores on the External Eating subscale. The
mean score for older girls was high when compared to scores among the controls in the Van Strien et al.
(1986) study. A significantly higher number of older girls reported eating problems, loss of control,
Table 3. COMPARISON BETWEEN YOUNGER (13-15 YEARS) AND OLDER (16-18 YEARS) GIRLS
Characteristic
<15 years
(n=139)
BMI
DBMI
Restrained Eating score
External Eating score
Emotional Eating score
>15 years
(n=370)
18,3
17,5
2,1
2,8
2
20
19,1
2,7
2,8
2,9
<15 years
Eating problems
Weight problems
Loss of control
Use of laxatives
Thinking a lot about food
Counting calories
Eating alone
Vomiting
p
0.000
0.000
0.000
0.822
0.000
>15 years
n
%
n
%
17
28
45
4
27
8
10
9
12
20
33
3
19
6
7
7
70
79
230
55
141
42
87
16
18
21
62
15
38
11
24
4
.040
.915
.000
.000
.000
.026
.000
.367
abuse of laxatives, thinking about food, counting calories, and eating alone when compared with the
younger group. In both groups, 1 in 5 girls indicated a weight problem in spite of a normal mean BMI.
There was a nonsignificant trend for a higher frequency of vomiting among younger girls than among
older girls.
We made a similar comparison for boys and, as shown in Table 4, a totally different picture
emerged. First, the desired BMI was higher than the current BMI in both age groups. Younger boys
showed a more pronounced restrained eating style than older boys, but these scores were normal for
both groups when compared with controls (Van Strien et al., 1986). For emotional eating, scores were
higher among older than among younger boys but were equally comparable to scores among controls. A
significantly higher number of older boys than younger boys reported that they ate when they were
externally or emotionally stimulated. With respect to eating patterns, significant differences between
younger and older boys were found for thinking about food, eating alone, and vomiting.
Table 5 shows a comparison of the numbers of students with high scores for restrained, external,
and emotional eating for the total group and for the different age- and gender-specific groups. High
scores for restrained and emotional eating were found more commonly among girls-more specifically,
among older girls. Among boys, an effect of age could be
Table 4. COMPARISON BETWEEN YOUNGER (13-15 YEARS) AND OLDER (16-18
YEARS) BOYS
Characteristic
Boys
BMI
DBMI
Restrained Eating score
External Eating score
Emotional Eating score
<15 years
(n=146)
>15 years
(n=127)
18
18,4
1,7
2,8
1,6
20,7
21,2
1,5
3
1,8
<15 years
Eating problems
Weight problems
Loss of control
Use of laxatives
Thinking a lot about food
Counting calories
Eating alone
Vomiting
p
.000
.000
.005
.008
.040
>15 years
n
%
n
%
11
14
51
6
32
3
28
7
7
10
36
4
22
2
19
5
5
6
58
3
46
2
45
0
4
5
46
2
37
2
36
0
.203
.089
.071
.521
.001
.917
.000
.002
Table 5. COMPARISON BY AGE
Girls
subscale
Boys
n
133
171
288
%
26
35
57
Restrained Eating
External Eating
Emotional Eating
n
21
49
25
Young Girls
%
15
35
18
n
112
122
263
Restrained Eating
External Eating
Emotional Eating
n
31
50
30
Young boys
%
21
34
21
n
13
60
40
Restrained Eating
External Eating
Emotional Eating
n
44
110
70
p
%
16
40
26
.000
.099
.000
%
30
35
71
.000
.999
.000
%
10
47
31
.002
.010
.016
Older Girls
Older boys
observed on the occurrence of high scores on the Restrained Eating (more common among younger
boys) and Emotional Eating (more common among older boys) subscales.
Discussion
The results of this large-scale survey of weight concerns and eating patterns among adolescents
clearly indicate first that current and desired body weights (as measured by means of body mass index)
very commonly are lower than ideal from a medical point of view. Therefore, it is not surprising that
restrained eating is very commonly reported, and that, to a lesser extent, adolescents additionally report
vomiting, laxative abuse, counting of calories, and skipping meals in order to lose weight. However, the
results of this study indicate that a restrained eating style commonly occurs in association with emotional
eating, because eating between meals, loss of control over eating, and eating under emotional
circumstances were commonly reported.
Second, the results show a marked effect of gender on these characteristics. Although girls and
boys reported current and desired BMIs that are lower than ideal from a medical point of view, the
desired BMI was lower than the current BMI among girls. On the contrary, boys indicated a higher
desired than current BMI. When compared with boys, girls far more commonly reported problems
related to eating and body weight, the occurrence of restrained eating with counting of calories, and
abuse of laxatives. Loss of control over eating was reported by more than half of the girls.
Third, an effect of age can be recognized. Among girls, the incidence of eating problems and
associated behavioral characteristics as described above clearly increased with age. .Among boys the
effect of age was less marked.
It is noteworthy, however, that in spite of a higher desired than current BMI, restrained eating and
vomiting were reported by boys but that the rate of these characteristics decreased with age. The
occurrence of externally or emotionally stimulated eating increased with age.
Before we discuss these results we should note that the study group is not representative of the
general population, because only adolescents at higher educational levels were included. This selection
bias may result in an overestimation of the occurrence of eating problems, as previous research has
shown a positive correlation between rates of eating disorders and educational level (Fombonne, 1995).
The overall picture emerging from this survey is that girls want to lose weight, whereas boys
indicate a desire to gain weight. Current BMI does not differ between boys and girls, but girls show.
more concern about their body weight and are at a clearly increased risk of developing behavioral
disorders associated with a restrained eating style and loss of control over eating under emotional
circumstances. This risk increases with age. The combination of restrained eating styles with eating in
emotional circumstances is likely to reflect a vicious circle resulting in persisting high levels of body
dissatisfaction.
The demonstrated association between female gender and weight related concerns and behaviors
indeed indicates the common existence of a dissatisfaction with the body shape among female
adolescents. This finding is in keeping with the results from previous studies (Attie & Brooks-Gunn,
1989; Huenemann et al., 1966; Paxton et al., 1991; Richards et al., 1990). As described earlier, this
dissatisfaction with body shape does not appear to exist for medical reasons. It is likely to be the result
of a perceived pressure exerted by society.
The present study adds to our current knowledge a similar difference between current and
desired BMIs among boys, albeit in an opposite way. In agreement with a previously demonstrated
negative appreciation of thinness among boys (Paxton et al., 1991), the present study shows that
adolescent boys actually desire to gain body weight. This may be due to the enhancement of self-esteem
associated with an increase in body weight and muscularity among boys. The difference between current
and desired BW among boys, however, does not appear to be associated with disturbed eating pat- terns.
Therefore, it appears that the desire to increase body weight does not induce disturbed eating patterns.
In conclusion, a large proportion of female adolescents shows disturbed eating patterns. For
some of these girls these symptoms may be risk factors for the development of eating disorders or
symptoms of a current eating disorder. For the other girls, the significant impairment that these
symptoms may bring cannot be underestimated. Therefore, the introduction of curriculum-based
programs to prevent eating disorders needs to be considered.
The results of this study indicate that the risk of developing eating disorders increases with age.
However, young girls already shows disturbances in eating patterns to such an extent that prevention
programs should start in the first years of secondary school.
References
Attie, I., & Brooks-Gunn, J. (1989). Development of eating problems in adolescent girls: A longitudinal study. Developmental
Psychology. 25. 70-79.
Dornbusch. S. M., Carlsmith, J. M., Duncan, P. D., Gross, R. T., Martin, J. A., Ritter, P. L., Siegel-Gorelick, B. (1984). Sexual
maturation, social class, and the desire to be thin among adolescent females. Developmental and Behavior Pediatrics, 5, 308314.
Dwyer, J. T., Feldman, J, J., Seltzer, C. C., & Mayer, J. (1969). Body image in adolescents: Attitudes toward weight and
perception of appearance. American Journal of Clinical nutrition. 20, 1045-1056.
Fombonne, E. (1995). Eating disorders: Time trends and possible explanatory mechanisms. In M Rutter & D. Smith (Eds.),
Psychosocial disorders in young people: Time trends and their causes
Gamer, D. M., Garfinkel, P. E., Rockert, W., & Olmsted, M. P. (1987). A prospective study of eating ilisturbances in the
ballet. Psychotherapy and Psychosomatics, 48, 170-175.
Gamer, D. M., Garfinkel, P. E., Schwartz, D., & Thompson, M. (1980). Cultural expectations of thinness in women.
Psychological Reports, 47, 483-491.
Gulliford, M. C., Rona, R. J., & Chinn, S. (1992). Trends in body mass index in young adults in England and Scotland from
1973 to 1988. Journal of Epidemiology and Community Health, 46, 187-190.
Hamilton, L. H., Brooks-Gunn, J., & Warren, M. P. (1985). Sociocultural influences on eating disorders in female professional
dancers. International Journal of Eating Disorders, 4, 465-477.
Huenemann, R. 1., Shapiro, L. R., Hampton, M. C., & Mitchell, B. W. (1966). A longitudinal study of gross body composition
and body conformation and their association with food and activity in a teenage population. American Journal of Clinical
Nutrition, 18, 325-338.
Johnson-Sabine, E., Wood, K., Patton, G., Mann, A., & Wakeling, A. (1988). Abnormal eating attitudes in London
schoolgirls-A prospective epidemiological study: Factors associated with abnormal response on screening questionnaires.
Psychological Medicine, 18, 615-622.
Kinoy, B. (1994). Eating Disorders: New Directions in Treatment and Recovery (p. 16). New York: Columbia University
Press.
Nylander, I. (1971). The feeling of being fat and dieting in a school population: Epidemiologic interview investigation. Acta
Sociomedica Scandinavica, 3, 17-26.
O'Neil, P. H., Currey, H. S., Hirsch, A. A., Malcolm, R. J., Sexauer, J. D., Riddle, F. E., & Taylor, C. I. (1979). Development
and validation of the Eating Behavior Inventory. Journal of Behavioral Assessment, 1, 123-132.
Patton, G. C., Johnson-Sabine, E., Wood, K., Mann, A. H., & Wakeling, A. (1990). Abnormal eating attitudes in London
schoolgirls-A prospective epidemiological study: Outcome at twelve month follow-up. Psychological medicine, 20, 383-394.
Paxton, S. J., Wertheim, E. H., Gibbons, K., Szmukler, G. I., Hillier, 1., & Petrovich, J. (1991). Body image satisfaction,
dieting beliefs, and weight loss behaviors in adolescent girls and boys. Journal of Youth and Adolescence, 20, 361-379.
Pudel, V., Metzdorff, M., & Oeting, M. (1975). The personality of the obese in psychological texts taking into account the
latent obesity. Journal of Psychosomatic Medicine and Psychoanalysis, 21, 345-361.
Richards, M. H., Boxer, A. M., Petersen, A. C., & Albrecht, R. (1990). Relation of weights to body image in pubertal girls and
boys from two communities. Developmental Psychology, 26, 313-321.
Shah, M., Hannan, P. J., & Jeffery, R. W. (1991). Secular trend in body mass index in the adult population of three
communities from the upper mid-western part of the USA. The Minnesota Heart Health Program. International Journal of
Obesity, 15, 499-503.
StatSoft. (1994). Statistica for the Macintosh [Computer software] Tulsa: StatSoft, Inc.
Striegel-Moore, R. H., Silberstein, L. R., & Rodin, J. (1989). A prospective study of disordered eating among college students.
International Journal of Eating Disorders, 8, 499-509.
Sullivan, P. F. (1995). Mortality in anorexia nervosa. American Journal of Psychiatry, 152, 1073-1074.
Szmukler, G. I., Eisloer, I., Gillies, C., & Hayward, M. E. (1985). The implications of anorexia nervosa in a ballet school.
Journal of Psychiatric Research, 19, 177-181.
Van Gaal, 1., Rillaerts, E., Creten, W., & De Leeuw, I. (1988). Relationship of body fat distribution pattern to atherogenic risk
factors in NIDDM. Preliminary results. Diabetes Care, 11(2) 103-106.
Van Strien, T. (1994). The increase in occurence of anorexia nervosa. Journal of ,Wental Health, 6, 647-652.
Van Strien, T., Frijters, J., Roosen, R., Knuiman-Mijl, D., & Defares, P. (1986). Eating behavior, personality traits and body
mass in women. Agricultural University, Wageningen, The Netherlands.
Wollersheim, J. P. (1970). Effectiveness of group therapy based upon learning principles in the treatment of overweight
women. Journal of Abnormal Psychology, 76, 462-474.
4. Eating-style and weight-concerns in young females3
In this study, attitudes towards eating among adolescent school-girls were compared to those among fashion models
and eating disorder patients. The results clearly demonstrate a preoccupation with body weight, even in school-girls.
A majority of the girls indicated a wish to lose weight, even when the current Body Mass Index was between 20
and 25. Eating disorder patients more commonly reported premorbid overweight. Furthermore, fashion models
tended to have an eating-style that was comparable to that of patients with eating disorders. The finding that the
mean current body weight of all girls was lower than before suggests that many girls developed a restrained eating
style. Vomiting, the use of anorectic drugs and laxatives, eating alone, and counting calories were reported by a
substantial proportion of the adolescent girls. Moreover, a substantial proportion of the girls experienced a loss of
control over eating. The combination of this eating-style and being overweight, can be considered as risk factor for
the development of eating disorders.
The culture of slimming in Western societies creates an important and increasing discrepancy
between the real shape and the ideal shape (Garner, Garfinkel, Schwartz, & Thompson, 1980).
Preoccupation with body weight and excessive concerns about body shape may induce eating patterns
that are similar to those of patients with eating disorders. It remains to be demonstrated under which
conditions such eating patterns develop into eating disorders.
Dissatisfaction with body weight and shape are very common among preadolescent and
adolescent girls.
It is particularly concerning that girls who show relatively unhealthy baseline eating
attitudes are more likely to fit in the category of the partial syndrome of eating disorders (PSED) at
follow-up (Button & Whitehouse, 1981). While PSED is not inevitably associated with the development
of anorexia or bulimia nervosa, it can, at the least, be regarded as similar to the first stage of Slade's
(1987) developmental model of eating disorders. The danger exists that any girl who has reached this
stage is prone to see low body weight and control as rewarding, and that she will then go on to develop a
more robust disorder as a consequence.
Thus, cultural factors may be a necessary condition in the development of eating disorders, or at
least act as a facilitating factor, especially as Western cultures also suggest that success and the approval
of others are solutions for problems (Wooley & Wooley, 1985). To be slim is a symbol of beauty, sexual
3
Vervaet, M., & van Heeringen, C. (2000). Eating Style and Weight Concerns in Young Females. Eating
Disorders: The Journal of Treatment and Prevention, 8: 233-240.
attractiveness, and success. Weight control is considered synonymous with discipline, personal strength
and willpower (Noordenbos, 1990).
Contemporary values such as perfectionism and control and
pressure on females to enhance their appearance induce social stresses. The question remains: To what
extent does such an internalisation process remain adaptive, or proceed beyond a certain limit and
develop into psychopathology? Knowledge of psychological factors contributing to the development of
pathological eating behaviors is indispensable for the identification of diagnostic criteria of the eating
disorders.
This study compared eating styles and weight concerns among schoolgirls, fashion models, and
patients diagnosed as suffering from eating disorders. The groups were chosen in order to assess the
association between eating behaviour, weight concerns, and eating disorders.
Method
Girls attending the fifth year of two large secondary schools participated in this study (n=333).
Questionnaires were filled in collectively. The questionnaire was also sent to 20 fashion models of a
national agency and to 40 patients with eating disorders (ED) admitted to the Department of Eating
Disorders (University Hospital Gent) in 1993 (31.0% anorectics in treatment, n = 10; 62.5% bulimics of
normal weight, n = 20; 6.3% overweight (BMI > 25) bulimics, n = 2). Items in the questionnaire
covered age, weight, desired weight, educational level, presence of a boyfriend, use of anorectic drugs
and laxatives, weight and eating problems (defined as self-criticism on weight and eating patterns,
perceived excessive bodyweight, or lack of control over eating), vomiting, eating-patterns, thinking about
eating (i.e. extent of preoccupation), eating alone (eating in secret), counting calories, preference for
sweet or salty foods, loss of control, and the frequency (exceptional, sometimes, daily) and severity
(<500Kcal, 1000-2000 Kcal, >2000 Kcal) of this loss of control. Moreover, the participants were asked
to fill in the Dutch Eating Behaviour Questionnaire (DEBQ; Van Strien, 1986) which consists of the
following subscales: emotional eating (eating elicited by emotional stimuli), restrained eating (the
tendency to eat to lose weight), and external eating (eating elicited by external stimuli).
Statistical analysis was performed using SPSS 9.0, and included a comparison of the
characteristics between the schoolgirls, models and ED patients, by means of chi-square analysis for
nominal variables and non-parametric tests for continuous variables.
Results
Questionnaires were returned by 333 schoolgirls (100 %), 11 fashion models (55 %), and 32 ED-patients
(80%). Table 1 shows mean values for age, weight, and body mass index (BMI= weight/length x length)
in the three groups.
Table 1: A Comparison of the Mean Values and Standard Deviation for Age, Weight and BMI
Among Schoolgirls, Fashion Models, and ED-patients.
Schoolgirls
Models
ED
n = 333
n = 11
n = 32
Mean (SD)
Mean (SD) Mean (SD)
_____________________________________________________________
Age (years)1
16.8 (0.8)ab
19 (0.9)ac
Weight (kg)2
56 (6.4)
57 (3.5)
BMI3
20 (1.9)
18 (1.O)
24 (5.2)bc
54 (12.6)
19 (4.1)
1
One-way ANOVA, F = 262.8; (df = 2); p < .0001
post-hoc comparison (Bonferroni) a p < .000; b p < .000; c p < .000
2
One-way ANOVA, F = .765; (df = 2); p = .466
3
One-way ANOVA, F = 1.5444; (df = 2); p = .215
There was a significant difference between the three groups in mean age, but not in mean weight and
BMI. Mean reported former weight was higher than mean current weight in all three groups (Table 2).
Table 2: A comparison of the Mean and Standard Deviation in Highest Weight, Desired Weight,
and Desired BMI among Schoolgirls, Models and ED-patients.
------------------------------------------------------------------------------------------------------------------------Schoolgirls
Models
ED
n = 333
n = 11
n = 32
_____________________________________________________________
Highest weight1
58 (6.9)ab
61 (5.6)ac
66 (16.5)bc
Desired weight2
54 (5.5)
55 (1.9)
52 (7.7)
Desired BMI3
19 (1.5)
18 (0.7)
19 (2.2)
1
One-way ANOVA, F = 12.9; (df = 2); p < .000
post-hoc comparison (Bonferroni) a p = .445; b p = .000 c p = .528
2
One-way ANOVA, F = .1.2; (df = 2); p = .297
3
One-way ANOVA, F = 2.5; (df = 2); p = .083
On the contrary, girls in the three groups indicated a desired weight that was lower than the ideal
BMI (63,5% of the schoolgirls want to lose weight, n = 212 versus 8,1% who want to gain weight, n =
27; 81,8% of the fashion models want to lose weight, n = 9 versus 9,1% who want to gain weight, n = 1;
62,5% of the eating disorder group want to lose weight, n = 20 versus 21,9% who want to gain weight, n
= 7). Mean reported highest weight was significantly higher in ED patients than for the other groups.
In the eating disorder group 40.6% (n = 13) reported a premorbid overweight, in contrast to 1,2% (n =
4) among the schoolgirls and 0% among the fashion models.
Significant differences between the three groups were found for educational level and for
reported weight and eating-problems (Table 3).
Table 3: A comparison of the frequency (%) of the Highest School Level, Relationship, Weight
Problems, and Eating Problems Among Schoolgirls, Models and ED Patients.
Models
ED
X2
p-value
Highest school level 74.4
27.3
62.5
20.120
0.000
Relationship
27.9
54.5
21.9
4.460
0.108
Weight problems
21.6
27.3
78.1
47.619
0.000
Eating problems
18.3
45.5
90.6
83.060
0.000
Schoolgirls
Fashion models had a lower educational level when compared to the other two groups. Although
the mean weight of attending schoolgirls was ideal, nearly one in four indicated problems with their
body weight. One in two fashion models and one in five schoolgirls experienced eating problems. No
significant association was found between having a boyfriend and belonging to one of the study groups.
It is noteworthy that approximately 10% of the ED patients denied having eating problems.
Table 4 shows the results regarding the use of more drastic methods to reduce body weight, i.e.
anorectic drugs, vomiting, or laxatives. It was found that 16 % of the schoolgirls used laxatives,
compared to 36 % of the models. Five percent of the schoolgirls used anorectic drugs, while 4 %
reported vomiting.
Table 4: A comparison of the Use of Anorectic Drugs, Vomiting and Laxatives Among
Schoolgirls, Models, and ED patients.
X2
p-value
Schoolgirls Models
ED
%
%
%
___________________________________________________________
Drugs
4.8
0
15.6
6.500
0.100
Vomiting
3.9
0
37.5
52.34
0.000
Laxatives
15.9
36.4
46.9
20.83
0.000
Eating patterns also were compared between the three groups. As shown in Table 5, no
significant differences in 'skipping breakfast' and 'experienced loss of control over eating' were found.
Table 5: Comparison of Eating Pattern Among Schoolgirls, Models and, ED Patients
Skipping
breakfast
Skipping
lunch
Skipping
dinner
Never
eating
between
meals
Eating
alone
Thinking
about food
Counting
calories
Loss of
control
once a day
(frequency)
>2000Kcal
(amount)
school-girls
%
10.2
Models
%
18.2
ED
%
21.9
X2-test
p-value
4.419
0.100
2.1
9.1
9.4
6.936
0.030
1.2
9.1
9.4
14.67
0.001
13.2
27.3
34.4
23
90.9
62.5
44.03
0.000
38.9
72.7
90.3
34.13
0.000
12
27.3
50
33.93
0.000
63
72.7
71.9
1.403
0.500
6.3
12.5
30.4
9.885
0.007
21.1
42.9
47.8
6.636
0.030
0.000
However, the severity and especially the frequency of loss of control differed significantly
between the groups. ED patients showed more frequent loss of control over eating and reported the
ingestion of larger amounts of food (in terms of Kcal). The significant character of the differences
regarding the other items was mainly due to a lower frequency of disturbed eating patterns among the
schoolgirls. However, even 12% of the schoolgirls counted calories, 40% thought about food during the
day, and 23 % reported frequent eating while being alone.
Mean scores on the items of the Dutch Eating Questionnaire are shown in Table 6.
Table 6: Comparison of the Mean Scores and Their Standard Deviation on the Dutch Eating
Questionnaire Among Schoolgirls, Models, and eating ED Patients.
School-girls
Models
ED
_____________________________________________________________
Restrained eating1
2.6 (0.9)ab
3.4 (1.0) ac
3.6 (0.9) bc
Diffuse emotions2
2.8 (0.8) ab
3.4 (0.7) ac
3.3 (1.2) bc
Clear emotions3
2.1 (0.7) ab
2.1 (0.7) ac
2.7 (1.2) bc
Total emotions4
2.3 (0.7) ab
2.5 (0.4) ac
2.8 (1.1) bc
External eating5
2.9 (0.5) ab
2.9 (0.5) ac
2.5 (0.7) bc
1
One-way ANOVA, F = 16,1; (df = 2); p = .000
post-hoc comparison (Bonferroni) a p = .028; b p =.000; c p =1.000
2
a
3
a
4
a
F = .7,8; (df = 2); p = .000
p = .058; b p =.003 c p =1.000
F = 8,7; (df = 2); p = .000
p = 1.000; b p =.000; c p =.101
F = 16,1; (df = 2); p = .001
p = 1.000; b p =.001; c p =.595
5;
a
F = 16,1; (df = 2); p = .001
p = 1.000; b p =.001; c p =.265
Significant differences (p = 0.001) in the occurrence of ‘restrained eating’, ‘emotional eating’ and
‘external eating’ were found between schoolgirls and ED patients, but no significant differences were
found between models and ED patients. The mean score for ‘restrained eating’ was significant lower for
schoolgirls than that of the fashion models.
Discussion and conclusion
This study in a large group of young women suggests a substantial preoccupation with body
weight, not only in patients diagnosed with eating disorders, but also in fashion models and in
schoolgirls. The means of desired weight are lower in all three groups so we may hypothesize that a
majority of girls in this study wanted to lose weight, even when their current BMI could be regarded as
ideal. The eating pattern of fashion models appears to resemble that of eating disordered patients.
Schoolgirls express severe concerns about their body weight, and one in four indicates problems related
to their body weight, although this apparently is not the case in view of girls’ normal BMIs. The
perceived problems induce counting calories and a restrained eating style, albeit to a lesser extent than in
fashion models and eating disordered patients. The results also show that fashion models do not report
to suffer from an eating disorder in spite of the fact that their eating patterns closely resemble those of
eating disordered patients. However, even one in ten ED patients does not report to suffer from a
disorder although she is currently being treated. In order to lose weight models commonly report the use
of laxatives while patients additionally report vomiting. Finally, the results indicate that the highest ever
mean body weight was reported by the patients suffering from an eating disorder. The finding of a
premorbid overweight in eating disordered patients is in keeping with the results from previous studies.
Two methodological aspects of this study should be addressed. First, the schools were not
randomly selected. Therefore, participating subjects cannot be considered to be representative of the
general population, and may actually have an increased risk of developing an eating disorder as the
schools were only attended by girls who belonged to higher social classes, who were obliged to wear
uniforms, and who were confronted with a very competitive spirit. Second, some questionnaires were
not returned by the fashion models and the patients, so some results may be due to a selection bias. The
low response rate in the model group may be due to distrust or lack of interest. The higher weight in
models in comparison with the schoolgirls may be due to the significant difference in mean age between
schoolgirls and fashion models. Finally, a number of schoolgirls and models may have actually been
suffering from an eating disorder.
Keeping these methodological limitations in mind, the findings from this study indicate that the
mean body weight in schoolgirls can be regarded as ideal, as far as the body mass index is a correct index
of body weight in this age group. In any case, the results demonstrate that there are no severe problems
regarding body weight in this group of young females. However, restrained eating, vomiting, and the use
of anorectic drugs or laxatives appear to be known as weight reducing strategies even among schoolgirls
and nearly one in five schoolgirls reports subjective problems with their body weight and eating.
Moreover, eating alone, thinking about food during the day, counting calories and experiencing of a loss
of control over eating are commonly experienced. In view of a demonstrated association between binge
eating and psychopathology (Telch and Agras, 1994), the finding that almost two-thirds of the
schoolgirls report a loss of control over eating is important. Six percent of the schoolgirls even report
loss of control to occur once a day, involving the ingestion of more than 2000 Kcal in more than 20%.
Equally important are the demonstrated similarities between patients and fashion models,
suggesting that the stronger the perceived pressure on body weight, the higher the risk of developing an
eating disorder might be. The fact that the models do not consider themselves as suffering from a
disorder may reflect the appreciation associated with their appearance, but might also be due to a denial
of the negative consequences of their job. In view of the strong impact of pictures of models in fashion
magazines (Field et al., 1999) our current findings indicate the necessity of providing information about
potential negative consequences of a restrained eating style to become underweight in terms of
developing psychopathology. As a conclusion, the results of this study suggest that being overweight
during adolescence is a risk factor for developing identity related problems in a Western society with a
slimming culture.
During the months following this study, 10 of the participating schoolgirls attended the
outpatient Department of Eating Disorders. Their symptoms fitted the criteria for an eating disorder
according to DSM-IV. Thus, this study not only resulted in the detection of potential risk factors for
eating disorders among schoolgirls, but also may have lowered the threshold for seeking treatment.
References
American Psychiatric Association. (1994). Diagnostic and Statistical Manual of Mental Disorders (4th ed.). Washington, DC: APA.
Button, E.J., Withouse, A.(1981). Subclinical anorexia nervosa. Psychological Medicine, 11, 509-516.
Field, A.E., Cheung, L., Wolf, A.M., Herzog, D.B., Gortmaker, S.L., Colditz, G.A.(1999). Exposure to the Mass Media and
Weight Concerns Among Girls. Pediatrics, Vol. 103, (3), 36-45.
Garner, D.M., Garfinkel, P.E., & Olmsted, M.P.(1983). An overview of sociocultural factors in the development of anorexia
nervosa. In: Darby, P.L., Garfinkel, P.E., Garner, D.M., & Coscina, D.V.(Eds.). Anorexia Nervosa. Recent Developments in
Research (pp. 65-82). New York: Alan R. Liss.
Garner, D.M., Garfinkel, P.E., Schwartz, D., Thompson, M. (1980). Cultural expectations of thinness in women. Psychological
Reports, 47, 483-491.
Noordenbos, G. (1990). Looking for the hidden identity behind a secret disorder. The recovery process of anorexia and
bulimia nervosa. In: Petherson, G., Essed, Ph., & Richardson, D. (Eds.), Between Selfhelp and Professionalism ( pp.197-212).
Amsterdam: The Moon Foundation The International Congress on Menthal Health Care for Women.
Slade, P.D.(1987). Early recognition and prevention: Is it possible to screen people at risk of developing an eating disorder?
In: D.Hardoff & E.Chigier (Eds). Eating Disorders in Adolescents and Young Adults. London: Freund.
Telch, C.F., Agras, W.S.(1994). Obesity, Binge Eating and Psychopathology: Are They Related? International Journal of Eating
Disorders, 15(1), 53-61.
Van Strien, T., Frijters, J., Roosen, R., Knuiman-Mijl D., Defares, P.(1986). Eating behavior, personality traits and body mass in
women. Wageningen, The Netherlands: Agricultural University .
Wooley, S.C., & Wooley, O.W.(1985). Intensive outpatient and residential treatment for bulimia. In: Garner D.M. &
Garfinkel P.E.(Eds.). Handbook of psychotherapy for anorexia nervosa and bulimia (p. 391). New York/London: Guilford Press.
PART II
The cognitive psychology of eating disorders:
personality, cognitions and behaviour.
Chapter 1: Theoretical background
1. Definition and epidemiology
An eating disorder (ED) can be defined as a syndrome, in which disturbed eating behaviour is
the central and meaningful characteristic (Vandereycken & Noordenbos, 2002). An ED thus can be
differentiated from disturbed eating behaviour as a symptom of other psychiatric disorders, such as a
mood disorder, schizophrenia, or obsessive compulsive disorder, or as a symptom of somatic
disturbances, including infectious, neoplastic and endocrine disorders or malabsorption. The central
characteristic of disturbed eating behaviour in syndromal eating disorders is associated with an extreme
worry about or preoccupation with body size and body weight. Disturbed eating behaviour may include
fasting, dieting and/or binge eating, and/or inappropriate compensating behaviour, including selfinduced vomiting or misuse of laxatives, diuretics, or enemas, and excessive exercise. Binge eating is
defined as eating, in a limited period of time (e.g., within a two-hour period), an amount of food that is
definitely larger than most people would eat during a similar period of time and under similar
circumstances, combined with a sense of lack of control over this eating behaviour. More than half of
the patients suffering from eating disorders have concomitant and secondary problems of anxiety and
disturbed mood.
Syndromal eating disorders can be ‘typical’, i.e. anorexia nervosa (AN) and bulimia nervosa (BN),
or ‘atypical’, i.e. eating disorders not otherwise specified (EDNOS). The latter do not meet all criteria
for a typical ED. For example, body weight may not have diminished to less than 85% of the expected
body weight in spite of restricting behaviour, so that a diagnosis of AN can not be made, even if patients
may not menstruate regularly. Bulimic women who binge and vomit weekly, but less than two times per
week, are also diagnosed with EDNOS. Within the group of EDNOS patients, there is a subgroup of
binge eaters who do not show compensating behaviour, and who are diagnosed with binge eating
disorder (BED). BED will probably be described as a separate diagnostic category in the following
edition of the DSM classification system of psychiatric disorders.
Estimated prevalence rates among young females aged 18-30 years are 0.3% and up to 3 % for
AN and BN, respectively, and ED are approximately 10 times more common in females than in males
(APA, 2000). EDNOS appears to be much more prevalent, and it is estimated that up to 4% of the
general population suffers from BED, but accurate epidemiological data are lacking. Assuming that
even studies with the most complete case finding methods yield an underestimate of the true prevalence,
the overall annual incidence of AN and BN can be estimated to be, at the least, 8 and 12 per 100 000
inhabitants, respectively. In 2000, primary care incidence rates were 4.7 and 6.6 per 100 000 population
for anorexia and bulimia nervosa (Currin, Schmidt, Treasure, & Jick, 2005). The incidence rate of AN
has a small global increase throughout the 20th century (Keel & Klump, 2003), particularly in females
aged 10-24 years, with a stable European incidence since the 1970s (Hoek & van Hoeken, 2003; Currin
et al., 2005). Overall there was an increase in the incidence of bulimia, at the least during the first five
years after BN was added to the DSM classification system, but rates declined after a peak in 1996
(Currin et al., 2005). For EDNOS, including BED, information regarding incidence rates is insufficient
(van Hoeken, Seidell, & Hoek, 2003).
Although the occurrence of ED is not associated with socio-economic status, individuals with
particular professions, including dancers, fashion models, actors or athletes, carry an increased risk of
ED. Possibly the choice of profession is related to a predisposition to ED.
It can be questioned whether anorexia nervosa is a culture-bound disorder, which is elicited by a
pervasive pressure to diet and which is rare or absent in non-Western cultures. First, there are historical
descriptions of cases of self-starvation without weight concern in cultures in which there was no
emphasis on slimness (Bemporad, 1996). Secondly, cross-cultural comparison has suggested that body
shape indeed is not the primary motivation in AN (Lee, 1996). Recent studies in South Africa (La
Grange, Telch & Tibbs, 1998; Wassenaar le Grange Winship, et al, 2000), Nigeria (Oyewumi &
Kazarian, 1992a, 1992b), Gana (Bennett, Sharpe, Freeman, & Carson, 2004), and Asia (Bhadrinath, 1990;
Khandelwal & Saxena, 1990; Lee, Ho & Hsu, 1993), suggest that AN may take different forms in
different cultures. The morbid self-starvation may have many motives, such as to atone for sins, to
achieve better results, or for religious reasons.
2. The complexity of the ED diagnosis
2.1. Categorical classification
As described above, eating disorders are classified in three categories, i.e. AN, BN and EDNOS
(DSM-IV; APA, 1994). Subgroups within the AN and BN have been defined on the basis of variations
in eating and compensatory behaviours. Thus, the AN category is subdivided in a restricting (RAN) and
binge-purging (BPAN) type. Individuals with BN are classified as a purging type (BP) when they show
binge eating and abuse laxatives, self-induce vomiting and/or use enemas, or as a non-purging type
(BNP) when they combine binge eating with fasting or extreme exercise. Although, by definition,
EDNOS means a failure to meet all criteria for a formal ED category, a diagnosis of EDNOS does not
necessarily reflect a lack of clinical significance (Anderson, Bowers, & Watson, 2001).
This categorical classification, predominantly based on descriptive behavioural and weight-related
characteristics, has a number of limitations. First, ED categories are heterogeneously composed, and
some but not all patients may shift from one category or type (e.g. restricting) to another (e.g. purging
and binging) in the course of their illness (Löwe et al., 2001; Wentz, Gillberg, Gillberg & Rastam, 2001).
Secondly, personality traits (Bulik, Sullivan, Weltzin, & Kay, 1995b; Bulik, Sullivan, Joyce, Carter, &
McIntosh, 1998; Podar, Hannus, & Allik, 1999; Rosenvinge, Martinussen, & Ostensen, 2000) or
personality disorders (Bulik, Sullivan, Joyce, & Carter, 1995a; Matsunaga et al., 2000; Muller et al., 2000)
may play a particular role in the emergence (Kay et al., 2000a) and maintenance of eating disorder
symptomatology (van Hanswijck de Jonge P, van Furth, EF, Lacey JH, & Waller G, 2003). ICD-10
(WHO, 1992) defines a personality disorder (Axis II) as a severe, long-term disorder in an individual’s
characterological constitution and behavioural tendencies, which usually extends to various aspects of
the personality and is nearly always associated with or results in serious personal and social disturbance.
As a consequence, the boundaries between Axis I and Axis II disorders are blurred in ED patients
(Webber, 1994).
Data suggest a greater incidence of Cluster B personality disorders, e.g. in particular borderline
personality disorder (Carroll et al., 1996; Wonderlich & Mitchell, 1997; Matsunaga et al., 2000) in bulimic
patients (compared to other ED) associated with behaviours such as self-harm, shoplifting and other
impulsive behaviours (Welch & Fairburn, 1996; Wiederman & Pryor, 1996). In that case, some authors
have suggested that a diagnosis of ‘multi-impulsive bulimia’ may be appropriate (Lacy, 1993; Lacy &
Read, 1993). Cluster C personality disorders, e.g. the avoidant personality disorders (Gillberg et al.,
1995; Roosenvinge e.a., 2000) were found more in anorectic individuals.
There is some evidence that
those with BPAN show higher rates of personality disorders than either RAN or BN patients (Piran et
al., 1988; Herzog et al., 1992). However, recent studies (Grilo, Sanislow, Shea, Skodo, Stout et al., 2003a;
Grilo, Sanislow, Skodel, Gunderson, Stout et al., 2003b) showed that patients with PD do not have
significantly more ED than patients with major depressive disorder but without PD. In addition,
patients with specific forms of PD do not differ in their frequencies of ED (Ilkjaer, Kortegaard,
Hoerder, Joergensen, Kyvik, & Gillberg, 2004). Nevertheless, rates of co-occurrence of ED and PD are
sufficiently high, especially for cluster C, to warrant careful consideration during routine assessment and
treatment planning stage, since diagnosable personality disorders occur, and they appear to be associated
with greater chronicity and poorer functioning (Skodol et al., 1993; Inceoglu et al., 2000; Johnson et al.,
1990). Moreover, it could be taken to mean that the PD, which is considered a more stable “trait” than
ED, which is usually regarded as a “state”, is heritable and precedes the onset of ED (Ilkjaer et al., 2004).
2.2. Dimensional classification and comorbidity
While the presence or absence of a personality disorder diagnosis reflects a categorical approach,
a dimensional model focuses on the extent to which personality traits are present, assessing the number
of personality disorder criteria that are present to an accentuated and/or pathological degree, regardless
of whether the patients has a full diagnosis. Nevertheless, it should be noted, that also the distinction
between EDs based on personality traits is by no means perfect, as studies have shown particular traits
to be present in AN and BN (Carroll et al., 1996; Inceoglu et al., 2000). Three personality clusters have
been identified in ED patients: a high functioning, self-critical, perfectionist group, which was mainly
associated with BN; a constricted, over-controlled group restricting pleasure, needs, emotions,
relationships and self-knowledge, which was associated with RAN; and an impulsive, under-controlled
and emotionally dysregulated group also associated with BN and with BED (Fahy & Eisler, 1993;
Goldner et al., 1999).
A useful and interesting dimensional approach differentiates the compulsive (or restrictive type,
RAN) and the impulsive type (or the bulimic, binging and purging patients, BPAN & BP) of ED
patients (Claes, Vandereycken & Vertommen, 2002; Polivy & Herman, 2002; Steiger & Seguin, 1999).
With regard to impulsivity, many components have been described (Whiteside and Lynam, 2001), but
two have been particularly studied in ED, i.e. urgency and lack of planning (Fischer, Smith, Anderson,
2003). Individuals high in urgency are likely to act rashly in order to cope with distress. Several studies
found that the bulimic symptoms ‘binge eating’ and ‘purging’ are related to urgency, since these
symptoms can be seen as reflecting mechanisms to cope with negative affect, which is relatively more
common in BN patients (Pryor & Wiederman, 1996; Stice, Killen, Hayward, & Taylor, 1998; Telch &
Stice, 1998; Tylka & Subich, 1999). Emotional states such as anxiety and depression have indeed been
shown to predict binge episodes (Arnow, Kenardy, & Agras, 1995). In contrast, several researchers have
found lack of planning to be within the normal range in bulimics (Bushnell, Wells, & Oakley Brown,
1996; Fahy & Eisler, 1993; Newton, Freeman, & Munro, 1993; Fischer et al., 2003).
Bulimic behaviour is thus associated with impulsivity, but obsessional features such as rigidity,
neatness, conscientiousness and preoccupation with rules and ethics characterize the restrictive anorexic
type. This pattern of responding was shown even at a basic perceptual level, with a rigid pattern of
responding in AN and an unstable or fluctuating style in BN patients (Tchanturia, Serpell, Troop, &
Treasure, 2002). If the latter characteristics are present to such an extent that they result in marked
impairment of social or occupational functioning over a considerable period of time, a diagnosis of
obsessive-compulsive personality disorder (OCPD) may be warranted (Serpell et al., 2002). A wealth of
clinical literature describes the cluster of rigidity, perfectionism and inflexible thinking, that is
characteristic of OCPD, in AN (Casper et al., 1992; Karwautz, Troop, Rabe-Hesketh, Collier, &
Treasure, 2003; Rosenvinge, Martinussen, & Ostensen, 2000; Strober, 1980; Vitousek & Hollon, 1990).
Estimates of the comorbidity of OCPD and ED vary from 3% (Piran et al., 1988) to 60% (Wonderlich
et al., 1990). Childhood OCPD personality traits also showed a high predictive value for the
development of ED (Brecelj et al., in press). Preliminary data from family studies indicate an increased
risk of OCPD in relatives of AN probands compared to controls (Lilenfeld et al., 1998). These findings
suggest the existence of a phenotype with core features of rigid perfectionism and propensity for
extreme behavioural constraint. Sohlberg and Strober (1994) have suggested that obsessional symptoms
are related to the state of starvation, while obsessional traits are stable personality features, which are
maintained after weight gain. Although phobic thoughts of food and weight repeatedly enter the mind
of AN patients, they are not regarded as senseless or unwanted (Mazure, Halmi, Sunday, Romano, and
Einhorn, 1994), which is in contrast to the typical obsessions and compulsions unrelated to eating that
also may occur in AN patients (Bastiani et al., 1996). Obsessions involving symmetry, such as ordering
and arranging, were found to be the most common obsessions in AN patients (Bastiani et al., 1996;
Matsunaga et al., 1999). The results of the most recent study of this type (Halmi, Sunday, Klump,
Strober, Leckman et al., 2003) with larger patient groups at all stages of illness, were remarkably similar
to those of the Bastiani study, with no significant difference between the RAN and BPAN women.
The neurobiological basis of the relationship between obsessive-compulsive disorder OCD and
ED remains unclear. Data from twin studies suggest that genetic vulnerability factors contribute to both
AN (Bulik, Sullivan, Wade, & Kendler, 2000; Klump, Miller, Keel, McGue, & Jacono, 2001; Kortegaard,
Hoerder, Joergensen, Gillberg, & Kybik, 2001; Wade et al., 2000) and OCD (Leckman, Zhang,
Asobrook, & Paus, in press). The few family aggregation studies suggest that these disorders may be
independently transmitted in families (Lilenfeld et al., 1998). Neuroimaging studies suggest that both
disorders are associated with alterations in the frontal cortex and in the subcortical and limbic regions
(Kaye et al., 2001; Saxena, Brody, Schwartz, & Baxter, 1998). This frontal-subcortical circuitry contains
complex direct and indirect pathways that are modulated by serotonin and dopamine. Pharmacologic
(DeVeaugh-Geiss, 1991; Halmi, 1999) and physiological (Lilenfeld et al., 1998) studies also indicate that
alterations in functional serotonin activity are present in both OCD and AN subjects. The common
nature of these phenotypical characteristics of AN and OCD patients may indicate that these disorders
share common brain behavioural pathways. However, the incomplete nature of the overlap between
these disorders suggests that they have different loci of pathology within these pathways (Halmi et al.,
2003).
Describing the restricting versus the bulimic group provides a good example of the overlap
between Axis-I ED diagnostic categories and between Axis-I ED diagnoses and Axis-II PD categories.
A dimensional approach may thus add information about traits and clinical phenomena to a categorical
diagnosis, offering the possibility of a more accurate and effective patient assessment and treatment
planning (Van Hanswijck, De Jonge et al., 2003).
3. Aetiology as a dynamic process: from trait- (vulnerability) to state- (eating disorder category)
dependent characteristics
3.1. Introduction
Although the aetiology of AN and BN is incompletely understood, a comprehensive aetiological
model is likely to include a combination of genetic and familial (Bulik et al., 2000; Treasure & Holland,
1995), personality and psychological (Vitousek & Manke, 1994), environmental and neurobiological
elements (Nasser, Katzman, & Gordon, 2001). A role of these factors in the development of ED can be
described in terms of their predisposing, precipitating (or eliciting: such as death of a loved one,
transition into puberty, dieting) and sustaining effect.
Genetic factors most probably contribute to the predisposition to ED. Twin and family studies
indeed suggest a substantial heritability for AN (Collier & Treasure, 2004; Lilenfeld LR, Kaye WH,
Greeno CG, Merikangas KR, Plotnicov K, Pollice C, et al., 1998).
Also in BN, family and twin studies point at a role of genetic factors in the predisposition (Collier &
Treasure, 2004; Hsu, 1990; Walters, Neale, Eaves, Lindon, & Heath, 1992), in addition to
-
biological factors such as reduced levels of beta-endorphin (Brewerton, Lydiard, Laraia, Shook,
& Ballenger, 1992), norepinephrine (Goldbloom, Garfinkel, & Shaw, 1991), and/or serotonin
(Jimmerson, Lesen, Kate, & Brewerton, 1992);
-
family factors such as poor communication (Hsu, 1990) and high expectations (Pike & Rodin,
1991);
-
individual factors such as perfectionism, maturity fears (Garner, Olmsted, Polivy, Garfinkel,
1984) and low self-esteem (Katzman & Wolchik, 1984);
-
sociocultural factors such as preoccupation with thinness and dieting at a societal level
(Brownell, 1991; Garner & Garfinkel, 1980).
More recently, a first study reported heritability of the core BED syndrome (Reichborn-Kjennerud,
Budlike, Tambs, & Harris, 2004), although the estimates of heritability are somewhat lower than those
reported for AN and BN (Budlike et al., 2000).
The focus of the studies as described in this thesis was on psychological factors as the link between
neurobiological characteristics and the overt behaviour of eating-disordered patients. Core psychological
traits and personality characteristics of ED patients were described as, among others, temperamental and
character dimensions which develop as the result of an interaction between genetic and learning
processes. In addition to these dimensions, three psychological characteristics were studied as they were
identified as core characteristics of ED patients in two recent transdiagnostic models of eating disorders,
i.e. negative self-esteem (inextricably related to body dissatisfaction) perfectionism/rigidity and
interpersonal difficulties (Fairburn, Cooper & Shafran, 2003; Serpell & Troop, 2003). These three
characteristics possibly reflect a premorbid vulnerability, and appear to be necessary (though possibly
not sufficient) conditions for the development of ED.
3.2. Low self-esteem and body dissatisfaction
Since the start of the systematic study of ED, the failure to develop a separate and integrated sense
of self, as the capacity for self-regulation, was found to be an important psychological factor in the
development of eating disorders (Bruch, 1973). Since then it has become clear that deficits in the self
also may become manifest as
•
disturbances in the ability to identify and modulate bodily cues and emotional experiences (de
Groot & Rodin, 1998; Bydlowski, Corcos, Jeammet, et al., 2005),
•
low self-esteem and pervasive feelings of ineffectiveness (Rosen, 1990), and
•
increased sensitivity to external evaluation, or fears of negative evaluation (Gilbert & Meyer,
2005).
ED patients thus lack positive self-schemata by means of which they organize information about the
self. In cognitive psychology, self-esteem refers to a cognitive evaluation of one’s competencies.
Longitudinal studies have suggested a relationship between low self-esteem and the subsequent
development of ED symptoms (e.g. Button et al., 1996; Wood et al., 1994). Retrospective reporting
suggests that negative self-evaluation during childhood may be more common among women with AN
or BN than among women in a non-psychiatric comparison group or among women with other
psychiatric disorders (Fairburn et al., 1997, 1999). However, follow-up studies suggest that self-esteem
improves with recovery of BN, but that it remains low in patients whose ED symptoms persist (e.g.
Troop et al., 2000).
Clinical observations appear to confirm theoretical considerations of an association between eating
disorders and disturbances in the mother-child relationship. These disturbances may include maternal
empathic failure and unresponsiveness to child-initiated cues that are thought to interfere with the
emerging sense of self. More specifically, studies have identified lower perceived maternal care (Calam,
Waller, Slade, & Newton, 1990; Haudek, Rorty, & Henker, 1999), greater maternal criticism (Dare,
LeGrange Eisler, & Rutherford, 1994), hostile maternal over-involvement (Humphrey, 1989; Rorty,
Yager, Rossotto, & Buckwalter, 2000), and a diminished sense of psychological separateness (Ogden &
Steward, 2000) as characteristics of the relationship between AN patients and their mothers. In addition,
dieting and body dissatisfaction have been found in girls whose mothers perceive their own autonomy as
low (Ogden & Steward, 2000). Self-esteem may thus be associated with a negative self-evaluation in
which environmental effects may be influential. It is not clear, however, to what extent this association
can be explained by genetic factors. Indeed, a significant proportion of the variance in self-esteem in the
population is due to genetic factors, which, in turn, may become manifest through temperamental
characteristics (Kendler, Gardner, & Prescott, 1998). Since personality has an effect on how the
environment is experienced, interpreted, and reacted to, children and adolescents with particular
temperaments, such as negative emotionality and low sociability, possibly interpret and experience life
events in a more negative way (see e.g. the social-information processing model of Crick & Dodge,
1994).
There is some evidence that particularly the strength of the association between self-esteem and
self-evaluation of weight and shape differentiates between individuals with ED and non-ED young
women (and those with other psychiatric disorders) (Serpell et al., submitted; Vitousek and Hollon,
1990). There is thus no doubt that the association between self-esteem and self-evaluation of the weight
and shape of the body is typical for eating disorders. It is not clear, however, when this association
between self-esteem and self-evaluation of weight and shape emerges in relation to the onset of ED.
Girls with a vulnerable sense of self may be at greater risk of linking their self-concept to the weight and
shape of their body if they live in familial environments that emphasize the importance of appearance,
and associate thinness with femininity, beauty and competence (Levine & Smolak, 1992). Self-concepts
and self-esteem emerge in a relational context in which the sense of self may be defined by relationships
with others and through evaluation by others, and this contextual effect appears to be more influential
among girls than among boys (Gilligan, 1993). This focus on external evaluation may place girls at
greater risk of adopting weight and shape as a gauge of their self-worth, especially in such families.
Negative self-evaluation may thus develop during the onset or after the onset of ED, and become a
symptomatic manifestation of low self-esteem.
On the other hand, body weight- and shape-related self-evaluation was the concept used to refer to
the process whereby an individual determines her self-worth based on an evaluation of her body weight
and shape (McFarlane, McCabe, Jarry, Olmsted, & Polivy, 2001).
The social comparison theory
(Festinger, 1954) suggested that individuals’ drive for self-evaluation can be met by comparison with
similar others. An upward social comparison can have negative effects on mood and self-esteem (Major,
Testa, & Bylsma, 1991). Exposure to images of thinness, which are idealized by mass media, can thus
have a consistent negative effect on body satisfaction, particularly among certain individuals (Groesz,
Levine, & Murnen, 2002), possibly more important among girls. A recent 16-month follow-up study
among adolescent boys and girls (McCabe & Ricciardelli, 2005) indeed showed an increase of perceived
messages to lose weight over time among the girls, whereas the boys perceived the messages as related to
increasing muscles. Among the girls, the strongest influences were mothers and best female friends,
while among the boys fathers play the most important role.
Trait-dependent psychological features (i.e. low self-esteem and perfectionism) and dysfunctional
information processes, which will be described later, may also lead to a disturbed body-image. This
disturbance can be viewed as a predisposing factor and as a maintaining factor of the disorder (Cooley &
Toray, 2001; Rosen, 1990; Tuschen-Caffier, Vögele, Bracht, & Hilbert, 2003; Stice, 2002; Wilson,
Fairburn, & Agras, 1997). Patients with a body-image disturbance are preoccupied with the appearance
of their body and show compulsive behaviours such as mirror checking and body measuring. Cognitive
models of eating disorders propose that this selective attention to appearance cues is due to underlying
knowledge structures (schemas) that filter information and direct attention. These schemata guide the
attention to stimuli, the memory for stimuli, and the interpretation of stimuli in ways that serve to
maintain the disorder (Ainsworth, Waller, & Kennedy, 2002; Hargreaves and Tiggemann, 2002; Viken,
Treat, Nosofsky, McFall, & Palmeri, 2002). It should be noted that many studies have used self-reports
to assess attentional processing, which may well reduce the reliability of findings. However, more direct
measures of attentional processing show that eating-disordered subjects allocate their attention more
towards a self-identified ugly body part, contrary to the focus of attention when looking at another body,
which is a beautiful body part. Normal controls do exactly the opposite (Jansen, Nederkoorn, &
Mulkens, 2005). These authors found an increase of attention in the eating-disordered patients when
they looked at their own body with activating negative appearance-related schemata as a consequence,
instead of the usually found avoidance behaviour.
3.3. Perfectionism as core trait
Perfectionists are anxious subjects with a strong tendency to overestimate the probabilities of
negative events and to over-predict threatening events, dangers, and damages (MacLeod, 1999;
Rachman, 1998). Anxious subjects spend much time worrying intensively about their fears (Borkovec,
Ray, & Stöber, 1998). Among perfectionists, the over-prediction of threatening events is associated with
an intensive fear of failure after important performances. In turn, this type of over-feared failure leads
to further damage in terms of decreased self-esteem and impaired social, familial and interpersonal
wellbeing. Perfectionists have an increased probability of experiencing failure in a stress situation,
because even minor shortfalls are tantamount to significant failures. Stress situations and major life
events negatively affect eating habits in human and animal models (Connan & Treasure, 1998). In turn,
perfectionism may facilitate the development of ED by increasing the impact of distressing
environmental events (Hewitt & Flett, 1993a; Hewitt et al., 1995). Therefore, perfectionists have a
tendency to worry about and to feel dissatisfied with perceived mistakes (e.g. regarding eating) and
imperfections (e.g. regarding body shape and weight) (Ruggiero et al., 2003).
Perfectionism is a salient trait in women with AN and BN during acute illness (Cockell, Hewitt, Seal,
Sherry, Goldner, Flett, & Remick, 2002; Fairburn, Cooper, Doll, & Welch, 1999; Goldner et al., 2002;
Halmi, Sunday, Strober, Kaplan, Woodside et al., 2000; Lilenfeld, Stein, Bulik, Strober, Plotnicov et al.,
2000; Stice & Shaw, 2002) and after recovery (Bastiani, Rao, Weltzin, Kaye, 1995; Bulik, Sullivan, Fear,
& Pickering, 2000; Halmi et al., 2000; Pia & Toro, 1999; Srinivasagam, Kaye, Plotnicov, Greeno,
Weltzin, Rao, 1995; Sutandar-Pinnock, Woodside, Carter, Olmsted, & Kaplan, 2003). Clinical (or
‘neurotic’) perfectionism, in which there is an inability to derive pleasure from one’s successes because
the performance is never good enough, (e.g. Kiemle et al., 1987; Ruggiero, Levi, Ciuna, Sassaroli, 2003;
Slade et al., 1990, 1991) is in particular accompanied by a tendency to evaluate one’s own behaviour in
an overly critical way (Frost, Marten, Lahart, & Rosenblate, 1990). “Clinical perfectionism” was defined
as “the overdependence of self-evaluation on the determined pursuit of personally demanding, selfimposed, standards in at least one highly salient domain, despite adverse consequences” (p. 778, Shafran,
Cooper, & Fairburn, 2002). In addition, the term perfectionism refers to
-
selective attention to and over-generalization of failure
-
stringent self-evaluations
-
a tendency to engage in ‘all or none’ thinking, whereby total success or total failure exist as
outcomes (Hewitt & Flett, 1991)
-
cognitive rumination over mistakes and imperfections
-
frequent automatic thoughts about attaining perfection (Hewett, Flett, Besser, Sherry, & McGee,
2002).
It should be noted, however, that studies are characterized by poor operational definitions and
assessments of perfectionism. As in the current studies, perfectionism is commonly measured using a
subscale of the Eating Disorder Inventory (EDI; Garner, Olmstead & Polivy, 1983), a 64-item, selfreport questionnaire that measures cognitive and behavioural characteristics of ED. The Perfectionism
subscale (EDI-P) consists of six items that emphasize personal standard setting and parental
expectations. Although performance on this subscale is expressed by means of one score, this subscale
measures both self-directed (3 items) and socially based (3 items) dimensions of perfectionism (Frost,
Marten, Lahart, Rosenblate, 1990; Hewitt & Flett, 1991; Wyatt & Gilbert; 1998; Sherry, Hewitt, Besser,
McGee, & Flett, 2004). Recent research (Sherry et al., 2004) emphasized that both the intrapersonal
(self-oriented) and interpersonal (other-oriented and socially prescribed) aspects of perfectionism are
independently implicated in the emergence and continuance of eating disorder symptoms.
This
conclusion is consistent with theoretical considerations (Bruch, 1981) and findings from some (Hewitt,
Flett & Edinger, 1995) but not all studies.
Self-oriented perfectionism with a tendency to interpret mistakes as failures is significantly associated
with the presence of AN and BN (Bulik, Tozzi, Anderson, Mazzeo, Aggen, & Sullivan, 2003; Cooper,
Cooper, & Fairburn, 1985). Socially prescribed perfectionism is positively associated with higher levels
of hopelessness and suicidal ideation and negatively associated with positive future thinking (Hewitt,
Flett & Turnbull-Donovan, 1992; Hewitt, Newton, Flett, & Callander, 1997, Hunter & O’Connor,
2003). This is not surprising, as socially prescribed perfectionism has been characterized as being driven
by the fear of failure or by the avoidance of punishment.
ED patients share high scores on the subscale for doubts about actions (describing the reduced
ability to accomplish tasks and obsessional aspects of perfectionism, as assessed by means of the ‘Frost
Multidimensional Perfectionism Scale’; Purdon, Antony & Swinson, 1999) with patients suffering from
anxiety disorders, possibly due to shared genetic factors. Although truly prospective studies have not
been conducted, retrospective clinical reports have frequently described premorbid perfectionism as a
risk factor for AN (Bruch, 1978; Halmi et al., 1977; Fairburn, Cooper, Doll, Welch, 1999; Rastam, 1992;
Slade, 1982; Srinivasagam et al., 1995). These studies have also provided evidence for a trait-dependent
nature of this characteristic, which is thus not simply due to the effects of the illness (e.g. starvation) but
which may reflect an underlying, whether or not genetically determined, vulnerability factor.
Few studies have assessed dimensions of temperament or cognitive/psychological domains, which
are believed to be important in the development of ED, among parents of ED patients. However,
elevated rates of perfectionism have been found in the mothers (and to a lesser extent fathers) of
individuals with AN (Woodside, Bulik, Halmi, Fichter, Kaplan et al., 2002), and in the first-degree
relatives of BN patients (Lilenfeld et al., 2000). Possibly, the trait perfectionism will be transmitted
through families and represent a vulnerability factor for the development of AN (Woodside et al., 2002).
Indeed, twin studies have provided preliminary evidence for the heritability of AN (Holland, Hall,
Murray, Russell, & Crisp, 1984; Holland, Sicotte, Treasure, 1988; Klump, Miller, Keel, McGue, &
Iacono, 2000). These findings support Strober’s (1991) genotypic foundation hypothesis of AN, with
harm avoidance, obsessiveness and self-doubting perfectionism as predisposing traits. Underweight and
weight-restored AN patients did not differ from normal controls regarding scores on ‘Parental
Expectations’ or ‘Other-Oriented Perfectionism’, while they showed only a trend in differing
significantly from normal controls on the ‘Doubt about Action’ and ‘Socially Prescribed Perfectionism’
dimensions (Bastiani et al., 1995). These results suggest that perfectionism in AN is particularly of a selfimposed nature.
Perfectionism could thus well be the behavioural expression of a biologically determined
vulnerability. Kaye and colleagues (1991) have provided evidence for such vulnerability by describing an
increased neuronal serotonin activity, which persists after long-term recovery of AN patients. The
related trait rigidity (related to obsessiveness) is also of interest (Goldner et al., 1999), functioning in
various neuropsychological domains, including perception, among AN patients (Tchanturia et al., 2002).
This perceptual rigidity appears to be also a stable trait, which persists after recovery from AN
(Tchanturia et al., in press). Rigidity may be specifically related to AN, since women with BN typically
show a fluctuation rather than rigidity in their perceptual processes (Tchanturia et al., 2002). Reduced
serotonergic activity has been associated with impulsive and aggressive behaviour (Coccaro, Kavoussi, &
Lesser, 1992; Spoont, 1992), that is opposite in character to the behavioural pattern of AN patients.
Indeed, in these patients control, or the absolute certainty of avoiding all the threatening events
predicted by perfectionists (Sassaroli & Ruggiero, 2002), is an important behavioural feature. This sense
of control often is obtained by monitoring continuously a particular parameter, such as body perception
in panic, or intrusive thoughts in obsessionality. For subjects suffering from ED, the parameters may be
related to eating and/or body weight and shape (Fairburn, Shafran, & Cooper, 1998). Therefore, ED’s
could be described as disorders of the sense of self-esteem and self-worth, which are without remedy
pervasively negative, if not lacking in such subjects. Achieving self-control is the ultimate goal of ED
individuals, who fear that they are not sufficiently worthy (Bruch, 1973; Button, 1985; Katzman & Lee,
1997). This general self-schema, a core cognitive characteristic of ED, is called “long-standing negative
self evaluation” (Vitousek & Hollon, 1990). Moreover, perfectionist subjects perceive their parents’ love
as being connected to parental expectations and critical evaluations (Patch, 1984). Subsequently, the
familial form of failure intensively feared by the perfectionist subject is the loss of parental love
(Ruggiero et al., 2003).
3.4. Perception of life events and the coping with life-events by individuals, characterized by
low self-esteem and clinical perfectionism
Serpell and Troop (2003) have recently discussed the presence of stressors and suboptimal
coping prior to the onset of eating disorders, while distinguishing between stressors that were temporally
distant from onset (i.e. occurring in childhood) and those occurring immediately prior to onset. In
general, ED patients appear to report trauma, including sexual abuse and parental antipathy, indifference
and over-control, more frequently than women without eating disorders. Within the group of patients
with ED, binging and purging patients (BPAN and BP) show the highest levels of childhood adversity
(Schmidt et al., 1997a). Based on retrospective reporting and thus subject to recall biases, Schmidt’s
(1993a, 1999) and Strober’s (1984) studies suggest that sufferers of the RAN subtype report relatively
little childhood adversity, but they report severe events and difficulties prior to onset. Women with
BPAN report high levels of childhood adversity, but low rates of events and difficulties prior to onset.
Relationship problems with a meaning of loss most commonly provoke the onset of eating disorders
(Schmidt et al., 1997b). Events related to pudicity, i.e. crises of a sexual nature that were perceived as
shameful, embarrassing or disgusting, were in particular significantly more common in patients
developing AN than in those developing BN and in non-psychiatric controls (24%, 3% and 8%,
respectively).
The coping response is important in determining the impact of life events and difficulties, i.e.
whether the life event or difficulty will result in high levels of stress. Research shows, in general, that
women with AN and BN display high levels of coping through avoidance when compared to non-ED
woman. Moreover, women with BN, but not AN, seek less support and are less confident (Bloks,
Spinhoven, Calewaert, Willems-Koning, & Turksma, 2001; Neckowitz & Morrison, 1990; Soukup et al.,
1991; Troop et al., 1994, 1998, Yager et al., 1995). Using a retrospective semi-structured interview,
Troop and Treasure (1997a) found that cognitive avoidance was associated with the onset of AN, while
cognitive rumination was associated with the onset of BN. In addition, the onset of an ED was related
to higher levels of helplessness in response to the provoking event/difficulty. These authors also found
higher levels of helplessness in girls who subsequently developed an ED, suggesting that helplessness is
related to the vulnerability for developing an ED. Overall, women with RAN reported lower levels of
helplessness than the other ED groups BN and BPAN. However, this may be due in part to the lower
levels of severe adversity in childhood in RAN women, since when only those women with two or more
adverse childhood experiences were included (e.g. sexual abuse, parental antipathy, parental indifference,
etc.) the levels of helplessness were rather similar for the ED subgroups, all of which were higher than
the levels found in non-ED women. Interestingly, Tiller and colleagues (1997) found differences in
structural and functional aspects of social support between ED subtypes. For example, women with AN
reported fewer support figures than non-ED women, but they were equally satisfied with the support
they received. BN women, however, reported a network of potential support figures of a similar size as
that of non-ED women, but they were considerably more dissatisfied. However, AN and BN women
reported fewer friends and more loneliness during their childhood than non-ED women (Fairburn et al.,
1997, 1999; Karwautz et al., 2001; Troop & Bifulco, 2002). Two-thirds of AN patients reported social
isolation, poor social interpersonal relationships and difficulties with relatives and therapists (Flament,
Godart, Fermanian & Jeammet, 2001). Bulik and colleagues (2000) reported significantly lower maternal
and paternal care scores in AN patients who were chronically ill. These associations can be interpreted in
different ways. While poor social support may indeed reflect the use of particular coping strategies that
may act as a vulnerability factor for ED, the long-standing presence of an ED may affect the family
system in an adverse way and/or may bias an individual’s perception of her parents. However, it appears
that the absence of adequate maternal and paternal care may contribute directly or indirectly to the
chronicity of an ED.
Based on these findings, it can be hypothesized that vulnerable individuals due to a low self-esteem,
associated with body dissatisfaction and perfectionism, cope with perceived threatening life-events by
avoidance or escape behaviour.
The perception and interpretation of those events is based on
neuropsychological and cognitive processes, which elicited those behaviours.
4. Information processing in eating disordered patients
4.1. Neuropsychological processes
When compared to healthy controls, AN patients show deficits in various neuropsychological
domains including verbal and visual memory, visuospatial ability, attentional skills (with a bias toward an
analytic and controlled information-processing mode) and executive functioning (Bowers, 1994; FrantzFox, 1981; Green, Elliman, Wakeling, & Rogers, 1996; Kaye, Bastiani, & Moss, 1995; Lauer, Gorzewski,
Gerlinghoff, Backmund, & Zihl, 1999; Mathias & Kent, 1998; Pendleton-Jones, Duncan, Brouwers, &
Mirsky, 1991; Strauss & Ryan, 1988; Szmukler et al., 1992; Thompson, 1993). Some (Kingston et al.,
1996; Lauer et al., 1999; Moser, Benjamin, Bayless et al., 2003; Szmukler et al., 1992), but not all (Green
et al., 1996) studies indicate that these neuropsychological deficits recover with treatment.
Among AN patients the attentional and perceptual deficits may be stimulus-specific with specific
difficulties in inhibiting irrelevant information, while perceiving stimuli related to body images, food and
weight (Cooper and Todd, 1997; Long, Hinton, & Gillespie, 1994; Perpina, Himsley, Treasure, & De
Silva, 1993; Rieger, Schotte, Touyz et al., 1998; Smeets, Smit, Panhuysen, & Ingelby, 1998; Smeets,
Ingelby, Hoek, & Panhuysen, 1999). The pathological preoccupation with body shape leads to an
intensive focus on the body and the search for perfection, which is typical of rigid personalities (Fassino,
Piero, Abbate Daga et al., 2002). Performance appears to be affected more when the situation or task is
relevant to the individual’s specific concern (Williams et al., 1997). However, methodological flaws
associated with the use of particular tasks (such as a modified Stroop colour-naming task) and validity
problems of the used questionnaires, hamper the interpretation of the results of studies in ED patients
(Mogg & Bradley, 1998).
Using an electrophysiological technique Dodin and Nandrino (2003) showed, that these deficits
extend to generic stimuli, irrespective of the task-complexity or to the task-specificity (e.g. requiring
attentional, perceptual or motor resources). Logically, it was hypothesized that food deprivation and/or
low BMI or the comorbid presence of depression were responsible, but this explanation was not
sufficient (Hamsher et al., 1981; Lauer et al., 1999; Kingston et al., 1996; Mathias & Kent, 1998; Moser
et al., 2003; Pendleton-Jones et al., 1991; Szmukler et al., 1992).
Parallel with the findings of
preoccupying cognitions in emotional disorders (Williams, Watts, MacLeod, & Mathews, 1997), the bias
towards a controlled processing mode could be related to anxiety with a systematically allocating high
level of attentional resources, impeding appropriate selective processing of relevant information (Green,
Elliman, & Rogers, 1997; Green & Rogers, 1995, 1998; Green, Rogers, Elliman, & Gatenby; 1994; Jones
& Rogers, 2003; Rogers & Green, 1993). Thus, Dodin and Nandrino (2003) explained this phenomenon
by the hyperarousal state of AN patients, characterized by a constant need to reassess new incoming
stimuli using their working memory. Working memory saturation would then be faster than normally
expected, reducing in this way the ability to learn in anorexic subjects. This failure to inhibit frequent
stimuli may correspond to an impaired learning process in association with a working memory deficit, as
suggested by Green and co-workers (1996). Even in simple tasks that could be carried out in a more
automatic fashion, patients may favour a controlled information-processing mode causing longer
perceptual decision times. Dieters and restrained eaters indeed displayed slower reaction times than
non-restrained eaters in the presence of a food-related cue reactivity manipulation (Green, Rogers,
Elliman, & Gatenby, 1994) and this effect was stronger during the earlier parts of the cognitive
processing measure (Green, Rogers, & Elliman, 2000). Non-clinical subjects scoring high on trait anxiety
measures showed interference during the automatic but not the controlled processing of emotional
material (MacLeod & Hagan, 1992).
Non-ED restrained eaters did not show distortions in the
processing of body shape and weights stimuli, nor an early automatic processing priority or a pattern of
strategic processing selectivity in Stroop studies (Jansen, Huygens, & Tenney, 1998). This finding might
point at a qualitative difference between normal restrained eaters and subjects with eating disorders of
clinical severity.
Slower information processing and deficiencies in the initiation of an adequate problem-solving
strategy appear to be present also in BN patients ((Black, Wilson, Labouvie, & Hefferman, 1997; Carter,
Bulik, McIntosh, & Joyce, 2000; Cooper & Fairburn, 1994; Hsu, Kaye, & Weltzin, 1993; Ferraro,
Wonderlich, & Jocic, 1997). Moreover, unsuccessful dieters, when compared to successful dieters, show
increased appetitive physiological responses to food stimuli and a greater vulnerability to disinhibition of
restraint and thus to overeating (Jones & Rogers, 2003). They also have more inflexible attitudes
towards food and eating (see review by Mela & Rogers, 1998). As a consequence, they may feel the
adverse effects of dietary violation more intensely, leading to a marked increase in preoccupation and
further impairment of task performance.
4.2 Cognitive processes
Cognitive-behavioural research has addressed cognitions that are relatively available to conscious
report (i.e., negative automatic thoughts and conditional assumptions, principally regarding food, shape,
and weight). However, there may also be a particular role for schema-level cognitive representations, or
core beliefs, which are not related to food, shape or weight, but which reflect unconditional negative
beliefs about the self, others, or the world. Indeed, the schematic level of cognitive representation
(unconditional core beliefs) may well be responsible for phenomena such as rapid mood swings (a result
of the triggering of unconditional core beliefs) and mood suppression (caused by the activation of
emotional inhibition beliefs) (see e.g., Young, 1994).
Although schema-level representations have
received attention particularly in terms of their capacity to explain personality disorder-related pathology,
they may also play a specific role in disorders with an impulsive component, such as bulimia, or with a
compulsive element, such as restriction (see e.g., Leung, Waller, & Thomas, 1999).
The cognitive model suggests that schemata relating to threat, particularly threats to self-esteem are
associated with bulimic attitudes and behaviours (Everill & Waller, 1995; Waller et al., 1996; Van Strien,
2000a; Vervaet, van Heeringen, & Audenaert, 2004; Gilbert & Meyer, 2005). These schemata are
activated prior to (or even without) conscious awareness of the threat and associated with an attentional
bias. Binge eating appears to be one way of reducing the activation or dominance of such threat-related
schemata. This phenomenon has been studied using a modified Stroop task, but the results of these
studies may have been biased as performance on this task may reflect a number of processes in addition
to attention (Foa, Feske, Murdock, Kozak, & McCarthy, 1991), and may be under some degree of
conscious control. Therefore, researchers such as Waller & Mijatovich (1998) have used subliminal visual
presentation of a threatening stimulus (Patton, 1992). The results from studies using both methods
confirm earlier conclusions of other models, i.e. that (1) binging serves the function of reducing
awareness of negative affect and cognitions (Lacey, 1986; Root and Fallon, 1989) or that (2) attention is
narrowed as a means of reducing awareness of threat, and that eating is disinhibited as a result of this
narrowing of attention (Heatherthon and Baumeister, 1991). Clinical experience suggests that both
mechanisms take place in the same individual at different times and to different degrees during the
development of bulimic disorder (McManus & Waller, 1995). There is evidence that the processes of
attentional bias and cognitive avoidance are not independent (de Ruiter & Brosschot, 1994). This
hypothesized process is similar to a recent model of anxiety. Beck and Clarke (1997) suggest that
information processing is initially automatic, but that it becomes a more strategic, purposeful responding
over time. When information is aversive, the initial automatic response (due to an attentional bias to
material that is strongly represented cortically) will be followed by a more purposeful form of processing
(avoidance of the aversive material). Bulimic psychopathology thus appears to be a cognitive “escape”
mechanism (Meyer, Waller, & Watson, 2000).
Using a semi-structured interview, it was found that the self-beliefs of ED patients, unlike those of
non-ED women, are negative, unconditional and concerned with themes such as abandonment and
uselessness (Cooper, Todd, & Wells, 1998). They were also invariably associated with negative early
experiences. Underlying assumptions were of two kinds, i.e. (1) weight and shape as a means to selfacceptance, and (2) weight and shape as a means to achieve acceptance from others. There were also
assumptions about eating. The interview also indicated that underlying assumptions provide a link
between negative self-beliefs and dieting behaviour. Assumptions appeared to be compensatory beliefs,
providing a way for the individual to overcome negative self-beliefs (Young, 1994). However, the
conclusions from this study were purely qualitative, and no information was provided regarding the
validity and reliability of the interview. Results of the study using a revised version of the interview
(Turner & Cooper, 2002) with a good inter-rater and test re-test reliability and promising concurrent
validity, in AN patients, non-symptomatic dieters and female controls were however comparable.
Patients experienced more eating-related negative automatic thoughts than dieters and controls, with
similar differences for duration, degree of belief and associated distress. Patients also reported more
eating-, weight- and shape-related thoughts than controls and had more underlying assumptions related
to eating, and weight and shape as a means to acceptance by self and others. Cooper and colleagues
(1998) have recently argued that both negative self-beliefs and underlying assumptions about weight,
shape and eating need to be present for the development of an ED. Successful dieting may reduce the
distress caused by negative self-beliefs and enhance self-esteem and the feeling of success. These beliefs
may thus function as ‘schema compensation beliefs’ (Young, 1990). The enhanced self-esteem is
however quickly negated by thoughts of inadequate dieting, which in turn reinforce negative self-beliefs.
This process may be similar to the ‘schema maintenance processes’ as identified by Young (1990).
The more common use of cognitive strategies involving punishment and worry among
individuals, who show a strong tendency of disinhibition, in order to control their thoughts parallels the
increased prevalence of these strategies in other clinical domains, such as the anxiety disorders (Wells &
Davies, 1994). Furthermore, a rigid and punitive cognitive style is characteristic of dieters and may serve
to control food intake as it was shown that the use of punishment correlates positively with ratings of
anxiety, distress, perceived thought frequency, and actual number of thoughts about food (Garner &
Bemis, 1982). It is unknown however, to what extent these strategies are adopted in response to
upsetting intrusive thoughts (Oliver & Huon, 2001).
Patients suffering from Binge Eating Disorder (BED) are characterized by substantially more
pathological core beliefs than normal controls. A recent study (Waller, 2003) revealed differences
between BED and BN for the nature of these core beliefs, but not for the extent of these beliefs, as in
previous research (e.g., Ardovini et al., 1999; Wilfley et al., 2000). In this study, patients with BED
showed particularly negative beliefs about their ability to experience or express emotions, their ability to
function independently, and their need to sacrifice their own needs for those of others. When compared
to the BN patients, BED patients reported however less pathological beliefs regarding the likelihood that
they would be abandoned. The absence of purging may thus be related to the lower level of
abandonment beliefs, and the presence rather than the extent of relatively negative abandonment beliefs
drives purging behaviours in BN (Patton, 1992).
4.3. Information processing and emotional arousal
In cognitive theories, emotion is a multifaceted phenomenon with cognitive processing of
stimuli, motivation, physiological activation, motor behaviour and subjective feeling state (Williams,
Watts, MacLeod, & Mathews, 1997).
Emotional disorders involve acute reactions with a strong
autonomic component but also long-term emotional disturbance and cognitive preoccupations. Some
individuals may adopt perfectionist standards as compensation for an underlying inferior sense of self
and shame-proneness (Miller, 1996), with early infantile narcissistic origins related to the fear of showing
one’s physical, intellectual or emotional defects to others (Jacobson, 1964). Shame is a complex emotion
in which the self is judged to have fallen short of an internalised set of standards. Even if experienced in
private it is as if the self is being judged by some external other. Shame can be considered as the
experience that the self is defective (see e.g. Tangney, 1993), while others conceptualise shame as a
psychological consequence of being judged to be low in social rank (see e.g. Gilbert, 1997). Implicit in
both these conceptualisations is the notion of social comparison (Lazarus, 1999). Shame, unfavourable
social comparison and submissive behaviour are associated with socially prescribed perfectionism,
suggesting that these individuals see themselves as rather lacking in status, and it may be this that is
particularly pathogenic (Wyatt & Gilbert, 1998).
In non-clinical samples shame-proneness is related to eating pathology (Sanftner et al., 1995). In
a diary study, Sanftner and Crowther (1998) showed that shame, in general, was more markedly present
in women who reported binge eating, but fluctuations in shame were not related to the occurrence of
binge episodes.
Interestingly, Waller and colleagues (2000) found that a core belief of
Defectiveness/Shame was related to the frequency of vomiting. At a group level, Defectiveness/Shame
was one of three core beliefs that differentiated between bulimic subgroups (BN, BPAN and BED) and
a non-ED comparison group, the other two core beliefs being Insufficient Self-Control and Failure to
Achieve.
Andrews (1997) found that bodily shame was a better predictor of BN than body
dissatisfaction and that bodily shame mediated the relationship between childhood physical or sexual
abuse and subsequent BN.
Similar to shame, jealousy is a complex emotion involving social comparison (Lazarus, 1999).
Two studies have used a sibling-comparison design to assess non-shared childhood environmental
effects on the development of AN (Murphy et al., 2000; Karwautz et al., 2001). Both studies found that
affected sisters reported having been more jealous of their unaffected sisters in childhood than the
unaffected sisters were of them. Women with BN, on the other hand, report their mothers to have been
jealous and competitive during their childhoods (Rorty et al., 2000a, 2000b). Thus, while the perception
of others being jealous of oneself may be a risk factor for AN and the jealousy of others may be a risk
factor in BN, these results suggest that the development of both disorders probably involves
competition in the context of social comparison.
The role of anger and hostility in ED has received less attention than other emotions. However,
these emotions occur more frequently among patients with ED than among non-ED comparison
women (e.g. Tiller et al., 1995). Milligan and Waller (2000) found that state anger, but not trait anger,
and anger suppression were related to bulimic pathology. Anger suppression was uniquely related to the
presence of binge eating, whereas state anger was uniquely related to the presence of vomiting. The
authors suggest that their findings support the functional role of bulimia in blocking unpleasant affective
states and, in particular, that different symptoms of bulimia may serve different functions. When
compared to normal controls, ED women had higher levels of state anger and anger suppression,
especially when they displayed bulimic symptoms (Waller, Babbs, Milligan, Meyer, Ohanian, & Leung,
2003). Considering specific symptoms, bingeing and vomiting were associated with trait anger, while
excessive exercise was associated with state anger, and laxative abuse was linked to anger suppression. It
can thus be hypothesized that bulimic behaviours serve different emotional functions, with a particular
contrast between the facets of anger that are influenced by “fast-acting” behaviours (bingeing, vomiting,
exercise) and those that are influenced by “slow-acting” behaviours (laxative abuse). When considering
the role of cognitions, unhealthy core beliefs were associated with higher levels of trait anger in both
groups but were relevant to anger suppression only in the ED patients.
Finally, but very interestingly, a specific impairment in the recognition of facial and vocal
expressions of emotion was found in ED patients (Kucharska-Pietura, Nikolaou, Masiak, & Treasure,
2004), which was possibly associated with their deficit in social functioning. This impairment may be
due to a disturbed emotional processing, which is common to people within the internalizing spectrum
of psychopathology (Uher, Murphy, Phillips & Dalgleish, 2001). Another possibility is that people with
emotional and interpersonal difficulties have an attention problem in social situations, comparable to the
attention deficit in people with social phobia (Chen, Ehlers, Clark, & Mansell, 2002).
4.4. From schemata to behaviour
Clinical investigators have described difficulties in identifying, verbally expressing, and regulating
a variety of physical tensions among ED patients (Bruch, 1973; Esplen, Garfinkel, & Gallop, 2000;
Troop, Schmidt, & Treasure, 1995).
According to Bruch, the confusion and apprehension in
recognizing and accurately responding to emotional states and the uncertainty in the identification of
certain visceral sensations related to hunger and satiety, tapped by the Interoceptive Awareness subscale
of the EDI, may result in a pattern of responding to negative mood by food intake, or ‘emotional
eating’. Interoceptive awareness is strongly associated with alexithymia (Taylor, Parker, Badbey, &
Bourke, 1996). Social self-doubt and unhappiness have been suggested as central elements in inducing
the eating pattern of emotional eaters. The escape theory of eating, as formulated by Heatherton and
Baumeister (1991), which incorporates elements of externality and psychosomatic theory, stated that a
shift to low levels of thinking would result in a reliance on immediate stimuli and in a dampening of
affect. Reduced affect and eating would then occur following escape from self-awareness. As described
by Van Strien (2000b), Slochower (1983) has also suggested that emotions and environment may operate
conjointly to produce overeating. The restraint theory is not valid for all dieters, but mainly for a
subpopulation with a strong tendency towards overeating (van Strien, Cleven & Schippers, 2000). Thus,
overeating following a preload occurred only in subjects with high scores on both restraint and
disinhibition, as measured by the ‘emotional eating’ and ‘external eating’ scales of the Dutch Eating
Behaviour Questionnaire (DEBQ; Van Strien, 1986) and the ‘bulimia’ subscale of the Eating Disorder
Inventory (EDI; Garner et al., 1983). A possible explanation is that anything that depletes restrained
eaters’ self-regulatory strength (as many everyday self-regulatory tasks) may disinhibit subsequent eating
(by undermining the ability to maintain cognitive regulation of the intake in the period following other
self-regulatory tasks) and disrupt attempts to diet (Kahan, Polivy, Herman, 2003). The false hope of
dieting may deplete the dieter’s resources due to the vicious circle of ill-advised attempts followed by
failure and self-recrimination (Polivy & Herman, 2000).
As described above, perfectionism/rigidity (as a particular risk for the restrictive disorders with overevaluation of achieving) and low self-esteem reflect a specific way of information processing, which may
make individuals vulnerable to develop an ED. Exposure to severe interpersonal life events (possibly at
least in part due to particular traits such as low sensitivity for social cues or impaired recognition of facial
and vocal expression of emotion) or to difficulties in combination with helplessness or inadequate
coping (another possible trait), in the presence of this predisposition or vulnerability, may precipitate the
development of specific core beliefs, such as negative self beliefs. These cognitions can be expressed by
a dysfunctional schema of body shape and weight-based self-esteem resulting in strict dieting, excessive
exercise and other weight-control behaviour such as purging (Fairburn et al., 2003). Binge eating can
then be a consequence of these restricting behaviours, or, as described above, it can be an escape
mechanism in the context of inevitable conflict situations.
Consistent with Stice’s (1994, 2001) dual pathway model of eating disorders, dieting and negative
affect independently predict the subsequent onset of binge eating (Shepherd & Ricciardelli, 1998; Stice et
al., 2000), though only in females. In contrast, experimental studies suggest an interactive effect, the socalled disinhibition of dietary restraint (Ruderman, 1986). Recently, cluster-analytic studies have yielded
two subtypes of eating disorders: pure dietary and mixed dietary-negative affect (Grilo, 2004). This last
type was characterized by a greater likelihood of binge eating, greater eating-related psychopathology,
greater body image dissatisfaction, greater personality disturbance and more commonly reported
concerns in clinical areas, including suicidality and childhood abuse. Polivy and Herman’s (1999) study
of the disinhibiting effects of emotion on dietary restraint provided no support for the “comfort
hypothesis”, which suggests that eating makes people feel better. However, strong support was found
for the “masking hypothesis” in which the dieter, by over-eating, misattributes her distress to the
problem of over-eating rather than to her real problems. In addition, the findings partially supported the
“learned helplessness hypothesis”, in which the experience of stress/distress generalises to all areas in
life including the ability to maintain a diet, and the “distraction hypothesis” in which restrained eaters
over-eat in order to distract themselves from feeling distressed.
Within a cognitive model, it has been proposed that overeating can serve the function of reducing
the awareness of threatening information and intolerable emotions (McManus & Waller, 1995). Such a
reduction in awareness corresponds with a lowering of activation of relevant cognitive representations
(schemata) through distraction or activation of other structures. At a preconscious level, and thus
automatic in nature, associations between abandonment and eating-related cognitions were found
(Meyer and Waller, 1999, 2000). At a conscious level, women with BN often report a significant event
involving the loss of a significant relationship prior to the onset of their disorder. These observations
may be causally associated through an outspoken need for approval and feelings of social isolation,
which are characteristic of bulimic psychopathology (Tiller et al., 1997). Based on their findings, Meyer
and Waller (2000) hypothesized that the core beliefs are more likely to focus on abandonment, whereas
negative automatic thoughts and dysfunctional assumptions are more likely to center on issues reflecting
food, shape, and weight. This leads to states experienced as a non-specific ‘extreme state of tension’, or
to feelings of emptiness and aloneness (Cross, 1993) combined with a lower level of soothing receptivity
(Glassman, 1988) and poorer capacity for evocative memory, and finally to a sense of loneliness and to
difficulties in the regulation of affect. This may offer an explanation for the limited effects of some
current therapies, i.e. those that only address the cognitive elements related to body distortion and
dieting behaviours, in treating disturbed regulation of affect (Arntz, 1994).
Taken together, theoretical considerations and empirical findings have suggested a variety of
reinforcing consequences that may shape and maintain disordered eating behaviours.
Specifically,
individuals may be more inclined to (1) respond to aversive internal and external events through
engagement in disordered eating behaviours that are, in turn, subsequently negatively reinforced as they
function to reduce or terminate these aversive events, and (2) engage in disordered eating as to
experience immediate gratification of needs or the attainment of immediate reinforcers, or to increase
the likelihood of attaining anticipated distal reinforcers (e.g. social approval for a slim appearance).
Possibly, reward sensitivity and responsiveness to reward and relief from aversion, and/or insensitivity
to signals of threat or punishment are important individual variables associated with the same underlying
trait, temperament dimension or brain system (Cloninger, 1987; Gray, 1987). Recently, an association
between reward sensitivity and purging behaviours has indeed been reported (Farmer, Nash, & Field,
2002).
Through their association with core psychopathological characteristics of ED patients, traitdependent measures may thus be useful for our understanding of the development and maintenance of
ED-related symptoms and for the prediction of eating-disordered behaviour. The following section will
describe a hypothetical dimensional trait model of ED-related characteristics based on Cloninger’s
psychobiological model of personality (Cloninger et al., 1993).
Cloninger proposes that specific
dimensions of temperament and character interact with one another to influence susceptibility to
emotional and behavioural disorders. Cloninger refers to temperament as emotional responses that are
moderately heritable, stable throughout life, and mediated by neurotransmitter functioning in the central
nervous system. Cloninger’s four proposed temperament dimensions include: novelty seeking (NS),
which reflects behavioural activation to pursue rewards and is posited to be related to decreased
dopaminergic activity; harm avoidance (HA), which is the tendency to inhibit behavior to avoid
punishment and is purported to be related to increased serotonergic activity; reward dependence (RD),
which reflects the maintenance of rewarded behaviour and is hypothesized to be mediated by decreased
noradrenergic activity; and persistence (P), which is perseverance without intermittent reinforcement
that is also purported to be related to decreased noradrenergic activity. Character, in contrast, refers to
self-concepts and individual differences in goals and values that develop through experience. The
character dimensions are: self-directedness (SD), which is the degree to which the self is viewed as
autonomous and integrated; cooperativeness (C), which reflects the degree to which the self is viewed as
a part of society; and self-transcendence (ST), which reflects the degree to which the self is viewed as an
integral part of the universe.
4. A hypothetical model for the prediction of eating-disordered behaviour
Although significant advances regarding the identification of individual risk factors have been made,
few prospective studies have tested a multivariate etiologic model that details how these individual risk
factors work in concert to promote the development of anorectic and bulimic symptoms. Two
prospective studies have provided support for a three-factor interactive model for bulimic symptoms in
which the confluence of perfectionism, body dissatisfaction and low self-esteem promotes the
development of bulimic symptoms (Vohs, Bardone, Joiner, Abramson, & Heatherton, 1999; Vohs,
Voelz, Pettit, Bardone, Katz, Abramson, Heatherthon, & Joiner, 2001). Although a replication study did
not support this model, the results confirmed those from previous prospective studies of the importance
and significant effect of body dissatisfaction (Shaw, Stice, & Springer, 2004).
According to the cognitive model of the maintenance of eating disorders (Fairburn, 1997), the core
psychopathology, even among anorectic patients (Carter, Blackmore, Sutandar-Pinnock, & Woodside,
2004) is the over concern with body shape and weight. Due to this over concern, self-worth is judged
largely or even exclusively in terms of satisfaction with weight and shape.
The function of this
overconcern is probably problem-avoidance. Taking into account the need for absolute self-control in
AN patients (Fairburn et al., 1999), food restriction in combination with excessive physical activity was
found to be highly reinforcing. This reinforcing effect is most probably related to the fact that these
behaviours increase circulating levels of endogenous opiates that activate dopamine in the brain’s
mesolimbic reward centres (Carter et al., 2004; Davis, Katzman, Kaptein, Kirsh, Brewer, Kalmbach,
Olmsted, Woodside, & Kaplan, 1997; Strober, Freeman, Morrell, 1997).
Many studies provide evidence for a strong relationship between impulsivity and eating-disordered
behaviour. A higher score on measures of impulsive behaviour has been described in eating disordered
individuals, especially in adolescents (Wonderlich, Connolly, & Stice, 2004). There is, however, a
difference between trait-oriented impulsivity and behavioural measures of impulsivity. It can be
hypothesized that the more outspoken behavioural impulsivity in behaviour among ED patients,
particularly in those showing binging-purging behaviours, is the expression of the temperament
dimension ‘Novelty Seeking’, whether or not in combination with a poorer character development as
measured by ‘Self-directedness’.
Based on a similar line of reasoning, it can be hypothesized that ED patients are characterised by a
high score on ‘Harm Avoidance’, expressed by their ‘Perfectionism’ and ‘restricting behaviour’ as a need
for control, and a low score on ‘Reward Dependence’, reflecting their rigidity or inability to cope with
(social) situations. A higher ‘Persistence’ among ED patients, when compared to normal controls, could
explain the persistent nature of avoidance behaviours, in spite of their adverse effects in the long run
after the short-term reinforcing effects. With regard to ‘Novelty Seeking’ especially differences between
the restricting type (RAN) and the binge-purging type (BPAN and BP) can be expected, expressed by
means of a more outspoken ‘body dissatisfaction’ and more frequent ‘emotional and external eating’,
combined with more ‘purging’ in the latter type. In view of the common high levels of helplessness, ED
patients can be expected to have lower scores on the character dimensions, in particular the ‘Selfdirectedness’ dimension, possibly reflecting low self-esteem. Scores on the self-directedness dimension
may even be lower among BN patients, as these individuals do not succeed in restricting and avoiding
and are conditioned with regard to their escape behaviours by binging or/and purging.
The following part of this thesis is constituted by studies of these hypothetical associations in the
context of the proposed dimensional trait model of factors predisposing to ED.
References
Ainsworth C, Waller G, & Kennedy F (2002). Threat processing in women with bulimia. Clinical Psychology Review, 22,
1155-1178.
Andersen AE, Bowers WA, & Watson T (2001). A slimming program for eating disorders not otherwise specified.
Reconceptualizing a confusing, residual diagnostic category. Psychiatric Clinics of North America, 24, 271-280.
Andreassi JL (2000).
Associates.
Psychophysiology.
Human behaviour and physiological respons.
London: Lawrence Erlbaum
Andrews B (1997) Bodily shame in relation to abuse in childhood and bulimia: A preliminary investigation. British Journal of
Clinical Psychology, 36, 41-49.
Ardovini C, Caputo G, Todisco P, & Grave RD (1999). Binge eating and restraint model: Psychometric analysis in binge
eating disorder and normal weight bulimia. European Eating Disorders Review, 7, 293-299.
Arnow B, Kenardy J, & Agras WS (1995). The emotional eating scale: The development of a measure to assess coping with
negative affect by eating. International Journal of Eating Disorders, 18, 79-90.
Arntz A (1994). Treatment of borderline personality disorder: A challenge for cognitive-behavioural therapy. Behavioural
Research and Therapy, 32, 419-430.
Bastiani AM, Altemus M, Pigott T, Rubenstein C, Weltzin TE, & Kaye WH (1996). Comparison of obsession and
compulsion in patients with anorexia nervosa and obsessive-compulsive disorder. Biological Psychiatry, 39, 966-969.
Bastiani, AM, Rao R, Weltzin T & Kaye W (1995) Perfectionism in anorexia nervosa. International Journal of Eating
Disorders, 17(2), 147-52.
Beck AT, & Clarke DA (1997). An information processing model of anxiety: Attentional bias or cognitive avoidance?
Behaviour Research and Therapy, 32, 315-319.
Bemporad J (1996). Self-starvation through the ages: reflexions on the pre-history of anorexia nervosa. International Journal
of Eating Disorders, 19, 217-237.
Bennet D, Sharpe M, Freeman C & Carson A (2004). Anorexia nervosa among female secondary school students in Ghana.
The British Journal of Psychiatry, 185, 312-317.
Bhadrinath ER (1990). Anorexia nervosa in adolescents of Asian extraction. British Journal of Psychiatry, 156, 565-568.
Bloks H, Spinhoven P, Calewaert I, Willemse-Koning C, & Turksma A (2001). Changes in coping styles and recovery after
inpatients treatment for severe eating disorders. European Eating Disorders Review, 9, 397-415.
Borkovec TD, Ray WJ, & Stöber (1998). Worry: A cognitive phenomenon intimately linked to affective, physiological, and
interpersonal behavioral processes. Cognitive Therapy and Research, 22, 561-567.
Brecelj M, Tchanturia K, Rabe-Hesketh S & Treasure JL (in press). Rigidity traits in the child- hoods of eating disorder
patients. American Journal of Psychiatry.
Brewerton TD, Lydiard BR, Laraia MT, Shook JE, & Ballenger JC (1992). CSF Betaendorphin and dynorphin in bulimia
nervosa. American Journal of Psychiatry, 149, 1086-1090.
Brownell KD (1991). Dieting and the search for the perfect body: Where physiology and culture collide. Behavior Therapy,
22, 1-12.
Bruch H (1973). Eating disorders: Obesity, anorexia nervosa, and the person within. New York: Basic Books.
Bruch H (1978). The golden cage: the enigma of anorexia nervosa. Cambridge, MA: Harvard University Press.
Bruch H (1981). Developmental considerations of anorexia nervosa and obesity. Canadian Journal of Psychiatry, 26, 212217.
Bulik CM, Sullivan PF, Fear JL, Pickering A. (2000). Outcome of anorexia nervosa: eating attitudes, personality, and parental
bonding. International Journal of Eating Disorders, 28(2), 139-47.
Bulik CM, Sullivan PF, Joyce PR, & Carter, F.A. (1995a). Temperament, character, and personality disorder in bulimia
nervosa. Journal of Nervous & Mental Disease, 183, 593-598
Bulik, C.M., Sullivan, P.F., Joyce, P.R., Carter, F.A., & McIntosh, V.V. (1998). Predictors of 1-year treatment outcome in
bulimia nervosa. Comprehensive Psychiatry, 39, 206-214.
Bulik, C.M., Sullivan, P.F., Wade, T.D. & Kendler, K.S. (2000) Twin studies of eating disorders: A review. International
Journal of Eating Disorders, 27, 2-20.
Bulik, C.M., Sullivan, P.F., Weltzin, T.E., & Kay, W.H. (1995). Temperament in eating disorders. International Journal of
Eating Disorders, 17, 251-261.
Bulik CM, Tozzi F, Anderson C, Mazzeo SE, Aggen S, Sullivan PF. (2003). The relation between eating disorders and
components of perfectionism. American Journal of Psychiatry, 160(2), 366-8.
Bushnell, JA, Wells, JE, & Oakley-Browne, MA (1996). Impulsivity in disordered eating, affective disorder, and substance use
disorder. Britisch Journal of Psychiatry, 169, 329-333.
Button E (1985). Eating disorders: A quest for control? In E.Button (Ed.), Persoanl construct theory and mental health (pp.
153-168). London: Croom Helm.
Button, E.J., Sonuga-Barke, E.J., Davies, J., & Thompson, M. (1996). A prospective study of self-esteem in the prediction of
eating problems in adolescent schoolgirls: Questionnaire findings. British Journal of Clinical Psychology, 35 (2), 193-203.
Bydlowski S, Corcos M, Jeammet P, Paterniti S, Berthoz S, Laurier C, Chambry J, & Consoli SM (2005). Emotion-processing
deficits in eating disorders. International Journal of Eating Disorders, 37, 4, 321-329.
Calam R, Waller G, Slade PD, & Newton T (1990). Eating disorders and perceived relationships with parents. International
Journal of Eating Disorders, 9, 479-485.
Carroll JM, Touyz SW & Beumont PJV (1996) Specjfic comorbidity between bulimia nervosa and personality disorders.
International Journal of Eating Disorders, 19 (2), 159-170.
Carter FA, Bulik CM, McIntosh VV, & Joyce PR (2000). Changes on the Stroop test following treatment: relation to word
type, treatment condition, and treatment outcome among women with bulimia nervosa. International Journal of Eating
Disorders, 28, 349-355.
Carter JC, Blackmore K, Sutandar-Pinnock, & Woodside (2004).
Psychological Medicine, 34, 671-679.
Relapes in anorexia nervosa: a survival analysis.
Casper RC, Hedeker D & McClough JF (1992) Personality dimensions in eating disorders and their subtyping. Journal of the
American Academy of Child and Adolescent Psychiatry, 31 (5), 830-840.
Chen YP, Ehlers A, Clark DM, & Mansell W (2002). Patients with generalized social phobia direct their attention awoy from
faces. Behaviour Research and Therapy, 40, 677-687.
Claes L, Vandereycken W, & Vertommen H (2002). Impulsive and compulsive traits in eating disordered patients compared
with controls. Personality and Individual Differences, 32, 707-714.
Cloninger CR, Svrakic DM & Przybeck TR (1993). A psychobiological model of temperament and character. Archives of
General Psychiatry, 50, 975-990.
Cloninger CR (1987a). Neurogenetic adaptive mechanisms in alcoholism. Science, 236, 410-416.
Cloninger CR (1987b). A systematic method for clinical description and classification of personality variants. Archives of
General Psychiatry , 44, 573-588.
Coccaro EF, Kavoussi RJ, & Lesser JC (1992). Self- and other-directed human aggression : The role of the central
serotonergic system. International Clinical Psychopharmacology, 6, 70-83.
Cockell SJ, Hewitt PL, Seal B, Sherry SB, Goldner EM, Flett GL, & Remick RA (2002). Trait and self-presentational
dimensions of perfectionism among women with anorexia nervosa. Cognitive Therapy and Research, 26, 745-758
Collier DA, & Treasure JL (2004). The aetiology of eating disorders. British Journal of Psychiatry, 185, 363-365.
Connan F, & Treasure J (1998). Stress, eating and neurobiology. In H.W. Hoeck, JL Treasure, & M Katzman (Eds.),
Neurobiology in the treatment of eating disorders (pp.211-236). Chichester, UK: Wiley.
Cooley E, & Toray T (2001). Disordered eating in college Freshman women: A prospective study. Journal of American
College Health, 49, 5, pp 229-236.
Cooper M, & Todd G (1997). Selective processing of three types f stimuli in eating disorders. British Journal of Clinical
Psychology, 36, 279-281.
Cooper, MJ, & Fairburn CG (1993). Confusion over the core psychopathology of bulimia nervosa. International Journal of
Eating Disorders, 13, 385-389.
Cooper MJ, Todd G, & Wells A (1998). Content, origin and consequences of dysfunctional beliefs in anorexia nervosa and
bulimia nervosa. Journal of Cognitive Psychotherapy, 12, 213-230.
Cooper Z, Cooper PJ, & Fairburn CG (1989). The validity of the Eating Disorder Examination and its subscales. British
Journal of Psychiatry, 154, 807-812.
Crick NR, & Dodge KA (1994). A review and reformulation of social nformation prosessing mechanisms in children’s social
adjustment. Psychological Bulletin, 113, 487-496.
Cross LW (1993). Body and self in feminine development: Implications for eating disorders and delicate self-mutilation.
Bulletin of the Menninger Clinic, 57, 41-68.
Currin L, Schmidt U, Treasure J, & Jick H (2005). Time trends in eating disorder incidence. British Journal of Psychiatry,
186, 132-135.
Dare C, LeGrange D, Eisler I, & Rutherford J (1994). Redefining the psychosomatic family: family process of 26 eating
disorder families. International Journal of Eating Disorders, 16, 211-226.
Davis C, Katzman DK, Kaptein S, Kirsh C, Brewer H, Kalmbach K, Olmsted MP, Woodside DB & Kaplan AS (1997). The
prevalence of high-level exercise in the eating disorders: etiological implications. Comprehensive Psychiatry, 38, 321-326.
DeGroot, J & Rodin G (1998). Coming alive: the psychotherapeutic treatment of patients with eating disorders. Canadian
Journal of Psychiatry, 43, 359-366.
De Ruiter C, & Brosschot JF (1994). The emotional Stroop interference effect in anxiety: attentional bias or cognitive
avoidance? Behaviour Research and Therapy, 32 (3), 315-319.
DeVeaugh-Geiss J (1991). Pharmacological treatment of obsessive-compulsive disorder. In J.Zohan, T.Insel, & S.
Rasmussen (Eds.), The psychobiology of obsessive-compulsive disorder (pp. 187-207). New York: Springer.
Dodin V, & Nandrino JL (2003). Cognitive processing of anorexic patients in recognition tasks: An event-related potentials
study. International Journal of Eating Disorders, 33 (3), 299-307.
Esplen MJ, Garfinkel P, & Gallop R (2000). Relationship between self-soothing, aloneness, and evocative memory in bulimia
nervosa. International Journal of Eating Disorders, 27, 96-100.
Everill J, & Waller G (1995). Dissociation and bulimia: Research and theory. European Eating Disorders Review, 3, 129147.
Fahy T, & Eisler I (1993) Impulsivity and eating disorders. British Journal of Psychiatry, 162, 193-197.
Fairburn CG (1997). Eating disorders. In D.M. Clark & C.G. Fairburn (Eds.), Cognitive behaviour therapy, Oxford
University press, New York.
Fairburn CG, Cooper Z, Doll HA & Welch SL (1999) Risk factors for anorexia nervosa: Three integrated case-control
comparison. Archives of General Psychiatry, 56, 468-476.
Fairburn CG, Cooper Z & Shafran R (2003). Cognitive behaviour therapy for eating disorders: A ‘transdiagnostic’ theory and
treatment. Behaviour Research and Therapy, 41, 509-528.
Fairburn CG, Cowen PJ, Harrison PJ. (1999). Twin studies and the etiology of eating disorders. International Journal of
Eating Disorders, 26(4), 349-58.
Fairburn CG, & Harrison PJ. (2003). Eating disorders. Lancet, 361 (9355), 407-16.
Fairburn CG, Shafran R & Cooper Z (1998). A cognitive behavioural theory of anorexia nervosa. Behaviour Research and
Therapy, 37, 1-13.
Fairburn CG, Welch SL, Doll HA, Davies BA & O'Connor ME (1997). Risk factors for bulimia nervosa. A community-based
case-control study. Archives of General Psychiatry, 54, 509-517.
Farmer RF, Nash HM, & Field CE (2002). Disordered eating behaviours and reward sensitivity. Journal of Behavior
Therapy and Experimental Psychiatry, 32, 211-219.
Fassino S, Piero A, Abbate Daga G, Leombruni P, Mortara P, & Rovera GG (2002). Attentional biases and frontal
functioning in Anorexia Nervosa. International Journal of Eating Disorders, 31, 274-283.
Ferraro FR, Wonderlich S, & Jocic Z (1997). Performance Variability as a New Theoretical Mechanism regarding eating
disorders an cognitive processing. Journal of Clinical Psychology, 53 (2), 117-121.
Festinger L (1954). A theory of social comparison processes. Human Relations, 7, 117-140.
Fisher S, Smith GT, Anderson KG (2003). Clarifying the orle of impulsivity in bulimia nervosa. International Journal of
Eating Disorders, 33, 406-411.
Flament MF, Godart NT, Fermanian J, & Jeammet P (2002). Predictive factors of social disablility in patients with eating
disorders. Eating and Weight Disorders, 6, 99-107.
Foa EB, Feske U, Murdock TB, Kozak MJ, & McCarthy PR (1991). Processing of threat-related information in rape victims.
Journal of Abnormal Psychology, 100, 156-162.
Frantz-Fox C (1981). Neuropsychological correlates of anorexia nervosa. International Journal of Psychiatry in Medicine, 11,
285-290.
Freeman R, Touyz S, Sara G, Rennie Ch, Gordon E, & Beumont P (1991). In the eye of the beholder: Processing body
shape information in anorexic and bulimic patients. International Journal of Eating Disorders, 6, 709-714.
Frost RO, Marten P, Lahart C, & Rosenblate R (1990). The dimensions of perfectionism. Cognitive Therapy and Research,
14, 449-468.
Garner DM, & Bemis KM (1982). A cognitve-behavioural approach to anorexia nervosa. Cognitive Therapy and Research,
6, 123-150.
Garner DM, & Garfinkel PE (1980). Socio-cultural factors in the development of anorexia nervosa. Psychological Medicine,
10, 647-656.
Garner DM, Olmstead MP, & Polivy J (1983). Development and validation of a multidimensional Eating Disorder Inventory
for anorexia nervosa and bulimia nervosa. International Journal of Eating Disorders, 2, 15-24.
Garner DM, Olmstead MP, Polivy J, & Garfinkel PE (1984). Comparison between weight-preoccupied woman and anorexia
nervosa. Psychosomatic Medicine, 46, 255-266.
Gilbert P (1997). The evolution of social attractiveness and its role in shame, humiliation, guilt and therapy. British Journal of
Medical Psychology, 70, 113-147.
Gilbert N, & Meyer C (2005). Fear of negative evaluation and the development of eating psychopathology: a longitudinal
study among nonclinical women. International Journal of Eating Disorders, 37, 4, 307-312.
Gillberg I, Rastam M & Gillberg C. (1995) Anorexia nervosa 6 years after onset: Part I. Personality disorders. Comprehensive
Psychiatry, 36 (I), 61-69.
Gilligan C (1993). In a Different Voice: Psychological Theory and Women’s Development. 2nd edn. Havard University
Press: Cambridge, MA.
Glassman EJ (1988). Development of a self-report measure of soothing receptivity. Unpublished doctoral dissertation.
Toronto: York University (GENERIC).
Goldbloom DS, Garfinkel PE, & Shaw BF (1991). Biochemical aspects of bulimia nervosa. Journal of Psychosomatic
Research, 35, 11-22.
Goldner EM, Cockell SJ & Srikameswaran S. (2002) Perfectionism and eating disorders. In P.L. Hewitt & G.L. Flett (Eds),
Perfectionism: Theory, Research and Interventions. APA Books: Washington DC.
Goldner EM, Srikameswara S, Schroeder ML, Livesley WJ, & Birmingham CL (1999).
personality pathology in patients with eating disorders. Psychiatric Research, 85, 151-159.
Dimensional assessment of
Gray JA (1987). The psychology of fear and stress (2nd ed). New York: Cambridge University Press.
Green MW, Elliman NA, & Rogers PJ (1997). Impaired cognitive performance in dieters: Failure of attentional focus or
resource capacity limitation? British Journal of Health Psychology, 2, 259-267.
Green MW, Elliman NA, Wakeling A, & Rogers PJ (1996). Cognitive functioning, weight change and therapy in anorexia
nervosa. Journal of Psychiatric Research, 30, 401-410.
Green MW, & Rogers PJ (1995). Impaired cognitive functioning during spontaneous dieting. Psychological Medicine, 25,
1003-1010.
Green MW, & Rogers PJ (1998). Impairments in working memory associated with spontaneous dieting behaviour.
Psychological Medicine, 28, 1063-1070.
Green MW, Rogers PJ, Elliman NA, & Gatenby SJ (1994). Impairment of cognitive performance associated with dieting and
high levels of dietary restraint. Physiology and Behavior, 55, 447-452.
Gregory RL (1998). OI_MRKOI_MRKEye and brain. The psychology of seeing. Oxford: Oxford University Press.
Grilo CM (2004). Subtyping female adolescent psychiatric inpatients with features of eating disorders along dietary restraint
and negative affect dimensions. Behaviour Research and Therapy, 42, 67-78.
Grilo CM, Sanislow CA, Shea MT, Skodol AE, Stout RL, Pagano ME, Yen S, & McGlashan TH (2003a). The natural course
of bulimia nervosa and eating disorder not otherwise specified is not influenced by personality disorders. International
Journal of Eating Disorders, 34, 319-330.
Grilo CM, Sanislow CA, Skodol AE, Gunderson JG, Stout RL, Shea MT, Zanarini MC, Bender DS, Morey LC, Dyck IR, &
McGlashan TH (2003b). Do eating disorders co-occur with personality disorders? Comparison Groups Matter, International
Journal of Eating Disorders, 33, 155-164.
Groesz LM, Levine MP, & Murnen SK (2002). The effect of experimental presentation f thin media images on body
satisfaction: A meta-analytic review. International Journal of Eating Disorders, 31, 1-15.
Halmi KA (1999). Eating disorders: Anorexia nervosa, bulimia nervosa and obesity. In K.E. Hales, S.C. Yodofsky, & J.
Talbot (Eds.), American psychiatric press textbook of psychiatry (3rd ed., pp. 983-1002). Washington, DC: American
Psychiatric Association.
Halmi K, Goldberg S, Eckert E, Casper R & Davis J. (1977) Pretreatment evaluation in anorexia nervosa. In R.A. Vigersky
(Ed.), Anorexia Nervosa. New York: Raven Press.
Halmi KA, Sunday SR, Klump KL, Strober M, Leckman JF, Fichter M, Kaplan A, Woodsid B, Treasure J, Berrettini WH,
Shabboat MA, Bulik C, & Kaye WH (2003). Obsessions and compulsions in Anorexia Nervosa Subtypes. International
Journal of Eating Disorders, 308-319.
Halmi KA, Sunday SR, Strober M, Kaplan A, Woodside DB, Fichter M, Treasure J, Berrettini WH, & Kay WH (2000).
Perfectionism in anorexia nervosa: variation by clinical subtype, obsessionality, and pathologic eating behaviour. American
Journal of Psychiatry , 157(11), 1799-1805.
Hamsher K, Halmi KA, & Benton AL (1981). Prediction of outcome in anorexia nervosa from neuro- psychological status.
Psychiatry Research, 4, 79-88.
Hargreaves D & Tiggemann M (2002). The role of appearance schematicity in the development of adolescent body
dissatisfaction. Cognitive Therapy and Research, 26 (6), 691-700.
Haudek C, Rorty M, & Henker B (1999). The role of ethnicity and parental bonding in the eating and weight concerns of
Asian-American and Caucasian college women. International Journal of Eating Disorders, 25, 425-433.
Heatherton TF, & Baumeister RF (1991). Binge eating as escape from self-awareness. Psychological Bulletin, 110, 86-108.
Hewitt PL, & Flett GL (1991). Perfectionism in the self and social contexts: Conceptualization, assessment, and association
with psychopathology. Journal of Personality and Social Psychology, 60, 456-470.
Hewitt PL, & Flett GL (1993). Dimensions of perfectionism, daily stress, and depression: A tst of the specific vulnerability
hypothesis. Journal of Abnormal Psychology, 102, 58-65.
Hewitt PL, Flett GL, Besser A, Sherry SB, & McGee B (2002). Perfectionism is multidimensional: a reply to Shafran, Cooper
and Fairburn. Behaviour Research and Therapy, 41, 1221-1236.
Hewitt PL, & Flett GL, & Edinger E (1995). Perfectionism traits and perfectionistic self-presentation in eating disorder
attitudes, characteristics, and symptoms. International Journal of Eating Disorders, 18, 317-326.
Hewitt PL, Flett GL, & Turnbull-Donovan W (1992). Perfectionism and suicide potential. British Journal of Clinical
Psychology, 31, 181-190.
Hilbert A, Tuschen-Caffier B, & Vögele C (2002). Effects of prolonged and repeated body image exposure in binge-eating
disorder. Journal of Psychosomatic Research, 52, 137-144.
Hoek HW, & van Hoeken D (2003). Review of the prevalence and incidence of eating disorders. American Journal of
Psychiatry, 152, 1272-1278.
Holland AJ, Hall A, Murray R, Russell GF & Crisp AH (1984). Anorexia nervosa: a study of 34 twin pairs and one set of
triplets. The British Journal of Psychiatry, 145, 414-419.
Holland AJ, Sicotte N & Treasure J (1988). Anorexia nervosa: evidence for a genetic basis. Journal of Psychosomatic
Research, 32 (6), 561-571.
Horne RL, Ferguson JM, Pope HJ, Hudson JI, Lineberry CG, Ascher J, Cato A (1988). Treatment of bulimia with bupropion:
a multicenter controlled trial. Journal of Clinical Psychiatry, 49, 262-266.
Hornyak LM, Baker EK (1989). Experiential Therapies for Eating Disorders. New York, Guilford Press.
Howard CE, & Porzelius LK (1999). The role of dieting in Binge Eating Disorder: Etiology and treatment implications.
Clinical Psycholgy Review, 19(1), 25-44.
Hsu LKG (1990). Eating Disorders. New York, Guilford Press.
Hsu LK, Kaye W & Weltzin T (1993). Are the eating disorders related to obsessive compulsive disorder? International
Journal of Eating Disorders, 14, 305-318.
Humphrey LL (1989). Observed family interactions among subtypes of eating disorders using struvtural analysis of social
behaviour. Journal of Consulting and Clinical Psychology, 57, 206-214.
Hunter EC, & O’Connor RC (2003). Hopelessness and future thinking in parasuicide: The role of perfectionism. British
Journal of Clinical Psychology, 42, 355-365.
Ilkjaer K, Kortegaard L, Hoerder K, Joergensen J, Kyvik K, & Gillberg C (2004). Personality Disorders in a Total Population
Twin Cohort with Eating Disorders. Comprehensive Psychiatry, 45, 261-267.
Inceoglu I, Franzen U, Backmund H & Gerlinghoff M. (2000) Personality disorders in patients in a day-treatment programme
for eating disorders. European Eating Disorders Review, 8, 67-72.
Jacobson E (1964). The self and the object world. New York: International Universities Press.
Jansen A, Nederkoorn C & Mulkens S (2005). Selective visual attention for ugly and beautiful body parts in eating disorders.
Behaviour Research and Therapy, 43, 2, 183-196.
Jansen A, Huygens K, & Tenney N (1998). No evidence for a selective processing of subliminally presented body words in
restrained eaters. International Journal of Eating Disorders, 24, 435-438.
Jimmerson DC, Lesem MD, Kate WH, & Brewerton TD (1992). Low serotonin and dopamine metabolite concentrations in
cerebrospinal fluid from bulimic patients with frequent binge episodes. Archives of General Psychiatry, 49, 132-138.
Johnson C, Tobin DL, Dennis A (1990). Differences in treatment outcome between borderline and non-borderline bulimics
at one-year follow-up. International Journal of Eating Disorders, 9, 616-627.
Jones N, & Rogers PJ (2003). Preoccupation, Food, and Failure: An Investigation of cognitive performance deficits in
Dieters. International Journal of Eating Disorders, 33, 185-192.
Kahan D, Polivy J, & Herman CP (2003). Conformity and dietary disinhibition: a tst of the ego-strenght model of selfregulation. International Journal of Eating Disorders, 33, 165-171.
Karwautz A, Rabe-Hesketh S, Hu X, Zhao J, Sham P, Collier DA & Treasure JL (2001) Individual-specific risk factors for
anorexia nervosa: A pilot study using a discordant sister-pair design. Psychological Medicine, 31, 317-329.
Karwautz A, Troop NA, Rabe-Hesketh S, Collier DA, & Treasure JL (2003).
dimensions in anorexia nervosa. Journal of Personality Disorders, 17 (1), 73-85.
Personality disorders and personality
Katzman AS, & Wolchik SA (1984). Bulimia and binge eating in college women: A comparison of personality and
behavioural characteristics. Journal of Consulting and Clinical Psychology, 52, 423-428.
Katzman MA, & Lee S (1997). Beyond body image: the integration of feminist and transcultural the-ories in the
understanding of self-starvation. International Journal of Eating Disorders, 22, 385-394.
Kay WH, Bastiani AM, & Moss H (1995). Cognitive style of patients with anorexia nervosa and bulimia nervosa.
International Journal of Eating Disorders, 18, 287-290.
Kaye WH, Frank GK, Meltzer CC, Price JC, McConaha CW, Crossan PJ, Klump KL & Rhodes L (2001). Altered serotonin
2A receptor activity in women who have recovered from bulimia nervosa. American Journal of Psychiatry, 158 (7), 11521155.
Kaye WH, Gwirtsman HE, George DT & Ebert MH (1991). Altered serotonin activity in anorexia nervosa after long-term
weight restoration. Archives of General Psychiatry , 48, 556-562.
Kaye WH, Lilenfeld LR, Berrettini WH, Strober M, Devlin B, Klump KL, Goldman D, Bulik CM, Halmi KA, Fichter MM,
Kaplan A, Woodside DB, Treasure J, Plotnicov KH, Pollice C, Rao R, McConaha CW. (2000). A search for susceptibility
loci for anorexia nervosa: methods and sample description. Biol Psychiatry, 47(9):794-803.
Kaye WH, Weltzin TE, Hsu LK, Bulik CM: An open trial of fluoxetine in patients with an-orexia nervosa. J Clin Psychiatry
1991; 52:464-471.
Keel PK, & Klump KL (2003). Are eating disorders culture-bound syndromes? Implications for conceptualizing their
etiology. Psychological Bulletin, 129, 747-769.
Kendler KS, Gardner CO, & Prescott CA (1998). A population-based twin study of self-esteem and gender. Psychological
Medicine, 28, 1403-1409.
Key A, George CL, Beattie D, Stammers K, Lacey H, & Waller G (2002). Body image treatment within an inpatient program
for anorexia nervosa: The role of mirror exposure in the desensitization process. International Journal of Eating Disorders,
31, 185-190.
Khandelwal S, & Saxena S (1990). Anorexia nervosa in people of Asian extraction. Britisch Journal of Psychiatry, 157, 783784.
Kiemle, G., Slade, P.D. & Dewey, M.E. (1987) Factors associated with abnormal eating attitudes and behaviors: Screening
individuals at risk of developing an eating disorder. International Journal of Eating Disorders, 6, 713-724.
Kingston K, Szmukler G, Andrewes D, Tress B, Desmond P (1996). Neuropsychological and struc-tural brain changes in
anorexia nervosa before and after refeeding. Psychological Medicine, 26, 15-28.
Klump KL, Bulik CM, Pollice C, Halmi KA., Fichter MM, Berrettini WH, Devlin B, Strober M, Kaplan A, Woodside DB,
Treasure J, Shabbout, M., Lilenfeld, L.R., & Plotnicov, K.H. (2000). Temperament and character in women with anorexia
nervosa. The Journal of Nervous and Mental Disease, 188 (9), 559-567.
Klump KL, Miller KB, Keel PK, McGue M & Iacono, WG (2001). Genetic and environmental influences on anorexia
nervosa syndromes in a population-based twin sample. Psychological Medicine, 31, 737-740.
Kortegaard LS, Hoerder K, Joergensen J, Gillberg C, & Kybik KO (2001). A preliminary population-based twin study of
self-reported eating disorder. Psychological Medicine, 31, 737-740.
Kucharska-Pietura K, Nikolaou V, Masiak M, & Treasure J (2004). The recognition of emotion in the faces and voice of
anorexia nervosa. International Journal of Eating Disorders, 35, 42-47.
Kuehnel RH, & Wadden TA (1994). Binge Eating Disorder, weight cycling, and psychopathology. International Journal of
Eating Disorders, 15 (4), 321-329.
Lacey JH (1986). Pathogenesis. In L.J. Downey & J.C. Malkin (Eds.), Current approaches: Bulimia nervosa (pp. 17-26).
Southampton: Duphar.
Lacey JH (1993) Self-damaging and addictive behaviour in bulimia nervosa. British Journal of Psychiatry, 163, 190-194.
Lacey JH, & Read T (1993) Multi-impulsive bulimia: description of an inpatient eclectic treatment programme and a pilot
follow-up study of its efficacy. European Eating Disorders Review, I, 22-31.
Lauer CJ, Gorzewski B, Gerlinghoff M, Backmund H, & Zihl, J. (1999). Neuropsychological assessments before and after
treatment in patients with anorexia nervosa and bulimia nervosa. Journal of Psychiatric Research, 33, 129-138.
Lazarus RS (1999). Stress and Emotion: A New Synthesis. London: Free Association Books.
Leckman JF, Zhang H, Alsobrook JP, & Pauls DL (in press). Symptom dimensions in obsessive-compulsive disorder:
Toward quantitative phenotypes. American Journal of Genetics.
Lee S (1996). Reconsidering the status of anorexia nervosa as a western culture-bound syndrome. Social Science and
Medicine, 42, 21-34.
Lee S, Ho P., & Hsu LKG.(1993). Fat phobic and non-fat phobic anorexia nervosa: A comparative study of 70 Chinese
patients in Hong Kong. Psychological Medicine, 23, 999-1017.
Leung N, Waller G, & Thomas G (1999). Core beliefs in anorexic and bulimic women. Journal of Nervous and Mental
Disease, 187, 736-741.
Le Grange D, Telch C & Tibbs J (1998). Eating attitudes and behaviours in 1435 South African Caucasian and NonCaucasian college students. American Journal of Psychiatry, 155, 250-254.
Lilenfeld LR, Devlin B, Bulik CM, Strober M, Berrettini W, Fichter M, Goldman D, Halmi K, Kaplan AS, Treasure J,
Woodside DB, & Kaye WH (2000). Deriving behavioural phenotypes in an international multicenter genetic study of eating
disorders. Psychological Medicine, 30, 1399-1410.
Lilenfeld LR, Kaye WH, Greeno CG, Merikangas KR, Plotnicov K, Pollice C, Rao R, Strober M, Bulik CM, Nagy L. (1998).
A controlled family study of anorexia nervosa and bulimia nervosa: psychiatric disorders in first-degree relatives and effects of
proband comorbidity. Archives of General Psychiatry, 55(7):603-10.
Lilenfeld LR., Stein D, Bulik CM, Strober M, Plotnicov K, Pollice C, Rao R, Merikangas KR, Nagy L, Kaye WH (2000).
Personality traits among currently eating disordered, recovered and never ill first-degree female relatives of bulimic and
control women. Psychological Medicine,30, 1399-1410.
Long CG, Hinton C, & Gillepsie NK (1994). Selective processing of food and body size words: application of the Stroop
test with obese restrained eaters, anorexics, and normals. International Journal of Eating Disorders, 15, 279-283.
Löwe B, Zipfel S, Buchholz C, Dupont Y, Reas DL & Herzog, W (2001). Long-term outcome of anorexia nervosa in a
prospective 21-year follow-up study. Psychological Medicine, 31, 881-890.
MacLeod C (1999). Anxiety and anxiety disorders. In T.Dalgleish & M. Power (Eds.), Handbook of cognition and emotion
(pp. 447-478). Chichester, UK: Wiley.
MacLeod C, & Hagan R (1992). Individual differences in the selective processing of threatening information, and emotional
responses to a stressful life event. Behaviour Research and Therapy, 30, 151-161.
Major B, Testa M, & Blysma WH (1991). Responses to upward and downward social comparisons: the impact of esteemrelevance and perceived control. In J. Suls & T.A. Ashby (Eds.), Social comparison: Contemporary theory and research (pp.
237-260). Hillsdale, NJ: Erlbaum.
Mathias JL, & Kent PS (1998). Neuropsychological consequences of extreme weight loss and dietary restriction in patients
with anorexia nervosa. Journal of Clinical and Experimental Neuropsychology, 20, 548-564.
Matsunaga H, Kaye W & McConaha S (2000) Personality disorders among subjects recovered from eating disorders.
International Journal of Eating Disorders, 27, 353-357.
Matsunaga H, Kaye WH, McConaha C, Plotnicov K, Pollice C, & Rao R (2000). Personality disorders among subjects
recovered from eating disorders. International Journal of Eating Disorders, 27, 353-357.
Matsunaga H, Miyaga A, Iwasaki H, Matsui T, Fujimoto K, & Kiriike N (1999). A comparison of clinical features among
Japanese eating-disordered women with obsessive-compulsive disorder. Comparative Psychiatry, 40, 337-342.
Mazure CN, Halmi KA, Sunday SR, Romano S, & Einhorn A (1994). The Yale-Brown Cornell Eating Disorder Scale:
Development, use, reliability and validity. Journal of Psychiatric Research, 28, 425-445.
McCabe MP, & Ricciardelli LA (2005). A prospective study of pressures from parents, peers, and the media on extreme
weight change behaviors among adolescent boys and girls. Behaviour Research and Therapy, 43, 653-668.
McManus F, & Waller G (1995). A functional analysis of binge-eating. Clinical Psychology Review, 15, 845-865.
McManus F, Waller G, & Chadwick P (1996). Biases in the processing of different forms of threat in bulimic and
comparison women. Journal of Nervous and Mental Disease, 184, 547-554.
Mela DJ, & Rogers PJ (1998). Food, eating and obesity: The psychobiological basis of appetite and weight control, London:
Chapman and Hall.
Meyer C, & Waller G (1999). The impact of emotion upon eating behavior: the role of subliminal visual processing of threat
cues. International Journal of Eating Disorders, 25, 319-326.
Meyer C, & Waller G (2000). Subliminal activation of abandonment- and eating-related schemata: relationship with eating
disordered attitudes in a nonclinical population. International Journal of Eating Disorders, 27, 328-334.
Meyer C, Waller G, & Watson D (2000). Cognitive avoidance and bulimic psychopathology: the relevance of temporal
factors in a nonclinical population. International Journal of Eating Disorders, 27, 405-410.
Miller SB (1996). Shame in context. London The Analytic Press.
Milligan RJ & Waller G (2000) Anger and bulimic psychopathology among nonclinical women. International Journal of
Eating Disorders, 28, 446-450.
Mogg K, Bradley BP, Hyare H, & Lee S (1997). Selective attention to food-related stimuli in hunger: are attentional biases
specific to emotional and psychopathological state, or are they also found in normal drive states? Behaviour Research and
Therapy, 36, 227-237.
Moser DJ, Benjamin ML, Bayless JD, BD, McDowell, Paulsen JS, Bowers WA, Arndt S, & Anderson AE (2003).
Neuropsychological functioning pretreatment and posttreatment in an inpatient eating disorders program. International
Journal of Eating Disorders, 33, 64-70.
Muller B, Herpertz S, Heussen N, Neudrorfl A, Wewetzer C, Remschmidt H, & Herpertz-Dahlmann B (2000). Personality
disorders and psychiatric morbidity in adolescent anorexia nervosa. Results of a prospective 10 year catmnesis. Z Kinder
Jungendpsychiatr Psycother, 28, 81-91.
Murphy F, Troop NA & Treasure JL (2000) Differential environmental factors in anorexia nervosa: A sibling-pair study.
British Journal of Clinical Psychology, 39, 193-203.
Neckowitz P, & Morrison TL (1991) Interactional coping strategies of normal-weight bulimic women in intimate and
nonintimate stressful situations. Psychological Reports, 69, 1167-1175.
Nasser MA, Katzman MA & Gordon RA (2001). Eating Disorders and Cultures in transition. Taylor & Francis: Andover,
Hants, pp 201.
Newton JR, Freeman CT, & Munro J (1993). Impulsivity and dyscontrol in bulimia nervosa: Is impulsivity an independent
phenomenon or a marker of severity? Acta Psychiatrica Scandinavia, 87, 389-394.
Ogden J, & Steward J (2000). The role of the mother-daugher relationship in explaining weight concern. International
Journal of Eating Disorders, 28, 78-83.
Oliver KG, & Huon GF (2001). Eating-related thought suppression in high and low disinhibitors. International Journal of
Eating Disorders, 30, 329-337.
Oyewumi LK & Kazarian SS (1992a). Abnormal eating attitudes among a group of Nigerian youths: I. Bulimic behaviour.
East African Medical Journal, 69, 663-666.
Oyewumi LK & Kazarian SS (1992b). Abnormal eating attitudes among a group of Nigerian youths: II. Anorexic behaviour.
East African Medical Journal, 69, 667-669.
Patch AR (1984). Reflections on perfection. American Psychologist, 39, 386-390.
Patton CJ (1992). Fear of abandonment and binge eating: A subliminal psychodynamic activation investigation. Journal of
Nervous and Mental Disease, 180, 484-490.
Pendleton-Jones B, Duncan CC, Brouwers P, & Mirsky AF (1991). Cognition in eating disorders. Journal of Clinical and
Experimental Neuropsychology, 13, 711-728.
Perpina C, Hemsley Treasure J, & De Silva P (1993). Is the selective information processing of food and body words specific
to patients with eating disorders? International Journal of Eating Disorders, 14, 359-366.
personality. Psychol Rep., 84(2):689-96.
Pia C, & Toro J (1999) Anorexia nervosa in a Spanish adolescent sample: An 8-year longitudinal study. Acta Psychiatrica
Scandinavica, 100, 441-446.
Pike KM, & Rodin J (1991). Mothers, daughters, and disordered eating. Journal of Abnormal Psychology, 100, 198-204.
Piran N, Lerner P, Garfinkel P, Kennedy S & Brouillette C (1988) Personality disorders in anorexic patients. International
Journal of Eating Disorders, 7, 589-599.
Podar I, Hannus A, & Allik J (1999). Personality and affectivity characteristics associated with eating disorders: a comparison
of eating disordered, weight-preoccupied, and normal samples. Journal of Personality Assessment, 73, 133-147.
Polivy J, & Herman CP (1999). Distress and eating: why do dieters overeat? International Journal of Eating Disorders, 26,
153-164.
Polivy J, & Herman CP (2000). The false-hope syndrome: Unfulfilled expectations of self-change. Current Directions in
Psychological Science, 9, 128-131.
Polivy J, & Herman CP (2002). Causes of eating disorders. Annual Review of Psychology, 53, 187-213.
Pryor T, & Wiederman MW (1996). Measurement of nonclinical personality characteristics of women with anorexia nervosa
and bulimia nervosa. Journal of Personality Assessment, 67, 414-421.
Purdon C, Antony MM, & Swinson RP (1999). Psychometric properties of the Frost Multidimensional Perfectionism Scale
in a clinical anxiety disorders sample. Journal of Clinical Psychology, 55, 1271-1286.
Rachman S (1998). The nature of anxiety. In S. Rachman (Ed.), Anxiety (pp. 1-26). Hve, UK: Psychology Press.
Rastam M (1992) Anorexia nervosa in 51 Swedish adolescents: Prernorbid problems and comorbid- ity. Journal of the
American Academy of Child and Adolescent Psychiatry, 31, 819-829.
Reichborn-Kjennerud T, Bulik CM, Tambs K, & Harris JR (2004). Genetic and Environmental influences on binge eating in
the absence of compensatory behaviours: a population-based twin study. International Journal of Eating Disorders, 36, 307314.
Rieger E, Schotte DE, Touyz SW, Beumont PJV, Griffiths R, & Russel J (1998). Attentional biases in eating disorders: A
visual probe detection procedure. International Journal of Eating Disorders, 23, 199-205.
Rogers PJ, & Green MW (1993). Dieting, dietary restraint and cognitive performance. British Journal of Clinical Psychology,
32, 113-116.
Root MPP, & Fallon P (1989). Treating the victimized bulimic. Journal of Interpersonal Violence, 4, 90-100.
Rorty M, & Yager J (1993). Why and how do women recover from bulimia nervosa? Int J Eat Disord, 14:249-260.
Rorty M, Yager J, Buckwalter JG, Rossotto E & Guthrie D (2000a) Development and validation of the Parental Intrusiveness
Rating Scale among bulimic and comparison women. International Journal of Eating Disorders, 28, 188-201.
Rorty M, Yager J, Rossotto E & Buckwalter G (2000b) Parental intrusiveness in adolescence recalled by women with a history
of bulimia nervosa and comparison women. International Journal of Eating Disorders, 28, 202-208.
Rosen JC (1990). Body image disturbances in eating disorders. In T.F. Cash, & T. Pruzinsky (Eds.), Body images.
Development, deviance and change (pp.190-214). New York: The Guilford Press.
Rosen JC, & Ramirez T (1998). A comparison of eating disorders and body dysmorphic disorder on body image and
psychological adjustment. Journal of Psychosomatic Research, 44, 441-449.
Rosen JC, Tracy B, & Howell D (1990). Life stress, psychological symptoms and weight reducing behavior in adolescent
girls: A prospective analysis. International Journal of Eating Disorders, 9, 17-26.
Rosenvinge JH, Martinussen M, & Ostensen E (2000). The comorbidity of eating disorders and personality disorders: A
meta analytical review of studies published between 1983 and 1998. Eating and Weight Disorders, 5, 51-62.
Ruggiero GM, Levi D, Ciuna A, & Sassaroli S (2003). Stress situation reveals an association between perfectionism and drive
for thinness. International Journal of Eating Disorders, 34, 220-226.
Sanftner JL, Barlow DH, Marschall DE & Tangney JP (1995). The relation of shame and guilt to eating disorder
symptomatology. Journal of Social and Clinical Psychology, 14, 315-324.
Sanftner JL, & Crowther JH (1998) Variability in self-esteem, moods, shame and guilt in women who binge. International
Journal of Eating Disorders, 23, 391-397.
Sassaroli S, & Ruggiero GM (2002). I costrutti dell’ansia: obbligo di controllo, perfezionismo patologico, pensiero
catastrofico, autovalutazione negative e intolleranza dell’ incertezza. (The constructs of anxiety: need for control,
perfectionism, catastrophic thought, negative self-evaluation, and intolerance of uncertainty) Psicoterapia Cognitiva e
Comprtamentale, 8, 45-60.
Saxena S, Brody AL, Schwartz JM, & Baxter LR (1998). Neuroimaging and frontal-subcortical circuitry in obsessivecompulsive disorder. British Journal of Psychiatry, 173, 26-37.
Schmidt U, Tiller J, Treasure J (1993b). Self-treatment of bulimia nervosa: a pilot study. International Journal of Eating
Disorder, 13:273-277.
Schmidt UH, Humfress H & Treasure JL (1997a) The role of general family environment and sexual and physical abuse in
the origins of eating disorders. European Eating Disorders Review, 5,184-207.
Schmidt UH, Jiwany A & Treasure JL (1993b) A controlled study of alexithymia in eating disorders. Comprehensive
Psychiatry, 34, 54-58.
Schmidt UH, Tiller JM, Andrews B, Blanchard M & Treasure JL (1997b) Is there a specific trauma precipitating onset of
anorexia nervosa? Psychological Medicine, 27, 523-530.
Schmidt UH, Tiller JM & Treasure JL (1993c) Setting the scene for eating disorders: Childhood care, classification and course
of illness. Psychological Medicine, 23, 663-672.
Schmidt UH, Troop NA & Treasure JL (1999) Stress and the onset of eating disorders: Correcting an "age-old" myth.
International Journal of Eating Disorders, 25, 83-88.
Serpell L, Livingstone A, Lask B & Neiderman M (2002) Anorexia nervosa: Obsessive compulsive disorder, obsessive
compulsive personality or neither. Clinical Psychology Review, 22, 647-669.
Serpell L, Neiderman M, Bird E, Rashid Z, Roberts V & Lask B (submitted) The shape and weight-based self-esteem
inventory (SAWBS) in Adolescent Girls with Eating Disorders and Adolescent Controls.
Shafran R, Cooper Z, Fairburn CG (2002). Clinical perfectionism: a cognitive-behavioural analysis. Behaviour Research and
Therapy, 40, 773-791.
Shafran R, Fairburn CG, Robinson P & Lask B (2003). Body checking and its avoidance in eating disorders. International
Journal of Eating Disorders, 35 (1), 93-101.
Shaw HE, Stice E, & Springer DW (2004). Perfectionism, Body Dissatisfaction, and Self-esteem in Predicting bulimic
symptomatology: lack of replication. International Journal of eating Disorders, 36, 41-47.
Shepherd H & Ricciardelli LA (1998) Test of Stice's dual pathway model: Dietary restraint and negative affect as mediators of
bulimic behaviour. Behaviour, Research and Therapy, 36, 345- 352.
Sherry SB, Hewitt PL, Besser A, McGee BJ, & Flett GL (2004). Self-oriented and socially prescribed perfectionism in the
Eating Disorder Inventory perfectionism subscale. International Journal of Eating Disorders, 35, 69-79.
Siegle GJ, Granholm E, Ingram RE, & Matt GE (2001). Pupillary and reaction time measures of sustained processing of
negative information in depression. Society of Biological Psychiatry, 49, 624-636.
Skodol A, Oldham J, Hyler S, Kellman HD, Doidge N & Davies M (1993) Comorbidity of DSM-III-R eating disorders and
personality disorders. International Journal of Eating Disorders, 14,403-416.
Slade PD (1982) Towards a functional analysis of anorexia nervosa and bulimia nervosa. British Journal of Clinical
Psychology, 21, 167-179.
Slade PD, Dewey ME, Kiemle G & Newton T (1990) Update on SCANS: A screening instrument for identifying individuals
at risk of developing an eating disorder. International Journal of Eating Disorders, 9, 583-584.
Slochower JA (1983). Excessive eating: The role of emotions and environment. New York: Human Sciences Press.
Slochower JA, Kaplan SP & Mann L (1981). The effects of life stress and weight on mood and eating. Appetite, 2, 115-125.
Smeets MAM, Ingleby JD, Hoek HW, & Panhuysen GEM (1999). Body size perception in anorexia nervosa: A signal
detection approach. Journal of Psychosomatic Research, 46(5), 465-477.
Smeets MAM, Smit F, Panhuysen GEM, & Ingleby JD (1998). Body size perception index: Benefits, pitfalls, ideas. Journal
of Psychosomatic Research, 44, 457-464.
Sohlberg S, & Strober M (1994). Personality in anorexia nervosa: An update and a theoretical integration. Acta Psychiatrica
Scandinavica, 89 (suppl. 378), 1-15.
Soukup VM, Beiler ME & Terrell F (1990) Stress, coping style and problem-solving ability among eating disordered
inpatients. Journal of Clinical Psychology, 46, 592-599.
Spoont MR (1992). Modulatory role of serotonin in neural information processing: Implications for human
psychopathology. Psychological Bulletin, 112, 330-350.
Srinivasagam NM, Kaye WH, Plotnikov KH, Greeno C, Weltzin TE & Rao R (1995) Persistent perfectionism, symmetry and
exactness after long term recovery from anorexia nervosa. American Journal of Psychiatry, 152, 1630-1634.
Steiger H, & Séguin JR (1999). Eating disorders : anorexia and bulimia nervosa. In: T. Millon, & P.H. Blaney (Eds.), Oxford
textbook of psychopathology (pp. 365-389). Toronto: Oxford Univ. Press. Lawrence Erlbaum Associates: Hillsdale, New
York.
Stern JA, & Dunham DN (1990). The ocular system. In J.T., Cacioppo, & LG Tassinary (Eds), Principles of
psychophysiology: Physical, social and inferential elements (pp. 513-553). Cambridge: Cambridge University press.
Stice E (1994) Review of the evidence for a socio-cultural model of bulimia nervosa and an exploration of the mechanisms of
action. Clinical Psychology Review, 14, 633-661.
Stice E (2001). A prospective test of the dual-pathway model of bulimic pathology: mediating effects of dieting and negative
affect. Journal of Abnormal Psychology, 110, 124-135.
Stice E (2002a). Risk and maintenance factors for eating pathology: A meta-analytic review. Psychological Bulletin, 128 (5), 825848.
Stice E (2002b). Sociocultural influences on body image and eating disturbance. In C.G. Fairburn & K.D. Brownell, Eating
disorders and obesity. Second edition. A comprehensive handbook (pp. 103-107). New York: Guilford Press.
Stice E, Akutagawa D, Gaggar A & Agras S (2000) Negative affect moderates the relation between dieting and binge eating.
International Journal of Eating Disorders, 27, 218-229.
Stice E, Killen JD, Hayward C, & Taylor CB (1998). Support for the continuity hypothesis of bulimic pathology. Journal of
Consulting and Clinical Psychology, 66, 784-790.
Stice E, & Shaw HE (2002). Role of body dissatisfaction in the onset and maintenance of eating pathology: a synthesis of
research findings. Journal of Psychosomatic Research, 53 (5), 961-962.
Strauss J, & Ryan RM (1988). Cognitive dysfunction in eating disorders. International Journal of Eating Disorders, 7, 19-27.
Strober M (1980). Personality and symptomatological features in young, nonchronic anorexia nervosa patients. Journal of
Psychosomatic Research, 24, 353-359
Strober M (1984). Stressful life events associated with bulimia in anorexia nervosa. Empirical findings and theoretical
speculations. International Journal of Eating Disorders, 3, 3-16.
Strober M (1991). Disorders of the self in anorexia nervosa: An organismic-developmental paradigm. In Psychodynamic
treatment of anorexia nervosa and bulimia (ed. C. Johnson), pp. 354-373. Guilford Press: New York.
Strober M (1995). Family-genetic perspectives on anorexia nervosa and bulimia nervosa. In Eating Disorders and Obesity
(ed. Brownell, K.D. and Fairburn, C.G.), pp. 212-218. The Guilford Press: New York
Strober M, Freeman R, Morrell W (1997). The long-term course of severe anorexia nervosa in ad-olescents: survival analysis
of recovery, relapse, and outcome predictors over 10-15 years in a prospective study. International Journal of Eating
Disorders, 22:339-360.
Sutandar-Pinnock K, Woodside DB, Carter JC, Olmsted MP, & Kaplan AS (2003). Perfectionism in anorexia nervosa: a 6-24
month follow-up study. International Journal of Eating Disorders, 33, 225-229.
Szmukler GI, Andrewes D, Kingston K, Chen L, Stargatt R, & Stanley R (1992). Neuropsychological impairment in anorexia
nervosa: Before and after refeeding. Journal of Clinical and Experimental Neuropsychology, 14, 347-352.
Tangney JP (1993) Shame and guilt. In C.G. Costello (Ed.), Symptoms of Depression (pp. 161-180). New York: John Wiley
& Sons.
Taylor GJ, Parker JDA, Badbey RM, & Bourke MP (1996). Relationships between alexithymia and psychological
characteristics associated with eating disorders. Journal of Psychosomatic Research, 41, 561-568.
Tchanturia K, Happé F, Godley J, Treasure J, Bara-Carril N, & Schmidt U (2004). ‘Theory of Mind’ in Anorexia Nervosa.
European Eating Diorders Review, 12, 361-366.
Tchanturia K, Morris RG, Surguladze S & Treasure JL (in press) An examination of perceptual and cognitive set shifting
tasks in acute anorexia and following recovery. Eating and Weight Disorders.
Tchanturia K, Serpell L, Troop N, & Treasure J (2002) Perceptual illusions in eating disorders: Rigid and fluctuating styles.
Behaviour Therapy and Experimental Psychiatry, 32, 107-115.
Telch CF, & Stice E (1998). Psychiatric comorbidity in women with Binge Eating Disorder: Prevalence rates from a nontreatment-seeking sample. Journal of Consulting and Clinical Psychology, 66 (5), 768-776.
Thompson SBN (1993). Implications of neuropsychological test results of women in a new phase of anorexia nervosa.
European Eating Disorders Review, 1, 152-165.
Tiller JM, Schmidt UH, Ali S & Treasure JL (1995). Patterns of punitiveness in women with eating disorders. International
Journal of Eating Disorders, 17, 365-371.
Tiller JM, Sloane G, Schmidt UH, Troop NA, Power M & Treasure JL (1997). Social support in patients with anorexia
nervosa and bulimia nervosa. International Journal of Eating Disorders, 21,31-38.
tional Journal of Eating Disorders, 17 (2), I 47~152.
Treasure JL & Holland A (1995). Genetic factors in eating disorders. In G. Szmukler, C. Dare & J. Treasure (Eds), Handbook
of Eating Disorders: Theory, Treatment and Research. Chichester: John Wiley & Sons.
Troop NA & Bifulco A (2002). Childhood social arena and cognitive sets in eating disorders. British Journal of Clinical
Psychology, 41, 205-211.
Troop NA, Holbrey A, & Treasure JL (1998). Stress, coping and crisis support in eating disorders. International Journal of
Eating Disorders, 24, 157-166.
Troop NA, Holbrey A, Trowler R & Treasure JL (1994) Ways of coping in women with eating disorders. Journal of Nervous
and Mental Disease, 182, 535-540.
Troop NA, Schmidt UH, & Treasure J (1995). Feelings and fantasy in eating disorders: A factor analysis of the Toronto
Alexitymia Scale. International Journal of Eating Disorders, 18, 151-157.
Troop NA, Schmidt UH, Turnbull S, & Treasure JL (2000) Self-esteem and responsibility for change in women with bulimia
nervosa. European Eating Disorders Review, 8, 384-393.
Troop NA, & Treasure JL (1997b). Setting the scene for eating disorders II: Childhood helplessness and mastery.
Psychological Medicine, 27,531-538.
Troop NA, & Treasure JL (1997a) Psychosocial factors in the onset of eating disorders: Responses to life events and
difficulties. British Journal of Medical Psychology, 70, 373-385.
Turner H, & Cooper M (2002). Cognitions and their origins in women with anorexia nervosa, normal dieters and female
controls. Clinical Psychology and Psychotherapy, 9(4), 242-252.
Tuschen-Caffier B, Vögele C, Bracht S, & Hilbert A (2003). Psychological responses to body shape exposure in patients with
bulimia nervosa. Behaviour Research and Therapy, 41, 573-586.
Tylka TL, & Subich LM (1999). Exploring the construct validity of the eating disorder continuum. Journal of Counseling
Psychology, 46, 268-276.
Uher R, Murphy T, Phillips M, & Dalgleish TT (2001). Perception of food and emotional stimuli in anorexia nervosa.
Neuroimage, 13, S1022-S1022.
Vandereycken W, & Noordenbos G (2002). Handboek eetstoornissen, De Tijdstroom, Utrecht.
Van Hanswijck, De Jonge P, Van Furth EF, Lacey JH, & Waller G (2003). The prevalence of DSM-IV personality pathology
among individuals with bulimia nervosa, binge eating disorder and obesity. Psychological Medicine, 33, 1311-1317.
Van Hoeken D, Seidell J, & Hoek HW (2003). Epidemiology. In: J. Treasure, U. Schmidt, & E. van Furth (Eds) Handbook
of Eating Disorders. (Second Edition),( pp. 11-35). Chichester, Wiley.
Van Strien T (1986). Eating behaviour, personality traits and body mass. Swets & Zeitlinger B.V.: Lisse
Van Strien T (2000a). Ice-Cream consumption, tendency toward overeating, and personality. International Journal of Eating
Disorders, 28, 460-464.
Van Strien T, Cleven A, & Schippers G (2000). Restraint, Tendency Toward Overeating and Ice Cream Consumption.
International Journal of Eating Disorders, 28, 333-338.
Viken RJ, Treat TA, Nosofsky R.M, McFall RM, & Palmeri TJ (2002). Modeling individual differences in perceptual and
attentional processes related to bulimic symptoms. Journal of Abnormal Psychology, 111, 598-609.
Vitousek K, & Hollon SS (1990). The investigation of schematic content and processing in eating disorders. Cognitive
Therapy and Research, 14, 191-214.
Vitousek K, & Manke F (1994). Personality variables and disorders in anorexia nervosa and bulimia nervosa. Journal of
Abnormal Psychology, 103, 137-147.
Vohs KD, Bardone AM, Joiner TE, Abramson LY, & Heatherton TF (1999). Perfectionism, perceived weight status, and
self-esteem interact to predict bulimic symptoms: A model of bulimic symptom development. Journal of Abnormal
Psychology, 108, 695-700.
Vohs KD, Voelz ZR, Pettit JW, Bardone AM, Katz J, Abramson LY, Heatherton TF, & Joiner TE (2001). Perfectionism,
body dissatisfaction, and self-esteem: An interactive model of bulimic symptom development. Journal of Social and Clinical
Psychology, 20, 476-497.
Wade TD, Bulik CM, Neale M, Kendler KS. (2000). Anorexia nervosa and major depression: shared genetic and
environmental risk factors. American Journal of Psychiatry (3), 469-71.
Waller G (2003). Schema-level cognitions in patients with binge eating disorder: a case control study. International Journal of
Eating Disorders, 33, 458-464.
Waller G, Babbs M, Milligan R, Meyer C, Ohanian V, & Leung N (2003). Anger and Core beliefs in the Eating Disorders.
International Journal of Eating Disorders, 34, 118-124.
Waller G, Mijatovich S (1998). Precounscious processing of threat cues: impact on eating among women with unhealthy
eating attitudes. International Journal of Eating Disorders, 24, 83-89.
Waller G, Ohanian V, Meyer C & Osman S (2000) Cognitive content among bulimic women: role of core beliefs.
International Journal of Eating Disorders, 28, 235-241.
Waller G, Watkins H, Shuck V, & McManus F (1996). Bulimic psychopathology and attentional biases to ego threats among
non-eating-disordered women. International Journal of Eating Disorders, 20, 169-176.
Walters EE, Neale MC, Eaves LJ, Lindon J, & Heath AC (1992). Bulimia nervosa and major depression: A study of common
genetic and environmental factors. Psychological Medicine, 22, 617-622.
Wassenaar D, le Grange D, Winship J, et al (2000). The prevalence of eating disorder pathology in a cross-ethnic population
of female students in South Africa. European Eating Disorders Review, 8, 225-236.
Webber EM (1994). Psychological characteristics of bingeing and non-bingeing obese woman. Journal of Consulting and
Clinical Psychology, 66, 768-776.
Wells A, & Davies MI (1994). The thought control questionnaire: A measure of indvidual differences in the control of
unwanted thoughts. Behaviour Research an Therapy, 32, 871-878.
Wentz E, Gillberg C, Gillberg IC, & Rastam M (2001). Ten-year follow-up of adolescent-onset anorexia nervosa: Psychiatric
Disorders and overall function scales. Journal of Child Psychology and Psychiatry and Allied Disciplines, 42, 613-622.
Whiteside SP, & Lynam Dr (2001). The Five Factor Model and impulsivity: Using a structural model of personality to
understand impulsivity. Personality and Individual Differences, 30, 669-689.
Wiederman MW, & Pryor T (1996). Multi-impulsivity in bulimia nervosa. International Journal of Eating Disorders, 20 (4),
359-365.
Wilfley DE, Schwartz MB, Spurrell EB, Fairburn CG (2000). EDI to identify the specific psychopathology of BED.
International Journal of Eating Disorders, 27, 259-269.
Williams JMG, Watts FN, Mac Leod C, & Mathews A (1997). Cognitive psychology and emotional disorders (2nd ed.).
Chichester: Wiley.
Wilson GT, Fairburn CG, & Agras WS (1997). Cognitive-behavioral therapy for bulimia nervosa. In D.M. Garner & P.E.
Garfinkel, Handbook of treatment for eating disorders. Second edition (pp. 67-93). New York: Guilford express.
Wonderlich SA, Connolly KM, & Stice E (2004). Impulsivity as a risk factor for eating disorder behaviour: Assessment
implications with adolescents. International Journal of Eating Disorders, 36, 172-182.
Wonderlich SA, Mitchell JE (1997). Eating disorders and comorbidity: empirical, conceptual and clinical implications.
Psychopharmacol Bull, 33:381-390.
Wonderlich SA, Swift WJ, Slotnick HB & Goodman S (1990) DSM-III-R personality disorders in eating disorders subtypes.
International Journal of Eating Disorders, 9, 607-616.
Wood A, Waller G, & Gowers S (1994). Predictors of eating psychopathology in adolescent girls. European Eating Disorders
Review, 2, 6-13.
World Health Organization (1992, 1993). The ICD-10 classification of mental and behavioral disorders. Clinical descriptions
and diagnostic guidelines. Genéve: Author.
Wyatt R, & Gilbert P (1998). Dimensions of perfectionism: a study exploring their relationship with perceived social rank
and status. Personality and Individual Differences, 24, 71-79.
Yager J, Rorty M. & Rossotto E. (1995). Coping styles differ between recovered and nonrecovered 1en with bulimia nervosa
but not between recovered women and non-eating disordered control subjects. Journal of Nervous and Mental Disease, 183,
86-94.
Young JE (1994). Cognitive therapy for personality disorders: A schema-focused approach (2nd ed.), Sarasota, FL:
Professional Resource Press.
PART II
The cognitive psychology of eating disorders:
personality, cognitions and behaviour.
Chapter 2: Personality characteristics as trait-dependent vulnerability: study
results
1. Binge Eating Disorder and Non Purging Bulimia: more similar than different?4
There is evidence of an overlap of symptoms in binge-eating disordered (BED) and bulimia nervosa non-purging
(BN-NP) patients. In addition, indications of an evolution from bulimia nervosa to BED along a continuum of
vulnerability have been found. However, DSM-IV categorizes BED and BN-NP as distinct disorders based on
clinical characteristics. In this study weight history and personality-related characteristics (TCI; Cloninger,
Svrakic, & Przybeck, 1993) were studied in 30 BED and 17 BN-NP patients. BED patients were older, and
had a longer duration of illness, a larger weight cycling, a higher current and previous BMI and a lower score for
the temperament dimension ‘Persistence’ than BN-NP patients. After correcting for age, differences between
weight variables remained, including comparatively
higher BMIs and larger weight fluctuations among the BED patients. A possible explanation is that this
difference is due to a genetic effect of the propensity to be overweight and the temperamental characteristic of
Persistence. This ‘morbid’ starting position and the lack of controlling mechanisms are associated with a more
trait- than state-dependent condition. Thus, restrained eating is not to be regarded as eliciting bingeing in BED
patients. Due to personality characteristics these patients are not able to restrain, which clearly differentiates them
from BN-NP patients.
Keywords: binge eating disorder, personality, bulimia nervosa non-purging type
Introduction
Patients diagnosed with Eating Disorders Not Otherwise Specified (EDNOS) are defined as
individuals who have an eating disorder of clinical severity but who do not meet diagnostic criteria for
anorexia nervosa or bulimia nervosa. Several studies (Mitchell, Pyle, Hatsukami, & Eckert, 1986;
Mitrany, 1992; Norvell & Cooley, 1986-1987, Mizes & Sloan, 1998; Spitzer et al., 1992; Williamson,
Gleaves, & Savin, 1992), which were mostly descriptive and based on relatively small sample sizes, have
suggested that patients suffering from binge eating disorder (BED) form a subgroup within this
EDNOS group. An important issue in the discussion of whether BED should be regarded as a
diagnostic entity, is the question whether patients with bulimia nervosa without purging (BN-NP) differ
from BED patients.
Based on results from a community sample, Striegel-Moore and collegues
suggested that BED does not represent a burned out form of BN (any type; Striegel-Moore et al., 2001).
4
Vervaet, M., van Heeringen, C., Audenaert, K. (2004). European Eating Disorders Review,
12, 27-33
DSM-IV criteria for BED imply the absence of inappropriate compensatory behaviours in BED
patients. BN-NP patients binge at least twice a week without compensatory behaviours, except for
fasting and excessive exercise. They appear to form a homogeneous group sharing however some
clinical characteristics with purging (BN-P) bulimics (Garfinkel et al., 1995; Kinzl, Traweger, Trefalt,
Mangweth, & Biebl, 1999) including age, gender, a similar determination to compensate for their
bingeing, and similar pathways to binge-eating. The main behavioural difference between non-purging
and purging bulimics is the frequently self-induced vomiting and/or misuse of laxatives and other drugs
to counteract the effects of binge-eating among the latter (Kinzl et al., 1999). In BN, the onset of binge
eating is very often preceded by dieting and weight loss (Mussell et al., 1997), whereas among patients
with BED, binge eating may be the cause, and not the consequence, of dieting behaviour (Marcus,
1995).
However, some cases of bulimia nervosa may evolve into BED, and accumulating evidence
indicates the existence of a continuum of vulnerability with a higher frequency of binge-eating reflecting
greater clinical severity among obese and bulimia nervosa patients (de Zwaan et al., 1994; Garfinkel et
al., 1995; Kendler et al., 1991; Striegel-Moore, Wilson, Wilfley, Elder, & Brownell, 1998). There is,
however, less evidence of an association between BMI and severity of binge-eating. Some studies, but
not all (Brody, Walsh, & Devlin, 1995; de Zwaan, Nutzinger, & Schoenbeck, 1992; Goldfein, Walsh,
LaChausse, Kissileff, & Devlin, 1993; Wilson, Nonas, & Rosenblum, 1993), have reported an association
(de Zwaan et al., 1994; Lowe & Caputo, 1991; Spitzer et al., 1993; Telch, Agras, & Rossiter, 1988).
Clinical observation and studies of personality characteristics and comorbidity indicate that BED
patients show more severe psychopathology than pure restricting anorexics. Moreover, their family
environment appears to be more similar to that of bulimic and anorectic purger/binger patients in terms
of conflict and chaos (Kanter, Williams, & Cummings, 1992; Marcus et al., 1990).
Thus, there is evidence of an overlap of symptoms in BED and BN-NP patients, and, in
addition, indications of an evolution from BN to BED along a continuum of vulnerability have been
found.
However, DSM-IV categorizes BED and BN-NP as distinct disorders based on clinical
characteristics.
This study aimed at investigating differences in personality-related characteristics
between BED and BN-NP patients.
Methods
Sample
A total of 409 patients who were consecutively referred to the in- and out-patient units of the Centre for
Eating Disorders at the Department of Psychiatry of the University Hospital Gent between December
1998 and April 2002 and who met the DSM-IV criteria for eating disorders, were enrolled in the study.
The study was compliant with the Code of Ethics of the World Medical Association (Declaration of
Helsinki) and carried out following the guidelines of the local ethics committee.
The referred group included 17 patients (4 per cent) with BN-NP, while 75 patients (18 per cent)
were diagnosed with EDNOS. In the BN-NP group, which consisted of 16 females and 1 male, the
mean age was 23.8 years (SD=7.2 years) and the mean BMI was 24.5 (SD=4.2). Among the EDNOS
patients, the mean age was 26.2 years (SD = 10.9 years) and the mean BMI was 26.7 (SD = 10.1).
Ninety-eight per cent (n = 72) of the EDNOS patients were female. Thirty-one patients of the EDNOS
group met the criteria for BED (female: 28; male: three). The data on one female of the BED group
were excluded from statistical analysis because of mental retardation which could have influenced the
reliability of the assessment. The mean age of BED patients was 33.1 years (SD = 10.7 years) with a
mean BMI of 37.7 (SD = 6.7).
Measures
Weight and height, highest and lowest adult weight ever and duration of illness were assessed carefully.
The body mass index (BMI) was calculated, as well the highest and lowest BMI (HBMI, LBMI), based
on the highest and lowest adult weight ever. Weight fluctuation was defined by the difference between
highest and lowest adult weight ever. Patients were asked to describe the frequency of their binging,
purging and restricting behaviours according to three categories: never, less than twice per week
(‘sometimes’), or more than twice per week (‘frequent’). Bingeing was described as the loss of control
over eating, not including any measurement of calories.
The Dutch version of the SCAN (Schedules
for Clinical Assessment in Neuropsychiatry) was used to assign diagnoses according to DSM-IV criteria
(Giel & Nienhuis, 1996). The validated Dutch version of the TCI (Duijsens, Spinhoven, Goekoop,
Spermon, & Eurelings-Bontekoe, 2000) was used to assess temperament and character characteristics.
The TCI is based on a psychobiological model of personality and assesses both temperament and
character. Temperamental aspects of personality are (at least partially) heritable, manifest early in life,
and involve preconceptual or unconscious biases in learning (Cloninger et al., 1993). The temperament
dimensions include novelty seeking (NS) reflecting behavioural activation, harm avoidance (HA), a
tendency toward behavioural inhibition, reward dependence (RD) reflecting behavioural attachment, and
persistence (PS), a measure of behavioural maintenance. Character aspects of personality are denoted by
individual differences in self-concepts, goals, and values.
The character dimensions include self-
directedness (SD), referring to a self-accepting, purposeful nature, cooperativeness (CO), a trait
associated with acceptance of other people and compassion, and self-transcendence (ST) reflecting
spirituality and an acceptance, identification, or spiritual union with nature and its source. Individuals
with the same temperament may behave differently as a result of differences in character development
(Cloninger et al., 1993). In addition to the self-report measurements, eating behaviours were assessed by
means of the Dutch Eating Behaviour Questionnaire (DEBQ; Van Strien, 1986). This questionnaire
measures the behavioural characteristics emotional eating (eating elicited by diffuse and clear emotional
stimuli), restrained eating (the tendency to diet in order to lose weight), and external eating (eating
elicited by external stimuli). Finally, patients were asked for feelings of sadness, sleeping disturbances
(without drugs), feelings of anxiety or phobia or panic attacks, feelings of depression, a history of
deliberate self-harm, and drug abuse.
Obesity or overweight in first degree family members was
assessed.
Statistical analysis was performed using SPSS 10.0. t-Tests were used to compare BN-NP with
BED patients with regard to demographic, clinical and behavioural (DEBQ) and personality (TCI)
characteristics.
Since a significant difference for age between the two patient groups was found, a
correction for age was applied in further statistical analysis.
Results
The study group included 17 BN-NP and 30 BED patients who all binged at least twice per week. Since
purging is an exclusion criteria for the BN-NP and BED diagnoses, patients were included only if they
vomited or used laxatives less than twice per week. The BN-NP group included one vomiting patient,
and one patient who used laxatives, while in the BED group eight patients reported vomiting and four
used laxatives, all less than twice a week. BN-NP patients reported food restriction very commonly
(more than twice per week, n=13), while BED patients tried to restrict, but failed (five patients reported
restricting more than twice per week). Since excessive exercise was assessed only in the last 14 patients,
only differences in restricting were calculated. As shown in Table 1 there are thus small numbers in
some cells. Consequently, data on excessive exercise were not included in further analysis.
Table 1: Significant differences for age, duration of illness, BMI, HBMI, LBMI and weightfluctuation characteristics between BN-NP and BED patients
BN-NP
n=17
BED
n=30
total
Never
Sometimes
Frequently
0
3
14
10
15
5
10
18
19
Excessive exercise Missing
Never
1
1
3
Frequently
13
6
20
7
33
2
1
3
Restricting
Sometimes
4
Sometimes, < twice a week; Frequently, >twice a week,
Pearson chi-square = 0.000
As shown in Table 2, BN-NP subjects were younger, and had a shorter duration of illness, when
compared to BED patients.
Table 2: Table 2: Significant differences for age, duration of illness, BMI, HBMI, LBMI,
weight-fluctuation, behavioural (DEBQ) and personality characteristics (TCI) characteristics
between BN-NP and BED patients
Age
Duration of illness
BMI
HBMI
LBMI
Weight fluctuation
Restrained Eating
Persistence
BN-NP
n=17
m
sd
23.8
7.2
4.1
3.5
24.5
4.2
27.1
5.5
19.3
4.1
21.7
12.6
4.0
0.8
5.4
2.1
BED
n=30
m
sd
33.1
10.7
11.4
7.5
37.7
6.7
39.7
7.6
25.4
3.7
40.6
22.1
2.9
0.6
3.4
2.1
t
p
-3.2
.002
-3.7
.001
-7.3
.000
-5.9
.000
-5,3
.000
-3.2
.002
4.8
.000
3.1
.004
The group of BN-NP patients had a mean lower BMI, adult HBMI and LBMI than BED
patients. BED patients showed significantly larger fluctuations in their body weight than patients of the
BN-NP group. Patients in the BN-NP group also had a higher score on ‘restrained eating’, than patients
in the BED group. With regard to personality dimensions, BN-NP patients scored higher on persistence
than BED patients.
After correction for age (Table 3), the described differences remained significant.
Table 3: Differences between BN-NP and BED after correction for age
BMI
HBM
LBMI
Weight
fluctuation
Restrained
eating
persistence
BN-NP
M
SE
26.2
1.4
29.1
1.6
19.1
1.0
27.6
4.4
BED
M
SE
36.7
1.0
38.5
1.2
25.5
0.7
37.1
3.2
R-squared
3.9
0.2
5.0
0.5
2.9
0.1
3.7
0.4
F
p-value
(Bonferroni)
.640
39.1
.000
.561
28.1
.000
.392
14.2
.000
.385
13.8
.000
.371
12.9
.000
.211
5.9
.006
ANOVA with Bonferroni post hoc comparison; corrected for age, evaluated at covariates appeared in the model: AGE =
29.72
There was a significant difference (Pearson chi-square = 0.007) in overweight or obesity in first
degree family members. Twenty-two of the BED patients (76 per cent) and seven of the 17 BN-NP
patients (47 per cent) reported that their mother or father was overweight. No differences were found
with regard to feelings of sadness, anxiety, depression, or the presence of sleep disturbances, deliberate
self-harm or drug abuse (Table 4).
Table 4: Clinical differences between BN-NP and BED patients
-------------------------------------------------------------------------------------------------------------------------
BN-NP
Sensitivity,
SleepFeelings Feelings of Deliberate Drug Overweight
tension, disturbances
of
Depression Self-harm abuse or obesity
sadness
anxiety
in family
14
7
5
13
3
0
7
N=17
BED
N=30
MannWhitney U
Asymp.Sig.
(twotailed)
27
19
13
24
9
4
22
217.0
176.5
192.5
209.0
184.5
180.0
161
.977
.233
.467
.740
.403
.129
.020
Finally, three different groups were compared according to the frequency of restricting food (Table 5).
Table 5. frequency of non-purging compensating behaviour in BN-NP and BED patients
Age
BMI
HBM
LBMI
Duration of
illness
Restrained
eating
persistence
Never
Restricting
M (SD)
(1)
35.5 (9.9)
Sometimes
Restricting
M (SD)
(2)
27.8 (9.9)
Frequently
Restricting
M (SD) (3)
F
p-value
(Bonferroni)
28.0 (10.9)
2.1
0.131
38.3 (5.1)
39.8 (6.1)
25.7 (3.6)
13.2 (8.0)
33.5 (8.0)
34.9 (8.6)
23.4 (7.1)
8.3 (5.9)
29.3 (9.7)
32.5 (10.6)
20.2 (4.5)
7.4 (7.5)
4.0
2.1
3.3
2.0
0.026
0.137
0.048
0.148
3<1
2.9 (0.8)
3.1 (0.6)
3.7 (0.9)
3.7
0.034
1,2<3
3.3 (1.5)
3.5 (2.5)
5.4 (2.0)
4.6
0.015
ANOVA with Bonferroni post hoc comparison
1,2<3
3<1
Significant differences between the groups were found for BMI, LBMI and the personality characteristic,
persistence.
Patients with frequent restricting behaviour had a mean lower BMI and LBMI ever
compared to patients who never restricted. The mean score for persistence was higher among the group
of frequently-restricting patients compared to the two other groups.
There was a significant association between restricting behaviour, when dichotomized to present
or absent, and persistence.
Discussion
This study shows that BED patients differ from BN-NP patients in being older and having a
longer duration of illness. The BED group has a mean BMI reflecting the obesity of these patients, in
contrast with the BN-NP patients, whose mean BMI can be described as reflecting overweight. The
finding that the lowest BMI ever among the BED patients was higher than the ideal level is noteworthy,
as this indicates overweight already during puberty. In contrast, the BN-NP patients, reported a highest
BMI ever indicating overweight, but these patients apparently succeed in becoming only slightly
overweight, although they binged. A possible explanation is that in BN patients, the onset of binge
eating is very often preceded by dieting and weight loss (Mussell et al., 1997), whereas among BED
patients binge-eating can be the cause, and not the consequence, of dieting behaviour (Marcus, 1995).
Moreover, BED patients have learned that dieting has little or no effect since they still remain
overweight and most of them have a history of yo-yo dieting. Comparing their weight cycling with the
BN-NP patients, there was a significant difference.
As previously described by Williamson and
colleagues (1992), the average score for ‘restrained eating’ was significantly lower in the BED group
when compared to the BN-NP group. As expected, there was no difference in ‘emotional eating’ or
‘external eating’ between the two groups. Noteworthy is the significant difference in ‘persistence’
between the study groups. A strong association between persistence and restricting eating behaviour, as
a manifestation of non-purging compensating behaviour was found and significantly more restricting
behaviour was found in the BN-NP group. Age has been shown to have an effect on the character
dimensions self-directedness and cooperativeness (Cloninger et al., 1993), which develop by means of
maturation. With regard to the current findings, however, differences in personality characteristics
between the patient groups were limited to the temperament dimension persistence, so that an effect of
age is unlikely. Given the possibility, that overweight and persistence are, at the least partially, genetically
determined, overweight youngsters with a rather high novelty seeking (compared to anorectic patients)
may binge due to a lack of control following exposure to external and emotional stimuli and may fail to
compensate, by restrained eating, due to a lack of persistence.
Although BED patients differ from BN-NP patients in a number of characteristics, there are also
some important shared features, indicating that BED is not merely a body weight-related problem.
Previous studies have shown a higher food intake even on non-binge days in BED patients compared to
obese non-bingers (Yanovski & Sebring, 1994). A history of more frequent weight fluctuations and a
greater amount of time spent dieting was shown in BED patients (Brody, Walsh, & Devlin, 1995;
Yanovski, 1993).
Moreover, obese BED patients show more psychiatric comorbidity and
psychopathology (Striegel-Moore et al., 1998; Telch & Agras, 1995; Yanovski, Nelson, Dubbert, &
Spitzer, 1993), and lower self-esteem (de Zwaan et al., 1994; Hawkins & Clement, 1980; Lowe & Caputo,
1991, Striegel-Moore et al., 1998). Striegel-Moore and colleagues (1998) even showed a lower selfesteem in BED patients than in subthreshold BED patients and overeaters.
Previous research has shown higher levels of thrill-seeking and excitability, affective instability
and impulsivity, and a tendency towards marked dysphoria in response to rejection or non-reward in
bulimic patients (Bulik, Beidel, Duchmann, Weltzin, & Kaye, 1992; Casper, Hedeker, & McKlough,
1992; Strober, 1995; Vitousek & Manke, 1994) which may predispose an individual to periodic loss of
control and eventual dietary chaos. Increased harm avoidance may be involved in the development of
both anorexia and bulimia nervosa, and persist, as a trait, following recovery from these disorders
(Casper, 1990; Kaye et al., 1998; Kaye, Strober, Stein, & Gendall, 1999; Srinivasagam et al., 1995). As
this study showed no differences between the two groups in scores on the temperament dimensions
novelty seeking, harm avoidance and reward dependence, it can be hypothesized that BED patients (and
BN-NP patients as well) differ from obese non-bingeing patients. This hypothesis is supported by the
absence of a difference in the clinical measures of feelings of sadness, sleeping disturbances (without
drugs), feelings of anxiety or phobia or panic attacks, feelings of depression, a history of deliberate selfharm, and drug abuse between the BN-NP and BED patients in this study.
The conclusion of this study is that BED patients share many behavioural and personality
characteristics with BN-NP patients. However, BED patients are older, and have a longer duration of
illness, greater weight cycling and a higher current and previous BMI than BN-NP patients. After
correcting for age, differences between restrained eating and weight variables remain together with less
restrained eating, higher BMIs and larger weight fluctuations among the BED patients. A possible
explanation is that this difference is due to a genetic effect of the propensity to be overweight and the
temperamental characteristic, persistence.
This ‘morbid’ starting position and lack of controlling
mechanisms are associated with a more trait- than state-dependent condition. Thus, restrained eating is
not to be regarded as eliciting bingeing in BED patients. Due to personality characteristics these
patients are not able to restrain, which clearly differentiates them from BN-NP patients. This could be
an important difference between the BN-NP and BED group and may support a categorical diagnostic
distinction. Further research on larger samples is clearly needed to confirm these findings. Moreover,
since only a small proportion of BED and BN-NP suffers come along to services, there is room for
doubt about extrapolation from clinic populations to the generality of those with the disorders.
References
Brody, M.L., Walsh, B.T., & Devlin, M.Y. (1995). Binge eating disorder: Reliability and validity of a new diagnostic categrory.
Journal of Consulting and Clinical Psychology, 62, 381-386.
Bulik, C.M., Beidel, D.C., Duchmann, E., Weltzin, T.E., & Kaye, W.H. (1992). Comparative psychopathology of women
with bulimia nervosa and obsessive-compulsive disorder. Comprehensive Psychiatry, 33, 262-268.
Casper, R.C. (1990). Personality features of women with good outcome from restricting anorexia nervosa. Psychosomatic
Medecine, 52, 156-170.
Casper, R.C., Hedeker, D., & McKlough, J.F. (1992). Personality dimensions in eating disorders and their relevance for
subtyping. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 830-840.
Cloninger, C., Svrakic, D., & Przybeck, T. (1993). A psychobiological model of temperament and character. Archives of
General Psychiatry, 30, 975-990.
de Zwaan, M., Mitchell, J.E., Seim, H.C., Specker, S.M., Pyle, R.L., Raymond, N.C., & Crosby, R.B. (1994). Eating related
and general psychopathology in obese females with binge eating disorder. International Journal of Eating Disorders, 15, 4352.
de Zwaan, M., Nutzinger,D.O., & Schoenbeck,,G. (1992). Binge eating in overweight women. Comprehensive Psychiatr,
33, 256-261.
Duijsens, I.J., Spinhoven, P., Goekoop, J.G., Spermon, T., & Eurelings-Bontekoe, E.H.M. (2000). The Dutch temperament
and character inventory (TCI): dimensional structure, reliability and validity in a normal and psychiatric outpatient sample.
Personality and Individual Differences, 28, 487-499.
Garfinkel, P.E., Lin, E., Goering, P., Spegg, C., Goldbloom, D.S., Kennedy, S., Kaplan, A.S., & Woodside, D.B. (1995).
Bulimia nervosa in a Canadian community sample: Prevalence and comparison of subgroups. American Journal of
Psychiatry, 152, 1052-1058.
Giel, R., & Nienhuis, F.J. (1996). Vragenschema’s voor de klinische beoordeling in de neuropsychiatrie. World Health
Organisation Mental Health, Geneva.
Goldfein, J.A., Walsh, B.T., LaChausse, J.L., Kissileff, H.R., & Devlin, M,Y. (1993). Eating behavior in binge eating
disorders. International Journal of Eating Disorders, 14, 427-431.
Hawkins, R.C., & Clement, P.F. (1980). Development and construct validation of a self-report measure of binge eating
tendencies. Addictive Behaviors, 5, 219-226.
Kanter, R., Williams, B., & Cummings, C. (1992). Personal and parental alcohol abuse, and victimization in obese binge
eaters and nonbingeing obese. Addictive Behaviors, 17, 439-445.
Kaye, W.H., Greeno, C.G., Moss, H., Fernstrom, J., Fernstrom, M., Lilenfeld, L.R., Weltzin, T.E.., & Mann, J.J. (1998).
Alterations in serotonin activity and psychiatric symptomatology after recovery from bulimia nervosa. Archives of General
Psychiatry, 55, 927-935.
Kaye, W.H., Strober, M., Stein, D., & Gendall, K. (1999). New Directions in Treatment Research of Anorexia and Bulimia
Nervosa. Biological Psychiatry, 45, 1285-1292.
Kendler, K.S., MacLean, C., Neale, M., Kessler, R., Heath, A., & Eaves, L. (1991). The genetic epidemiology of bulimia
nervosa. American Journal of Psychiatry, 148, 1627-1637.
Kinzl, J.F., Traweger, C., Trefalt, E., Mangweth, B., Biebl, W. (1999). Binge eating Disorder in Females: a population-based
investigation. International Journal of Eating Disorders, 25, 287-292.
Lowe, M.R., & Caputo, G.C. (1991). Binge eating in obesity: Toward the specification of predictors. International Journal
of Eating Disorders, 10, 49-55.
Marcus, M., Wing, R., Ewing, L., Kern, E., Gooding, W. & McDermott, M. (1990). Psychiatric disorders among obese binge
eaters. International Journal of Eating Disorders, 9, 69-77.
Marcus, M.D. (1995). Binge eating and obesity. In K.D. Brownell & C.G. Fairburn (Eds.), Eating disorders and obesity. A
comprehensive handbook (pp. 441-444). New York: Guilford Press.
Mitchell, J.E., Pyle, R.L., Hatsukami, D., & Eckert, E.D. (1986). What are atypical eating disorders? Psychosomatics, 27, 2128.
Mitrany, E. (1992). Atypical eating disorders. Journal of Adolescent Health, 13, 400-402.
Mizes, J.S., Sloan, D.M. (1998). An empirical analysis of Eating Disorder, Not Otherwise Specified: preliminary support for a
distinct subgroup. International Journal of Eating Disorders, 23, 233-242.
Mussell, M.P., Mitchell, J.E., Fenna, C.J., Crosby, R,D., Miller, J.P., & Hoberman, H.M. (1997). A comparison of onset of
binge eating versus dieting in the development of bulimia nervosa. International Journal of Eating Disorders, 21, 353-360.
Norvell, N., & Cooley, E. (1986-1987). Diagnostic issues in eating disorders: Two cases of atypical eating disorder.
International Journal of Psychiatry Medicine, 16, 317-323.
Spitzer, R.L., Devlin, M.J., Walsh, B.T., Hasin, D., Wing, R., Marcus, M., Stunkard, A., Wadden, T., Yanovski, S., Agras, S.,
Mitchell, J., & Nonas, C. (1992). Binge eating disorder: A multisided trial of the diagnostic criteria. International Journal of
Eating Disorders, 11, 191-203.
Spitzer, R.L., Yanovski, S., Wadden, T., Wing, R., Marcus, M., Stunkard, A., Devlin, M.J., Mitchell, J., Hasin, D., & Horne,
R.L. (1993). Binge eating disorder: Its further validation in a multiside study. International Journal of Eating Disorders, 13,
137-153.
Srinivasagan, N.M., Plotnicov, K.H., Greeno, C., Weltzin, T.E., & Rao, R. (1995). Persistent perfectionism, symmetry, and
exactness in anorexia nervosa after long-term recovery. American Journal of Psychiatry, 152, 1630-1634.
Striegel-Moore, R.H., Wilson, G.T., Wilfley, D.E., Elder, K.A., Brownell, K.D. (1998). Binge eating in an obese community
sample. International Journal of Eating Disorders, 23, 27-37.
Strober, M. (1995). Family-genetic perspectives on anorexia nervosa and bulimia nervosa. In K.D Brownell, and C.G.
Fairburn (Eds), Eating Disorders and Obesity, 212-218. New York: The Guilford Press.
Telch, C.F., & Agras, W.S. (1995). Obesity, binge eating and psychopathology: Are they related? International Journal of
Eating Disorders, 15, 53-62.
Telch, C., Agras, W.S., & Rossiter, E.M. (1988). Binge eating increases with increasing adiposity. International Journal of
Eating Disorders, 7, 115-119.
Van Strien, T. (1986). Eating behaviour, personality traits and body mass. Swets & Zeitlinger B.V.: Lisse.
Vitousek K., Manke F. 1994. Personality variables and disorders in anorexia nervosa and bulimia nervosa. Journal of
Abnormal Psychology 103 (1), 137-47.
Williamson, D.A., Gleaves, D.H., & Savin, S.S. (1992). Empirical classification of Eating disorder, Not Otherwise Specified:
Support for DSM-IV changes. Journal of Psychopathology and Behavioral Assessment , 14, 201-216.
Wilson, G.T., Nonas, C., & Rosenblum, G,D. (1993). Assessment of binge-eating in obese patients. International Journal of
Eating Disorders, 13, 25-34.
Yanovski, S.Z. (1993). Binge eating disorder: Current knowledge and future directions. Obesity Research, 1, 306-324.
Yanovski, S.Z., & Sebring, N.G. (1994). Recorded food intake of obese women with binge eating disorders before and after
weight loss. International Journal of Eating Disorders, 15, 135-150.
Yanovski, S.Z., Nelson, J.E., Dubbert, B.K., & Spitzer, R.L. (1993). Association of binge eating disorder and psychiatric
comorbidity in the obese. American Journal of Psychiatry, 150, 1472-1479.
2. Is Drive for Thinness in Anorectic Patients associated with Personality
Chararteristics?5
Abstract
Objective: The objective was to compare clinical and personality features in anorectic patients (AN) with a high
and low drive for thinness (DT). Method: The samples comprised 244 AN in- and out-patients at the
Department of Psychiatry and Medical Psychology (University of Ghent) in Belgium. Subjects were assessed on
clinical and psychometric parameters. Results: 27% (n=62) of the subjects had low DT as measured by the
Eating Disorder Inventory (EDI) of whom 48 were restricting anorectic patients (ANR). This atypical anorectic
group appeared to have less severe psychopathology with a lower Harm Avoidance and higher Self Directedness as
subscales of the Temperament and Character Inventory (TCI). Discussion: Weight concerns is an important
diagnostic criterion, but may have other motivations than a culture-bound drive for thinness. This differentiation
may have therapeutic consequences.
Introduction
Weight phobia is a main criterion to distinguish patients suffering from eating disorders (EDs)
from those with other psychiatric diagnoses and from non-clinical populations (Russell, 1970, 1979;
DSM-IV, 1994). In anorexia nervosa (AN), this intense fear of fatness perseveres in the face of
emaciation and remains present even after weight restoration (Bastiani, Rao, Weltzin, Kaye; 1995). The
morbid fear of fat is often measured by clinical means and self-report as the drive for thinness (DT;
Ramacciotti, Dell’Osso, Paoli, et al., 2002). Thus, while this feature is considered an important element
in the diagnosis of eating disorders, it is surprising to note that fat phobia or a drive for thinness is
absent in a substantial proportion of non-Western (Lee, Ho & Hsu, 1993) and Western (Ramacciotti et
al., 2002; Strober, Freeman & Morell, 1999) patients. The absence of fat phobia in AN patients has been
explained by the comorbid presence of a conversion disorder (Garfinkel, Kaplan, Garner, & Darby,
1983), by the egosyntonic nature of emaciation (Theander, 1995; Lasègue, 1873/1997), as a consequence
of the denial of illness, and even as a feature of grandiosity (Orimoto & Vitousek, 1992). Furthermore,
Lee et al. (2001) explained the diversity of rationales for food refusal in AN patients as congruous with
5
Vervaet, M., Audenaert, K., & van Heeringen, C. (2004). European Eating Disorders
Review, 12, 375-379.
historical, clinical, and community studies showing that attributions regarding weight and shape were not
static. Instead, they varied with situations (Lee, 1995), across the lifespan (Tiggemann & Stevens, 1999),
and with the body weight (Fairburn, Shafran, & Cooper, 1999).
We recently showed an association between a substantial number of cognitive and behavioural
characteristics and personality traits in ED patients (Vervaet, Audenaert, & van Heeringen, 2003). It
can be questioned whether DT is also associated with particular personality characteristics. Recent
studies of the personality of ED patients have commonly used Cloningers Temperament and Character
Inventory (TCI; Cloninger, Przybeck, Svrakic, & Wetzel, 1994), showing a comparatively high score on
Harm Avoidance and low score on Novelty Seeking and Reward Dependence, the data concerning the
last dimension not being equivocal (Brewerton, Hand, & Bishop, 1993; Bulik, Sullivan, Weltzin, & Kay,
1995; Cloninger et al., 1994; Klump, Bulik, Pollice et al., 2000), and by low scores on Self-Directedness
and high scores on Persistence (Diaz-Marsa, Carrasco, Hollander, Cesar, & Saiz-Ruiz, 2000).
The present study aimed at investigating whether the presence or absence of DT is associated
with personality characteristics in patients with anorexia nervosa.
Methods
Subjects
The study group consisted of patients who were consecutively referred to the in- and out-patient units of
the Centre for Eating Disorders at the Department of Psychiatry of the University Hospital Gent
between December 1998 and March 2003, and who met the DSM-IV criteria for eating disorders. All
patients gave informed consent compliant with the Code of Ethics of the World Medical Association
(Declaration of Helsinki) and the study was conducted following the approval of the local ethics
committee.
Assessments
Weight and height were measured during the first consultation, while highest and lowest adult weight
ever and duration of illness were assessed by self-report. The current body mass index (BMI) was
calculated, as well the highest and lowest lifetime BMI (HBMI, LBMI), based on the highest and lowest
adult weight ever. Age of onset was defined as the age at which eating behaviour changed. Patients were
asked to report the presence (i.e. two or more times per week) or absence of bingeing and/or purging
behaviours.
The Dutch version of the SCAN (WHO-Schedules for Clinical Assessment in Neuropsychiatry)
was used to assign diagnoses according to DSM-IV criteria (Giel & Nienhuis, 1996). Patients also
completed the Eating Disorders Inventory (EDI; Garner, et al., 1983), the Dutch Eating Behaviour
Questionnaire (DEBQ; Van Strien, 1986) and the validated Dutch version of the Temperament and
Character Inventory (TCI; Duysens, Spinhoven, Goekoop, Spermon, & Eurelings-Bontekoe, 2000).
On the basis of the score obtained on the EDI subscale ‘Drive for thinness’ (DT) and calculated
using Garner’s (1991) item-transformation, we divided the sample in two groups. The first group
comprised patients with a DT higher than 7 (the “typical” group) and the second group consisted of
patients with a DT up to 7 (the “atypical” group). The cutoff score of 7 was similar to that in previous
studies (e.g. Ramacciotti et al., 2002) in order to allow for comparison of our results. The six-point
Likert scale was recalculated in a score of 0-3 with a range of the total score between 0 and 21.
Results
Among the total group of referred patients (n=531), 244 (46.0 percent) were diagnosed with anorexia
nervosa, including 167 restrictors (68 percent of the AN patients). Assessment data were available for
226 AN patients (93 percent). Using the above-mentioned EDI-DT cut-off score, the “atypical” group
comprised 62 (27 percent) AN patients, while 164 (73 percent) AN patients constituted the “typical”
group.
The atypical group was significantly larger among restricting AN patients (n=48) than among
binging/purging anorexics (n= 14; Pearson χ² = 20; p < .001). No significant difference in the
proportion of atypical patients was found between in-patients (n=34) and out-patients (n=28; Pearson χ²
= .025; p =.874 ).
Further statistical analysis pursued the comparison between atypical and typical AN patients. As
shown in Table 1, no significant differences were found for the characteristics age, BMI, highest lifetime
BMI and duration of illness. Atypical patients reported a later age of onset of their eating disorder and a
lower lifetime BMI.
Table 1: Clinical characterics, DEBQ and TCI variabels between atypical and typical AN
Atypical AN
(N=62)
Typical AN
(N=164)
T-test
statistics
Mean (SD)
Mean (SD)
23.7 (7.3)
21.9 (7.7)
1.6
BMI
15 (1.5)
15.1 (1.5)
-0.5
HBMI
20.7 (3.1)
21.2 (3.7)
-1.1
LBMI
13.9 (1.8)
14.5 (1.7)
-2.4*
Duration of illness
4.0 (5.0)
3.9 (6.1)
0.1
Age of onset
19.6 (4.8)
18.0 (4.5)
2.3*
Clinical Characteristics
Dutch Eating Behaviour Questionnaire (DEBQ)
Restrained Eating
3.1 (0.9)
4.3 (0.9)
-9.3***
External Eating
3.2 (0.7)
2.9 (1.1)
0.1
Emotional Eating
2.4 (0.9)
2.6 (1.2)
0.2
Temperament en Character Inventory (TCI)
Novelty Seeking (NS)
15.9 (6.3)
16.2 (6.9)
0.8
Harm Avoidance (HA)
21.8 (6.8)
24.8 (6.6)
-3.0**
Reward Dependence (RD)
16.6 (3.6)
16.2 (3.8)
0.5
Persistence (P)
5.9 (2.0)
5.6 (1.9)
0.4
Self-Directedness (SD)
25.3 (7.0)
21.1 (7.4)
3.8***
Cooperativeness (C)
33.4 (4.5)
31.8 (6.7)
0.1
Self-transcendence (ST)
12.3 (6.6)
12.7 (6.4)
0.7
P< 0.05; **P<0.005; ***P<0.001
BMI= body mass index; HBMI = highest adult (>16 years) BMI ever;
LBMI = lowest adult (>= 16 years) BMI ever
Atypical AN patients were also found to score lower on the ‘restrained eating’ subscale of the
Dutch Eating Behaviour Questionnaire (DEBQ). No significant differences were found for scores on
the ‘external eating ‘ and ‘emotional eating’ subscales. With regard to personality characteristics, atypical
patients scored significantly lower on the temperament dimension ‘harm avoidance’ and significant
higher on the character dimension ‘self-directedness’ (Table 1).
While no significant difference was found with regard to the occurrence of binging behaviour,
there were comparatively fewer atypical patients (n= 29; 47 percent) than typical patients (103; 63
percent) who reported purging (Pearson χ² = 4.759; p < 0.05).
Discussion
This study aimed at investigating the occurrence and personality-related correlates of a low drive
for thinness among anorexia nervosa patients by comparing their characteristics with those of anorexia
nervosa patients with a high drive for thinness. The findings indicate that a low drive for thinness is
present in more than one-quarter of these patients, and particularly common among those of the
restricting type. The findings also demonstrate that a low drive for thinness is associated with a higher
age of onset of the eating disorder and with less severe behavioural manifestations such as purging and
restrained eating. Also, with regard to their personality profile, anorexic patients with a low drive for
thinness showed comparatively less severe disturbances, i.e. a relatively less increased harm avoidance
and a relatively less decreased self-directedness, than anorexic patients with a high drive for thinness.
With regard to the occurrence of a low drive for thinness, the current findings are in keeping
with those from previous studies using the same diagnostic criteria for drive for thinness (Ramacciotti et
al., 2002; Strober, Freeman & Morrell, 1999). In accordance with the findings of Lee and colleagues
(Lee, Lee, Ngai, Lee, & Wing, 2001), no differences between the two groups were found regarding BMI,
age at referral and duration of illness. We could not demonstrate a significantly lower premorbid BMI in
association with a low drive for thinness.
It thus appears that a low drive for thinness among anorexia nervosa patients is associated with
less eating-related pathology (lower frequency of purging and less restrained eating) and less severe
psychopathology (lower harm avoidance and higher self-directedness). Strober, Freeman and Morrell
(1999) have stated in a similar way that atypical anorexics have a comparatively smaller chance of
progressing to chronic morbidity, a faster rate of full clinical recovery, and a lower risk of developing a
first onset of binge eating. According to current cognitive behavioural theory, an extreme need to
control eating is the central feature of AN, with a superimposed tendency to judge self-worth in terms of
shape and weight in Western societies (Fairburn, Shafran & Cooper, 1998; Fairburn, Cooper & Shafran,
2003).
This need to control eating has been attributed to fat phobia, but recent research findings
suggest that reinforcing effects of food restriction per se play a crucial role. Kaye et al. (2003) hypothesize
that starvation in anorexia nervosa patients serves to reduce 5-HT neuronal activity in response to their
trait-related (i.e. premorbid and persisting after recovery) increase in serotonergic (5-HT) neuronal
transmission.
This increased 5-HT signal transmission does not respond to normal regulatory
mechanisms, and thus contributes to uncomfortable core symptoms such as obsessionality,
perfectionism, harm avoidance, and anxiety. Starvation is associated with a dietary-induced reduction of
tryptophan (TRP; the precursor of 5-HT), and thus may temporarily reduce this dysphoric behavioural
state. The influence of bingeing or purging on the anxiolytic effect of starvation in anorexia nervosa
patients is currently not known. Our present findings indicate an association between a low drive for
thinness and restricting rather than binging/purging behaviour in anorexia nervosa patients.
The drive for thinness in anorexia nervosa patients may in general thus reflect a drive for food
restriction as a compensatory mechanism for increased anxiety. In view of the comparatively less severe
eating disorder-related symptoms, this mechanism appears to be relatively effective in patients with a low
drive for thinness. Our findings suggest that this relative effectiveness is associated with a comparatively
lower harm avoidance and a higher self-directedness. Low self-directedness is indeed associated with an
external locus of control, and thus with a more outspoken susceptibility to external influences. Knowing
that individuals with character traits denoting low self-directedness and high self-transcendence may be
particularly reactive and susceptible to societal messages referring to the ideology of slenderness
(Gendall, Joyce, Sullivan and Bullik, 1998), it can be hypothesized that typical anorexia nervosa patients
translate their food phobia into a weight phobia, characterized by behavioural compensatory
mechanisms such as more restrained eating and purging.
Ramacciotti et al. (2002) suggest that the treatment of the non-fat phobic group of anorexia
nervosa patients should be less cognitively based and less focused on cultural tyranny and fat. However,
there are several reasons to include cognitive strategies in the treatment of anorexia nervosa patients
with a low drive for thinness. The important interaction between an extreme need for control and the
use of food restriction to judge self-worth in order to cope with anxiety in anorexia nervosa patients
(Fairburn et al., 1998, 2003) requires cognitive restructuring procedures. Such strategies should be added
to behavioural interventions aiming at increasing body weight, perhaps through in vivo exposure to food
to attain the extinction of the anxiety-food connection. In order to prevent relapse, and in keeping with
previous findings (see e.g. Kaye, Barbarich, Putnam et al., 2003), the current study indicates that traitdependent anxiety regulation should also be addressed. In view of the well-documented role of 5-HT in
the modulation of harm avoidance (Cloninger, 2000), serotonergic drugs may be particularly indicated
(Frank, Kaye, Weltzin, et al., 2001; Kaye, Greeno, Moss, et al., 1998).
References
American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). DSM IV, Washington DC:
Author.
Bastiani, A.M., Rao, R:, Weltzin, T. & Kaye, W. (1995) Perfectionism in anorexia nervosa. International Journal of Eating
Disorders, 17(2), 147-52.
Brewerton, T.D., Hand, L.D., & Bishop, E.R. (1993). The Tridimensional Personality Questionnaire in eating disorder
patients. International Journal of Eating Disorders, 14, 213-218.
Bulik, C.M., Sullivan, P.F., Weltzin, T.E., & Kay, W.H. (1995). Temperament in eating disorders. International Journal of Eating
Disorders, 17, 251-261.
Cloninger, C.R., Przybeck, T.R., Svrakic, D.M., & Wetzel, R.D. (1994). The Temperament and Character Inventory (TCI): A guide to
its development and use. St. Louis, MO: Center for Psychobiology of Personality, Washington University.
Cloninger, C.R. (2000). Biology of personality dimensions. Current opinion in Psychiatry, 13, 611-616.
Diaz-Marsa, M., Carrasco, J.L., & Saiz-Ruiz, J. (2000). A study of temperament and personality in anorexia and bulimia
nervosa. Journal of Personal Disorders , 14(4), 352-359.
Duijsens, I.J., Spinhoven, P., Goekoop, J.G., Spermon, T., & Eurelings-Bontekoe, E.H.M. (2000). The Dutch temperament
and character inventory (TCI): dimensional structure, reliability and validity in a normal and psychiatric outpatient sample.
Personality and Individual Differences, 28, 487-499.
Fairburn, C.G., Shafran, R., & Cooper, Z. (1998). A cognitive behavioural theory of anorexia nervosa. Behaviour Research and
Therapy, 37, 1-13.
Fairburn, C.G., Cooper, Z., & Shafran, R. (2003). Cognitive behaviour therapy for eating disorders: a “transdiagnostic”
theory and treatment. Behaviour Research and Therapy, 41, 509-528.
Frank, G.F., Kaye, W.H., Weltzin, T.E., Perel, J., Moss, H., McConaha, C., & Pollice, C. (2001). Altered response to metachlorophenylpiperazine in anorexia nervosa: support for a persistent alteration of serotonin activity after short-term weight
restoration. International Journal of Eating Disorders, 30, 57-68.
Garfinkel, P.E, Kaplan, A.S., Garner, D.M., & Darby, P.L. (1983). The differentiation of vomiting and weight
loss as a conversion disorder from anorexia nervosa. American Journal of Psychiatry, 140, 1019-1022.
Garner, D.M. (1991). Eating Disorder Inventory-2 Manual. Odessa: Psychological Assessment Resourses, Inc.
Garner, D.M., Olmstead, M.P, & Polivy, J. (1983). The Eating Disorders Inventory: A measure of cognitive-behaviroural
dimensions of anorexia and bulimia. In P. L. Darby (Ed.), Anorexia Nervosa: Recent developments in research (pp. 173-184). New
York: Alan R. Liss.
Garner, D.M., Olmstead, M.P., & Polivy, J. (1985). Development and validation of a multidimensional eating disorder
inventory for anorexia nervosa and bulimia. International Journal of Eating Disorders, 2, 15-34.
Gendall, K.A., Joyce, P.R., Sullivan, P.F., & Bulik, C.M. (1998). Personality and dimensions of dietary restraint. International
Journal of Eating Disorders, 24, 371-379.
Giel, R. & Nienhuis, F.J. (1996). Vragenschema’s voor de klinische beoordeling in de neuropsychiatrie. World Health Organisation
Mental Health, Geneva.
Hsu, L.K., Lee, S. (1993). Is weight phobia always necessary for a diagnosis of anorexia nervosa? American Journal of psychiatry,
150 (10), 1466-71.
Humphrey, L.L. (1991). Object relations and the family system: An integrative approach to understanding and treating eating
disorders. In C. Johnson (Ed.), Psychodynamic treatment of anorexia nervosa and bulimia (pp. 322-353). New York: Guilford Press.
Kaye, W.H., Greeno, C.G., Moss, H., Fernstrom, J., Fernstrom, M., Lilenfeld, L.R., Weltzin, T.E., & Mann, J.J. (1998).
Alterations in serotonin activity and psychiatric symptomatology after recovery from bulimia nervosa. Archives of General
Psychiatry, 55, 927-935.
Kaye, W.H., Barbarich, N.C., Putnam, K., Gendall, K.A., Fernstrom, J., Fernstrom, M., McConaha, C.W., & Kishor, A.
(2003). Anxiolytic effects of acute tryptophan depletion in anorexia nervosa. International Journal of Eating Disorders, 33, 257267.
Kleifield, E.I., Sunday, S., Hurt, S.W., & Halmi, K.A. (1993). Psychometric validation of the Tridimensional Personality
Questionnaire: Application to subgroups of eating disorders. Comprehensive Psychiatry , 249-253.
Klump, K.L., Bulik, C.M., Pollice, C., Halmi, K.A., Fichter, M.M., Berrettini, W.H., Devlin, B., Strober, M., Kaplan, A.,
Woodside, D.B., Treasure, J., Shabbout, M., Lilenfeld, L.R., & Plotnicov, K.H. (2000). Temperament and character in
women with anorexia nervosa. The Journal of Nervous and Mental Disease, 188 (9), 559-567.
Lasègue, E.C. (1997). On hysterical anorexia. Obesity Research, 5, 492-497. (Original work published in 1873).
Lee, S., Ho, P., & Hsu, L.K.G. (1993). Fat phobic and non-fat phobic anorexia nervosa: A comparative study of 70 Chinese
patients in Hong Kong. Psychological Medicine, 23, 999-1017.
Lee, S. (1995). Self-starvation in contexts: Towards the culturally sensitive understanding of anorexia nervosa. Social Science
and Medicine, 41, 25-36.
Lee, S., Lee, A.M., Ngai, E, Lee, D.T.S, & Wing, Y.K. (2001). Rationales for food refusal in Chinese patients with anorexia
nervosa. International Journal of Eating Disorders, 29, 224-229.
Orimoto, L., & Vitousek, K.B. (1992). Anorexia nervosa and bulimia nervosa. In P. H. Wilson (Ed.), Principles and practice of
relapse prevention (pp. 85-127). New York: Guilford Press.
Ramacciotti, C.E., Dell’Osso, L., Paoli, R.A., Ciapparelli, A., Coli, E., Kaplan, A.S., & Garfinkel, P.E. (2002). Characteristics
of eating disorder patients without a drive for thinness. International Journal of Eating Disorders, 32, 206-212.
Regier, E., Touyz, S.W., Swain, T., & Beumont, P.J.V. (2001). Cross-cultural research on anorexia nervosa: Assumptions
regarding the role of body weight. International Journal of Eating Disorders, 29, 205-215.
Russell, G.F.M. (1970). Anorexia nervosa; Its identity as an illness and its treatment. In J.H. Price (Ed.), Modern trends in
psychological medicine (Vol.2, pp. 131-164). London: Butterworths.
Russell, G.F.M. (1979). Bulimia nervosa: An ominous variant of anorexia nervosa. Psychological Medicine, 9, 429-448.
Strober, M., Freeman, R., & Morell, W. (1999). Atypical anorexia nervosa: separation from typical cases in course and
outcome in a long-term prospective study. International Journal of Eating Disorders, 25, 135-142.
Tellegen, A. (1985). Structures of mood and personality and their relevance to assessing anxiety with an emphasis on selfreport. In Tuma, A.H. & Maser, J.D (Eds), Anxiety and anxiety disorders (pp. 681-706). Stad-uitgeverij.
Tiggemann, M., & Stevens, C. (1999). Weight concern across the life-span: Relationship to self-esteem. International Journal
of Eating Disorders, 26, 103-106.
Theander, S. (1995); The essence of anorexia nervosa: Comment on Gerald Russell’s Anorexia nervosa through time.” In G.
Szmukler, C. Dare, & J. Treasure (Eds.), Handbook of eating disorders: Theory, treatment and research (pp. 19-24). London: Wiley.
Van Strien, T. (1986). Eating behaviour, personality traits and body mass. Swets & Zeitlinger B.V.: Lisse.
Van Strien, T., Frijters, J.E.R., Bergers, G.P.A., & Defares, P.B. (1986). The Dutch Eating Behaviour Questionnaire (DEBQ)
for assessment of restrained, emotional and external eating behaviour. International Journal of Eating Disorders, 5, 295-315.
Vervaet, M., Audenaert, K., & van Heeringen, C. (2003). Cognitive and behavioural characteristics are associated with
personality dimensions in patients with eating disorders. European Eating Disorders Review, 11, 1-16.
Vitousek, K. (1996) The current status of cognitive-behavioral models of anorexia nervosa and bulimia nervosa. In P.
Salkovskis (Ed.), Frontiers of Cognitive Therapy (pp. 383-418). New York: Guilford Press.
Waller, D.A., Gullion, C.M., Petty, F., Hardy, B.W. & al. (1993). Tridimensional Personality Questionnaire and serotonin in
bulimia nervosa. Psychiatry Research , 48 9-15.
3. Cognitive and behavioral characteristics are associated with personality
dimensions in patients with eating disorders6
DSM-IV categorizes eating disorders according to behavioural and cognitive characteristics. Based on personalityrelated and biological research, hypotheses have been formulated to explain differences in the symptomatology
between the various types of eating disorders. Therefore, the study of the association between personality-related
characteristics and behavioural and cognitive characteristics may contribute to our understanding of the causes and
course of eating disorders. This study aimed, first, at describing personality characteristics (using Cloninger’s
Temperament and Character Inventory) in a group of eating disordered patients (n= 272) according to the type of
eating disorder. Three groups were compared: restricting anorexics (n=71), purging anorexics (n=84) and
bulimics (n=118). Secondly, the association between personality characteristics and cognitive and behavioural
aspects, using the Eating Disorders Inventory and the Dutch Eating Behaviour Questionnaire, was measured. In
bulimics, positive correlations were found between novelty seeking on the one hand and external and emotional
eating and bulimia on the other. Contrary to expectation, there was no significant correlation between novelty
seeking and body dissatisfaction in bulimics. The significant difference between the restricting and purging type of
anorexics regarding self-directedness, and restrained and emotional eating and drive for thinness was corresponding
with the significant negative correlation between these characteristics.
Introduction
Evidence is accumulating that stable personality traits play a major role in the development of
eating disorders. It has been shown with remarkable consistency that restricting-type anorexia nervosa,
in particular, is characterized by a cluster of such traits. These temperamental characteristics include
emotional restraint, avoidance of novelty, anxious worry and self-doubt, weight- and shape- related
anxiety, compliancy, obsessionality, rigidity, over-control, perfectionism, and perseverance in the face of
non-reward (Beumont, George, & Smart, 1976; Bruch, 1978; Halmi et al., 2000, Lilenfeld, Kaye, &
Strober, 1997; Lilenfeld & Kaye, 1998; Pryor & Wiederman, 1996; Strober, 1980, 1995). Retrospective
studies indeed suggest that these characteristics commonly predate the onset of the eating disorder, and
remain present even after long-term weight restoration (Pollice, Kaye, Greenco, & Weltzin, 1997;
Srinivasagan, Kaye, Plotnicov, Greeno, Weltzin, & Rao, 1995; Strober, 1980).
6
Vervaet, M., Audenaert, K., & van Heeringen, C. (2003). European Eating Disorders
Review, 11 (5), 363-379.
Although the clinical presentation of bulimia nervosa is less consistent than the symptomatology
of restricting-type anorexia nervosa, the involvement of a number of behavioural traits in the
development of this disorder has been shown to be equally prevalent. Such traits include thrill-seeking
and excitability, affective instability and impulsivity, and a tendency towards marked dysphoria in
response to rejection or non-reward (Bulik, Beidel, Duchman, Weltzin, & Kaye, 1992; Casper, Hedeker,
& McKlough, 1992; Diaz-Marsa, Carrasco, & Saiz, 2000; Vitousek & Manke, 1994).
These
characteristics may protect individuals against sustained dietary restriction, and, thus, predispose an
individual to periodic loss of control and eventual dietary chaos. Some traits may be involved in the
development of both anorexia and bulimia nervosa, as over-concern with body image and thinness,
increased harm avoidance, dysphoria, obsessions about symmetry or exactness, and perfectionism may
persist following recovery from these disorders (Anonymous, 2001; Casper, 1990; Diaz-Marsa et al.,
2000; Kaye et al., 1998; Kaye, Strober, Stein, & Gendall, 1999; Srinivasagam et al., 1995).
Research on brain neurotransmitter systems has supported the hypothesis that an underlying
biological diathesis and temperament may place someone at risk for developing anorexia (Kaye, 1997).
For example, increased levels of 5-HIAA, the major metabolite of serotonin, have been found in the
cerebrospinal fluid (CSF) of anorexia and bulimia nervosa patients which persist after long-term clinical
recovery from (Kaye, Gwirtsman, George, & Ebert, 1991; Kaye et al., 1998). It has been suggested that
increased levels of CSF 5-HIAA reflect an increased activity of the serotonergic system that could
contribute to behavioural constraint, obsessionality, and inhibition of appetite (Soubrie, 1986; Spoont,
1992). Increased serotonin activity could make people specifically vulnerable to developing an eating
disorder as well as certain core phenotypic aspects of these disorders, including anxious dysphoria,
obsessional thinking, perseverance, and cognitive distortions of the aversive consequences of eating and
weight gain (Kay and Strober, 2003). These processes could be further enhanced by malnutritiontriggered changes in hypothalamic neuropeptides, that modulate conditional learning (Demitrack et al.,
1990).
Cloninger (1986, 1987a, 1987b) has developed a psychobiological model of personality including
clearly defined traits or personality dimensions. The initial model included three temperamental
dimensions which are thought to be independently heritable and mediated by separate neurobiological
mechanisms. Novelty seeking (NS) reflects behavioural activation, a tendency toward frequent
exploratory activity and excitement in response to novel stimuli. Harm avoidance (HA) describes the
tendency to respond to aversive stimuli and thus to inhibit behaviour to avoid punishment or frustrating
non-reward. Reward dependence (RD) reflects the maintenance of behaviour that has been previously
rewarding, especially in the interpersonal sphere.
Normative studies using the TPQ confirmed the structure of temperament with the exception
that persistence (P) emerged as distinct fourth temperamental dimension, describing perseverance
despite frustration or fatigue (Cloninger, Svrakic, & Przybeck, 1993). Further observations suggested
that the TPQ did not measure aspects of personality that are related to dimensions of character, or the
development of self-concepts. The character dimensions include self-directedness, cooperativeness, and
self-transcendence. Self-directedness (SD) is characterized by responsibility and resourcefulness in
initiating and organizing steps to achieve personal goals. Cooperativeness (C) describes social tolerance,
empathy, helpfulness, compassion, and moral principles.
Self-transcendence (ST) involves the
spontaneous feeling of participation in one’s surroundings as a united whole.
These additional
dimensions were included in the “seven factor model”, that can be assessed by means of the
Temperament and Character Inventory (Cloninger et al., 1993; Svrakic, Whitehead, Przybeck, &
Cloninger, 1993).
The diagnosis of eating disorders according to criteria such as those in the DSM classification
system is based mainly on cognitive and behavioural characteristics. It might, however, be interesting to
study the association between these characteristics and personality dimensions for the following reasons.
First, a growing body of evidence supports the existence of separate genetic and neurobiological
underpinnings of personality characteristics such as Cloninger’s temperament dimensions. For example,
an association between serotonergic dysfunction and the temperamental dimension HA has been
described, and evidence of a genetic contribution to the variation in NS is increasing (Kaye et al., 2001).
Insight in the association between such personality characteristics and eating disorders can therefore be
expected to contribute to our knowledge of the genetic and neurobiological aspects of eating disorders.
Second, insight into the role of personality characteristics in the development of eating disorders may
provide new approaches in treatment and prevention.
Therefore, this study aimed, first, at describing personality dimensions and eating-disordered
related cognitive and behavioural aspects in patients who suffer from eating disorders according to the
type of eating disorder. Secondly, this study aimed at describing the association between core cognitive
and behavioural characteristics of eating disorders and these personality dimensions.
Methods
Subjects
Three hundred eighteen patients who were consecutively referred to the in- and out-patient
Eating Disorders Unit at the Department of Psychiatry of the University Hospital Gent between
December 1998 and June 2001 and who met the DSM criteria of Eating Disorders were enrolled in the
study. Research was compliant with the Code of Ethics of the World Medical Association (Declaration
of Helsinki) and performed following the guidelines of the local ethics committee.
Clinical measures
Weight and height, highest and lowest weight ever and duration of illness were carefully checked.
The body mass index (BMI) was calculated, as well the highest and lowest body mass index (HBMI,
LBMI), based on the highest and lowest weight ever.
Instruments
The Dutch version of the SCAN (Schedules for Clinical Assessment in Neuropsychiatry) was
used as a structured clinical interview to assign a diagnosis according to DSM-IV criteria (Giel &
Nienhuis, 1996). The Dutch translation of the Eating Disorders Inventory was used (EDI; Garner,
Olmstead, & Polivy, 1983) with subscales assessing the drive for thinness, bulimia, body dissatisfaction,
ineffectiveness, perfectionism, interpersonal distrust, interceptive awareness and maturity fears. The
validated Dutch version of the TCI (Duysens, Spinhoven, Goekoop, Spermon, Eurolings-Bontekoe,
2000) was used as a personality questionnaire to assess temperament and character characteristics. The
Dutch Eating Behaviour Questionnaire (DEBQ; Van Strien, 1986) was used to assess the behavioural
characteristics: emotional eating (eating elicited by diffuse and clear emotional stimuli), restrained eating
(the tendency to diet in order to lose weight), and external eating (eating elicited by external stimuli).
Statistics
Statistical analysis was performed using SPSS 9.0. One way ANOVA with post hoc Bonferroni
comparision was used to compare three diagnostic subgroups: anorectic restrictors (AN-R), anorectic
binge-eating/purging type (AN-P) and bulimics (B). These groups were compared with regard to
demographic, clinical and behavioural (DEBQ), cognitive (EDI) and personality (TCI) characteristics.
Correlations between personality dimensions and scores on the EDI and DEBQ were measured by
calculating Pearson correlation coefficients.
Results
The referred group consisted of 318 patients, including 154 (48,4%) anorectic patients of whom
70 (22 %) were restrictor-type anorectics (AN-R) and 84 (26,4 %) were purging-type anorectics (AN-P).
Among the bulimic patients (B=118; 37,1 %), 100 (31,4 %) were purging-type bulimics and 18 (5,7 %)
were non-purging type bulimics. The category of eating disorders not otherwise specified (EDNOS),
contained 46 (14,4 %) patients of whom 16 (5.0 %) met the criteria of binge eating disorder (BED).
This paper will report on the findings in anorectic and bulimic patients. In view of the specific nature of
the findings in EDNOS patients, these will be reported in a forthcoming paper (Vervaet et al.,
unpublished data).
As no differences were found between the purging and non-purging bulimics,
bulimics (B) were described as one group and compared to ‘anorectic restrictors’ (AN-R) and ‘purging
anorectics‘ (AN-P). The group of 272 patients contains 268 females (age range: 13 to 49 years; mean =
22.3; sd = 7.0) and 4 males, 1 restricting-anorectic and 3 purging bulimics (age range: 14 to 44 years;
mean = 25.5; sd =12.9).
Table 1: Age, BMI and duration of illness, by type of eating disorder.
Variable
Age(years)
BMI
(kg/m2)
LowestBMI
After 16
HighestBMI
After 16
Duration of
ED (years)
AN-R
N= 70
M
SD
21,17
6,49
14,64b
1,50
AN-P
N= 84
M
SD
23,11
7,66
15,32c
1,34
B
N= 118
M
SD
22,11
6.88
20,09bc
3,35
13,73b
1,68
19,78ab
2.20
3,23
3,52
14,41c
1,66
21.42ac
3.14
4,67
5,12
18,27bc
2,82
25.12bc
4.34
4,06
4,20
F
p
1.51
0.222
206.58
0.000
116.66
0.000
56.194
0.000
2.103
0.124
ED = eating disorder; AN-R = anorexia nervosa of the restricting type
AN-P = anorectics of the purging type; B = bulimic women
ANOVA with Bonferoni post hoc comparison (significant p<0.05 level)
a = comparison between AN-R and AN-P
b = comparison between AN-R and B
c = comparison between AN-P and B
When comparing B patients to AN-R and AN-P patients, there was no difference
regarding age and duration of illness. As expected, the BMI at admission (AN-R: m=14.6; sd=1.5; ANP: m=15.3; sd=1.3), lowest BMI ever (AN-R: m=13.7; sd=1.7; AN-P: m=14.4; sd=1.7) and highest BMI
ever (AN-R: m=19.8; sd=2.2; AN-P: m=21.4; sd=3.1) were significantly lower (p<0.001) in the ANgroup than in the B-group (BMI: m=20.1; sd=3.3; LBMI: m=18.3; sd=2.8; HBMI: m=25.1; sd=4.3).
The only difference between the restricting and purging anorexics was a significant higher BMI ever
among patients in the latter group (p=0.014).
Comparing the behavioural characteristics, there was no difference regarding eating with diffuse
or clear emotions. Thus, only scores on ‘total emotional eating’ were included in the further analyses.
Table 2: Behavioural characteristics by type of eating disorders.
AN-R AN-P
N= 67 N= 81
Variable
Restrained
eating
External
eating
Total
emotional
eating
M
SD
3.59ab
1.16
2.96b
0.94
2.15ab
1.00
M
SD
4.20a
1.10
3.02c
0.92
2.79ac
1.18
B
N=
109
M
SD
4.24b
0.81
3.57bc
1.01
3.76bc
1.00
F
p
9.80
0.000
11.56
0.000
51.19
0.000
ED = eating disorder; AN-R = anorexia nervosa of the restricting type; AN-P = anorectics of the purging type; B = bulimic
women
ANOVA with Bonferoni post hoc comparison (significant p<0.05 level)
a = comparison between AN-R and AN-P; b = comparison between AN-R and B; c = comparison between AN-P and B
Scores on restrained eating were lower in the AN-R group (p=.000; m=3.6; sd= 1.2) than in the
AN-P group (m=4.2; sd=1.1) and the B-group (m=4.24; sd=0.81). Anorexics had a lower score on
external eating (p=.000; AN-R: m=3; sd= 0.9; AN-P: m=3; sd=0.9)) in comparison with the bulimic
group (m=3.6; sd= 1). The scores on the emotional (p=.000) subscale of the DEBQ were lowest for
the AN-R group (m= 2.1; sd=1) and lower for the AN-P group (m=2.8; sd=1.2) when comped to the
B-group (m=3.8; sd=1).
For the cognitive characteristics only significant differences were found for the ‘drive for
thinness’ (p=.000), ‘bulimia’ (p=.000) and ‘body dissatisfaction’ (p=.000), subscales of the EDI.
Table 3: Cognitive characteristics by type of eating disorders.
Variable
EDI
Drive
thinness
Bulimia
for
Body
dissatisfaction
Ineffectiveness
Perfectionism
Interpersonal
distrust
Interceptive
awareness
Maturity fears
AN-R
N= 70
M
SD
9.94ab
7.12
0.76ab
1.49
11.50b
6.51
11.50
7.59
7.13
4.95
5.90
4.58
9.33
5.31
7.57
5.67
AN-P
N= 83
M
SD
13.75a
6.54
4.37ac
5.32
13.48c
7.87
13.34
7.49
8.19
4.79
6.94
4.58
10.69
5.66
6.73
5.21
B
N= 115
M
SD
15.49b
5.27
9.52bc
5.80
17.02bc
7.46
12.45
8.18
7.25
5.27
5.55
4.43
10.90
5.86
7.34
5.95
F
p
17.55
0.000
74.19
0.000
13.34
0.000
1.05
0.352
1.11
0.331
2.36
0.097
1.81
0.165
0.46
0.628
ED = eating disorder; AN-R = anorexia nervosa of the restricting type; AN-P = anorectics of the purging type; B = bulimic
women
ANOVA with Bonferoni post hoc comparison (significant p<0.05 level)
a = comparison between AN-R and AN-P; b = comparison between AN-R and B; c = comparison between AN-P and B
The ‘drive for thinness’ was lower in the AN-R group (m=9.9; sd=7.1) when compared to the AN-P
group (m=13.7; sd=6.5) and the bulimic group (m=15.5; sd=5.3). Scores on the ‘bulimia’ subscale were
lowest (p=.000) in the AN-R group (m=0.8; sd=1.5), and lower among the AN-P patients (m=4.4;
sd=5.3) than in the bulimics (m=9.5; sd=5.8). Finally, ‘body dissatisfaction’ was lower (p=.000) in the
anorectic group (AN-R: m=11.50; sd=6.51; AN-P: m=13.5; sd=7.9), than in the bulimic group (m=17;
sd=7.5).
The scores on the Temperament and Character Scales are shown in Table 4.
Table 4: Personality characteristics by type of eating disorder
Variable
TCI
Novelty
seeking(NS)
Exploratory
excitability (NS1)
Impulsiveness
(NS2)
Extravagance
(NS3)
Harm avoidance
(HA)
Reward
Dependence
(RD)
Persistence (P)
Self-directedness
(SD)
Enlightened
Second Nature
(SD5)
Cooperativeness
(CO)
Selftranscendence
(ST)
AN-R
N= 70
M
SD
15.37b
6.14
5.06
2.79
3.04b
2.15
2.79ab
2.27
23.72
6.90
16.32
3.98
AN-P
N= 84
M
SD
16.33c
7.09
4.68c
2.53
3.19c
2.48
3.96ac
2.63
24.94
6.29
16.35
3.19
B
N= 109
M
SD
19.49bc
6.62
5.63c
2.59
4.13bc
2.51
4.84bc
2.40
23.85
7.09
16.39
3.84
5.81b
1.99
23.25ab
7.56
5.59
2.09
20.30a
7.28
6.47ab
2.89
32.60
7.27
12.66
6.81
F
p
9.59
0.000
3.14
0.045
5.54
0.004
14.80
0.000
0.77
0.462
0.01
0.994
5.03b
1.95
19.61b
7.01
3.65
0.027
5.56
0.004
5.38a
2.40
4.56b
2.18
12.75
0.000
31.79
5.64
12.99
6.22
31.68
6.07
11.85
7.13
0.49
0.610
0.71
0.495
ED = eating disorder; AN-R = anorexia nervosa of the restricting type; AN-P = anorectics of the purging type; B = bulimic
women
ANOVA with Bonferoni post hoc comparison (significant p<0.05 level)
a = comparison between AN-R and AN-P; b = comparison between AN-R and B; c = comparison between AN-P and B
The temperament dimensions ‘Novelty Seeking’ (p=.000) and ‘Persistence’ (p=.027) differed
significantly between anorectic and bulimic patients.
‘Novelty Seeking’ and the ‘impulsiveness’
subdimension (p=.004) were lower among patients in the AN-R group (NS: m=15.4; sd=6.1; NS2: m=3;
sd=2.1) than among those in the AN-P group (NS: m=16.3; sd=7.1; NS2: m=3.2; sd=2.5) and among
bulimic patients (NS: m=19.5; sd=6.6; NS2: m=4.1; sd=2.5). ‘Exploratory excitability’ was lower
(p=.045) in the AN-P group (m=4.7; sd=2.5) than in the B group (m=5.6; sd=2.6). The scores on
‘Extravagance’ were lowest (p=.000) in the AN-R group (m=2.8; sd=2.3), but also lower in the AN-P
(m=4; sd=2.6) than in the B group (m=4.8; sd=2.4). Persistence was significantly higher in the AN-R
group (m=5.8; sd=2) in comparison with bulimic patients (m=5; sd=1.9).
Character dimensions differed with regard to ‘Self-directedness’, with a highest score (p=.004)
for the restrictor-type of Anorexia Nervosa (m=23.2; sd=7.6), especially due to a higher ‘Enlightened
Second Nature’ (p=.000) in this latter group (m=6.5; sd=2.9) compared to the other groups (AN-P:
m=5.4; sd=2.4; B: m=4.6; sd=2.2).
The group of restrictors (n=71) may not have been homogeneous with regard to duration of
illness, so that this specific group was split into a ‘chronic’ group, with a duration of illness of 5 years
and more, and an ‘acute’ group with less than 5 years duration of illness. The ‘chronic’ group (n = 18)
differed from the ‘acute’ group (n = 53) only in a higher score on reward dependence (m=18.6; sd=3.7
versus m=15.6; sd=3.7; p=.011; df=2). The difference seems to be caused more specifically by a higher
score on the subscale ‘attachment’ (m=5.6; sd=2.5 versus m=4; sd=2.2; p=.048; df=2). The same
distinction was made for bulimics, but revealed no differences. Bulimics were also divided in two weight
groups, with a cut-off score of BMI 20 without showing any differences in personality characteristics
between the bulimics with lower and higher weight.
Further statistical analyses pursued the assessment of correlations between personality
dimensions, cognitive aspects and behavioural characteristics (Table 5).
Table 5: Correlations between personality dimensions and cognitive and behavioural
characteristics of eating disordered patients
NS
HA
RD
P
SD
CO
ST
Bulimia
.26**
-.02
-.07
-.09
-.11
-.12
.02
Drive for
thinness
Dissatis—
faction
Ineffecti
veness
Perfecti
onism
Distrust
.12
.30**
-.02
.01
-.44**
-.12
.23*
-.04
.36**
.10
.09
-.46**
-.03
.16
-.2 9**
.60*
-.03
.01
-.50**
.02
-.03
-.28**
.18
.14
.43**
-.10
.05
.11
-.28**
.34**
-.41**
-.09
-.32**
-.12
-.03
Interoceptiveness
-.05
.43**
-.09
.09
-.40**
-.08
.18
Maturity
-.14
.36**
-.03
.10
-.30**
-.09
.07
Restrained
eating
External
eating
Total
emotional
-.01
.28**
.05
.19
-.26**
-.10
.12
.22*
-.14
-.08
-.18
-.05
-.10
.12
.235*
.082
-.161
-.075
-.219*
-.252
-.126
* = p < . 05, ** = p < . 01
The scores on personality dimensions correlated significantly with a number of those rating
cognitive and behavioural characteristics. Temperament factors correlated in particular strongly with
cognitive characteristics. Novelty Seeking was found to correlate with ‘bulimia’, ‘ineffectiveness’,
‘perfectionism’ and ‘distrust’, characteristics in particular, reflecting a loss of control, as found in
behavioural characteristics such as emotional and external eating. Harm Avoidance particularly
correlated with characteristics reflecting as ‘drive for thinness’, ‘dissatisfaction’, ‘ineffectiveness’,
‘distrust’, ‘interoceptiveness’ and ‘maturity’ and behavioural inhibition. Reward Dependence correlated
significantly with ‘distrust’, Persistence with ‘perfectionism’, and Self-Transcendence with ‘drive for
thinness’.
Discussion
The main findings from this study can be summarized as follows. First, within the group of
eating disordered patients, personality characteristics differ between types of eating disorders to such an
extent that, when compared to bulimic patients, anorectic patients have significantly lower scores on
novelty seeking, more specifically on the subdimensions ‘impulsiveness’ and ‘extravagance’.
The
findings regarding novelty seeking and impulsiveness are in keeping with those from previous studies
(Brewerton, Dorn, & Bishop, 1992. Brewerton, Hand, & Tellegen, 1993; Bulik, Sullivan, Weltzin, &
Kaye, 1995; Kleifield, Sunday, Hurt, & Halmi, 1993; Tellegen, 1985; Waller et al., 1993). Purging
anorectics also differ from bulimics in lower ‘exploratory excitability’, which parallels previous findings
on the role of impulsivity in BN. Restricting anorexics score higher on the character scale Selfdirectedness and the subscale of ‘enlightened second nature’, in comparison with the purging type of
anorexia. The scores of this latter group are higher on ‘extravagance’ compared to the restrictor-type of
anorexia nervosa. The higher score of the ‘chronic’ anorectic restrictor group on reward dependence is
in keeping with the study of Bulik and colleagues (1995).
Secondly, the types of eating disorders studied differ with regard to cognitive and behavioural
characteristics. In general, bulimic patients show higher scores on measures of behavioural
characteristics, including eating induced by emotional and external stimuli, and more restrained eating
when compared to the restrictor type of anorexia. Higher scores are also found for cognitive
characteristics such as ‘bulimia’ and ‘body dissatisfaction’, compared to anorexics, and a higher ‘drive for
thinness’, compared to the restrictor type. Within the group of anorectic patients, the restricting type
scores lower on restrained and emotional eating and on the drive for thinness and bulimia when
compared to the purging type.
Thirdly, the study of the association between personality characteristics and cognitive or
behavioural characteristics shows three main patterns of correlations. Novelty seeking correlates
positively with behavioural characteristics, such as eating following emotional or external triggers, and
with bulimia, while negative correlations are found with cognitive factors, including ineffectiveness,
perfectionism and distrust. Harm avoidance correlates positively with all assessed cognitive
characteristics, except for bulimia and perfectionism with restrained eating. Reward Dependence
correlates negatively with interpersonal distrust, and Persistence positively with perfectionism. Finally,
self-directedness correlates negatively with nearly all behavioural (except for external eating) and
cognitive characteristics (except for bulimia and perfectionism), and self-transcendence positively with
the drive for thinness. This latter finding corresponds with the results of a recent study in a group of
101 women in a random general population sample, using the TCI, showing that individuals with
character traits denoting low ‘Self-directedness’ and high ‘Self-transcendence’ may be particularly reactive
and susceptible to societal messages referring to the ideology of slenderness (Gendall, Joyce, Sullivan, &
Bulik, 1998).
There is a paucity of studies on the association between personality characteristics, using the
TCI, and cognitive or behavioural aspects. Our finding of patterns of correlations between, on the one
hand, novelty seeking and self-directedness, and, on the other hand, the assessed behavioural and
cognitive characteristics as described above, are in keeping with clusters of characteristics found in
bulimics such as higher novelty seeking, more external and emotional eating, and bulimia. However,
contrary to expectations no significant correlation between novelty seeking and body dissatisfaction in
bulimics can be demonstrated. The significant difference between the restricting and purging type of
anorexics corresponds with the significant negative correlation between self-directedness, restrained and
emotional eating and drive for thinness. The lower score on extravagance, a subscale of novelty seeking,
can probably explain the lower bulimia, since the tendency toward extravagance may reflect a liability to
spend money on food or the ‘all or nothing’ thoughts (I’ve taken a bite/blown my diet, so I may as well
binge) that characterize disinhibition (Gendall et al., 1998).
With regard to the cognitive and behavioural characteristics, we found, as expected, that eating
induced by emotions or external stimuli is more commonly reported by bulimic than by anorectic
patients, and that, among the anorectic patients, emotional eating is more common among the purging
type than the restricting anorectics. The finding that mean scores on restrained eating are higher among
the purging than among the restricting anorectic patients was not expected. This can however, be
explained by the lower drive for thinness in the latter group. Clinical experience indeed suggests that the
wish to eat as little as possible is more consciously present among girls who show loss of control over
eating. Purely anorectic patients commonly do not even experience the fact that they eat so little. The
more outspoken body dissatisfaction among bulimic when compared to anorectic patients is probably
related to this finding. Clinical experience and the scarce literature on the subject suggest a difference in
the meaning of dieting between restricting and bulimic patients. The former group of patients may
regard dieting as an achievement, like doing something that others are not able to do, while the motive
for dieting among the latter group of patients may include a wish to be reinforced as a person by having
an attractive body. Among anorectic patients the denial of bodily needs is more prominent than
dissatisfaction with their appearance. Due to a similar dissatisfaction bulimic patients experience an
increasing wish for slenderness following loss of control, based on the fear of not being regarded as
beautiful (conform social pressure), and extremely afraid of being overweight (as before). Among
purging anorectics, loss of control may induce feelings of guilt concerning their perceived indolence.
The greater body dissatisfaction experienced by bulimics can of course, also be an expression of a low
self-esteem, characterized by emotional chaos.
It appears that the combination of high Harm
Avoidance, compared to normals, and higher Novelty Seeking among bulimics (Waller et al., 1993),
compared to anorexics, becomes manifest through the instability of affects and impulses, as seen in
bulimics (Humphrey, 1991). In case of the anorexics, Strober (1991) postulated in a similar way that the
“core of Anorexia Nervosa lies in genotypic personality structures that predispose…to rigid…avoidance
behaviours with marked obsessional, anxious-depressive colouring” (Steiger & Séguin, 1999).
As described above, the implications for treatment and prevention are an important impetus for
the study of personality characteristics in eating disordered patients. Cloninger and colleagues (1993)
have described therapeutic implications of their psychobiological model by stating that, assuming that
character and temperament involve concept-based and percept-driven memory, respectively, stable
personality change probably requires that conceptual insights modify habits by discipline practice,
perhaps facilitated by combined pharmacotherapy. Personality change has both rational and emotional
components (Cloninger, et al., 1993). This means that behavioural and cognitive techniques, aiming at a
normalization of eating patterns and at an increase in self-esteem and in social skills by promoting
conflict-handling and problem solving capacities have their place in cognitive behavioural treatment of
eating disorders, if they include perceptual (i.e. temperamental) and conceptual (i.e. character-based)
learning processes. By including the potential of perceptual learning, i.e., repeated exposure in
combination with control, predictability and efficacy could thus be effective components of cue
exposure to binge food, or systematic desensitisation using lists of forbidden food.
As indicated by Cloninger and colleagues (1993), combined pharmacotherapy could well have a
facilitating effect on such learning procedures. As biological underpinnings of several of these
dimensions have been demonstrated, including associations between novelty seeking and the
dopaminergic system, and between harm avoidance and the serotonergic system (Cloninger, 1987b),
eating disordered patients could thus benefit from such pharmacological facilitative effects. The benefits
of serotonergic drugs in eating disordered patients have indeed been demonstrated (Mayer & Walsh,
1998), although the mechanism of action is not yet clear. The results of the present study suggest that
personality dimensions should be included as outcome parameters in psychopharmacological studies in
ED patients. The role of drugs targeting the dopaminergic system in the treatment of eating disorders is
yet to be established, and particularly their effect on cognitive and behavioural characteristics as
identified in this study.
References
APA: Anonymous. (2001). Deriving behavioural phenotypes in an international, multi-centre study of eating disorders.
Psychological Medicine, 31(4): 635-645.
Beumont, P.J.V., George, G.C.W., Smart, D.E. (1976). ‘Dieters’ and ‘vomiters and purgers’ in anorexia nervosa. Psychological
Medicine , 6, 617-622.
Brewerton, T.D., Dorn, L.J., Bishop, E.R. (199). The Tridimensional Personality Questionnaire in eating disorder patients.
Biological Psychiatry , 31, 91A.
Brewerton, T.D., Hand, L.D., Bishop, E.R. (1993). The Tridimensional Personality Questionnaire in eating disorder patients.
International Journal of Eating Disorders, 14, 213-218.
Bruch, H. (1978). The golden cage. Cambridge: Harvard University Press.
Bulik, C.M., Beidel, D.C., Duchmann, E., Weltzin, T.E., Kaye, W.H. (1992). Comparative psychopathology of women with
bulimia nervosa and obsessive-compulsive disorder. Comprehensive Psychiatry, 33, 262-268.
Bulik, C.M., Sullivan, P.,F., Weltzin, T.E., Kaye, W.H. (1995). Temperament in Eating Disorders. International Journal of Eating
Disorders, 17 (3), 251-261.
Casper, R.C. (1990). Personality features of women with good outcome from restricting anorexia nervosa. Psychosomatic
Medicine, 52, 156-170.
Casper, R.C., Hedeker, D., McKlough, J.F. (1992). Personality dimensions in eating disorders and their relevance for
subtyping. Journal of the American Academy of Child and Adolescent Psychiatry, 31, 830-840.
Cloninger, C.R. (1986). A unified biosocial theory of personality and its role in the development of anxiety states. Psychiatric
Developments, 3, 167-226.
Cloninger, C.R. (1987a) . Neurogenetic adaptive mechanisms in alcoholism. Science, 236, 410-416.
Cloninger, C.R. (1987b). A systematic method for clinical description and classification of personality variants. Archives of
General Psychiatry, 44, 573-588.
Cloninger, C.R, Svrakic, D.M., Przybeck, R. (1993). A psychobiological model of temperament and character. Archives of
General Psychiatry, 50, 975-990.
Demitrack, M.A., Lesem, M.D., Listwak,, S.J., Brandt, H.A., Jimerson, D.C., Gold, P.W. (1990). CSF oxytocin in anorexia
nervosa and bulimia nervosa: clinical and pathophysiologic consideration. American Journal of Psychiatry, 147, 882-886.
Diaz-Marsa, M., Carrasco, J.L., Saiz, J. (2000). A study of temperament and personality in anorexia and bulimia nervosa.
Journal of Personal Disorders, 14(4), 352-359.
Duijsens, I.J., Spinhoven, P., Goekoop, J.G., Spermon, T., Eurelings-Bontekoe, E.H.M. (2000). The Dutch temperament and
character inventory (TCI): dimensional structure, reliability and validity in a normal and psychiatric outpatient sample.
Personality and Individual Differences, 28, 487-499.
Garner, D.M., Olmstead, M.P., Polivy, J. (1983). The Eating Disorders Inventory: A measure of cognitive-behaviroural
dimensions of anorexia and bulimia. In Anorexia Nervosa: Recent developments in research (ed. PL Darby), pp. 173-184. New
York: Alan R. Liss.
Gendall, K.A., Joyce, P.R., Sullivan, P.F., Bulik, C.M. (1998). Personality and dimensions of dietary restraint. International
Journal of Eating Disorder, 24(4), 371-9.
Giel R, Nienhuis FJ. 1996. Vragenschema’s voor de klinische beoordeling in de neuropsychiatrie. World Health Organisation
Mental Health, Geneva.
Halmi, K.A., Sunday, S.R., Strober, M., Kaplan, A., Woodside, D.B, Fichter, M., Treasure, J., Berrettini, W.H., Kay, W.H.
(2000). Perfectionism in anorexia nervosa: variation by clinical subtype, obsessionality, and pathologic eating behaviour.
American Journal of Psychiatry, 157(11), 1799-1805.
Humphrey, L.L. (1991). Object relations and the family system: An integrative approach to understanding and treating eating
disorders. In Psychodynamic treatment of anorexia nervosa and bulimia (ed. C Johnson), pp. 322-353. New York: Guilford Press.
Kaye, W.H., Gwirtsman, H.E., George, D.T., Ebert, M.H. (1991). Altered serotonin activity in anorexia nervosa after longterm weight restoration. Archives of General Psychiatry, 48, 556-562.
Kaye, W.H. (1997). Anorexia nervosa, obsessional behavior, and serotonin. Psychopharmacological Bulletin, 33(3), 335-344.
Kaye, W.H., Greeno, C.G., Moss, H., Fernstrom, J., Fernstrom, M., Lilenfeld, L.R., Weltzin, T.E., & Mann, J.J. (1998).
Alterations in serotonin activity and psychiatric symptomatology after recovery from bulimia nervosa. Archives of General
Psychiatry, 55, 927-935.
Kaye, W.H., Strober, M., Stein, D., Gendall, K. (1999). New Directions in Treatment Research of Anorexia and Bulimia
Nervosa. Biological Psychiatry, 45: 1285-1292.
Kaye, W.H., Strober, M. (2003). Neurobiology of eating disorders. In D. Charney, E., E. Nestler, & W. Bunney (Eds.),
Neurobiological Foundations of Mental Illness. Oxford: Oxford University Press (in press).
Kaye, W.H., Frank, G.K., Meltzer, C.C., Price, J.C., McConaha, C.W., Crossan, P.J., Klump, K.L., Rhodes, L. (2001).
Altered serotonin 2A receptor activity in women who have recovered from bulimia nervosa. American Journal of Psychiatry,
158(7): 1152-1155.
Kleifield, E.I., Sunday, S., Hurt, S.W., Halmi, K.A. (1993). Psychometric validation of the Tridimensional Personality
Questionnaire: Application to subgroups of eating disorders. Comprehensive Psychiatry, 34 (4): 249-253.
Lilenfeld, L.R., Kaye, W.H., Strober, M. (1997). Genetics and family studies of anorexia nervosa and bulimia nervosa. In D.
C. Jimerson, & W.H. Kaye (Eds.), Bailliere’s Clinical Psychiatry. Eating Disorders (Vol. 3 pp.177-197). London: Bailliere Tindall.
Lilenfeld, L.R., Kaye, W.H. (1998). Genetic Studies of Anorexia and Bulimia Nervosa. In H.W. Hoek, J.L. Treasure, &
M.A. Katzman (Eds), Neurobiology in the Treatment of Eating Disorders. Chichester: Wiley & Sons.
Mayer, L.E.S., Walsh, B.T. (1998). Pharmacotherapy of eating disorders. In H.W. Hoek, J.L. Treasure, & M.A. Katzman
(Eds), Neurobiology in the Treatment of Eating Disorders. Chichester: Wiley & Sons.
Pollice, C.P., Kaye, W.H., Greeno, C.G., Weltzin, T.E. (1997). Relationship of depression, anxiety, and obsessionality to
state of illness in anorexia nervosa. International Journal of Eating Disorder, 21, 367-376.
Pryor, T., Wiederman, M.W. (1996). Measurement of nonclinical personality characteristics of women with anorexia nervosa
and bulimia nervosa. Journal of Personality Assessment, 67, 414-421.
Soubrie, P. (1986). Reconciling the role of central serotonin neurosis in human and animal behavior. Behavioural Brain Science ,
9, 319-363.
Spoont, M.R. (1992). Modulatory role of serotonin in neural information processing: implications for human
psychopathology. Psychological Bulletin, 112, 330-350.
Srinivasagan, N.M., Kaye, W.H., Plotnicov, K.H., Greeno, C., Weltzin, T.E., & Rao, R. (1995). Persistent perfectionism,
symmetry, and exactness in anorexia nervosa after long-term recovery. American Journal of Psychiatry, 152, 1630-1634.
Steiger, H., Séguin, J.R. (1999). Eating disorders : anorexia and bulimia nervosa. In T. Millon, & P.H. Blaney (Eds), Oxford
textbook of psychopathology (pp. 365-389). Toronto: Oxford University Press.
Strober, M. (1980). Personality and symptomatological features in young, nonchronic anorexia nervosa patients. Journal of
Psychosomatic Research, 24, 353-359.
Strober, M. (1991). Disorders of the self in anorexia nervosa: An organismic-developmental paradigm. In C. Johnson (Ed.),
Psychodynamic treatment of anorexia nervosa and bulimia (pp. 354-373). New York: Guilford Press.
Strober, M. (1995). Family-genetic perspectives on anorexia nervosa and bulimia nervosa. In K.D. Brownell, & C.G.
Fairburn (Eds), Eating Disorders and Obesity (pp. 212-218). New York: The Guilford Press.
Svrakic DM, Whitehead C, Przybeck TR, Cloninger CR. 1993. Differential diagnosis of personality disorders by the seven
factor model of temperament and character. Archives of General Psychiatry 50, 991-999.
Tellegen, A. (1985). Structures of mood and personality and their relevance to assessing anxiety with an emphasis on selfreport. In A.H. Tuma, & J.D. Maser (Eds), Anxiety and anxiety disorders (pp. 681-706). Hillsdale, NJ: Lawrence Erlbaum
Associates.
Van Strien, T.(1986). Eating behaviour, personality traits and body mass. Swets & Zeitlinger B.V.: Lisse
Vitousek, K., & Manke, F. (1994). Personality variables and disorders in anorexia nervosa and bulimia nervosa. Journal of
Abnormal Psychology, 103 (1), 137-47.
Waller, D.A., Gullion, C.M., Petty, F., Hardy, B.W., Murdock, M.V., & Rush, A.J. (1993). Tridimensional Personality
Questionnaire and serotonin in bulimia nervosa. Psychiatry Research, 48 (1), 9-15.
4. Personality-Related Characteristics in Restricting versus Binging and Purging Eating
Disordered Patients7
Abstract
The current study sought to examine differences in personality-related characteristics between restricting anorexia
nervosa (RAN), binging/purging anorexia (BPAN), and purging bulimia nervosa (BN) patients. Scores on the
Temperament and Character Inventory (TCI) and on the Dutch Eating Behaviour Questionnaire (DEBQ) were
compared for 166 RAN, 78 BPAN and 151 BN patients. Bingers/purgers showed a higher score for
restrained, external and emotional eating and a lower score for a subscale of ‘selfdirectedness’ compared to patients
who never binge and purge. Personality differences were most marked between RAN and BN patients, while
personality characteristics of BPAN patients tended to be similar to those of BN patients. BN patients showed
higher scores on ‘novelty seeking’ and the subscales ‘exploratory excitability’, ‘impulsivity’ and ‘extravagance’, and
lower scores on ‘self-directedness’, compared to restricting patients. Moreover RAN patients also showed higher
scores on subscales of character dimensions, compared to BN patients. The higher the scores on novelty seeking, the
lower the scores on several character scales, which has important implications for the reinforcement of behaviour and
the treatment of eating disorders.
According to current diagnostic nosological convention, eating disorders comprise two major
categories, i.e. anorexia nervosa (AN) and bulimia nervosa (BN) (DSM-IV, 1994). However an
alternative diagnostic approach has been proposed, which distinguishes between eating disordered
patients who restrict food intake without binging and purging (i.e. always anorexic) and those who binge
and purge (i.e. sometimes anorexic, sometimes bulimic; DaCosta & Halmi, 1992). This distinction
between restrictors and bingers/purgers is thought to correspond to important phenomenological and
aetiological differences, including those related to predominant personality features, family-interaction
styles, neurobiological abnormalities, and patterns of genetic transmission. Such differences imply that
the restrictor versus binger/purger distinction may delineate subgroups of eating disorders in a more
meaningful way with regard to treatment and prevention than the distinction between AN and BN
(Steiger & Séguin, 1999).
There is a paucity of studies of a distinction between restrictors and
bingers/purgers based on personality characteristics which could however lead to innovative treatment
approaches.
Vervaet M, van Heeringen C, & Audenaert K (2004). Personality-related characteristics in restricting versus
binging and purging eating disordered patients. Comprehensive Psychiatry, 45 (1), 37-43.
Conventional treatments for bulimic syndromes usually include cognitive-behavioural elements
that encourage patients to decrease attitudinal and behavioural restraints upon eating behaviour. As in
the restraint theory, the assumption is that this will ultimately reduce the pressure to binge (Fairburn et
al., 1993b). Indeed, a substantial number of controlled trials have shown that such interventions are
effective (Laessle, Zoettle & Pirke, 1987; Fairburn et al., 1993a; Garner et al., 1993; Mitchell et al., 1993).
On the other hand, other studies have consistently found that bulimic symptoms in highly impulsive
bulimics can hardly be influenced by treatment (Keel & Mitchell, 1997). In these individuals, the urge to
binge may indeed be attributable rather to generalized impulse dysregulation than to the effects of
dietary overcontrol (Lacey, 1984; Vitousek & Manke, 1994; Yates et al., 1989, Steiger et al., 1999). The
study of Van Strien (1997) among highly restrained eaters resulted in a similar way in a distinction
between patients with low and those with high susceptibility toward failure of restraint, the differences
being associated with many features of psychopathology. As Van Strien (2000b) explained, the escape
theory of eating (Heatherton & Baumeister, 1991) incorporates elements of two major theories about
the aetiology of binging: the externality theory (Schachter & Rodin, 1974) and the psychosomatic theory
(Bruch, 1973). According to the escape theory, a shift to low levels of thinking will result in a reliance
on immediate stimuli, as well as a dampening of affect. Following escapes from self-awareness, eating
and a reduced affect co-occur (Heatherton & Baumeister, 1991).
It thus appears that the occurrence of binging or, on the contrary, sustaining restricting is
associated with personality characteristics. This study aimed at further exploring the effect of
personality characteristics on the occurrence of binging/purging in eating disorder patients.
Methods
Sample
Five hundred twenty-seven patients who were consecutively referred to the inpatient and
outpatient units of the Centre for Eating Disorders at the University Department of Psychiatry of the
Ghent University Hospital between December 1998 and January 2003 and who met the DSM-IV criteria
for Eating Disorders were enrolled in the study. The assessments were done during the first week
following referral before start of the treatment. Research was compliant with the Code of Ethics of the
World Medical Association (Declaration of Helsinki) and performed following the guidelines of the local
ethics committee.
The referred group included 244 (46 %) anorectic patients of whom 166 were restrictor-type
anorectics (RAN), while 78 were purgers/bingers (BPAN). Among the bulimic patients (B=179; 34 %),
151 were purgers/bingers (BN) and 28 were non-purging type bulimics.
The group of patients
diagnosed with eating disorders not otherwise specified (EDNOS) contained 104 (20 %) patients of
whom 38 met the criteria for binge eating disorder (BED).
The current study focused on patients of the RAN, BPAN and BN group, with respectively 3
and 7 males in the RAN and in the BN group. All bulimic/purging patients met the criteria of binging
(large amounts of food with a sense of lack of control) and purging (self-induced vomiting or the misuse
of laxatives, diuretics, or enemas) at least twice per week for three months. In the RAN group, only 115
patients reported to never binge or purge, while 51 patients reported some bulimic and/or purging
behaviour, but with a lower frequency than twice a week or involving smaller, and thus subjective binges.
This latter group is described in this paper as the RAN* group.
Measures
Weight and height, highest and lowest adult weight, and duration of illness were assessed
carefully. The body mass index (BMI) was calculated, as well the highest and lowest lifetime BMI
(HBMI, LBMI), based on the highest and lowest adult weight (16 years). HBMI and LBMI can thus
reflect an underestimation as current lengths were used to calculate these indexes; patients were not
reliable in remembering their precise length at the moment of their highest and lowest weight. Patients
were asked to describe the frequency of their binging, purging and restricting eating according to three
categories: never, more than two times per week, or less than two times per week. Binging was described
as losing control over eating, not including any measurement of calories, but as ‘involving larger
amounts of food than most people would eat during a similar period of time and under similar
circumstances’. The Dutch version of the Schedules for Clinical Assessment in Neuropsychiatry (SCAN)
was used as a structured clinical interview to assign a diagnosis according to DSM-IV criteria (Giel &
Nienhuis, 1996).
The validated Dutch version of the Temperament and Character Inventory (TCI; Duysens et al.,
2000) was used to assess temperament and character characteristics.
The TCI is based on a
psychobiological model of personality and assesses both temperament and character. Temperamental
aspects of personality are (at least partially) heritable, manifest early in life, and involve preconceptual or
unconscious biases in learning (Cloninger et al., 1993).
The temperament traits include “novelty
seeking” reflecting behavioural activation, “harm avoidance”, a tendency toward behavioural inhibition,
“reward dependence” reflecting behavioural attachment, and “persistence”, a measure of behavioural
maintenance. Characterologic aspects of personality are denoted by individual differences in selfconcepts, goals, and values. The character traits are “self-directedness”, referring to a self-accepting,
purposeful nature, “cooperativeness”, a trait associated with acceptance of other people and
compassion, and “self-transcendence” reflecting spirituality and an acceptance, identification, or spiritual
union with nature and its source. Individuals with the same temperament may behave differently as a
result of differences in character development (Cloninger et al., 1994).
The Dutch Eating Behaviour Questionnaire (DEBQ; Van Strien, 1986) was used to assess the
behavioural characteristics “emotional eating” (eating elicited by diffuse and clear emotional stimuli),
“restrained eating” (the tendency to diet in order to lose weight), and “external eating” (eating elicited by
external stimuli).
Statistics
Statistical analysis was performed using SPSS 10.0 (Spss Inc., Chicago, IL). One-way analysis of
variance ANOVA comparison was used to compare the three diagnostic subtypes: RAN, BPAN, BN.
When significant, a post hoc Bonferroni comparison was used with alpha set at 0.05.
comparison between two specific subtypes, the t test for independent samples was used.
For the
Results
As shown in Table 1, restricting and binging/purging patients differed on a number of
behavioural characteristics and weight variables.
Table 1: Age, weight-related characteristics, duration of illness, behavioural and personalityrelated characteristics in eating disorder patients, by type of eating disorder1
Binging/
F
p
Restricting Purging PurgingBonf
post
hoc
Anorexia Anorexia Bulimia
comparison
RAN
BPAN
BN
N=166
N=78
N=151
Age
21.5
24.3
22.7
3.6 .027
RAN < BPAN
7.6
7.8
7.1
BMI
14.8
15.7
20.7
326.5 .000
RAN < BPAN < BN
1.5
1.1
3.4
HBMI ever had
20.3
22.4
24.5
50.2 .000
RAN < BPAN < BN
2.9
4.1
4.0
LBMI ever had
14.1
14.8
18.4
110.0 .000
RAN, BPAN < BN
1.7
1.6
2.4
Duration of illness
3.0
5.4
3.8
5.0 .007
RAN < BPAN
5.3
6.1
4.9
Restrained eating
3.7
4.1
4.1
6.0 .003
RAN < BPAN, BN
1.2
1.0
0.9
External eating
2.9
3.3
3.7
32.5 .000
RAN < BPAN < BN
0.9
1.1
0.8
Emotional
eating
2.2
3.2
3.8
107.2 .000
RAN < BPAN < BN
(total)
1.0
1.1
0.9
Novelty seeking (NS)
15.9
17.0
19.8
13.2 .000
RAN, BPAN < BN
6.5
6.8
6.9
Exploratory
4.8
4.8
5.6
3.6 .027
RAN < BN
excitability (NS1)
2.8
2.5
2.6
Impulsiveness (NS2)
3.2
3.5
4.3
7.1 .001
RAN < BN
2.4
2.5
2.5
Extravagance (NS3)
3.3
3.8
5.0
17.1 .000
RAN, BPAN < BN
2.4
2.4
2.5
Selfdirectedness (SD)
23.3
21.6
20.2
6.5 .002
BN < RAN
7.7
8.0
7.1
Enlightened Second
6.6
5.5
4.9
18.1 .000
BN, BPAN < RAN
Nature (SD5)
2.7
2.7
2.2
Helpfulness (C3)
6.5
6.1
6.1
3.6 .029
1.3
1.5
1.5
Compassion (C4)
8.0
7.8
7.0
5.7 .004
BN < RAN
2.2
2.8
3.0
Transpersonal
3.0
2.7
2.4
3.5 .032
BN < RAN
Identification (ST2)
2.1
2.4
2.0
NOTE: Values are mean (SD). Only characteristics with significant differences between subtypes are included in the
table; * ANOVA with Bonferoni post hoc comparison, with level of significance set at P < .05
Characteristics
ED; n=395
When compared to binging/purging (BPAN and BN) patients, RAN had a lower BMI and
lifetime HBMI, and showed a significant lower score on restrained, external and emotional eating. RAN
and BPAN patients did not differ with regard to scores on personality dimensions, except for a higher
score on the “Enlightened Second Nature” subscale of the character dimension “self-directedness”.
Scores on personality dimensions of the BPAN patients tended to be more similar to those of BN
patients than to those of AN patients. BPAN patients differed from BN patients only by having a lower
score on the dimension “novelty seeking” and its subscale “extravagance”.
Differences on personality dimensions between RAN patients and BN patients were more
marked. Patients of the RAN group showed a comparatively lower score on the dimension “novelty
seeking” and nearly all its subscales, e.g. “exploratory excitability”, “impulsiveness” and “extravagance”,
and a higher score on the dimension self-directedness and its subscale “enlightened second nature”. In
addition, the comparison between these two groups revealed higher scores on the “helpfulness” and
“compassion” subscales of the cooperativeness dimension and for the “transpersonal identification”
subscale of self-transcendence.
When comparing RAN and BPAN patients, a significant difference was found for age and
duration of illness. Patients in the latter group were older and reported a longer duration of illness.
A comparison of the characteristics of the RAN* group and those of the other patients groups
revealed a number of differences. When compared to RAN patients, RAN* patients reported a longer
duration of illness (RAN: mean 2.4, SD 5.0; RAN*: mean 4.4, SD 5.8; P = .030), a higher score on the
“extravagance” subscale of “novelty seeking” (RAN: mean 3.0, SD 2.2; RAN*: mean 4.2, SD 2.6; P =
.003), and a lower score on the “self-acceptance” subscale of “self-directedness” (RAN: mean 6.6, SD
2.6; RAN*: mean 5.6, SD 2.6; P = .029). When compared to BPAN patients, RAN* patients showed
differences on behavioural and weight-related characteristics (see Table 2).
Table 2: Significant difference in age, weight-related characteristics, duration of illness,
behavioural and personality-related characteristics in anorectic patients by difference in
frequency and/or amount of binging and purging
Characteristics
Restricting
Binging/ t
Anorexia with
Purging
Some binging and Anorexia
purging
RAN*
N=51
BMI
HBMI ever had
LBMI ever had
External eating
Emotional eating (total)
15.1
1.5
20.6
3.0
14.1
2.0
3.0
1.0
2.3
1.0
BPAN
N=78
15.7
1.1
22.4
4.1
14.8
1.6
3.3
1.1
3.2
1.1
p
Bonf post hoc comparison
2.5 .012
RAN* < BPAN
2.6 .010
RAN* < BPAN
2.2 .026
RAN*, BPAN
2.2 .032
RAN *< BPAN
4.7 .000
RAN *< BPAN
NOTE. Values are mean (SD). * t-test with independent variables P < .05.
Finally, when comparing the characteristics of the “pure” RAN patients (i.e. those without any
binging and/or purging) with those of the BPAN and BN patients, similar differences were found,
except for a significant higher score (P = .047) for the dimension “persistence” in patients of the RAN
group (mean 5.8, SD 1.9) compared to patients of the BN group (mean 5.2, SD 1.9), and a higher score
(P = .012) for the subscale ‘”self-acceptance” (SD4) for this pure RAN group (mean 6.6, SD 2.6)
compared with patients of the BN group (mean 5.6, SD 2.6).
Discussion
This study aimed at investigating an alternative approach to the classification of eating disorders,
based on behavioural characteristics and their association with dimensions of personality. The findings
from this study indeed indicate that a distinction between restricting and binging/purging eating
disordered patients parallels behavioural and personality-related characteristics. These findings may lead
to a better understanding of eating disorders, and thus to innovative approaches to their treatment and
prevention.
AN patients as a group differed from BN patients only in having a lower adult BMI and in lower
scores on external eating, emotional eating and the temperamental dimension “novelty seeking”.
However, the subdivision of eating disordered patients in general, and AN patients in particular, on the
basis of their eating behavior revealed a number of important additional behavioral and personalityrelated differences. When compared to binging/purging patients, restricting patients showed lower
scores on external eating and emotional eating, and had a lower current BMI, while their highest BMI
ever was lower than that in binging/purging patients. Among AN patients, a binging/purging eating
pattern was associated not only with being older and having a longer duration of illness, but also with
higher scores on emotional eating and external eating and on a subscale of the character dimension selfdirectedness, when compared to RAN. Moreover, BPAN had a higher BMI at the moment of the
assessment and a higher BMI ever than RAN.
Differences on personality characteristics were most outspoken between RAN and BN patients:
bulimic patients showed relatively higher scores on “novelty seeking” and most of its subscales, and
lower scores on “self-directedness” and its subscale “enlightened second nature”, lower scores on the
“helpfulness” and “compassion” subscales of “cooperativeness”, and finally a lower score on the
“transpersonal identification” subscale of the dimension “self-transcendence”. When a subgroup of
RAN patients who showed limited binging/purging behaviour was compared to purely restricting
anorectic patients, it was shown that even this limited binging/purging behaviour was associated with
personality characteristics, i.e. with higher scores on the “extravagance” subscale of “novelty seeking”
and with lower scores on “self-directedness”.
Preceding a discussion of these findings, a number of limitations of this study should be noted.
First, there was no accounting for an effect of malnutrition. Mood (Smoller et al., 1987; Wing et al.,
1984) and personality (Keys et al., 1950) may indeed be influenced by malnutrition, although this was
not confirmed in other studies (Tuschl et al., 1989; Koeppl et al., 1992; Klump et al., 2000). Second,
scores on personality dimensions may be influenced by mood. Particularly harm avoidance scores covary
with mood (Svrakic et al, 1992).
The results of this study suggest that a diagnostic classification of eating disorders based on a
behavioural distinction (i.e. restricting versus binging/purging) is, at the least, as useful as the current
categorisation approach (i.e. AN, restricting and binging/purging subtypes, v BN) for the understanding
and treatment of eating disorders. The usefulness of a delineation of subtypes of anorectic patients has,
however, been questioned because of ambiguous diagnostic differences in early studies and possible
changes in subgroup status, as predominant symptoms may change over time (Pryor, Wiederman, &
McGilley, 1996; Eddy et al., 2002). Although cross-sectional in nature, the current study provides some
support for this latter argument. When compared to RAN patients, BPAN patients were older and
reported a longer duration of illness. Moreover, RAN* patients shared a substantial number of cognitive,
behavioural and personality-related characteristics with PBANs. Patients may thus move along a
continuum from a purely restricting type to a binging/purging type of anorexia nervosa. The current
data suggest that novelty seeking is involved in the evolution from anorexia nervosa with limited
binging/purging to higher frequencies (more than 2 times a week as in BPAN patients). Indeed, while
no significant difference in novelty seeking scores between RAN and BPAN was found, RAN* patients
had a higher score on a subscale of novelty seeking than purely RAN. This score was not significantly
different from that in BPAN patients, which suggests that relatively higher scores on novelty seeking (or
its subscales), in combination with low scores on character dimensions such as self-directedness, among
RAN may predispose them to develop the binging purging type of AN. The current findings indeed
indicate that binging/purging is associated with a relatively lower score on (subscales of) selfdirectedness, cooperativeness and self-transcendence, with higher scores on behavioural characteristics
such as emotional and external eating, and, consequently, with a higher current and lifetime BMI. Thus it
appears that the higher the score on novelty seeking is, the higher the probability of failure of selfcontrol with increased restrained, emotional and external eating as a consequence.
These findings are in keeping with the results of previous studies. More pronounced impulsivity
in bulimic patients compared to patients with other eating disorders was found in a number of studies
(Diaz-Marsa, Carrasco & Saiz, 2000; Nagata et al., 2000; Steiger et al., 2001; Fassino, et al., 2002). The
association between novelty seeking and disinhibition, as assessed by external and emotional eating in
this study, is in keeping with findings in female BN patients (Brewerton, Hand & Bishop, 1993; Kleifield
et al., 1994; Bulik et al., 1995) and restrained binge eaters (Edwards & Nagelberg, 1986). Another study
showed that RAN indeed differed notably from purging AN and BPAN by having a low score on
novelty seeking (Klump et al., 2000).
Poor impulse control, excitability, and the desire for sensory stimulation are likely to be
counterproductive in the maintenance of inhibition over eating, particularly when confronted with
palatable food, in the context of dysphoric mood or alcohol intoxication.
The tendency toward
extravagance, a novelty seeking subscale, may reflect a liability to spend money on food or to the ‘all or
nothing’ thoughts (such as “I’ve taken a bite/blown my diet, so I may as well binge”), which characterize
disinhibition (Gendall et al., 1998). The finding that novelty seeking may play an important role in the
disability to sustain dietary restraint can be explained in biological and cognitive-behavioural ways.
Steiger and collegues (1999) postulated in their study that highly impulsive binge eaters suffer from a
syndrome due to a marked serotonergic (5-HT) dysregulation, and that this explains the concurrent
propensities toward problems of impulse control and satiation in these patients. If outspoken, 5-HT
dysregulation may be sufficient to disrupt normal satiety mechanisms, in the absence of antecedent
episodes of excessive dietary restraint. Second, these authors hypothesized that individuals, once aware
of an increased urge to binge, might be expected to increase dietary control in an effort to maintain
control over impending dysregulation. In other words, people may become more vigilant about eating in
an attempt to keep the mounting impulse to eat under control. An increasing urge to binge in these
individuals may have been balanced by no corresponding increase in inhibitory controls (i.e., dietary
restraint). Because character is believed to develop during life in contrast with temperament (Cloninger
et al., 1993), individuals may not be temperamentally predisposed towards dietary restraint, but rather
‘learn’ or become susceptible to restrained eating patterns as a function of their character development,
and attempt to control their emotions. Dependent of their temperament dimension “novelty seeking”,
they may or may not sustain this restraint. In the absence of impulsivity, as in restrictors, refraining
from eating is rewarding, since their negative emotions can be denied. Due to a deficient impulse control
in bulimics and owing to the rewarding effects of binging and purging, these eating patterns become
strategies to cope with tension. As known already from the early laboratory work of Herman and
colleagues in the 1970s and 1980s there indeed is evidence for a link between dietary restraint and binge
eating (Herman & Polivy, 1975, 1980, 1988, 1990).
However, several studies have shown that dieting is not a necessary condition for binge eating to
occur in patients with either BN (Bulik, Sullivan, Carter, & Joyce, 1997; Mussell et al., 1997) or BED
(Abbott et al., 1998; Berkowitz, Stunkard, & Stallings, 1993; Grilo & Masheb, 2000; Spitzer, Devlin,
Walsh, & Hasin, 1992; Spitzer, Stunkard, et al., 1993; Spitzer, Yanovski, et al., 1993; Spurrel, Wilfley,
Tanofsky, & Brownell, 1997; Wilson, Nonas, & Rosenblum, 1993). Other studies found that violations
of dietary restraint do not necessarily lead to binge eating in normal weight women (Charnock, 1989)
and obese subjects (Ruderman & Wilson, 1979; Spencer & Fremouw, 1979). In addition to the argued
notion of purging as a reinforcer of binge eating (by decreasing anxiety about weight gain), other
explanations are possible. The suggestion of Byrne and McLean (2002) that the initial impetus for the
binge-purge cycle may come from purging rather than from binge eating was in keeping with the results
of previous studies (Leitenberg, Gross, Peterson, & Rosen, 1984; Leitenberg & Rosen, 1989; Leitenberg,
Rosen, Gross, Nudelman, & Vara, 1988; Rosen & Leitenberg, 1982, 1985, 1988). According to this
hypothesis purging triggers the bulimic cycle, because purging can control anxiety about weight gain, and
this removes inhibitions against a binge.
Finally, our findings suggest that restraining and binging are associated in case of a low score on
novelty seeking. Moreover, the higher the novelty seeking, the lower the self-directedness and the more
restraining, binging and purging.
In that way, impulsive bulimics may show poor response to
interventions which focused only on relaxing dietary restraint, because such treatments target a
dimension, that is only peripheral to the maintenance of such individuals’ binge eating behaviours.
Interventions that target impulsivity (and its implications upon eating behaviours) may thus be pertinent.
In view of the above mentioned roles of 5-HT and impulse control, we suggest (a) adjunctive
pharmacotherapy (Brewerton, 1995) with anti-impulsive/anti-bulimic agents (like selective serotonin
reuptake inhibitors) and/or (b) interventions aimed at improving self-control as exposure and response
prevention and impulse-control skills, like those suggested by Linehan and collegues (1991) for the
treatment of borderline personality disorder.
References
Abbott DW, de Zwaan M, Mussell MP, Raymond NC, Seim HC, Crow SJ, Crosby RD, & Mitchell JE. Onset of binge eating
and dieting in overweight women: Implications for etiology, associated features and treatment. J Psychos Res, 1998; 44 (3-4) :
367-374.
Berkowitz R, Stunkard AJ, & Stallings VA. Binge-eating disorder in obese adolescent girls. An NY Acad of Sc 1993; 699:
200-206.
Brewerton TD, Hand LD, & Bishop ER. The Tridimensional Personality Questionnaire in eating disorder patients. Int J Eat
Disord 1993; 14: 213-8.
Brewerton TD. Toward a unified theory of serotonin dysregulation in eating and related disorders. Psychoneuroendocr
1995; 20:561-590.
Bruch H. Eating Disorders. New York: Basic Books, 1973.
Bulik CM, Sullivan PF, Weltzin TE, & Kay WH. Temperament in eating disorders. Int J Eat Disord 1995; 17: 251-261.
Bullik CM, Sullivan PF, Carter FA, & Joyce PR. Initial manifestations of disordered eating behaviour: Dieting versus binging.
Int J Eat Disord 1997; 22: 195-201.
Byrne SM, & McLean NJ. The Cognitive-Behavioral Model of bulimia nervosa: A direct evaluation. Int J Eat Disord 2002;
31: 17-31.
Charnok DJK . A comment on the role of dietary restraint in the development of bulimia nervosa. Br J Cl Psych 1989; 28:
329-340.
Cloninger CR, Przybeck TR, Svrakic DM, & Wetzel RD. The Temperament and Character Inventory (TCI): A guide to its
development and use. St. Louis, MO: Center for Psychobiology of Personality, Washington University, 1994.
Cloninger CR, Svrakic DM, & Przybeck TR. A psychobiological model of temperament and character. Arch Gen Psychiatr
1993; 50: 975-990.
DaCosta M, & Halmi KA. Classification of anorexia nervosa: Question of subtypes. Int J Eat Disord, 1992; 11: 305-313.
Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. Washington DC: American Psychiatric Association: 1994; 539545.
Diaz-Marsa M, Carrasco JL, & Saiz J. A study of temperament and personality in anorexia and bulimia nervosa. J Personal
Disord 2000,14: 352-9.
Duijsens IJ, Spinhoven P, Goekoop JG, Spermon T, & Eurelings-Bontekoe EHM. The Dutch temperament and character
inventory (TCI): dimensional structure, reliability and validity in a normal and psychiatric outpatient sample. Pers and Ind
Diff 2000;28: 487-499.
Eddy KT, Keel PK, Dorer DJ, Delinsky SS, Franko DL & Herzog DB. Longitudinal comparison of anorexia nervosa
subtypes. Int J Eat Disord 2002; 31: 191-201.
Edwards FE, & Nagelberg DB. Personality characteristics of restrained/binge eaters versus unrestrained/nonbinge eaters.
Add Beh 1986; 11: 207-211.
Fairburn CG, Jones R, Peveler RC, Hope RA, O'Connor M: Psychotherapy and bulimia nervosa: longer-term effects of
interpersonal psychotherapy, behavior therapy, and cognitive behavioral therapy. Arch Gen Psychiatry 1993a; 50: 419-428.
Fairburn CG, Marcus M, & Wilson GT. Cognitive-behavioral therapy for binge eating and bulimia nervosa: A
comprehensive treatment manual. In C. Fairburn & G.T. Wilson (Eds.): Binge eating: nature, assessment and treatment.
New York: Guilford, 1993b, 361-404.
Fassino S, Abbate-Daga G, Amianto F, Leombruni P, Boggio S, & Rovera GG. Temperament and character profile of eating
disorders: a controlled study with the temperament and character inventory. Int J Eat Disord 2002; 32: 412-425.
Garner DM, Olmstead MP & Polivy J. The Eating Disorders Inventory: A measure of cognitive-behaviroural dimensions of
anorexia and bulimia. In Anorexia Nervosa: Recent developments in research (ed. P. L. Darby), pp. 173-184. New York:
Alan R. Liss, 1983.
Garner DM, Rockert W, Davis R, Garner MV, Olmsted MP, Eagle M: A comparison of cog-nitive-behavioral and
supportive-expressive therapy for bulimia nervosa. Am J Psychiatry 1993; 150: 37-46.
Garner DM. Eating Disorders Inventory-2. Professional manual. Odessa, FL: Psychological Assessment Resources, 1990.
Gendall KA, Joyce PR, Sullivan PF, & Bulik CM. Personality and dimensions of dietary restraint. Int J Eat Disord 1998; 24:
371-379.
Giel R & Nienhuis FJ. Vragenschema’s voor de klinische beoordeling in de neuropsychiatrie. World Health Organisation
Mental Health, Geneva, 1996.
Grilo CM, & Masheb RM. Onset of dieting versus binge eating in outpatients with binge eating disorder. Int J Obes and Rel
Metab Dis 2000; 24 (4): 404-409.
Heatherton TF & Baumeister RF. Binge eating as escape from self-awareness. Psychol Bull 1991; 110: 86-108.
Herman CP & Polivy J. Anxiety, restraint and eating behaviour. J Abn Psych 1975; 84: 666-672.
Herman CP, & Polivy J. Stress-induced eating and eating-induced stress: A response to Robbins and fray. Appetite 1980; 1:
135-139.
Herman CP, & Polivy J. Psychological factors in the control of appetite. In M. Winick (Ed.), Control of appetite. Current
concepts in nutrition (Vol. 16, pp. 41-51). New York: Wiley, 1988.
Herman CP, & Polivy J. From dietary restraint to binge eating: Attaching causes to effects. Appetite 1990; 14 (2): 123-125.
Keel PK & Mitchell JE. Outcome in bulimia nervosa. Am J of Psych 1997; 154: 313-321.
Keys A, Brozek J, Honschel A, Mickelson O & Taylor HL. The biology of human starvation. Minneapolis: University of
Minnesota Press, 1950.
Kleifield EE, Sunday S, Hurt S & Halmi KA. The tridimensional personality questionnaire: An exploration of personality
traits in eating disorders. J of Psych Res 1994; 28: 413-423.
Klump K, Bulik CM, Pollice C et al. Temperament and character in women with anorexia nervosa. J Nerv Ment Dis 2000;
188 (9): 559-567.
Koeppl PM, Heller J, Bleecker ER, Meyers DA, Goldberg AP & Bleecker ML. The influence of weight reduction and
exercise regimens upon the personality profiles of overweight males. J Clin Psych 1992; 48: 463-471.
Lacey JH. Moderation of bulimia. J Psychosom Res 1984; 24: 259-269.
Laessle RG, Zoettle C, Pirke KM: Meta-analysis of treatment studies for bulimia. Int J Eat Disord 1987; 6: 647-654.
Leitenberg H, & Rosen JC. Cognitive-behavioral therapy with and without exposure plus response prevention in treatment
of bulimia nervosa: comment on Agras, Schneider, Arnow, Raeburn and Telch. J Cons Clin Psych 1989; 57: 776-777.
Leitenberg H, Gross J, Peterson J, & Rosen JC. Analysis of an anxiety model and the process of change during exposure plus
response prevention treatment of bulimia nervosa. Beh Ther 1984; 15: 3-20.
Leitenberg H, Rosen JC, Gross J, Nudelman S, & Vara LS. Exposure plus response-prevention treatment of bulimia
nervosa. J Cons Clin Psych 1988; 56: 535-541.
Linehan MM, Armstrong HE, Suarez A, Allmon D & Heard HL. Cognitive-behavioral treatment of chronically parasuicidal
borderline patients. Arch Gen Psych 1991; 48: 1060-1064.
Mitchell JE, Pyle RL, Pomeroy C, Zollman M, Crosby R, Sein H, Eckert ED, Zimmerman R: Cognitive-behavioral group
psychotherapy of bulimia nervosa: importance of logistical variables. Int J Eat Disord 1993; 14: 277-287.
Mussell MP, Mitchell JE, Fenna CJ, Crosby RD, Miller JP, & Hoberman HM. A comparison of onset of binge eating versus
dieting in the development of bulimia nervosa. Int J Eat Disord 1997; 21: 353-360.
Nagata T, Kawarada Y, Kiriike N, & Iketani T. Multi-impulsivity of Japanese patients with eating disorders : primary and
secondary impulsivity. Psychiatry Res 2000; 94: 239-50.
Pryor T & Wiederman MW. Measurement of nonclinical personality characteristics of women with anorexia nervosa and
bulimia nervosa. J of Pers Assess 1967; 414-421.
Rosen JC, & Leitenberg H. Bulimia nervosa: Treatment with exposure and response prevention. Beh Ther 1982; 13: 117124.
Rosen JC, & Leitenberg H. Exposure plus response prevention treatment of bulimia. In D.M. Garner & P.E. Garfinkel
(Eds.), A handbook of psychotherapy for anorexia nervosa and bulimia (pp. 193-209). New York: Guilford Press, 1985.
Rosen JC, & Leitenberg H. The anxiety model of bulimia nervosa and treatment with exposure plus response prevention. In
KM Pirke, W Vandereycken, & D Ploog (Eds.), The psychobiology of bulimia nervosa (pp. 146-151). Berlin: SpringerVerlag, 1988.
Ruderman AJ, & Wilson GT. Weight, restraint, cognitions and counterregulation. Beh Res Ther 1979; 17 (6): 581-590.
Schachter S & Rodin J. Obese humans and rats. Washington, DC: Erlbaum/Halsted, 1974.
Smoller JW, Wadden TA & Stunkard AJ. Dieting and depression: A critical review. Journal of Psychos Res 1987; 31: 429440.
Spencer JA, & Fremouw WJ. Binge eating as a function of restraint and weight classification. J Abn Psych 1979; 88: 262267.
Spitzer RL, Devlin MJ, Walsh BT, Hasin D, Wing R, Marcus M, Stunkard A, Wadden T, Yanovski S, Agras S, Mitchell J, &
Nonas C. Binge eating disorder: A multisided trial of the diagnostic criteria. Int J Eat Disord, 1992; 11: 191-203.
Spitzer RL, Stunkard A, Yanovski S, Marcus MD, Wadden T, Wing R, Mitchell J, & Hasin D. Binge eating disorder should
be included in DSM-IV: A reply to Fairburn et al.’s “the classification of recurrent overeating: The binge eating disorder
proposal. Int J Eat Disord 1993; 13: 161-169.
Spitzer RL, Yanovski S, Wadden T, Wing R, Marcus M, Stunkard A, Devlin MJ, Mitchell J, Hasin D, & Horne RL. Binge
eating disorder: Its further validation in a multiside study. Int J Eat Disord 1993; 137-153.
Spurrell EB, Wilfley DE, Tanofsky MB, & Brownell KD. Age of onset for binge eating: Are there different pathways to
binge eating? Int J Eat Disord 1997; 21: 55-65.
Steiger H & Séguin JR. Eating disorders : anorexia and bulimia nervosa. In: T. Millon, & P.H, 1999.
Steiger H, Lehoux PM & Gauvin L. Impulsivity, dietary control and the urge to binge in bulimic syndromes. Int J Eat
Disord 1999b; 26: 261-274.
Steiger H, Young SN, Kin NM, Koerner N, Israel M, Lageix P, & Paris J. Implications of impulsive and affective symptoms
for serotonin function in bulimia nervosa. Psychol Med 2001; 31: 85-95
Svrakic DM, Przybeck TR, & Cloninger CR. Mood states and personality traits. J Affect Dis 1992; 24:217-226.
Tuschl RJ, Laessle RG, Kothaus BC & Pirke KM. Behavioral and biological correlates of restrained eating. Ann NY Acad Sc
1989; 575: 580-581.
Van Strien T, Cleven A & Schippers G. Restraint, Tendency Toward Overeating and Ice Cream Consumption. Int J Eat
Disord 2000a; 28: 333-338.
Van Strien T, Frijters JER, Bergers GPA & Defares PB. The Dutch Eating Behaviour Questionnaire (DEBQ) for
assessment of restrained, emotional and external eating behaviour. Int J Eat Disord 1986; 5: 295-315.
Van Strien T. The concurrent validity of a classification of dieters with low versus high susceptibility toward failure of
restraint. Add Beh 1997; 22: 587-597.
Van Strien T. Ice-Cream Consumption, Tendency Toward Overeating, and Personality. Int J Eat Disord 2000b; 28: 460-464.
Vitousek K & Manke F. Personality variables and disorders in anorexia nervosa and bulimia nervosa. J Abn Psych 1994;
103: 137-147.
Wilson GT, Nonas C, & Rosenblum, GD. Assessment of binge-eating in obese patients Int J Eat Disord 1993; 13: 25-34.
Wing RR, Epstein LH, Marcus MD & Kupfer DJ. Mood changes in behavioral weight loss programs. J Psychosom Res
1984; 28: 189-196.
Yates WR, Sieleni B & Bowers WA. Clinical correlates of personality disorder in bulimia nervosa. Int J Eat Disord 1989; 8:
473-477.
5. Attempted suicide and personality in eating disorders8
Abstract
Objective: To assess the occurrence and associated characteristics of attempted suicide in eating disorders.
Method: The study group consisted of 300 ED in- and out-patients at the Department of Psychiatry
(University Hospital of Ghent) in Belgium. Personality dimensions, and behavioural and cognitive characteristics
were compared between ED patients with and these without a history of attempted suicide (AS).Results: A
history of suicide attempts was reported by 44 (14.6 %) patients. Suicide attempts were more common among
bulimia nervosa (BN, 23%) patients than in anorexia nervosa (AN, 13.5%) or EDNOS patients (7%). AS
among AN patients appeared to differ from that in BN or EDNOS patients in terms of associated personality
dimensions and behavioural and cognitive characteristics. Conclusion: The findings support a stress-diathesis
model for attempted suicide and provide guidelines for the prevention of AS among ED patients, using a
psychotherapeutic approach, perhaps facilitated by psychopharmacological strategies.
Eating disorders – attempted suicide – personality dimensions
Introduction
Eating disorders are associated with a strongly increased mortality. The mortality rate for
anorexia nervosa (AN) is 5.6% per decade, and major causes of death are starvation and suicide
(Sullivan, 1995). Indeed, most (Patton, 1988; Eckert, Halmi, Marchi, Crove, & Crosby, 1995; MollerMadsen, Nystrup, & Nielsen, 1996; Nielsen, Moller-Madsen, Isager, Jorgensen, Pagsberg, & Theander,
1998; Apter & Ofek, 2001) though not all (Coren & Hewitt, 1998) studies in AN patients suggest that
suicide is the main cause of increased mortality rates, with an increased risk of premature death
occurring up to 8 years after the initial assessment (Patton, 1988; Nielsen et al., 1998). AN may indeed
have the highest standardized mortality ratio (SMR) for suicide among all psychiatric disorders (Harris &
Barraclough, 1997). The crude mortality rate in BN is lower than that in AN, ranging from 0.3 to 0.9%
(Keel & Mitchel, 1997; Herzog et al, 2000). Studies of suicide in bulimia nervosa (BN) are fewer in
number. A recent review of the deaths among BN patients in multiple studies showed that 29% were the
result of suicide (Franko et al, 2004).
8
Vervaet M, van Heeringen C, & Audenaert K. Journal of Affective Disorders (submitted 2005).
There are very few reports of (attempted) suicide among patients suffering from atypical eating
disorders, i.e. eating disorders not otherwise specified (EDNOS). Fullerton and co-workers (1995)
reported a prevalence rate of 23.2 %.
Attempted suicide (AS) is regarded as the most robust clinical predictor of suicide (Sakinofsky,
2000), and the study of the occurrence and risk factors of AS may thus contribute to the prevention of
suicide among eating disordered patients. In a large series of eating disordered outpatients, 13% reported
at least one suicide attempt (Favaro & Santonastaso, 1996, 1997). A recent longitudinal study showed
that 15% of ED patients reported a history of AS characterized by at least some intent to die during the
8.6-year follow-up period, including 22.1% of AN patients and 10.9% of BN patients, with severity of
depressive symptoms and drug use predicting AS in AN and a history of drug use and laxative use
predicting AS in BN (Franko et al, 2004).
The prevalence of AS among outpatient anorexics was recently estimated at 11.3% (Sansone &
Levitt, 2002). No data are available with regard to the occurrence of AS among inpatient anorexics. Bulik
and colleagues (1999) found that the occurrence of AS among women with AN was independent of a
lifetime history of major depression, although for bulimia, those women with comorbid depression may
be at greater risk. Favaro and Santonastaso (1997) reported that anorexic subjects who attempted suicide
were older, had a longer duration of illness, weighed less, and were more likely to use substances, as
compared to non-attempters. In addition, Corcos and co-workers (2002) found that a history of
attempted suicide among AN patients was associated with more severe depressive symptoms and
impulsive behaviours. With regard to EDI-measured characteristics, AN patients attempting suicide
during a follow-up period differed from those who did not attempt suicide only by a higher score on the
‘Ineffectiveness’ subscale (Franko et al, 2004).
The lifetime prevalence of AS in BN has been estimated at 22%, with attempts commonly being
multiple and serious (Keel, Dorer, Eddy, Franko, Charatan, & Herzog, 2003; Sansone & Levitt, 2004).
Contrary to the findings from retrospective studies in AN patients (Favaro & Santonastaso, 1996;
Pompili, Mancinelli, Girardi, Ruberto, & Tatarelli; 2004), the risk of AS among BN patients appeared to
be independent of the presence or severity of core ED symptoms such as binging and purging, but
associated with the duration of illness, more severe depressive symptoms, and impulsive behaviours
including a history of drug use (Corcos, Taïeb, Benoit-Lamy, Paterniti, Jeammet, & Flament, 2002;
Franko et al, 2004). With regard to EDI-measured characteristics, BN patients attempting suicide during
a follow-up period differed from those who did not attempt suicide by higher scores on the
‘Ineffectiveness’, ‘Interpersonal distrust’, ‘Interoceptive Awareness’, and ‘Maturity fears’ subscales
(Franko et al, 2004).
These studies have thus demonstrated that suicidal behaviour is relatively common among ED
patients and that its occurrence may be related to axis-I disorders, to core ED-symptoms and to
personality characteristics. It has recently become clear that suicidal behaviour is to be regarded as the
consequence of an interaction between stressors and a diathesis or predisposition to suicidal behaviour.
These stressors may be disease-related, e.g. due to depression or other axis-I disorders. With regard to
the diathesis a role of trait-dependent impulsivity and aggression has been suggested (Mann et al, 1997).
Also in ED it has been suggested that among anorexic and bulimic patients suicide attempts are part of a
cluster of impulsive behaviours (Franko et al, 2004).
Cloninger’s TCI has been used to study trait-dependent temperamental correlates of AS,
suggesting a role of increased harm avoidance and decreased reward dependence in the development of
attempted suicide (Van Heeringen et al, 2000; 2003). In addition, the temperament and character traits of
high persistence, low self-directedness and high self-transcendence are associated with a reported history
of SA in the ED diagnostic groups (Bulik et al., 1999).
Cloninger and co-workers (unpublished
manuscript and cited in Bulik et al., 1999) have indicated that self-transcendence makes an important
contribution to both positive and negative aspects of mental health, and that the valence of the
contribution is determined by the configuration of the other character traits. For example, high selftranscendence combined with low self-directedness and low cooperativeness is associated with increased
schizotypy, psychosis-proneness and depression, whereas high self-transcendence combined with high
self-directedness and high cooperativeness leads to hyperthymia or cheerful creativity.
The current study was undertaken in an attempt to fill a number of gaps in our knowledge of the
role of personality-related risk factors for AS among ED patients. First, a majority of previous studies
were conducted in the USA, due to which the definition of AS differs from the definition used in
Europe. Indeed, according to US definitions AS is characterized by an intent to die, which is not the
case in definitions used in European research. It is therefore unclear to what extent previous findings are
applicable to European ED patients. Secondly, as little information is available on the occurrence and
risk factors for AS among EDNOS patients, these patients were included in the current study. Thirdly,
this study aimed at assessing whether these personality characteristics are involved in the previously
described effect of ED-related cognitive and behavioural characteristics (see above) on the occurrence of
AS among ED patients by studying (1) the association between AS and ED-related cognitive and
behavioural characteristics, and (2) the correlation between the TCI personality traits and these cognitive
and behavioural characteristics in the three types of ED.
Patients and methods
The study group consisted of ED patients, who were consecutively referred for inpatient or
outpatient treatment to the Center for Eating Disorders of the University Department of Psychiatry at
the University Hospital in Gent, Belgium. Psychiatric diagnoses were assigned according to DSM-IV
criteria.
A history of attempted suicide was assessed carefully. Attempted suicide was defined as an act
with a non-fatal outcome, in which an individual initiates a non-habitual behaviour that will cause self
harm, or deliberately ingests a substance in excess of the prescribed or generally recognized therapeutic
dosage, or ingests a substance which is not meant for human consumption. Motives or suicidal intent are
thus not included in the definition of attempted suicide, which is in keeping with the definition of
attempted suicide as used in the “WHO/EURO Multicentre Study of Suicidal Behaviour” (Schmidtke,
Weinacker, Apter, et al., 1999).
Weight and height, highest and lowest lifetime weight, and duration of illness were assessed
carefully. Body mass index (BMI) and the highest and lowest lifetime BMI (HBMI, LBMI) were
calculated, the latter based on the highest and lowest adult weight (i.e. 16 years or older). Patients were
asked to describe the frequency of their binging, purging and restricting eating patterns. Binging was
defined as losing control over eating, not including any measurement of calories, but involving ‘larger
amounts of food than most people would eat during a similar period of time and under similar
circumstances’.
The Dutch Eating Disorders Inventory (EDI; Garner, Olmstead & Polivy, 1983) was used to
assess cognitive characteristics including drive for thinness, bulimia, body dissatisfaction, ineffectiveness,
perfectionism, interpersonal distrust, interoceptive awareness and maturity fears.
The validated Dutch version of the TCI (Duijsens, Spinhoven, Goekoop, Spermon & EurelingsBontekoe, 2000) was used to assess temperament and character dimensions. The TCI is based on a
psychobiological model of personality and assesses both temperament and character. Temperamental
aspects of personality are (at least partially) heritable, manifest early in life, and involve pre-conceptual or
unconscious biases in learning (Cloninger, Svrakic & Przybeck, 1993). The temperament traits include
novelty seeking (NS) reflecting behavioural activation, harm avoidance (HA), i.e. a tendency toward
behavioural inhibition, reward dependence (RD) reflecting behavioural attachment, and persistence (PS),
which is a measure of behavioural maintenance. Character dimensions are denoted by individual
differences in self-concepts, goals, and values. The character traits in the TCI are self-directedness (SD),
referring to a self-accepting and purposeful nature, cooperativeness (CO), a trait associated with
acceptance of other people and compassion, and self-transcendence (ST) reflecting spirituality and
acceptance, identification, or spiritual union with nature and its sources. Individuals with the same
temperament may behave differently as a result of differences in character development (Cloninger,
Przybeck, Svrakic & Wetzel, 1994).
The Dutch Eating Behaviour Questionnaire (DEBQ; Van Strien, Frijters, Bergers & Defares,
1986) was used to assess the behavioural characteristics ‘emotional eating’ (eating elicited by emotional
stimuli), ‘restrained eating’ (the tendency to diet in order to lose weight), and ‘external eating’ (eating
elicited by external stimuli).
The validated Dutch translation (Van der Does, 2002) of the Beck Depression Inventory (BDIII-NL; Beck AT, Steer RA, & Brown GK, Swets & Zeitlinger), was used to assess the severity of
depressive symptoms.
Results
The study group consisted of 300 patients, including 96 AN patients (32 %), 104 BN patients
(34.6 %), and 100 EDNOS patients (33.3 %). The patient group consisted of 290 females (96.6 %) and
10 males (3.4 %). In view of the small proportion of males, statistical analyses were performed without
stratification by gender.
A history of AS was reported by 44 (14.6 %) ED patients. AS was significantly more commonly
reported by BN patients (n= 24; 23.1 %) than by AN patients (n= 13; 13.5 %) or EDNOS patients (n=
7; 7%; df = 2; χ² = 10.671; p = .005).
In the anorectic group, no differences were found for scores on the BDI-II between patients
with and those without a history of suicide attempt. BN and EDNOS patients with a history of AS had
higher scores on the BDI-II (35,7 and 39,5 respectively), than those without such a history (27, 8 and
21.7; p=.007 and p = .003 respectively).
As shown in Table 1, a history of AS among AN patients was associated with a higher score on
novelty seeking. Patients diagnosed with BN or EDNOS with a history of AS had a significantly higher
score on harm avoidance and a significantly lower score on self-directedness than those without such a
history.
Table 1: Scores on personality dimensions according to type of eating disorder and to history of
attempted suicide
Personality
AN
BN
EDNOS
dimension
AS-
AS+
AS-
AS+
AS-
AS+
Novelty seeking
14.8
19.9**
20.7
20.5
19.8
19.4
Harm avoidance
24.9
25.5
23.3
27.7**
21.8
29.7**
Reward dependence
15.6
16.8
17.1
16.2
17.1
14.7
5.7
5.1
4.9
4.9
4.8
4.6
Self-directedness
22.9
19.5
20.1
13.7**
24.4
29.1
Cooperativeness
31.4
29.9
32.2
30.9
32.1
30.7
Self-transcendence
10.3
11.1
10.7
10.7
11.9
13.7
Persistence
* p < .05 ** p < .001
Among ED patients with a history of AS, BN patients had significantly lower scores on SD than
AN patients. No other differences between ED categories on TCI-dimensions were found among ED
patients with a history of AS.
ED patients without a history of AS showed more differences according to type of ED. AN patients
scored significantly lower than BN and EDNOS patients on novelty seeking and reward dependence,
higher than EDNOS patients on harm avoidance, and higher than BN and EDNOS patients on
persistence. BN patients scored significantly lower on self-directedness than EDNOS patients.
Table 2 shows the scores on cognitive and behavioural characteristics of patients according to
their type of ED and to the presence or absence of a history of AS. Among the AN patients, a history of
AS was not associated with cognitive and behavioural characteristics. BN patients with a history of AS
showed higher scores on ineffectiveness, interoceptive awareness and maturity fears. Finally, EDNOS
patients with a history of AS differed from those without such a history in that they showed relatively
higher scores on drive for thinness, body dissatisfaction, ineffectiveness and perfectionism, and a lower
score on eating due to external stimuli.
Table 2: Scores on cognitive and behavioural characteristics according to type of ED and to
history of AS
Cognitive/behavioural
AN
BN
EDNOS
characteristic
AS-
AS+
AS-
AS+
AS-
AS+
drive for thinness
12.7
12.5
16.7
15.6
11.7
17.1*
bulimia
1.4
2.2
11.0
12.0
4.1
3.7
body dissatisfaction 12.3
15.1
29.6
20.7
16.0
22.1*
ineffectiveness
12.4
14.5
12.7
19.6**
9.4
19.6**
perfectionism
6.5
6.6
5.9
8.5*
5.8
9.7*
interpers distrust
6.6
6.7
4.9
7.3*
4.5
4.1
interocept. awar.
1.1
9.0
10.7
15.0**
7.7
13.3*
maturity fears
6.9
7.4
5.3
9.5**
4.9
6.6
restrained eating
4.0
3.9
3.8
3.8
3.5
3.8
external eating
2.4
2.4
3.5
3.7
3.0
2.0**
emotional eating
2.2
2.2
4.0
4.1
3.0
1.9*
* p < .05 ** p < .001
Finally, statistical analysis pursued the study of the correlation between scores on TCIpersonality dimensions with an effect on the occurrence of AS and cognitive or behavioural
characteristics in the ED categories.
Among AN patients, scores on novelty seeking correlated negatively with those on ineffectiveness (r = .237; p = .020), interpersonal distrust (r = -.287; p = .005) and interoceptive awareness (r = -.230; p=
.024).
Table 3: Significant correlations between personality dimensions and cognitive characteristics
in AN patients
Ineffectiveness
Novelty
Seeking
r (p)
-.237 (.020)
Interpersonal
Distrust
r (p)
-.287 (.005)
Interoceptive
awareness
r (p)
-.230 (.024)
Among BN patients, scores on harm avoidance correlated significantly with those on drive for
thinness (r = .205; p = .036), body dissatisfaction (r = 321; p = .001), ineffectiveness (r = .541; p =
.000), perfectionism (r = .294; p = .002), interpersonal distrust (r = .400; p = .000), interoceptive
awareness (r = .425; p = .000) and maturity fears (r = .362; p = .000). Scores on self-directedness among
BN patients correlated significantly with scores on bulimia (r = -.321; p = .001), ineffectiveness (r = .504; p = .000), perfectionism (r = -.361; p = .000), interpersonal distrust (r = -.409; p = .000),
interoceptive awareness (r = -.375; p = .000), maturity fears (r = -.310; p = .001), external eating (r = .245; p = .012) and emotional eating (r = -.335; p = .001).
Table 4: Significant correlations between personality dimensions and cognitive characteristics
in BN patients
DT
r
(p)
B
r
(p)
BD
r
(p)
INE
r
(p)
P
r
(p)
IP
r
(p)
IA
r
(p)
MF
r
(p)
EE
r
(p)
EME
r
(p)
Harm
Avoidance
.205
(.036)
-
321
(.001)
.541
(.000)
.294
(.002)
.400
(.000)
.425
(.000)
.362
(.000)
-
-
Self
directedness
-
-.321
(.001)
-
-.504
(.000)
-.361
(.000)
-.409
(.000)
-.375
(.000)
-.310
(.001)
-.245
(.012)
-.335
.001
DT = drive for thinness; B = bulimia; BD = body dissatisfaction; INE = ineffectiveness; P = perfectionism; IP =
interpersonal distrust; IA = interoceptive awareness; MF = maturity fears; EE = external eating; EME =
emotional eating
Scores on harm avoidance among EDNOS patients correlated significantly with those on drive
for thinness (r = .404; p = .000), bulimia (r = .279, p = .005), body dissatisfaction (r = .578; p = .000),
ineffectiveness (r = .755, p = .000), perfectionism (r = .293; p = .003), interpersonal distrust (r = .436; p
= .000), interoceptive awareness (r = .543, p = .000), maturity fears (r = .365, p = .000) and emotional
eating (r = .312, p = .002). Finally, scores on self-directedness among EDNOS patients correlated
significantly with those on drive for thinness (r = -.249; p = .013), bulimia (r = -.307; p = .002), body
dissatisfaction (r = -.461; p = .000), ineffectiveness (r = -.599; p = .000), interpersonal distrust (r = -.351;
p = .000), interoceptive awareness (r = -.401; p = .000), maturity fears (r = -.337; p = .001) and
emotional eating (r = -.316; p = .001).
Table 5: Significant correlations between personality dimensions and cognitive characteristics
in EDNOS patients
Harm
Avoidance
Self
directedness
DT
r
(p)
.404
(.000)
B
r
(p)
.279
(.005)
BD
r
(p)
.578
(.000)
INE
r
(p)
.755
(.000)
P
r
(p)
.293
(.003)
IP
r
(p)
.436
(.000)
IA
r
(p)
.543
.000
MF
r
(p)
.365
(.000)
EE
r
(p)
-
EME
r
(p)
.312
(.002)
-.249
(.013)
-.307
(.002)
-.461
(.000)
-.599
(.000)
-
-.351
.000)
-.401
(.000)
-.337
(.001)
-
-.316
.001
DT = drive for thinness; B = bulimia; BD = body dissatisfaction; INE = ineffectiveness; P = perfectionism; IP =
interpersonal distrust; IA = interoceptive awareness; MF = maturity fears; EE = external eating; EME =
emotional eating
Discussion
The results from this study can be summarized as follows. First, 14.6 % of this large group of
eating disordered patients reports a history of attempted suicide, with a significant effect of the type of
eating disorder involved, as such a history is more common among bulimia nervosa patients (23 %) than
among anorexia nervosa (13 %) or atypical eating disorder patients (7 %). Secondly, a history of
attempted suicide is associated with trait-dependent personality characteristics, reflecting increased
novelty seeking among anorexia nervosa patients and increased levels of harm avoidance and reduced
levels of self-directedness among patients suffering from bulimia nervosa or an eating disorder not
otherwise specified. Thirdly, among patients with a history of suicide attempt, bulimic patients scored
lower than anorectic patients on self-directedness. Finally, these personality characteristics correlate
significantly with a number of eating disorder-related cognitive and behavioural characteristics, which
have previously been shown to be involved in the occurrence of attempted suicide among eating
disordered patients.
Taken together, these findings indicate an important effect of personality characteristics on the
occurrence of attempted suicide among the three major categories of eating disordered patients, and
thus suggest that a stress-diathesis model can be used to explain the development of suicidal behaviour
in association with eating disorders. While the ‘stress’ component of the model was not assessed in this
study, the findings indicate that the ‘diathesis’ component of this model can be described in terms of
personality characteristics, and that previously described risk factors for attempted suicide among eating
disordered patients, such as cognitive and behavioural characteristics, actually reflect the effect of these
personality characteristics.
The results of the current study may have been biased by the small number of patients reporting
a history of attempted suicide in the three categories of eating disorders and by its retrospective nature.
However, the proportion of eating disordered patients reporting a history of attempted suicide in the
current study is in keeping with that in previous retrospective studies. A recent longitudinal study,
however, showed a higher rate of attempted suicide in anorexia nervosa than bulimia nervosa (Franko et
al, 2004). It should be noted that attempted suicide in this prospective study was defined by at least some
intent to die. Thus, while the current study suggests that risk factors for attempted suicide in terms of
personality characteristics in anorexia nervosa differ from those in bulimia nervosa, these findings
indicate that attempted suicide in anorexia nervosa may also differ from that in bulimia nervosa by a
relatively more marked intent to die. Unfortunately, intent to die was not assessed in the current study.
The current findings confirm previous reports of a common occurrence of attempted suicide
among ED patients. It appears that the impact of the difference in operational definitions between
Europe and the USA on prevalence rates of AS in ED is limited. It is currently not clear how this
common occurrence can be explained. It has been suggested that eating disorders themselves constitute
a version of self-harm and may exist along a continuum with other self-harm behaviours (Anderson &
Bulik, 2004). AS and ED share a more common prevalence among females, their onset often occurs
during adolescence, and both behaviours can be used as a means of taking control over one’s own body
(Anderson & Bulik, 2004). However, the current study also showed that the occurrence of AS among
ED patients is associated with a particular temperamental make-up, which may constitute a diathesis for
attempted suicide among eating disordered patients.
The diathesis among anorexia nervosa patients appears to differ from that in bulimia nervosa and
EDNOS patients. More particularly, it appears that a disturbed trait-dependent regulation of anxiety, or
increased behavioural inhibition, in combination with a low score on self-directedness is involved in
suicidal behaviour among the latter categories of eating disorders but not in anorexia nervosa. The lower
score on self-directedness indicates a reduced ability to control, regulate and adapt behaviour to fit the
situation in accordance with individually chosen goals, and a limited development of skills and
confidence in solving problems (Cloninger et al., 1993). The current findings indicate that increased
harm avoidance and low self-directedness among eating disordered patients may become manifest
through cognitive and behavioural problems including increased drive for thinness, bulimia, body
dissatisfaction, ineffectiveness, perfectionism, interpersonal distrust, interoceptive awareness, maturity
fears and emotional eating. While no causal interpretation of this association can be inferred from the
data, the results suggest that these characteristics can be regarded as cognitive coping strategies reflecting
a shift from the interpersonal to the personal domain and from a psychological to a somatic focus in an
attempt to increase perceived control.
A combination of low novelty seeking and high harm avoidance will lead to increased behavioral
inhibition due to which behaviours will not be reinforced by external stimuli but instead be repetitive
and automatic. The results suggest a pivotal role for novelty seeking. Increased levels of harm
avoidance reflect behavioural inhibition, but may nevertheless be associated with cognitive and
behavioural disinhibition when combined with increased levels of novelty seeking. This appears to be
the case in AN patients who show increased levels of harm avoidance and, in case of a history of AS,
additionally increased levels of novelty seeking. The scarce literature and case reports indeed suggest an
important effect of anxiety on the development of suicidal behaviour in general, and in anorexia nervosa
in particular. For example, Ellen West described the role of anxiety in the development of suicidal
behaviour in association with anorexia nervosa in a compelling way in her diary (summarized by Bruch,
1979). Before committing suicide, this anorexia nervosa patient wrote that ‘the most horrible thing about
my life is that it is filled with fear. Fear of eating, but also fear of hunger and fear of fear itself. Only
death can liberate me from this dread’. In the same line of reasoning, Williams and Pollock (2001) have
pointed at the role of Gilbert’s (1989) ethological concept of ‘arrested flight’ in the development of
suicidal behaviour, describing the behaviour of a bird experiencing entrapment and the lack of escape,
and the similarities between this concept and the effect of increased behavioural inhibition have been
described elsewhere (Van Heeringen, 2001). It is tempting to point at the similarities between Gilbert’s
description of a bird in a cage experiencing ‘arrested flight’ and Hilde Bruch’s ‘The Golden Cage’ (1979),
suggesting that suicidal behaviour may indeed be the only escape from anxiety and entrapment. Taking
into account the stress-diathesis model of suicidal behaviour, the current findings suggest that the
anxiety involved in the development of suicidal behaviour in anorexia nervosa relates more to illnessrelated stress than to the trait-dependent diathesis for suicidal behaviour.
Although more research is clearly needed to support the application of the stress-diathesis model
to suicidal behaviour among eating disordered patients, a number of implications for treatment and
prevention can be formulated. From a psychotherapeutic point of view, the current findings suggest that
an increase in self-directedness or self-control should be an important issue in the treatment of eating
disordered patients. Fairburn and colleagues (1998) have described a cognitive behavioural approach to
enhance self-control in eating disordered patients. The findings from the current study suggest that such
an approach is particularly important in preventing attempted suicide.
From a psychopharmacological point of view, the current findings suggest a role of serotonergic
agonists in the prevention of attempted suicide among eating disordered patients, particularly in patients
suffering from bulimia nervosa and EDNOS in view of the role of harm avoidance in the development
of attempted suicide in these types of eating disorders. Indeed, using a functional neuro-imaging
approach we have recently demonstrated a reduced prefrontal binding potential of prefrontal serotonin
(5-HT)-2a receptors in association with attempted suicide (Audenaert, Goethals, Van Laere, van
Heeringen & Dierckx, 2002), which correlated negatively with levels of harm avoidance (Van Heeringen
et al., 2003). There might, however, also be a role for these pharmacological agents in the treatment of
anorexia nervosa as we could show in another study that anorexia nervosa patients have a lower 5-HT2a
receptor binding in the left prefrontal cortex, in the left and right parietal cortex and the left and right
occipital cortex (Audenaert et al., 2002). An association between these findings and the occurrence of
attempted suicide or related cognitive and behavioural characteristics as assessed in the current study
remains however to be demonstrated. Moreover, as both attempted and completed suicide appear to be,
at least in part, under genetic control, further study is needed with regard to genetic influences on the
occurrence of suicidal behaviour in eating disordered patients. The genetic effects of 5-HT2a receptor
functioning might provide a focus for such studies. The results of studies of the effect of a 5-HT2a
receptor polymorphism on the development of anorexia nervosa have not been equivocal (Ohara, Nagai,
Tsukamoto, Tani, Suzuki & Ohara, 1998; Fairburn, Shafran & Cooper, 1998), but its effect on the
occurrence of suicidal behaviour among eating disordered patients clearly needs more study.
In conclusion, this study shows that attempted suicide is a common problem among eating
disordered patients and that its occurrence is associated with personality characteristics, which in turn
may become manifest as cognitive and behavioural problems related to eating disorders. The findings
thus provide support for the application of a stress-diathesis model of suicidal behaviour, and indicate
that the diathesis for attempted suicide among anorexia nervosa patients differs from that in patients
suffering from bulimia nervosa and atypical eating disorders.
References
Audenaert, K., Van Laere, K., Goethals I., Lahorte, P., Brans, B., Beelaert, B., van Heeringen, C., & Dierckx, R. (2002).
SPECT neuropsychological activation procedure with the verbal fluency test in depressed suicide attempters. Nuclear
Medicine Communications, 23, 907-916.
Bruch, H. (1979). The golden cage: the enigma of anorexia nervosa. New York, Vintage.
Bulik, C., Sullivan, P.F., & Joyce, P.R. (1999). Temperament, character and suicide attempts in anorexia nervosa, bulimia
nervosa and major depression. Acta Psychiatrica Scandinavica, 100, 27-32.
Cloninger, C.R., Przybeck, T.R., Svrakic, D.M., & Wetzel, R.D. (1994). The Temperament and Character Inventory (TCI): A
guide to its development and use. St. Louis, MO: Center for Psychobiology of Personality, Washington University.
Cloninger, C.R, Svrakic, D.M, & Przybeck, T.R. (1993). A psychobiological model of temperament and character. Archives
of General Psychiatry, 50, 975-990.
Corcos, M., Taïb, O., Benoit-Lamy, S., Paterniti, S., Jeammet, P., & Flament, M.F. (2002). Suicide attempts in women with
bulimia nervosa: frequency and characteristics. Acta Psychiatrica Scandinavica, 106, pp 381-386.
Coren, S., & Hewitt, P.L. (1998). Is anorexia nervosa associated with elevated rates of suicide? American Journal of Public
Health, 88, 1206-1207.
Duijsens, I.J., Spinhoven, P., Goekoop, J.G., Spermon, T., & Eurelings-Bontekoe, E.H.M. (2000). The Dutch temperament
and character inventory (TCI): dimensional structure, reliability and validity in a normal and psychiatric outpatient sample.
Personality and Individual Differences, 28, 487-499.
Eckert, E.D., Halmi, K.A., Marchi, P., Crove, E., & Crosby, R. (1995). Ten-year follow-up study of anorexia nervosa: clinical
course and outcome. Psychological Medicine, 25, 143-156.
Fairburn, C.G., Shafran, R., & Cooper, Z. (1998). A cognitive behavioural theory of anorexia nervosa. Behaviour Research
and Therapy, 37, 1-13.
Favaro, A. & Santonastaso, P. (1996). Purging behaviors, suicide attempts, and psychiatric symptoms in 398 eating
disordered subjects. International Journal of Eating Disorders, 20, 99-103.
Favaro, A. & Santonastaso, P. (1997). Suicidality in eating disorders: clinical and psychological correlates. Acta Psychiatrica
Scandinavica, 95, 508-514.
Franko DL, Keel PK, Dorer DJ, Blais MA, Delinsky SS, Eddy KT, Charat V, Renn R, & Herzog (2004). What predicts
suicide attempts in women with eating disorders ? Psychological Medicine, 34, 843-853.
Fullerton, D.T., Wonderlich, S.A., & Gosnell, B.A. (1995). Clinical characteristics of eating disorder patients who report
sexual or physical abuse. International Journal of Eating Disorders, 17, 243-249.
Garner, D.M., Olmstead, M.P, & Polivy, J. (1983). The Eating Disorders Inventory: A measure of cognitive-behaviroural
dimensions of anorexia and bulimia. In: DARBY PL, ed. Anorexia Nervosa: Recent developments in research.. New York:
Alan R. Liss.
Gilbert, P. (1989). Human nature and suffering. Hove and London, Lawrence Erlbaum Associates.
Keel, P.K., Dorer, D.J., Eddy, K.T., Franko, D., Charatan, D.L., & Herzog, D.B. (2003). Predictors of mortality in eating
disorders. Archives of General Psychiatry, 60, pp 179-183
Mann, J.J., Waternaux, C., Malone, K., …. (1997?) Towards a clinical model of suicidal behaviour in psychiatric patients.
American Journal of Psychiatry, ….
Moller-Madsen, S., Nystrup, J. & Nielsen, S. (1996). Mortality in anorexia nervosa in Denmark during the period 1970-1987.
Acta Psychiatrica Scandinavica, 94, 454-459.
Nielsen, S., Moller-Madsen, S., Isager, T., Jorgensen, J., Pagsberg, K. & Theander, S. (1998). Standardized mortality in eating
disorders: a quantitive summary of previously published studies and new evidence. Journal of Psychosomatic Research, 44,
413-434.
Ohara, K., Nagai, M., Tsukamoto, T., Tani, K., Suzuki, Y., Ohara, K.
polymorphism – 1438G/A and mood disorders. Neuroreport, 9, 1139-1141.
(1998).
5-HT2A receptor gene promoter
Patton, G.C. (1988). Mortality in eating disorders. Psychological Medicine, 18, 947-951.
Pompili M, Mancinelli I, Girardi P, Ruberto A, & Tatarelli R (2004). Suicide in Anorexia Nervosa: A Meta-Analysis.
International Journal of Eating Disorders, 36: 99-103.
Sakinofsky, I. (2000) Repetition of suicidal behaviour. In: Hawton K. & Van Heeringen C, eds. The international
handbook of suicide and attempted suicide, Wiley, England.
Sansone, R.A., & Levitt, J.L. (2002). Self-harm behaviors among those with eating disorders. Eating Disorders: The Journal
of Treatment & Prevention, 10, 205-213.
Sansone, R.A., & Levitt, J.L. (2004). The prevalence of self-harm behavior among those with eating disorders. In: L. Levitt,
R.A. Sansone & L. Cohn (eds). Self-harm behavior and eating disorders: dynamics, assessment, and treatment. New York:
Brunner & Routledge.
Schmidtke, A., Weinacker, B., Apter, A., Batt, A., Berman, L., Bille-Brahe, U., Botsis, A., De Leo, D., Doneux, A., Goldney,
R., Grad, O., Haring, K., Hawton, K., Hjelmeland, H., Kelleher, M., Kerkhof, A., Leenaars, A., Lönnqvist, J., Michel, K.,
Ostamo, A., Salander-Renberg, E., Sayil, I., Takahashi, Y., Van Heeringen, C., Vrnik, A., & Wasserman, D. (1999). Suicide
rates in the world: an update. Archives of Suicide Research, 5, 81-89.
Sullivan, P.F. (1995). Mortality in anorexia nervosa. American Journal of Psychiatry, 152, 1073-1074.
Van Heeringen C. (2001). Understanding suicidal behaviour: the suicidal process approach to research, treatment and
prevention. Chichester, Wiley.
Van Heeringen, C., Audenaert, K., Van Laere, K., Dumont, F., Slegers, G., Mertens, J., & Dierckx, R.. (2003). Prefrontal 5HT2a receptor binding index, hopelessness and personality characteristics in attempted suicide. Journal of Affective
Disorders, 74, 149-158.
Van Strien, T., Frijters, J.E.R., Bergers, G.P.A. & Defares, P.B. (1986). The Dutch Eating Behaviour Questionnaire (DEBQ)
for assessment of restrained, emotional and external eating behaviour. International Journal of Eating Disorders, 5, 295-315.
Wildman, P., Lilenfeld L.R.R., & Marcus M.D. (2004). Axis I comorbidity Onset and parasuicide in women with eating
disorders. International Journal of Eating Disorders, 35, 190-197.
Williams, J.M.G. & Pollock, L. (2001). Psychological aspects of the suicidal process. In Van Heeringen C. (ed.)
Understanding suicidal behaviour: the suicidal process approach to research, treatment and prevention. Chichester, Wiley.
PART II
The cognitive psychology of eating disorders:
personality, cognitions and behaviour.
Chapter 3: Integration of personality characteristics in a psychobiological model of eating
disorders: general outcome (paper in preparation)
Introduction
This chapter will describe the association between ED and personality dimensions in a large
sample of ED- patients. The findings will be discussed in the context of the hypothetical model for the
prediction by eating-disordered behaviour as it was described in the last sections of Part I. Based on the
differences of the personality characteristics between the subcategories of ED patients and the measured
clinical differences between these groups, it could be expected that the higher the Novelty Seeking
(positive correlation) and the lower the Self-directedness (negative correlation), the higher the BMI,
HBMI, the higher the scores on external and emotional eating and on drive for thinness, bulimia and
body dissatisfaction, and the higher the number of patients who vomited and/or abused laxative, will be,
since these characteristics scored highest in the BP group.
Methods
Eight hundred patients who were consecutively referred to the in- and out-patient units of the
Centre for Eating Disorders at the University Department of Psychiatry of the Ghent University
Hospital between December 1998 and September 2004 and who met the DSM-IV criteria for Eating
Disorders were enrolled in the study. The assessments were done during the first week following
referral before start of the treatment. Research was compliant with the Code of Ethics of the World
Medical Association (Declaration of Helsinki) and performed following the guidelines of the local ethics
committee.
The referred group included 329 (41 %) anorectic patients of whom 239 were restrictor-type
anorectics (RAN), while 90 were purgers/bingers (BPAN). Among the bulimic patients (B=273; 34 %),
225 were purgers/bingers (BP) and 48 were non-purging type bulimics (B-NP). The group of patients
diagnosed with eating disorders not otherwise specified (EDNOS) contained 198 (25 %) patients of
whom 58 met the criteria for binge eating disorder (BED). Most of the patients were female as only 3,5
% (n = 28) were male, with 5 male patients in the RAN group, 1 in the BPAN, 9 in the BP group, 3 in
the B-NP and 10 in the EDNOS group of whom 3 were BED patients. The control group (n = 326)
consisted of 178 female students in the first year of their training in Psychology or Medicine, and 148
women from a general population sample (van Heeringen & Meerschaert, unpublished data) (see Table
1).
Table 1. Frequencies of study population
N
%
RAN
239
29.9
BPAN
90
11.3
BP
225
28.1
B-NP
48
6.0
EDNOS
140
17.5
BED
58
7.3
ED
800
100
Measures
Weight and height, highest and lowest adult weight and duration of illness were assessed
carefully. The body mass index (BMI) was calculated, as well the highest and lowest lifetime BMI
(HBMI, LBMI), based on the highest and lowest adult weight (16 years or older). HBMI and LBMI can
thus reflect an underestimation as current body lengths were used to calculate these indices, as patients
may not be reliable in remembering their precise length at the moment of their highest and lowest
weight. Patients were asked to describe the frequency of their binging, purging and restricting eating
according to three categories: never, more than two times per week or less than two times per week.
Binging was described as losing control over eating, not including any measurement of calories, but as
‘involving larger amounts of food than most people would eat during a similar period of time and under
similar circumstances’.
As in the five studies described before, the validated Dutch version of the TCI (Duysens et al.,
2000) was used to assess temperament and character characteristics. The Dutch Eating Behaviour
Questionnaire (DEBQ; Van Strien, 1986) was used to assess the behavioural characteristics ‘emotional
eating’ (eating elicited by diffuse and clear emotional stimuli), ‘restrained eating’ (the tendency to diet in
order to lose weight), and ‘external eating’ (eating elicited by external stimuli). The Eating Disorder
Inventory (EDI; Garner et al., 1983) was used to assess body dissatisfaction, perfectionism and
interpersonal distrust. Statistical analysis was performed using SPSS 10.0.
The reliability and validity of the assessment of symptoms and diagnoses using self-administered
questionnaires is variable. Self-reports can be associated with demand characteristics, response bias and
defensiveness (Vitousek & Orimoto, 1993).
With regard to eating disorders, studies in different
populations have consistently shown that self-report generates higher scores than the Eating Disorders
Examination (EDE; Fairburn & Cooper, 1993), which is the golden standard for the assessment of
complex features such as binge eating and concerns about shape, weight, and dietary restraint (Celio,
Wilfley, Crow, Mitchell, Walsh, 2004; De Zwaan, Mitchell, Swan-Kremeier, McGregor, Howell, Roerig,
Crosby, 2004). The EDE is advantageous because it includes a detailed description of binge episodes and
thus provides more valid assessments of the amount of food eaten, feelings of loss of control, and
frequency of episodes that are essential to diagnose a clinical disorder. However, the assessment of
eating disorders by means of self-reports is brief, inexpensive, and highly efficient. Drawbacks in using
the EDE indeed include the amount of time it takes to administer (30-60 min) and the extensive training
of personnel that is required (Goldfein, Devlin, Kamenetz, 2005).
Although the current study used self-reports, the data can be regarded as reliable. All patients
were treated in the same department so that obvious discrepancies between self-reported and clinical
data were corrected during the first weeks of treatment. Moreover the main target was the study of the
relationship between usually measured cognitive and behavioural characteristics and personality
dimensions in order to the construction of a hypothetical neuro-bio-psychological model associated with
eating disordered symptoms.
Results
In this part of the study, data on typical ED patients (RAN, BPAN, BP and B-NP) were
compared to those of control women. First age and personality characteristics were compared between
AN and B patients and control women (CW) (see table 2).
Table 2: Age and personality characteristics in eating disordered patient compared to control
women
Variable
AN
N=32
9
(320)
m
sd
22.5
8.1
16.1
6.5
4.7
2.6
3.3
2.4
3.5
2.4
4.5
2.1
24.0
6.5
B
N=273
(264)
m
sd
CW
N=326
(326)
m
sd
23.1
7.2
20.0
6.8
5.6
2.6
4.4
2.6
5.0
2.1
4.9
2.1
23.8
7.2
23.4
8.4
20.3
6.2
6.7
2.3
4.4
2.7
5.1
2.0
4.2
2.2
17.1
7.0
Persistence (P)
7.7
2.4
5.2
1.7
5.3
2.2
5.8
2.4
16.1
3.6
7.4
2.0
4.2
2.3
4.6
1.2
5.6
1.9
7.8
2.5
4.9
2.0
5.1
2.4
5.9
2.4
16.3
3.6
7.3
2.0
4.5
2.3
4.5
1.1
5.1
2.0
Selfdirectedness
22.6
7.6
19.8
7.1
Age
Novelty
seeking(NS)
Exploratory
excitability (NS1)
Impulsiveness
(NS2)
Extravagance
(NS3)
Disorderliness
(NS4)
Harm
Avoidance(HA)
Anticipatory worry
(HA1)
Fear of uncertainty
(HA2)
Shyness (HA3)
Fatigability (HA4)
Reward
dependence (RD)
Sentimentality
(RD1)
Attachment (RD3)
Dependence (RD4)
F
p
1.0
.360
ns
32.0
.000
AN < B, CW
41.3
.000
AN < B < CW
14.2
.000
AN < B, CW
46.0
.000
AN < B, CW
10.0
.000
AN, CW < B
103.1
.000
CW < ED
5.0
2.6
4.5
1.8
4.0
2.3
3.5
2.2
18.5
3.4
7.9
1.7
6.2
2.0
4.5
1.1
4.4
2.0
121.0
.000
CW < ED
11.9
.000
CW < ED
30.6
.000
CW < ED
103.6
.000
CW < ED
45.1
.000
ED < CW
7.5
.001
ED < CW
75.3
.000
ED < CW
.352
.725
ns
34.0
.000
CW < ED
B < AN
31.4
7.1
210.0
.000
ED < CW
B < AN
(SD)
Responsibility
(SD1)
Purposefulness
(SD2)
Resourcefulness
(SD3)
Self-acceptance
(SD4)
Enlightened
Second Nature
(SD5)
Cooperativeness
(C)
Social acceptance
(C1)
Empathy (C2)
Helpfulness (C3)
Compassion (C4)
Pure-hearted
Conscience (C5)
Selftranscendence
(ST)
Self-forgetful (ST1)
Transpersonal
identification(ST2)
Spiritual
Acceptance (ST3)
3.9
2.2
4.1
1.9
2.2
1.6
6.2
2.7
6.2
2.7
3.5
2.2
3.9
2.0
2.1
1.6
5.7
2.5
4.6
2.4
6.0
2.0
5.7
1.9
3.6
1.3
7.1
2.4
8.9
2.4
122.3
.000
ED < CW
79.8
.000
ED < CW
106.6
.000
ED < CW
24.6
.000
223.8
.000
ED < CW
B < AN
ED < CW
B < AN
31.8
6.7
31.3
6.4
34.4
5.2
23.0
.000
ED < CW
6.5
1.7
5.0
1.6
6.3
1.5
7.7
2.6
6.5
1.5
12.4
6.3
6.4
1.7
5.1
1.5
6.2
1.4
7.2
2.8
6.4
1.6
11.2
6.6
7.2
1.2
5.9
1.2
6.9
1.3
7.6
2.5
6.8
1.5
13.0
6.7
26.0
.000
ED < CW
36.2
.000
ED < CW
27.9
.000
ED < CW
2.6
.074
ns
5.9
.003
ED < CW
5.5
.004
B < CW
4.6
2.7
2.7
2.1
4.7
3.1
4.6
2.7
2.3
2.0
4.3
3.4
4.9
2.5
2.6
2.1
5.5
3.4
1.1
.323
ns
3.1
.047
B < AN
9.5
.000
ED < CW
AN = Anorectic patients; B = Bulimic patients; CW = Control women; ED = AN + B
ED patients showed comparatively high scores on HA (on all the sub-dimensions) and low
scores on SD (on all the sub-dimension). Mean scores on RD and cooperativeness in all ED categories
were lower than the mean scores of control women except for the RD4 ‘dependence’ and C4
‘compassion’ sub-dimensions. To the contrary, ED patients showed a comparatively higher score on the
temperament dimension Persistence (P). ED patients also showed a comparatively lower score on the
sub-dimension ‘Exploratory excitability’ (NS1) of the ‘Novelty Seeking’ temperament dimension (NS)
and a comparatively lower score on the sub-dimension ‘Spiritual Acceptance’ (ST3).
Differences between the anorectic and bulimic categories of ED patients included a lower score
on Novelty Seeking among AN patients than among bulimic patients. Bulimic patients had also a lower
score on Persistence (P), when compared to AN patients. Furthermore, lower scores were found for
bulimic patients for ‘Self-directedness’ (SD), especially for the sub-dimensions ‘Self-acceptance’ (SD4)
and ‘Enlightened Second Nature’ (SD5). Bulimic patients showed lower scores on ‘Self-Transcendence’
(ST) compared to control women, and lower scores on ‘Transpersonal Identification’ (ST2) compared to
anorectic patients.
Comparing diagnostic subtypes of ED’s, excluding the non-purging bulimics, significant
differences were mentioned in Table 3.
Table 3: Significant differences in personality characteristics between eating disordered patients
Variable
Novelty seeking(NS)
Exploratory
excitability (NS1)
Impulsiveness (NS2)
Extravagance (NS3)
Disorderliness (NS4)
Persistence (P)
Selfdirectedness (SD)
Responsibility (SD1)
Self-acceptance (SD4)
Enlightened Second
Nature (SD5)
RAN
N=23
9
(232)
M
15.7
6.4
4.7
2.7
3.2
2.3
3.4
2.3
4.3
2.0
5.7
1.8
23.1
7.4
BPAN
N=90
(88)
SD
BP
N=225
(218)
M
17.1
6.8
4.7
2.5
3.5
2.5
4.0
2.4
4.9
2.4
5.5
2.1
21.4
8.0
3.9
2.2
6.3
2.6
6.5
2.7
F
p
20.0
609
5.6
2.6
4.4
2.6
5.0
2.5
5.0
2.2
5.1
2.0
19.6
7.0
23.9
.000
6.9
.001
12.8
.000
AN < BP
AN < BP
26.5
.000
AN < BP
5.7
.004
RAN < BP
5.2
.006
BP < RAN
12.5
.000
BP < RAN
3.7
2.3
3.3
2.1
3.9
.020
BP < RAN
5.9
2.8
5.5
2.7
5.6
2.5
4.6
2.4
4.5
.011
BP < RAN
28.7
.000
AN < BP
BP < BPAN < RAN
Although all anorectic patients scored lower than bulimics on the Novelty Seeking dimension,
the scores of the restrictor group (RAN) were lower than those of the BP group only on the subdimension ‘Disorderliness’ (NS4). This was combined with higher scores, though only for the RAN
patients, on all dimensions of the ‘Self-directedness’ and ‘Persistence’. Finally, the scores of the RAN
patients were even higher than those of the BPAN group on the sub-dimension ‘Enlightened Second
Nature’ (SD5).
Further statistical analysis included the calculation of correlations between the measured
personality characteristics and cognitive and behavioural aspects related to the eating pathology. Major
findings regarding these aspects are summarized in Table 4 and Table 5.
Table 4: Age, weight-related characteristics, duration of illness, behavioural and cognitive
characteristics in eating disorder patients, by type of eating disorder.
BP
RAN BPAN
p
N=239 N=90 N=225 F
m
m
m
sd
sd
sd
Age
21.9
24.1
23.0
2.7 .07
ns
8.2
7.7
7.3
Duration of illness
3.9
5.3
4.6
2.0 .137
ns
6.3
6.2
6.2
Age at onset
18.0
18.8
18.3
0.9 .40
ns
5.1
4.8
5.0
BMI
15.0
15.6
21.1 373.4 .000
AN < B-P
1.5
1.1
3.5
Highest life time BMI
20.5
22.2
24.9
68.4 .000 RAN < BPAN < B-P
3.0
4.0
5.0
Lowest life time BMI
14.3
14.8
18.5 153.1 .000
AN < B-P
1.8
1.5
3.6
Restrained eating
3.8
4.1
4.0
4.6 .011
RAN < BPAN
1.1
1.0
0.8
External eating
2.5
2.9
3.4
86.7 .000 RAN < BPAN < B-P
0.7
0.9
0.7
Emotional eating
2.2
3.2
3.8
183.2 .000 RAN < BPAN < B-P
1.0
1.1
0.9
Drive for thinness
11.6
13.5
15.6
23.2 .000 RAN < BPAN, B-P
7.2
6.6
5.1
Bulimia
1.1
6.5
10.9 268.8 .000 RAN < BPAN < B2.5
6.0
5.5
P
Body dissatisfaction
11.8
13.0
17.9
36.9 .000
AN < B-P
7.6
7.8
8.1
Ineffectiveness
12.0
12.9
12.9
1.04 .353
ns
7.3
7.5
7.6
Perfectionism
7.0
7.1
7.0
0.02 .980
ns
4.6
4.6
4.8
distrust
6.2
6.6
5.5
2.3 .100
ns
4.5
4.5
4.4
Interoceptive awareness 10.2
10.9
11.1
1.8 .171
ns
5.2
5.5
5.4
Maturity fears
7.2
6.5
6.6
1.1 .347
ns
Characteristics
5.5
5.0
5.3
ANOVA with Bonferoni post hoc comparison, (df =2), with level of significance set at p < .05
Table 5: Compensatory behaviour by type of eating disorder
RAN BPAN
BP
N=239 N=90 N=225
N
N
N
%
%
%
p
Purging
40
17
90
100
225
100
.000
Vomiting
19
7
24
10
69
29
73
81
21
23
15
17
181
80
85
38
58
26
.000
Laxative abuse
Excessive exercise
.000
.050
Pearson Chi-Square
No significant differences between the three ED groups were found for age, duration of illness,
age of onset, ineffectiveness, distrust, interoceptive awareness and maturity fears.
AN patients had a lower current BMI, as expected, but also a lower highest and lowest lifetime
BMI, and lower scores on external and emotional eating, bulimia and body dissatisfaction. Among AN
patients, the RAN group, showed the lowest scores on external and emotional eating, bulimia and the
highest lifetime BMI. Restrictive anorectic patients (RAN) scored lower compared to both
binger/purger groups (BPAN and BP) on ‘restrained eating’ and lower compared to the BPAN group
on ‘drive for thinness’. As shown in Table 5, patients in the three ED categories differed significantly
with regard to the presence of vomiting, purging, abusing laxatives and excessive exercise more than two
times per week.
Table 6 shows the correlations between scores on personality dimensions and those on
cognitive and behavioural characteristics.
Table 6: Correlations between personality dimensions and cognitive and behavioural
characteristics
NS
HA
RD P
SD
CO
ST
.18**
.07
.09* -.23** -.10** -.02
.09*
.10** .03
-.17** -.09*
-.04
-.11**
.19**
.02
-.24** -.05
-.04
-.10**
-.08*
.34** .03
-.12**
BMI
HBMI
.06
LBMI
.06
-.31** -.04
.005
Drive for thinness
Bulimia
.22** .07*
Body dissatisfaction .01
-.00 -.14** -.30** -.10** -.03
.37** .06
-.05
-.36** -.06
-.07
-.13** -.02
.02
Restrained
eating
-.15** .18** -.02 .18**
External
eating
.24** -.01
Total
emotional
.18**
.11** -.04 -.11** -.32** -.09*
-.07
Laxative abuse
-.02
.14** .03
.04
-.13** -.02
-.01
Vomiting
.15**
.02
.00
-.05
-.15** -.02
.06
Excessive
exercise
-.02
-.04
-.05 .09**
.04
-.02
-.06 -.15** -.18** -.11** .05
.01
* Correlation is significant at the 0.05 level (2-tailed)= p < . 05
** Correlation is significant at the 0.01 level (2-tailed) = p < . 01
A number of correlations between key characteristics of ED, i.e. body dissatisfaction,
perfectionism and interpersonal distrust, and personality dimensions were found. As shown in Table 7,
body dissatisfaction correlated positively with HA and negatively with self-directedness, while
perfectionism correlated positively with HA, RD, P and ST and negatively with NS and SD.
Interpersonal distrust correlated negatively with NS, RD, SD and C, and positively with HA and P
Table 7: Positive and Negative correlations between specific cognitive characteristics and
personality dimensions
NS
HA
RD
P
SD
+
Body Dissatisfaction
C
ST
-
Perfectionism
-
+
+*
+
-
Interpersonal distrust
-
+
-
+*
-
+
-
Correlation is only significant at the 0.05 level (2-tailed)= p < . 05
The correlations between personality dimensions and behavioural and cognitive characteristics
according to ED categories are shown in Table 8, 9 and 10.
Table 8 : Correlations between personality dimensions and cognitive and behavioural
characteristics in the RAN group
NS
Body dissatisfaction
HA
RD
+0..33**
SD
-0.38**
Perfectionism
-0.14*
Interpersonal
distrust
-0.39** +0.39** -0.46**
* Correlation is significant at the 0.05 level (2-tailed)= p < . 05
** Correlation is significant at the 0.01 level (2-tailed) = p < . 01
+0.14*
P
+0.16* +0.39** -0.19**
-0.24**
C ST
Table 9 : Correlations between personality dimensions and cognitive and behavioural
characteristics in the BPAN group
NS
HA
Body dissatisfaction
Perfectionism
RD
P
SD
+0.51**
-0.38**
-0.24*
Interpersonal
distrust
C ST
+0.44** -0.26*
-0.50**
+0.30**
-0.34**
* Correlation is significant at the 0.05 level (2-tailed)= p < . 05
** Correlation is significant at the 0.01 level (2-tailed) = p < . 01
Table 10 : Correlations between personality dimensions and cognitive and behavioural
characteristics in the BP group
NS
Body dissatisfaction -0.14*
HA
RD
P
SD
C
ST
+0.38**
-0.21**
Perfectionism
-0.27** +0.32**
-0.35**
Interpersonal
distrust
-0.30** +0.42** -0.51** +0.15* -0.41** -0.23** -0.17**
* Correlation is significant at the 0.05 level (2-tailed)= p < . 05
** Correlation is significant at the 0.01 level (2-tailed) = p < . 01
A correlation between body dissatisfaction and HA (+) and SD (-) was found in the three
diagnostic groups (RAN, BPAN and BN). Only among the BP patients there was a negative correlation
between NS and body dissatisfaction. A positive correlation was found between perfectionism and HA
(not for BPAN), RD (not for BPAN and BP), P (not for BP), and ST (not for RAN and BP). A negative
correlation between perfectionism and NS and SD was found in the three groups.
Finally, for
interpersonal distrust a negative correlation was found with NS and RD in all three groups, and
additionally with SD (except for the BPAN group) and with, C (only for the BP group). A positive
correlation was found between interpersonal distrust and HA (not for BPAN) and only with P for the
BP group.
Finally correlations between cognitive and behavioural characteristics were calculated.
Table 11: Correlations between cognitive and behavioural characteristics
BMI
.02
Restrained
eating
.62**
Emotional
eating
.18**
vomiting
.18**
Laxative
abuse
.31**
Excessive
exercise
.11**
.32**
-.03
.72**
.44**
.17**
-.03
Body
dissatisfaction
Ineffectiveness
.37**
.26**
.25**
.10**
.24**
.07
-.02
.19**
.14**
.06
.17**
.04
Perfectionism
-.07
.21**
.03
.03
.20**
.01
Interpersonal
distrust
Interoceptive
Awareness
Maturity
fears
-.03
.10*
.02
.04
.09*
.01
-.02
.23**
.19**
.10**
.18**
.07*
-.08*
.17**
.06
-.02
.04
.02
Drive for
Thinness
Bulimia
* Correlation is significant at the 0.05 level (2-tailed)= p < . 05
** Correlation is significant at the 0.01 level (2-tailed) = p < . 01
Table 11 shows that only positive correlation between the eating pathology-related cognitive and
behavioural characteristics were found, with the exception of a negative correlation between maturity
fears and BMI. More specifically, ‘Drive for thinness’ and ‘Interoceptive awareness’ were positively
correlated with emotional eating and all assessed compensatory behaviours: restrained eating, vomiting,
laxative abuse and excessive exercise, bulimia correlated with BMI, emotional eating, vomiting and
laxative abuse. ‘Body dissatisfaction’ was positively correlated with BMI, restrained and emotional
eating, vomiting, laxative abuse but not with excessive exercise.
‘Ineffectiveness’ correlated with
restrained and emotional eating and laxative abuse, and Perfectionism with restrained eating and with
laxative abuse. Although a strong correlation was found between ‘interpersonal distrust’ and most TCI
personality dimensions, no correlation between this cognitive factor and the behavioural dimensions was
found except for restrained eating and laxative abuse and this only at the p < 0.05 level. Finally,
‘Maturity Fears’ was correlated positively with restrained eating.
Discussion
ED patients showed comparatively high scores in HA and low scores on SD These personality traits
might thus describe the basic personality of the “ED’s spectrum” (Brewerton, Hand, & Bishop, 1993;
Bulik, Sullivan, Weltzin, & Kay, 1995; Cloninger, Przybeck, Svrakic, & Wetzel, 1994; Diaz-Marsa,
Carrasco, & Saiz-Ruiz, 2000; Klump, Bulik, Pollice et al., 2000; Mizushima, Ono, & Asai, 1998; Nagata
et al., 2003) and appear to have a negative prognostic value (Bulik, Sullivan, Joyce, Carter, & McIntosh,
1998). HA is a temperamental trait strictly linked to the individual’s predisposition to react to stressful
situations with behavioural inhibition, fear, anxiety, and depression (Cloninger & Svrakic, 1999). A high
HA is usually found in depressive and anxiety disorders (Cloninger et al., 1994). The fact that EDs are
characterized by a higher HA than the controls may mean that patients with EDs have a temperamental
predisposition toward the development of an ED as a reaction to stressors (Cloninger & Svrakic, 1999).
ED patients show a comparatively high score on all sub-dimensions ‘Anticipatory Worrying’ (HA1),
‘Fear of uncertainty’ (HA2), ‘Shyness’ (HA3) and ‘Fatigability’ (HA4), which indicates that they are
cautious, nervous, timid, doubtful, discouraged, insecure, passive, negativistic, or pessimistic even in
situations that do not worry other people. They have less energy and a strong tendency to tiredness
when compared to other people, with a slow recovery from stressors and minor illnesses (Cloninger et
al., 1994). This temperamental predisposition is associated with a low serotonergic tone (Cloninger et
al., 1994; Diaz-Marsa et al., 2000; Waller, Petty, Hardy, Gullion, Murdock, & Rush, 1993) and might
represent a factor which predisposes to EDs through a familial transmission (Fassino, Abbate-Daga,
Amianto, Leombruni, Boggio, & Rovera, 2002a; Fassino, Svrakic, Abbate Daga, Amianto, Leombruni, &
Stanic, 2002b; Kaye, Strober, Stein, & Gendall, 1999; Strober, Freeman, Lampert, Diamond, & Kaye,
2000).
On the other hand, a comparatively low Self-Directedness reflects a character element which promotes
expression of eating disorder (Bulik et al., 1995; Bulik, Sullivan, Joyce, & Carter, 1995; Cloninger, 2000;
Diaz-Marsa, Carrasco, Hollander, Cesar, & Saiz-Ruiz, 2000; Svrakic, Whitehead, Przybeck, & Cloninger,
1993). Individuals displaying low Self-Directedness are described as immature, self-humbling, and
unable to fix and pursue goals (Cloninger et al., 1994). Low Self-Directedness is associated with
personality disorder in a high percentage of individuals (Svrakic, et al., 1993; Cloninger, 2000) and
appears to be a negative prognostic factor for the effect of psychotherapy in EDs (Bulik et al., 1998).
ED patients are in particular characterized by a tendency to consider other people and situations
responsible for their frustrations through the perception that their behaviour is largely determined by
influences beyond their control or free will (SD1 significantly lower in all ED groups; Fassino et al.,
2002). Such individuals might be characterized by a tendency to anticipate pain and failure with
pessimistic thoughts and by not being able to bear humbling and embarrassing experiences, to which
they would react with long lasting “ruminations” (Cloninger et al., 1994). The lower scores on
‘purposefulness’ (SD2) display a marked detachment from social relationships (Diaz-Marsa et al., 1998).
It is possible that the difficulty in pursuing self-chosen goals and values and the tendency to look for an
external guide - which are characteristics of poorly self-directing individuals (Cloninger et al., 1994),
represent elements promoting the expression of what Gendall and co-workers defined (1998) as “ a
susceptibility to social messages on thinness”. Partially recovered, chronically ill anorexics reported
significantly higher HA (controlled for the prevalence of lifetime major depression or depression at the
time of follow-up), lower SD and lower CO than either healthy controls or fully recovered AN patients
(Bulik, Sullivan, Fear, & Pickering, 2000). These authors found that high SD is associated with a good
outcome (Bulik, Sullivan, Carter, McIntosh, & Joyce, 1998) and predicts an rapid response to cognitivebehavioural therapy also in bulimic patients (Bulik, Sullivan, Carter, McIntosh, & Joyce, 1999). It has
been suggested that low character development is a fundamental psychopathologic factor for all EDs
(Bulik et al., 1998; Diaz-Marsa et al., 1998; 2000).
Mean scores on RD (the data about this dimension are controversial; Brewerton, Hand, &
Bishop, 1993) and cooperativeness in all ED categories were lower than the mean scores of control
women except for the RD4 ‘dependence’ and C4 ‘compassion’ sub-dimensions. ED patients thus
showed a greater tendency to intolerance, criticism, and opportunism than controls. They can be
described as social insensitive and as having difficulties in finding something in common with other
people showing less worry about other people’s feelings, and allowing higher levels of aggressiveness
toward other people and the external environment. Low scorers enjoy getting revenge on people who
hurt them, either overt (active-aggressive behaviour) or disguised (passive-aggressive), while showing a
tendency to treat other people unfair, in a biased, self-serving manner that usually reflects their own
profit.
To the contrary, ED patients showed a comparatively higher score on the temperament
dimension Persistence (P) was found. A highly persistent individual tends to be a perfectionist, and
when contingencies change rapidly, perseveration becomes maladaptive.
ED patients also showed a comparatively lower score on the sub-dimension ‘Exploratory excitability’
(NS1) of the ‘Novelty Seeking’ temperament dimension (NS) compared to control females. ED patients
thus usually demand very good practical reasons before they are willing to change the way they do
something.
Finally, ED patients showed a comparatively lower score on the sub-dimension ‘Spiritual Acceptance’
(ST3). This is a disadvantage when facing situations over which there is no control or possibility for
evaluation by rational objective means, such situations may include inevitable death, suffering, or unjust
punishments.
Differences between the anorectic and bulimic categories of ED patients included a lower score
on Novelty Seeking among AN patients than among bulimic patients (Brewerton et al., 1993; Casper,
1990; Casper, Hedeker, & McClough, 1992; Bulik et al., 1995a; 1995b; Nagata, Oshima, Wada, Yamada,
Iketani, & Kiriiki, 2003; Waller et al., 1993) and compared to control women (Klump et al., 2000).
Bulimic patients are thus in general, less organized, methodical, and systematic than AN patients.
Although other studies found AN patients to be similar to non-patient controls with regard to NS
(Kleifield, Sunday, Hurt, & Halmi, 1993; Kleifield, Sunday, Hurt, & Halmi, 1994; Brewerton et al., 1993;
Bulik, Sullivan, Weltzin, et al., 1995), we only found this similarity for the sub-dimension ‘Disorderliness’
(NS4).
Bulimic patients had also a lower score on Persistence (P), when compared to AN patients.
Furthermore, lower scores were found for bulimic patients for ‘Selfdirectedness’ (SD), especially
for the sub-dimensions ‘Self-acceptance’ (SD4) and ‘Enlightened Second Nature’ (SD5). This means that
bulimic patients tend to manifest behaviours, which are unfavourable in pursuit of their goals, and show
a poor strength of will, thus being unable to resist their temperamental impulses (Diaz-Marsa et al., 1999;
Klump et al., 2000).
Usually they are described as manipulative. Bulimic patients showed lower scores
on ‘Self-Transcendence’ (ST) compared to control women, and lower scores on ‘Transpersonal
Identification’ (ST2) compared to anorectic patients. In that way, they are less able to tolerate ambiguity
and uncertainty, rather materialistic, and unable to be satisfied with what they have.
Although studies comparing traits between diagnostic subtypes of ED’s are scarce, it seems that
RAN and BP patients have some opposite traits and BPAN patients share features with RAN and BP
patients (Van der Ham, Meulman, Van Strien, & Van Engeland, 1997). Patients of the B-NP group
were excluded from the following comparative analysis, since they were studied in comparison with the
BED patients separately (paper above) and they are rather low in frequency.
These results show that personality characteristics of patients with eating disorders differ from
those of healthy control females. Anorectic and bulimic patients differed from control women by
having relatively higher scores on HA and P and lower scores on RD. This temperament constellation
was combined with a poor character development as reflected by lower scores on SD and C.
When comparing patients in the ED categories with control women, particularly for AN patients
differences on the scores of temperament dimensions were found. Besides higher scores on HA and P
and lower scores on RD, AN patients and particularly the RAN group, also scored lower on Novelty
Seeking,. On the contrary, no difference for this dimension was found between bulimics and healthy
controls. Bulimic patients scored lower than the AN patients, particularly the RAN group, on character
dimensions, including SD and its sub-dimension SD5, and the ‘Transpersonal identification’ subdimension of ST.
No significant differences between the three ED groups were found for age, duration of illness,
age of onset, ineffectiveness, distrust, interoceptive awareness and maturity fears. Although for the
anorectic group, a higher score on perfectionism was found by Garner and colleagues (1993), no
difference between the categories was found in this study. As we have mentioned in earlier described
results (Part4article3), the motive for fasting can be different in the RAN group, since there lower score
for restrained eating and drive for thinness.
The hypothesis, as formulated in the introduction of this chapter, was confirmed with the
exception of a negative correlation between drive for thinness and NS, and the absence of a correlation
between body dissatisfaction and NS. The negative correlation between cognitive and behavioural
characteristics and SD, also supports this hypothesis. Since the RAN group has the highest score on
Persistence, a negative correlation with HBMI, Restrained, External and Emotional Eating, drive for
thinness and bulimia was hypothesized. This was also confirmed except for a positive relation between
Persistence and restrained eating and the absence of a correlation between persistence and drive for
thinness. Of interest was also the positive correlation between excessive exercise (mostly seen in the
RAN group) and Persistence.
It can thus be concluded that the three key characteristics of eating disorders show a clear
correlation with relevant personality dimensions. As hypothesized, body dissatisfaction plays a central
role in the basic spectrum of all three ED categories and correlated especially with HA (+) and SD (-).
Perfectionism appears to play a more important role in the RAN type, whereas interpersonal distrust
correlated with all personality dimensions in the BP group. As mentioned before, the BPAN group
shares features with the RAN and the BP group.
There is a paucity of studies on the association between personality characteristics, using the
TCI, and cognitive or behavioural aspects. Our finding of patterns of correlations between, on the one
hand, novelty seeking and self-directedness, and, on the other hand, the assessed behavioural and
cognitive characteristics as described above, are in keeping with findings of clusters of characteristics
found in bulimics such as increased novelty seeking, more outspoken external and emotional eating, and
bulimia.
The current findings suggest that the occurrence of AN, especially the RAN group, is
determined more by temperamental factors, i.e. predisposition, while the occurrence of BP is influenced
more by immature character development.
A comparable conclusion was formulated in a recent
Japanese study (Nagata et al., 2003), suggesting the importance of environmental factors in the
pathogenesis of bulimic symptoms in a culture, which differs much from Western ones. This could
clarify why cognitive behavioural therapy (CBT) is (more) effective in the treatment of bulimia nervosa,
since CBT is based on increasing self-control and changing maintaining factors. However, personality
development is not static and little is known about the interaction between distinct temperament
characteristics and the environment. Only one study using a longitudinal design to examine the role of
childhood temperament in the later development of eating concerns (Martin, Wertheim, Prior, Smart,
Sanson, & Oberklaid, 2000). It was found that high negative emotionality (negative reactivity) and low
task persistence assessed during childhood, were the factors most strongly associated with the risk of the
later development of eating disorders, particularly among girls. Another study found that bulimic
individuals were found more likely than control subjects to perceive their fathers as less affectionate and
more controlling toward them than they were toward their siblings (Wonderlich, Ukestad, & Perzacki,
1994). Very interesting is the study of Berg and colleagues (2000), in which the relationship between
temperament and perception of non-shared environment in BN patients was measured.
Among
bulimics, high levels of Harm Avoidance were more likely to be associated with increased maternal
affection and decreased levels of maternal control. One possible explanation for this association is that
in families of bulimic individuals, increased HA in the bulimic child is responded to with a rather
protective and non-demanding maternal response. Similarly, high levels of NS were more likely to be
associated with decreased paternal control (i.e. discipline). Again, it is plausible that these findings reflect
a pattern in which fathers of bulimic individuals respond to temperamental extremes with less limiting
and structuring behaviour. Johnson and Connors (1987) also reported parental under-involvement in
the families of bulimic individuals.
In summary of this study it can be stated that eating-disordered patients describe themselves as
more anxious and less socially sensitive, self-directed and cooperative than healthy volunteers of similar
age and educational level. AN patients show a lower score than BP patients and healthy volunteers on
NS. RAN patients score higher than BP patients on persistence and self-directedness. Scores on the
temperamental dimension NS correlate positively with levels of body dissatisfaction and negatively with
levels of perfectionism and interpersonal distrust, while sores on persistence correlate positively with
levels of perfectionism.
Scores on the character dimension self-directedness correlate negatively with the cognitive
attitudes body dissatisfaction, perfectionism and interpersonal distrust.
Lower scores on NS in combination with increased scores on P and SD become manifest
through behaviour that is less reactive to external and emotional stimuli, which in turn may lead to a
comparatively lower BMI.
A major outcome of these studies is that the demonstrated associations between core cognitive
and behavioural symptoms and these personality dimensions create the possibility to bridge the gap
between psychological theories and neurobiological functioning of eating-disordered patients.
Consequently, there was an impetus for further psychobiological research, which takes into account the
nurture-related temperamental and the development-related character dimensions of eating disorders in
general, and RAN and BP in particular. Part 3 describes two such studies followed by conclusions and
suggestions for further research.
References
Berg ML, Crosby RD, Wonderlich SA, & Hawley D (2000). Relationship of temperament and perceptions of non-shared
environment in bulimia nervosa. International Journal of Eating Disorders, 28, 148-154.
Brewerton TD, Hand LD, & Bishop ER (1993). The Tri-dimensional Personality Questionnaire in eating disorder patients.
International Journal of Eating Disorders, 14, 213-218.
Bulik C, Sullivan P, Carter FA, McIntosh VV, Joyce PR (1998). The role of exposure with response prevention in the
cognitive-behavioral therapy for bulimia nervosa. Psychological Medicine, 28, 611-623.
Bulik CM, Sullivan PF, Carter FA, McIntosh VV, Joyce PR (1999). Predictors of rapid and sustained response to cognitivebehavioral therapy for bulimia nervosa. International Journal of Eating Disorders, 26, 611-623.
Bulik CM, Sullivan PF, Fear JL, Pickering A (2000). Outcome of anorexia nervosa: eating attitudes, personality, and parental
bonding. International Journal of Eating Disorders, 28(2), 139-47.
Bulik CM, Sullivan PF, Joyce PR, & Carter FA (1995). Temperament, character, and personality disorder in bulimia nervosa.
Journal of Nervous & Mental Disease, 183, 593-598.
Bulik CM, Sullivan PF, Joyce PR, Carter FA, & McIntosh VV (1998). Predictors of 1-year treatment outcome in bulimia
nervosa. Comprehensive Psychiatry, 39, 206-214.
Bulik CM, Sullivan PF, Weltzin TE, & Kay WH (1995). Temperament in eating disorders. International Journal of Eating
Disorders, 17, 251-261.
Casper RC (1990). Personality features of women with good outcome from restricting anorexia nervosa. Psychosomatic
Medicine , 52, 156-170.
Casper RC, Hedeker D, & McClough JF (1992). Personality dimensions in eating disorders and their subtyping. Journal of the
American Academy of Child and Adolescent Psychiatry, 31 (5), 830-840.
Celio AA, Wilfley DE, Crow SJ, Mitchell J, Walsh BT. A comparison of the Binge Eating Scale, Questionnaire for Eating and
Weight Patterns-Revised, and Eating Disorder Examination Questionnaire with Instructions with the Eating Disorder
Examination in the assessment of binge eating disorder and its symptoms. International Journal of Eating Disorders 2004; 36:
434-444.
Cloninger CR, Svrakic DM. (1997).
Psychiatry, 60(2), 120-41.
Integrative psychobiological approach to psychiatric assessment and treatment.
Cloninger CR, Svrakic DM, & Przybeck TR (1993). A psychobiological model of temperament and character. Archives of
General Psychiatry, 50, 975-990.
Cloninger CR (1987b). A systematic method for clinical description and classification of personality variants. Archives of
General Psychiatry , 44, 573-588.
Cloninger CR (2000). A practical way to diagnosis personality disorders: a proposal. Journal of Personality Disorders, 14, 99108.
Cloninger CR, Przybeck TR, Svrakic DM, & Wetzel RD (1994). The Temperament and Character Inventory (TCI): A guide
to its development and use. St. Louis, MO: Center for Psychobiology of Personality, Washington University.
Cloninger CR, & Svrakic DM (1999). Personality Disorders. In B.J. Sadock & V.A. Sadock (Eds.), Kaplan and Sadock’s
comprehensive textbook of psychiatry (7the ed.). London: Lippincott Williams & Wilkins.
Cloninger CR, Svrakic DM, & Przybeck TR (1993). A psychobiological model of temperament and character. Archives of
General Psychiatry, 50, 975-990.
De Zwaan M, Mitchell JE, Swan-Kremeier L, McGregor T, Howell ML, Roerig JL, Crosby RD. A comparison of different
methods of assessing the features of eating disorders in post-gastric bypass patients: a pilot study. European Eating Disorders
Review 2004; 12(6): 380-386.
Diaz-Marsa M, Carrasco JL, Hollander E, Cesar J, & Saiz-Ruiz J (2000). Decrease platelet monoamine oxidase activity in
female anorexia nervosa. Acta Psychiatrica Scandinavica, 101, 226-230.
Diaz-Marsa M, Carrasco JL, Prieto Lopez R, & Saiz -Ruiz J (1999). Personality profile of eating disorders, Actas Esp
Psiquiatr, 27, 43-50.
Diaz Marsa M, Carrasco JL, Lopez-Ibor JJ, Saiz J (1998). A study of personality in eating disorders. Article in Spanish. Actas
Luso Esp Neurol Psiquiatr Cienc Afines, 26(5), 288-96.
Diaz-Marsa M, Carrasco JL, & Saiz-Ruiz J (2000). A study of temperament and personality in anorexia and bulimia nervosa.
Journal of Personal Disorders, 14(4), 352-359.
Duijsens IJ, Spinhoven P, Goekoop JG, Spermon T, & Eurelings-Bontekoe EHM (2000). The Dutch temperament and
character inventory (TCI): dimensional structure, reliability and validity in a normal and psychiatric outpatient sample.
Personality and Individual Differences 28, 487-499.
Fairburn CG, & Cooper Z (1993). The eating disorders examination (12th ed.). In C.G. Fairburn & G.T. Wilson (Eds.),
Binge eating: Nature, assessment, and treatment (pp. 317-360). New York: Guilford Press.
Fassino S, Abbate-Daga G, Amianto F, Leombruni P, Boggio S, & Rovera GG. (2002a). Temperament and character profile
of eating disorders: a controlled study with the temperament and character inventory. International Journal of Eating
Disorders, 32, 412-425.
Fassino S, Svrakic D, Abbate Daga G, Amianto F, Leombruni P, & Stanic S (2002b).
temperament and character data. Comprehensive Psychiatry, 43(2), 114-120.
Anorectic family dynamics:
Garner DM, Olmstead MP, & Polivy J (1983). Development and validation of a multidimensional Eating Disorder Inventory
for anorexia nervosa and bulimia nervosa. International Journal of Eating Disorders, 2, 15-24.
Garner DM, Rockert W, Davis R, Garner MV, Olmsted MP, Eagle M (1993). A comparison of cognitive-behavioral and
supportive-expressive therapy for bulimia nervosa. American Journal of Psychiatry, 150, 37-46.
Gendall KA, Joyce PR, Sullivan PF, & Bulik CM (1998). Personality and dimensions of dietary restraint. International
Journal of Eating Disorders, 24, 371-379.
Goldfein JA, Devlin MJ, Kamenetz C. Eating Disorder Examination-Questionnaire with and without Instruction to assess
binge eating in patients with binge eating disorder. International Journal of Eating Disorders 2005; 37: 107-111.
Humphrey LL (1991). Object relations and the family system: An integrative approach to understanding and treating eating
disorders. In: Psychodynamic treatment of anorexia nervosa and bulimia (ed. C. Johnson), pp. 322-353. New York: Guilford
Press.
Johnson C, & Connors ME. The Etiology and Treatment of Bulimia Nervosa. New York, Basic Books, 1987.
Kaye WH, Strober M, Stein D, & Gendall K (1999). New Directions in Treatment Research of Anorexia and Bulimia
Nervosa. Biological Psychiatry, 45, 1285-1292.
Kleifield E, Sunday S, Hurt SW, & Halmi KA (1993). Psychometric validation of the Tri-dimensional Personality
Questionnaire: Application to subgroups of eating disorders. Comprehensive Psychiatry , 34 (4), 249-253.
Kleifield E, Sunday S, Hurt S, & Halmi KA (1994). The tri-dimensional personality questionnaire: An exploration of
personality traits in eating disorders. Journal of Psychiatric Research, 28, 413-423.
Klump KL, Bulik CM, Pollice C, Halmi KA, Fichter MM, Berrettini WH, Devlin B, Strober M, Kaplan A, Woodside DB,
Treasure J, Shabbout M, Lilenfeld LR, & Plotnicov KH (2000). Temperament and character in women with anorexia
nervosa. The Journal of Nervous and Mental Disease, 188 (9), 559-567.
Martin GC, Wertheim EH, Prior M, Smart D, Sanson A, & Oberklaid F (2000). A longitudinal study of the role of childhood
temperament in the later development of eating concerns. International Journal of Eating Disorders, 27, 150-162.
Mayer LES, & Walsh BT (1998). Pharmacotherapy of eating disorders. In: Neurobiology in the treatment of eating disorders
(ed. Hoek, H.W., Treasure, J.L. & Katzman, M.A.) Wiley & Sons.
Mizushima H, Ono Y, & Asai M, (1998). TCI temperamental scores in bulimia nervosa patients and normal women with and
without diet experiences. Acta Psychiatrica Scandinavica, 98, 228-30.
Nagata T, Oshima J, Wada A, Yamada H, Iketani T, & Kiriike N (2003). Temperament and Character of Japanese Eating
Disorder Patients. Comprehensive Psychiatry, 44, 142-145.
Steiger H, & Séguin JR (1999). Eating disorders : anorexia and bulimia nervosa. In: T. Millon, & P.H. Blaney (Eds.), Oxford
textbook of psychopathology (pp. 365-389). Toronto: Oxford Univ. Press. Lawrence Erlbaum Associates: Hillsdale, New
York.
Strober M (1991). Disorders of the self in anorexia nervosa: An organismic-developmental paradigm. In Psychodynamic
treatment of anorexia nervosa and bulimia (ed. C. Johnson), pp. 354-373. Guilford Press: New York.
Strober M, Freeman R, Lampert C, Diamond J, & Kaye W (2000). Controlled family study of anorexia nervosa and bulimia
nervosa: Evidence of shard liability and transmission of partial syndromes. American Journal of Psychiatry, 157, 393-401.
Svrakic DM, Whitehead C, Przybeck TR, & Cloninger CR (1993). Differential diagnosis of personality disorders by the
seven factor model of temperament and character. Archives of General Psychiatry , 50, 991-999.
Van der Ham T, Meulman JJ, Van Strien DC, & Van Engeland H (1997). Empirically based subgrouping of eating disorders
in adolescents: a longitudinal perspective. British Journal of Psychiatry, 170, 363-368.
Van Strien T.(1986). Eating behaviour, personality traits and body mass. Swets & Zeitlinger B.V.: Lisse.
Vitousek KB, & Orimoto L (1993). Cognitive behavioural models of anorexia nervosa, bulimia nervosa, and obesity. In K.S.
Dobson, & P.C. Kendall (Eds.), Psychopathology and Cognition (pp.191-243). San Diego, CA: Academic Press.
Waller DA, Petty F, Hardy BW, Gullion CM, Murdock MV, & Rush AJ (1993). Tridimensional Personality Questionnaire
and serotonin in bulimia nervosa. Psychiatry Research, 48, 9-15.
Wonderlich SA, Ukestad L, & Perzacki R (1994). Perceptions of non-shared childhood environment in bulimia nervosa.
Journal of the American Academy of Child and Adolescent Psychiatry, 33, 740-746.
PART III
Further study of the psychobiological model of eating disorders
1. Introduction
Based on the demonstrated differences in personality dimensions and the related cognitive and
behavioural characteristics between healthy volunteers and types of eating disorders, the final aim was to
study the association between these psychological findings and neurobiological functioning.
The
extensive research into the neurobiology of eating disorders has focused on neuropeptide and
monoamine (especially serotonin, or 5-HT) systems thought to be central to the physiology of eating and
weight regulation. Of the various central and peripheral abnormalities reported, many are likely to be
secondary to aberrant eating behaviours and associated weight loss. However, some aspects of 5-HT
function remain abnormal after recovery, suggesting that a trait monoamine abnormality might
predispose individuals whether or not due to its association with characteristics such as perfectionism.
Furthermore, normal dieting in healthy women alters central 5-HT function, providing a potential
mechanism by which eating disorders might be precipitated in women who are vulnerable for other
reasons (Fairburn, 2003; Kay & Strober, 1999; Kaye, Frank, Meltzer et al., 2001; Frank, Kaye, Meltzer, et
al., 2002).
The final part of this thesis includes two studies comparing cortical 5-HT2A receptor binding
between respectively anorectic and bulimic patients and healthy volunteers. Further research addresses a
comparison of 5-HT2A binding between subcategories of anorexia nervosa and the associations between
temperament dimensions and the 5-HT2A binding index.
2. Decreased 5-HT2a Receptor Binding in Patients with Anorexia Nervosa9
Abstract
Indirect estimations of brain neurotransmitters in patients with anorexia nervosa (AN) and low weight have
demonstrated a reduction in brain serotonin (5-HT) turnover in general and led to hypotheses about dysfunction in
the 5-HT2a receptor system. It was our aim to investigate the central 5-HT2a receptor binding index using
SPET brain imaging. Methods: The 5-HT2a receptor of low weight patients with AN were studied by means
of the highly specific radio-iodinated 5-HT2a receptor antagonist 4-amino-N-[1-[3-(4-fluorophenoxy)propyl]-4methyl-4-piperidinyl]-5-iodo-2-methoxybenzamide or 123I-5-I-R91150. Fifteen patients with the clinical
diagnosis of AN and 11 age-matched healthy volunteers received intravenous injections of 185 MBq 123I-5-IR91150 and were scanned with high-resolution brain SPECT. Results: Compared to healthy volunteers,
patients with AN had a significantly reduced 5-HT2a binding index in the left frontal cortex, in the left and
right parietal cortex, and the left and right occipital cortex. A significant left-right asymmetry was noted in the
frontal cortex (left < right). Conclusion: These results are in accordance with diminished metabolic and
perfusion of frontal and parietal cortices reported in recent neuroimaging studies and imply localized disturbed
serotonergic function. The data are discussed in the light of possible confounding factors related to the low-weight
AN status. A regional cortical reduction in 5-HT2a binding index is not likely to be caused by a general
reduction in serotonergic function due to the possible confounding factors. Suggestions for further research are given.
Key words: Anorexia nervosa, serotonin, serotonin-2A receptor, SPECT
The essential features of Anorexia Nervosa (AN) are that the individual refuses to maintain a
minimally normal body weight and is intensely afraid of gaining weight. Weight loss can be accomplished
primarily through excessive physical exercise and through voluntarily reduction in total food intake,
sometimes accompanied by purging behaviour (i.e. self-induced vomiting or the misuse of laxatives or
diuretics). In addition, a disturbance in the perception of body shape and weight is an essential
neuropsychological feature of AN (1).
Psychological and biological mechanisms appear to play key roles in the pathogenesis of AN.
Neuropsychological investigations have indicated cognitive deficits in frontal cortex and in parietal
cortex (2,3).
Perceived distortion of body image has been associated specifically with parietal
dysfunctions (4). Functional brain imaging with PET and SPET has shown reduced parietal and frontal
cortex metabolism (5) and cerebral perfusion (6).
9
Audenaert K, Van Laere K, Dumont F, Vervaet M, Goethals I, Slegers G, Mertens J, van Heeringen C, Dierckx
R (2003). Decreased 5-HT2a receptor binding in patients with anorexia nervosa. European Journal of Nuclear
Medicine, 44, 163-169.
In past decades, the involvement of serotonin as a neurotransmitter in AN was largely indicated
through indirect estimations of brain serotonergic function.
Impaired serotonin turnover and function
were demonstrated through plasma measurements of tryptophan, the precursor of 5-hydroxytryptamine
(5-HT) (7) or 5-hydroxyindole acetic acid (5-HIAA, the metabolite of 5-HT), in cerebrospinal fluid
(CSF) of low weight AN patients (8). Elevated CSF 5-HIAA concentrations have been reported in longtime-weight-restored AN patients (8) . Another indication of reduced serotonergic function in lowweight AN patients was blunted physiological responses to the administration of selective
pharmacological agonists (9-11). Again, these findings normalized after weight restoration (10).
The involvement of the 5-HT2a receptor in the pathophysiology of AN was demonstrated
indirectly via blood platelet studies, both through an enhanced mobilization of intracellular platelet
calcium content, mediated by 5-HT2 receptors (12), and through enhanced platelet serotonin 5-HT2a
binding, measured in vitro with 3H-lysergic acid diethylamide (13). Recently, studies with PET and 18Faltanserin as a tracer showed a reduced 5-HT2a binding in the orbitofrontal cortex in recovered bulimic
patients (14). Some recent molecular genetic studies in patients with eating disorders have demonstrated
an increased frequency of one of the alleles on the promotor region of the 5-HT2a gene (15). Also, twin
and family studies suggest a genetic vulnerability to AN, and the hypothesis has been put forward that
this vulnerability may be expressed in the central serotonergic system (16).
Functional imaging techniques, such as PET and SPECT, using specific 5-HT2 receptor ligands,
make it possible to evaluate in vivo receptor binding in patients with AN. Preliminary research in
healthy subjects has indicated that 4-amino-N-[1-[3-(4-fluorophenoxy)propyl]-4-methyl-4-piperidinyl]-5iodo-2-methoxybenzamide ( 123I-5-I-R91150) is a suitable ligand for imaging 5-HT2a receptors in vivo. It
binds reversibly and with high affinity in vitro to 5-HT2a receptors (17). On average, 2% of a bolus dose
of
123
I-5-I-R91150 is taken up by the brain (18). Effective blockade of 5-HT2a receptors in vivo was
demonstrated in a study of patients with schizophrenia who were treated with risperidone or clozapine
(19).
The aim of this study was to evaluate the 5-HT2a binding index (BI) in patients with AN.
MATERIALS AND METHODS
Patients
Fifteen patients were included in the study. All were right handed, 16-30 y old, and diagnosed as
having AN according to the criteria of the fourth edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-IV) (1). Patients were recruited from an inpatient eating disorder unit in a university
psychiatric hospital. Patients were selected by a senior psychiatrist and a senior psychologist after DSMIV-based structured clinical interviews. To create a group of patients with consistent disease status, only
symptom-fixed patients who stayed in the hospital as a result of resistance of the disease to treatment
were included. Exclusion criteria were a comorbid psychiatric, major medical, or neurological disorder;
antidepressant, neuroleptic or electroconvulsive therapy in the preceding year; substance abuse;
pregnancy or lactation, and a Mini-Mental State Examination score < 28. Menstrual status was noted in
female patients.
The patients were compared with 11 age-matched healthy volunteers, (7 women, 4 men), who
were recruited from hospital staff. These individuals had no history of psychiatric treatment or
significant medical events. None used psychotropic drugs or other relevant medication, and none abused
illegal drugs. All had normal physical examination findings.
Ethical approval for the study was granted by the local ethics committee. Both patients and
healthy individuals provided written informed consent to participate in this study.
Scanning Procedure
SPECT scanning was performed using
123
I-5I-R91150 as a radioligand. This tracer was synthesized by
electrophilic substitution on the 5-position of the methoxybenzamide group of R91150, followed by
purification with high-performance liquid chromatography. The product had a radiochemical purity > 99
% and was negative for bacteria and pyrogen tests. A specific activity of 370 GBq/µmol was obtained.
The tracer is a 5-HT2a antagonist with high affinity (Kd = 0.11 nmol) and selectivity for 5-HT2a
receptors. The selectivity of the ligand for 5-HT2a receptors is at least 50 times that of other receptors,
such as other 5-HT receptors including 5-HT2c, dopamine receptors, adrenoreceptors, and histamine
receptors (17).
Thyroid blockade was achieved by administration of a single oral dose of 100 mg potassium
iodine before injection. All subjects received an intravenous injection of 185 MBq
123
I-5-I-R91150 in
normal sitting conditions. SPECT scanning was performed using a triple-headed high-resolution gamma
camera GCA-9300 (Toshiba Medical Systems, Oetwil am See, Switzerland) with fanbeam collimation.
For 123I, the resulting transaxial image resolution is 9.5 mm in full width at half maximum.
Because sequential dynamic SPECT brain scans have shown that the corticocerebellar ratio
reaches a plateau between 90 and 110 min, reflecting pseudoequilibrium, and remains stable thereafter
for up to 8 h (18), acquisition was started between 110 and 140 minutes after tracer injection, according
to previous protocols (20). A transmission scan was acquired before the emission scan, using 3 153Gd rod
sources. This scan was used for subsequent image coregistration to stereotactic coordinates. Emission
images were acquired during a 40 min-period. The whole-brain volume was acquired within the single
scanning session. Images were reconstructed using filtered backprojection and corrected for scatter and
nonuniform attenuation (21).
Analysis of the scans was performed without knowledge of patient status after automatic image
coregistration to stereotactic space using the transmission image (BRASS, Nuclear Diagnostics Ltd.,
Stockholm, Sweden) (22).
The method for coregistration of SPECT receptor data using transmission images has been
published previously (22). In short, the sequential acquisition of transmission and emission image can be
use to anatomically standardize the emission image using the same linear parameters as those used for
the transmission image. The latter is first reoriented to a template in Talairach space, and the same
transformation is then given to the emission images. On the Talairach templates, a predefined volumeof-interest (VOI) set can be constructed (originally performed on perfusion SPECT images), which
allows a user-independent sampling of the whole-brain volume of different patients without a previously
available structural information.
A diagram of the VOI map (22,23) is shown in Figure 1 and a description of VOIs is provided in Table
1.
TABLE 1
Description of Retained Volumes of Interest
with
Radioactivity estimates
in the cortex were
Corresponding Brodmann Areas
Volumes of interest
Brodmann’s areas
assumed to represent
total ligand binding
(1) Left and (2) right
6, 8, 9, 10, 11, 44,
45, 47 nonspecific binding plus
(specific
plus frontal cortex
(3) Left and (4) right
free
ligand)
(18). sensorimotor
Because, very few 5cortex
1, 2, 3, 4
20, 21, 22, 37, 38, the
cerebellum
HT2a receptors are in (5) Left and (6) right
temporal cortex
41, 42
5, 7, 39, 40
compared with the (7) Left and (8) right
cortex
(24),
the
parietal cortex
17, 18, 19
cerebellar region can be (9) Left and (10) right
considered to represent
occipital cortex
non-specific
activity. (11) Left and (12) right
Calculation of relative
cerebellum
indices of specific BI was performed by VOI normalisation to the activity per volume element in the
cerebellum. Under these pseudoequilibrium circumstances, this binding index is directly related to the in
vivo receptor density (Bmax) and affinity (KD).
BI was defined as:
target activity – background activity in brain
(background activity)
which was operationally estimated as:
[(counts/pixel in frontal cortex) – (counts/pixel in cerebellum)]
(counts/pixel in cerebellum)
Statistical methods
The equality of age and body mass index (BMI) distributions between diagnostic categories was
evaluated using the Mann Whitney test, and the equality of sex distributions was evaluated using the
Fischer exact test. As BIs were normally distributed (Kolmogorov-Smirnov testing), t statistics were
used to compare mean levels between categories. Correlation analyses were used to examine any
relationships among BI, BMI, and disease duration.
RESULTS
Demographic and physical variables
The 26 individuals in this study were on average 23.8 y old (SD = 4.1), with ages ranging from 16 to
30 y. Mean ages were not significantly different (Mann-Whitney test = 52.5; p= 0.12) between the two
study groups, with 22.5 y (SD = 2.5) for patients with AN and 25.6 y (SD = 4.7) for healthy volunteers.
A significant difference in sex (Fisher exact test; P = 0.02) existed between the group of healthy
volunteers (7 female; 4 male) and patients with AN (15 females).
The BMI in patients with AN was 14.9 (SD = 1.6; range, 11.9-16.9) which was significantly different
(Mann-Whitney test = 0; P < 0.0001) from the BMI of the healthy volunteers (mean, 22.3; SD = 1.4;
range, 20.5-24.5). The number of years of presence of disease was 4.3 (SD = 4.48; range, 1-14 y). All
patients were postmenarcheal and amonorrheic. These variables are summarized in Table 2.
Binding index
Patients with AN had a significantly reduced 5-HT2a binding potential in the left frontal cortex,
in the left and right parietal cortex, and the left and right occipital cortex when compared with healthy
volunteers (see Table 3). Figure 2 shows an example of a 25-y-old patient compared with the
anatomically standardized normal control population used for this study. Additional adjustment for
age did not alter either the magnitude or the statistical significance of the observed difference
between the groups.
Individual values of left frontal and biparietal BI are plotted in Figure 3. Because of the significant
difference in sex distribution in the patients and volunteers, individual values of male volunteers are
indicated with arrows.
All male patients fell in the same range as the female volunteers. Moreover, there is no statistical
significance in BI in any of the regions between the male and female healthy volunteers (all P > 0.5).
There was a significant difference in the left-to-right ratio in the frontal cortex of patients with eating
disorders when compared with healthy volunteers (Table 4).
Correlation analyses did not reveal significant relationships between regional cortical BIs, BMI and
disease duration.
DISCUSSION
In this in vivo study of cortical 5-HT2a receptors in patients with AN, a significantly reduced 5-HT2a
BI in the left frontal, bilateral parietal, and occipital cortices was demonstrated in comparison with that
observed in healthy volunteers. A significant difference also was demonstrated in the left-right BI, (left
< right) in the frontal cortex .in patients with AN.
When evaluated in the light of indirect studies assessing serotonergic function and 5-HT2a
binding status in low weight AN patients, the reduction in regional cortical BI is in keeping with the
findings of neuroendocrine challenge tests and blood platelet studies that demonstrated a possible 5-HT2
involvement in the pathogenesis of AN (11-13).
The reduction in BI was not present in all cortical regions but was restricted to the left frontal,
bilateral parietal, and occipital cortices. This may be in accordance with functional imaging studies that
have assessed cerebral blood flow or metabolism in patients with AN that have shown a regional
hypometabolism in frontal and parietal cortices (5,6). The occipital cortex was not evaluated in these
reports.
Neuropsychological studies have identified a disturbed body image perception in anorectic
patients (4), a cognitive function that is attributed to parietal cortex. Others also have reported deficits
in attention (3) and problem solving abilities (2,3), which are mediated by the frontal cortex, and deficits
in digit symbol test (25), visual-spatial construction (2,26) and mental arithmetic (27), which are related
to parietal functions.
However, it remains unclear whether this reduction in BI is a cause or a consequence of AN and
whether this reduction is trait or state dependent. Many of the biological findings in low-weight AN
patients normalized or were even inversely disturbed after long-term weight restoration (8,10,28) and
were state dependent and possibly caused by the low weight or neuroendocrine status.
A reduction in 5-HT2a BI can be caused by reduced estrogen concentrations.
It has been
demonstrated that estrogen increases 5-HT2a receptor expression (29). We did not evaluate estrogen
concentrations in the patients in our study. However, because all the women were in a postmenarcheal
amenorrheic state, it is probable that estrogen concentration was low and, directly or indirectly, could be
the driving force behind the reduction in 5-HT2a expression.
Another important confounding factor is reduced food intake, especially reduced intake of
protein, because the essential amino acid tryptophan is the precursor of serotonin. Alternatively, a third
possible confounding factor is that a reduced BI can occur as a compensatory response to chronic
overrelease of 5-HT. Physical hyperactivity, which is common among AN patients, may cause lipolysis
of intermuscular lipids, resulting in the release of free fatty acids. These fatty acids displace tryptophan
from albumin, leading to an increase in free tryptophan and in 5-HT turnover in the brain (30). All the
aforementioned variables -estrogen, protein reduction and physical hyperactivity, can be responsible for
the reduction in 5-HT2a BI in our study. However, one would then expect a global reduction in 5-HT2a
BI, which is contrary to the regional reduction with a clear sparing of the left and right temporal cortex
as found in our study.
Our findings also can be confounded by mood status, because depression
is a common
comorbid disorder among AN patients. This possibility cannot be ruled out; however, no functional
imaging study of the 5-HT2a receptor in depressed (31,32) or attempted-suicide patients (20) showed a
reduction in parietal BI, a finding that was significantly present in our study. Nor was a frontal
asymmetry present in any of these studies of depressed individuals.
As a potential methodological limitation of our study, the difference in sex distribution may be a
possible confounding factor. However, it is unlikely, because sex differences in BI were not reported
with this tracer (33), in agrees with our own (unpublished) data, and because male BI values fell in the
range of the female healthy volunteers, as is shown in Figure 2 (see original paper).
Because of lack of structural matching, another potential confounding factor in this study may be
the result of partial volume averaging. It is known that substantial (and partially reversible) brain volume
loss may accompany low-weight status in patients with AN. Therefore, neocortical activity per unit brain
volume may have been underestimated for the patient group. It would be unlikely, however, that such a
process is location specific and could account for the regional differences in the frontal and parietal
neocortex only.
In this subgroup, no dynamic SPET acquisitions were made. Hence, the assumption that the
imaging outcome measure (the BI) is comparable among patient and control subjects cannot not be
made. The pseudoequilibrium conditions for the tracer under consideration were defined with regard to
the rate of washout from receptor-rich regions (18). Our own measurements in healthy volunteers (20)
have shown that the relative activity in neocortical specific regions with regard to aspecific binding in the
cerebellum gradually decreases after 90 minutes after injection and thereafter can be approximated by a
linear decrease during the first hours, with a stable specific-to-aspecific activity ratio. The time of
measurement after injection (start 110-140 min after injection) lies well after the onset of probable
pseudoequilibrium. Therefore, although not directly proven in this population, it can be expected that
the neocortical equilibrium of the tracer in AN patients would be found approximately at the same time,
even with 20-30 % slower kinetics (i.e. reaching of the plateau phase). Moreover, because several
neocortical regions (predominantly temporal areas) are normal in patients with AN when compared with
those of healthy volunteers, it is unlikely that a very altered kinetic distribution is present within the
affected areas that would invalidate the assumption of pseudo-equilibrium at the time the measurements
were performed after injection.
In addition, without full kinetic modeling, the contribution of altered perfusion and tracer
delivery from altered density of binding sites cannot be distinguished. Hence, the possibility can not be
excluded that some portion of the demonstrated changes may not involve serotonergic binding deficits,
but altered influx to the brain (KI) particularly in light of previous studies in anorexic patients with
perfusion deficits in the frontal and parietal neocortex (6,34). Therefore, this study assumes implicitly
that the tracer kinetics are in the pseudo-equilibrium state after an hour and are not altered by regional
changes in K1 but by specific binding properties. Investigations in a small subset of patients with
complete kinetic modeling should be conducted to validate this assumption. It should also be taken into
account that, in addition to serotonin, other neurotransmitter system or hormones have altered or
disturbed metabolism in patients with AN. At least theoretically, this is possible with neurotransmitter
systems (e.g. norepinephrine and dopamine effects on the serotonergic system) or neurohormonal
systems (e.g., cortisol and cortisol-releasing factor effects on the serotonergic system). Because the
estimation of the
123
I-5I-R91150 BI is based on the assumption of pseudo-equilibrium, the effects of
these intrinsic and neuronal interactions could alter tracer kinetics.
Another limitation lies in the fact that the specific-to-nonspecific activty ratio is around 2.0 (BI =
1.0) in the age groups studied. The spread in healthy volunteers, which is the combination of intrinsic
interindividual physiological differences as well as uncertainties in tracer delivery (kinetics, distribution,
Poisson noise etc.), is fairly high (18,33), whereas the uncertainty of the BI of 1.0 is about 0.2-0.3 (or 2030 %). This uncertainty, however, is incorporated in the study because reference to a group of healthy
volunteers was included.
CONCLUSION
A specific regional reduction in BI of the 5-HT2a receptors is demonstrated in low-weight AN
patients when compared with healthy volunteers. State-dependent variables of AN may be causal
factors in the BI reduction. To address these variables, future work should aim to replicate the findings
of this study in the same diagnostic group and in other eating disorder subgroups. A follow-up study of
AN patients with a reevaluation of the 5-HT2a BI at long-term weight restoration could help in
determining whether this status is state dependent or a trait variable.
ACKNOWLEDGMENT
The authors gratefully acknowledge logistic support from Nuclear Diagnostics Ltd.
References
1.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington DC: American
Psychiatric Association; 1994: 539-545.
2.
Szmukler G, Andrewes D, Kingston K, Chen L, Stargatt R, Stanley R. Neuropsychological impairment in anorexia
nervosa: before and after refeeding. J Clin Exp Neuropsychol. 1992;14:347-352.
3.
Lauer C, Gorzewski B, Gerlinghoff M, Backmund H, Zihl J. Neuropsychological assessments before and after treatment
in patients with anorexia nervosa and bulimia nervosa. J Psychiatr Res. 1999;33:129-138.
4.
Horne R, Van-Vactor J, Emerson S. Disturbed body image in patients with eating disorders. Am J Psychiatry.
1991;148:211-215.
5.
Delvenne V, Goldman S, De Maertelaer V, Lotstra F. Brain glucose metabolism in eating disorders assessed by positron
emission tomography. Int J Eating Dis. 1999;25:29-37.
6.
Nozoe S, Naruo T, Yonekura R, et al. Comparison of regional cerebral blood flow in patients with eating disorders. Brain
Res Bull. 1995;36:251-255.
7.
Coppen AJ, Gupta RK, Eccleston EG, Wood KM, Wakeling A. Plasma tryptophan in anorexia nervosa. Lancet.
1976;1(7966): 961.
8.
Kaye W, Gwirtsman H, George D, Ebert M. Altered serotonin activity in anorexia nervosa after long term weight
restoration: Does elevated cerebrospinal fluid 5-hydroxyindolacetic acied level correlate with rigid and obsessive
behaviour? Arch Gen Psychiatry. 1991;48:556-562.
9.
Brewerton T, Jimerson D. Studies of serotonin function in anorexia nervosa. Psychiatry Res. 1996;62:31-42.
10. O'Dwyer ALJ, Russell G. Serotonin activity in anorexia nervosa after long-term weight restoration: response to Dfenfluramine challenge. Psychol Med. 1996;26:353-359.
11. Monteleone P, Brambilla F, Bortolotti F, La Rocca A, Maj M. Prolactin response to d-fenfluramine is blunted in people
with anorexia nervosa. Br J Psychiatry. 1998;172:438-442.
12. Berk M, Kessa K, Szabo CP, Butkow N. The augmented platelet intracellular calcium response to serotonin in anorexia
nervosa but not bulimia may be due to subsyndromal depression. Int J Eat Disord. 1997;22:57-63.
13. Spigset O, Andersen T, Hagg S, Mjondal T. Enhanced platelet serotonin 5-HT2A receptor binding in anorexia nervosa
and bulimia nervosa. Eur Neuropsychopharmacol. 1999;9:469-473.
14. Kaye W, Frank F, Meltzer C, et al. Altered serotonin 2A receptor activity in women who recovered from bulimia
nervosa. Am J Psychiatry 2001;158, 1152-1155.
15. Collier D, Arranz M, Li T, Mupita D, Brown N, Treasure J. Association between the 5-HT2A gene promotor
polymorphism and anorexia nervosa. Lancet. 1997;350 (9075):412.
16. Treasure J, Campbell I. The case for biology in the aetiology of anorexia nervosa. Psychol Med. 1994;24:3-8.
17. Mertens J, Terriere D, Sipido V, Gommeren W, Janssen P, Leysen J. Radiosynthesis of a new radioiodinated ligand for
serotonin-5HT2-receptors, a promising tracer for gamma-emission tomography. J Labelled Compounds Radiopharmaceuticals.
1994;34:795-806.
18. Busatto G, Pilowsky L, Costa D, et al. Initial evaluation of 123I-5-I-R91150, a selective 5-HT2A ligand for single-photon
emission tomography, in healthy subjects. Eur J Nucl Med. 1997;24:119-124.
19. Travis M, Busatto G, Pilowsky L, et al. 5-HT2a receptor blockade in patients with schizophrenia treated with risperidone
and clozapine. A SPET study using the novel 5-HT2a ligand 123I-5-I-R-91150. Br J Psychiatry. 1998;173:236-241.
20. Audenaert K, Van Laere K, Dumont F, et al. Decreased frontal serotonin 5-HT2a receptor binding index in deliberate
self harm patients. Eur J Nucl Med. 2000;27:1800-1808.
21. Van Laere K, Koole M, Kauppinen T, Monsieurs M, Bouwens L, Dierckx R. Non-uniform transmission in brain SPET
using 201-Tl, 99m-Tc and 153-Gd static line sources: antropomorphic dosimetry studies and brain quantification. J Nucl
Med. 2000;41:2051-2062.
22. Van Laere K, Koole M, D'Asseler Y, et al. Automated stereotactic standardization of brain receptor data using singlephoton transmission images. J Nucl Med. 2001;42:361-375.
23. Van Laere K, Versijpt J, Audenaert K, et al. 99mTc-ECD brain perfusion SPET: variability, asymmetry and effects of age
and gender in healthy adults. Eur J Nucl Med. 2001; 28: 873-887.
24. Pazos A, Probst A, Palacios J. Serotonin receptors in the human brain-IV. Autoradiographic mapping of serotonin-2
receptors. Neuroscience. 1987;21:123-139.
25. Palazidou E, Robinson P, Lishman W. Neuroradiological and neuropsychological assessment in anorexia nervosa. Psychol
Med. 1990;20:521-527.
26. Mathias J, Kent P. Neuropsychological consequences of extreme weight loss and dietary restriction in patients with
anorexia nervosa. J Clin Exp Neuropsychol. 1998;20:548-564.
27. Hamsher K, Halmi K, Benton A. Prediction of outcome in anorexia nervosa from neuropsychological status. Psychiatry
Res. 1981;4:79-88.
28. Delvenne V, Goldman D, De Maertelaer V, Simon Y, Luxen A, Lotstra F. Brain hypometabolism of glucose in anorexia
nervosa: normalization after weight gain. Biol Psychiatry. 1996;40:761-768.
29. Connan F, Treasure J. Stress, eating and neurobiology. In: Hoek H, Treasure J, Katzman M, eds. Neurobiology in the
treatment of eating disorders. Chicester: John Wiley & Sons; 1998:211-234.
30. Fisher G, Hollman W, De Meirleir K. Exercise changes in plasma tryptophan fraction and relationship with prolactin. Int
J Sports Med. 1991;12:487-489.
31. Biver F, Wikler D, Lotstra F, Damhaut P, Goldman S, Mendlewicz J. Serotonin 5-HT2 receptor imaging in major
depression: focal changes in orbito-insular cortex. Br J Psychiatry. 1997;171:444-448.
32. Massou JM, Trichard C, Attar-Levy D, et al. Frontal 5-HT2A receptors studied in depressive patients during chronic
treatment by selective serotonin reuptake inhibitors. Psychopharmacology (Berl). 1997;133:99-101.
33. Baeken C, D'Haenen H, Flamen P, et al. 123I-5-I-R91150, a new single-photon emission tomography ligand for 5-HT2a
receptors: influence of age and gender in healthy subjects. Eur J Nucl Med. 1998;25:1617-1622.
34. Delvenne V, Goldman D, De Maertelaer V, Wikler D, Damhaut P, Lotstra F. Brain glucose metabolism in anorexia
nervosa and affective disorders: influence of weight loss or depressive symptomatology. Psychiatry Res. 1997;74:83-92.
3. Comparison of Cortical 5-HT2A Receptor Binding in Bulimia Nervosa Patients and healthy
volunteers. 10
ABSTRACT
Objective: Bulimia nervosa has been associated with alterations in central serotonergic (5-HT) function. This
study investigated iodine-labelled 4-amino-N-[1-[3-(4-fluorophenoxy)propyl]-4-methyl-4-piperidinyl]-5-iodo-2methoxybenzamide (123I-5-I-R91150) binding to the 5-HT2A receptor in the brain by using single photon
emission computed tomography (SPECT) in acutely ill bulimia nervosa patients. Method: Cortical 123I-5-IR91150 binding in 10 normal-weight patients with bulimia nervosa, purging type, was compared with that of 11
healthy volunteers. Results: The 5-HT2A binding index of the bulimia nervosa patients, with and without
correction for age, was not significantly different from that of the comparison group. Conclusions: As a group,
acutely ill BN patients cannot be discriminated from healthy subjects on the basis of cortical 123I-5-I-R91150
binding index.
Bulimia nervosa is characterized by binge eating and inappropriate compensatory behaviours to
avoid weight gain.
The aetiology of bulimia nervosa likely involves interactions among genetic,
psychological and biological variables. Of interest is the attention given to neurobiological alterations.
Several authors have addressed the role of the serotonin (5-HT) neurotransmitter system in bulimia
nervosa. In the majority of these studies, indirect measurements of central 5-HT function were used,
and contradictory results were reported (1). Single photon emission computed tomography (SPECT)
allows for a more direct exploration of the central 5-HT system. The SPECT radiopharmaceutical,
iodine-labelled
4-amino-N-[1-[3-(4-fluorophenoxy)propyl]-4-methyl-4-piperidinyl]-5-iodo-2-
methoxybenzamide (123I-5-I-R91150), specifically binds to the 5-HT2A receptor in the brain (2).
Recently, we used
123
I-5-I-R91150 and SPECT to compare 5-HT2A receptor availability in anorexia
nervosa patients and healthy comparison subjects and found lower 5-HT2A receptor availability in the left
frontal, bilateral parietal and occipital regions in the anorexia nervosa patients (3). The present study
reports on 123I-5-I-R91150 binding in acutely ill bulimia nervosa patients.
10
Goethals I, Vervaet M, Van De Wiele C, Audenaert K, Slegers G, van Heeringen C, Dierckx R (2004). Binding
potential of cortical 5-HT2A receptors is not different in bulimia nervosa patients and healthy volunteers. American
Journal of Psychiatry. 161:10, 1916-1918.
METHOD
We studied 10 normal-weight patients who met the DSM-IV criteria for bulimia nervosa, purging
type without a history of anorexia nervosa (nine women, one man). Duration of the eating disorder
varied between 1 and 4 years. None of the patients had a concomitant psychiatric disorder. Patients
were free of psychotropic medication for at least 1 year. Additional exclusion criteria were a history of
major medical or neurological disorder, previous ECT, current pregnancy or lactation, and abnormal
menstrual function. Depressive symptoms were rated with the Beck Depression Inventory.
Eleven medication-free healthy volunteers (seven women, four men) without a personal or
family (first-degree relatives) history of neurological and psychiatric disorder, served as the comparison
group. Detailed characteristics of this group were described elsewhere (3). This study was approved by
the local ethics committee. Written informed consent was obtained from each subject.
All subjects had the same standardized, low-protein breakfast on the morning of the study.
Thyroid blockade was achieved by oral administration of 100 mg potassium chloride. Subjects received
185 MBq of
123
I-5-I-R91150 intravenously as a single bolus. Transmission and emission SPECT scans
were performed at pseudoequilibrium (2). After automatic image coregistration to stereotactic space, a
predefined volume-of-interest analysis was performed. Radioactivity estimates in the cortex represent
total ligand binding. Since the cerebellum contains only a small number of 5-HT2A receptors (4), and
therefore represents non-specific activity, calculation of binding index was performed by volume-ofinterest normalization to the activity-per-volume element in the cerebellum.
As
binding index values were normally distributed, between-group comparisons of mean
binding index were made by using two-tailed group t tests. Since 5-HT2A binding was shown to decline
with age (5), between-group comparisons were recalculated using the general linear model procedure
with age as a covariate. Correlation analyses were used to examine relationships between binding index
values and psychopathological data.
RESULTS
The 21 individuals in this study had an average age of 23.6 years (SD=3.5; range= 16.9-29.3).
Mean ages were significantly different between the two study groups (patients: mean=21.3 years (SD
3.2); healthy volunteers: mean=25.6 years (SD 2.5)) (U=18, p=0.01). The two groups did not differ
significantly in gender (p=0.30, Fisher’s Exact test) or body mass index (U=34.5, p=0.25). None of the
patients met criteria for a major depressive episode nor for any other comorbid psychiatric disorder at
the moment of the SPECT scanning. The Beck Depression Inventory score was below 10 in all
patients.
Correlation analysis, in the bulimia nervosa patients as well as in the healthy subjects, revealed a
significant (at the 5% level) negative relationship between age and binding index in the prefrontal cortex.
In addition, a nonsignificantly negative correlation between age and binding index was found in the
temporal , parietal, and occipital regions. Further, there were no significant relationships between
binding index values and gender, body mass index, or disease duration. The mean 5-HT2A binding index
in the bulimia nervosa patients, with and without correction for age, was not significantly different in any
predefined cortical brain region from the mean binding index values in the healthy comparison subjects
(Table 1).
DISCUSSION
In this study, no changes in cortical 5-HT2A receptor binding, assessed by
123
I-5-I-R91150 and
SPECT, were observed in acutely ill bulimia nervosa patients, relative to healthy comparison subjects. In
addition, a significant negative relationship between binding index and age in the prefrontal cortex
indicated that in bulimia nervosa patients, as well as in healthy subjects, an age-related decline in 5-HT2A
receptor availability was preserved. These results agree with those of the literature (5). In a previous
(indirect) study, no significantly difference in CSF levels of 5-hydroxyindoleacetate acid (5-HIAA) was
found between bulimia nervosa patients and healthy comparison subjects (6). This finding could
indicate that central 5-HT turnover is not disturbed in acutely ill bulimia nervosa patients. Yet, in
another study using
123
I- -CIT and SPECT, a reduction of available binding sites in 5-HT transporter-
rich areas was documented in 10 medication-free female patients with bulimia, compared with 10 agematched healthy female subjects (7). Although decreased
123
I- -CIT binding may reflect central 5-HT
dysfunction, secondary changes may involve the postsynaptic 5-HT2A receptor as well. In a positron
emission tomography study using 18F-altanserin, a ligand for the postsynaptic 5-HT2A receptor, reduced
binding in the orbital frontal cortex was found in patients who recovered from bulimia nervosa (8).
Based on the observation that recovered bulimia nervosa patients have elevated CSF 5-HIAA
concentrations (9) and in agreement with in vitro studies (10), the authors postulated that 5-HT2A
receptors were down-regulated. Based on our findings, acutely ill bulimia nervosa patients are not
characterized by altered cortical 5-HT2A receptor binding in specific (prefrontal) brain regions. These
results clearly differ from those in acutely ill AN patients (3), suggesting that different biological
mechanisms are involved in patients with different types of eating disorders.
In reporting our findings we are aware of several limitations. A major limitation of this study was the
small number of subjects. Consequently, we did not correct for a large number of potential
confounding factors, such as psychopathological variables.
References
The authors thank Koen Van Laere, M.D., Ph.D., Dr.Sc. for comments on the manuscript and Erik
Nolf, M.Sc. for technical advise.
1. Walsh BT, Devlin MJ: Eating disorders: progress and problems. Science 1998; 280:1387-1390
2. Busatto GF, Pilowsky LS, Costa DC, Mertens J, Terriere D, Ell PJ, Mulligan R, Travis MJ, Leysen JE, Lui D, Gacinovic S,
Waddington W, Lingford-Hughes A, Kerwin RW: Initial evaluation of 123I-5-I-R91150, a selective 5-HT2A ligand for singlephoton emission tomography, in healthy human subjects. Eur J Nucl Med 1997; 24:119-124
3. Audenaert K, Van Laere K, Dumont F, Vervaet M, Goethals I, Slegers G, Mertens J, van Heeringen C, Dierckx RA:
Decreased 5-HT2a receptor binding in patients with anorexia nervosa. J Nucl Med 2003; 44:163-169
4. Pazos A, Probst A, Palacios JM: Serotonin receptors in the human brain--IV. Autoradiographic mapping of serotonin-2
receptors. Neuroscience 1987; 21:123-139
5. Baeken C, D'haenen H, Flamen P, Mertens J, Terriere D, Chavatte K, Boumon R, Bossuyt A: 123I-5-I-R91150, a new
single-photon emission tomography ligand for 5- HT2A receptors: influence of age and gender in healthy subjects. Eur J
Nucl Med 1998; 25:1617-1622
6. Kaye WH, Ballenger JC, Lydiard RB, Stuart GW, Laraia MT, O'Neil P, Fossey MD, Stevens V, Lesser S, Hsu G: CSF
monoamine levels in normal-weight bulimia: evidence for abnormal noradrenergic activity. Am J Psychiatry 1990; 147:225229
7. Tauscher J, Pirker W, de Zwaan M, Asenbaum S, Brucke T, Kasper S: In vivo visualization of serotonin transporters in the
human brain during fluoxetine treatment. Eur Neuropsychopharmacol. 1999; 9:177-179
8. Kaye WH, Frank GK, Meltzer CC, Price JC, McConaha CW, Crossan PJ, Klump KL, Rhodes L: Altered serotonin 2A
receptor activity in women who have recovered from bulimia nervosa. Am J Psychiatry 2001; 158:1152-1155
9. Kaye WH, Greeno CG, Moss H, Fernstrom J, Fernstrom M, Lilenfeld LR, Weltzin TE, Mann JJ: Alterations in serotonin
activity and psychiatric symptoms after recovery from bulimia nervosa. Arch Gen Psychiatry 1998; 55:927-935
10. Barnes NM, Sharp T: A review of central 5-HT receptors and their function. Neuropharmacology 1999; 38:1083-1152
General conclusions
Eating disorders have emerged as clinical problems of growing relevance due to their increasing
prevalence, substantial somatic and psychiatric co-morbidity, increased mortality, frequent relapse and
common failure of treatment.
Eating disorders occur predominantly during adolescence or early
adulthood, and the ‘core psychopathology’ can be described as an over-concern about body-shape and
body-weight resulting in eating-disordered thinking and behaviour. This over-evaluation of body-shape
and body-weight is probably based on an extreme need for control, expressed as self-starvation in
anorectic patients, or on a fear of rejection, which motivates bulimic patients to strive for ideal body
shapes. During the past decades, aetiological models have to a varying extent, emphasized the role of a
balance between nature and nurture but increasing insight, have not yet clarified the association between
body dissatisfaction and self-esteem on the one hand and unsuccessful dieting on the other hand.
The first three papers in Part 1 of this thesis examine factors, which may place individuals at risk
of ‘weight concerns’ and ‘dieting’, and describe the relation between these factors and the development
of eating disorders. The risk of disturbed eating behaviour associated with a focus on dieting was studied
five years after treatment for obesity, combining cognitive-behavioural treatment with a very low calorie
diet (VLCD) or a low calorie diet (LCD). Significantly more patients in the VLCD-group than in the
LCD-group reported bingeing. More than half of the successfully treated women (BMI ≤ 30) reported
binge eating, and restrained eating was as common in successfully treated as in unsuccessfully treated
women. Better treatment outcome was associated with less external and emotional eating, and with a
smaller quantity of food intake in the case of bingeing.
The second study clearly showed a
dissatisfaction with body shape among female adolescents, as desired body weights were clearly lower
than current BMI’s and the medical standard. Consequently, it is not surprising that female adolescents
commonly reported restrained eating and, to a lesser extent, vomiting, laxative abuse, counting of
calories, and skipping meals in order to lose weight. This restrained eating style was frequently associated
with emotional eating. On the contrary, boys reported a higher desired than current BMI. Although
restrained eating and vomiting was also found in boys, the occurrence of these characteristics decreased
with age, which was not the case in girls.
A preoccupation with body weight in school-girls was
confirmed in the third study, in which their attitudes towards eating were compared to those among
fashion models and eating disordered patients.
Vomiting, the use of anorectic drugs and laxatives,
eating alone, counting calories and the experience of a loss of control were reported by a substantial
proportion of adolescent girls. Fashion models tended to have an eating-style that was comparable to
that of patients with eating disorders. The main differences were a more outspoken intensity of
disturbed eating patterns and the more commonly reported premorbid overweight in ED patients.
Probably, this overweight is a risk factor for developing eating-related psychopathology in a Western
society with a slimming culture.
Without denying the importance of contextual variables, further research targeted the study of a
vulnerability, which may place individuals at an increased risk of developing an eating disorder. In
addition, it was studied whether there were differences in vulnerabilities between and within the eating
disorder categories. Evidence of an overlap of symptoms in binge-eating disordered (BED) and bulimia
nervosa non-purging (BN-NP) patients was indeed found. In our study population, BED patients were
older and had a longer duration of illness, a larger weight cycling, a higher current and previous BMI,
and a lower score on the temperament dimension ‘Persistence’ than BN-NP patients. After correcting
for age, the differences for weight variables remained, including comparatively higher BMIs and larger
weight fluctuations among the BED patients. These differences may well be due to a genetically
determined propensity to be overweight and to the temperamental characteristic of Persistence. Due to
personality characteristics these patients are apparently indeed not able to restrain, which clearly
differentiates them from BN-NP patients.
Also within the group of anorectic patients, understanding of this restrained eating style is not
straight forward. Indeed, an intense fear of increasing weight, even when underweight, is one of the
core features of AN patients. A low or absent drive for thinness in more than one-quarter of our AN
patients, particularly among those of the restricting type, is therefore, at the least, remarkable. A low
drive for thinness was associated with a higher age of onset of the eating disorder, less eating-related
pathology (lower frequency of purging and less restrained eating) and less severe psychopathology (lower
harm avoidance and higher self-directedness). Weight concerns may thus have other motivations than a
culture-bound drive for thinness. Historical descriptions of cases of self-starvation without weight
concerns in cultures, in which there was no emphasis on slimness, and cross-cultural comparison have
suggested that AN does not necessarily follow the accepted Western format of thinness. It could well be
that reinforcing effects of food restriction per se play a crucial role. Indeed starvation in AN patients
could serve to reduce serotonergic neuronal activity in response to their trait-related (i.e. premorbid and
persisting after recovery) increase in 5-HT neuronal transmission. In support of this hypothesis, we
demonstrated an association between a low drive for thinness and restricting rather than
binging/purging behaviour. Thus, this mechanism appears to be relatively effective in RAN patients, in
view of the comparatively less severe eating disorder-related symptoms associated with a comparatively
lower harm avoidance and a higher self-directedness. From a therapeutic point of view, the use of food
restriction to judge self-worth, in order to cope with anxiety, requires cognitive restructuring procedures,
perhaps facilitated by a pharmacologic (i.e. serotonergic) reduction of trait-dependent anxiety.
The current findings suggest also a role of serotonergic agonists in the prevention of attempted
suicide among eating disordered patients. Attempted suicide and eating disorders share a more common
prevalence among females, while their onset often occurs during adolescence. Both behaviours can be
used as a means of taking control over one’s own body. Previous studies have demonstrated that suicidal
behaviour is relatively common among eating disordered patients and that its occurrence may be related
to co-morbid axis-I disorders, to core ED-symptoms and to personality characteristics. In our study, a
history of suicide attempt was more common among BN patients than among AN patients or EDNOS
patients. The diathesis among AN patients appears to differ from that in BN and EDNOS patients.
First, and in keeping with the results of previous studies in AN and BN patients, co-morbidity with
depression appears to be a specific risk of attempted suicide in BN, but not in AN. Secondly, an
increased risk of attempted suicide is associated with a combination of specific dimensions of
personality, i.e. high harm avoidance, moderate to high novelty seeking and low self-directedness. In
case of AN, commonly characterized by a lower novelty seeking compared to the two other diagnostic
groups, a higher scores on novelty seeking was indeed associated with a higher frequency of attempted
suicide.
The current findings indicate that the combination of moderate to high novelty seeking,
increased harm avoidance and low self-directedness among eating disordered patients may become
manifest through cognitive and behavioural problems including increased drive for thinness, bulimia,
body dissatisfaction, ineffectiveness, perfectionism, interpersonal distrust, interoceptive awareness,
maturity fears and external and emotional eating. While no causal interpretation of this association can
be inferred from the data, the results suggest that these characteristics can be regarded as cognitive
coping strategies reflecting a shift from the interpersonal to the personal domain and from a
psychological to a somatic focus in an attempt to increase perceived control. Taking into account the
stress-diathesis model of suicidal behaviour, the current findings suggest that the anxiety and low selfdirectedness involved in the development of eating disorders, in absence of the rigidity due to a low
novelty seeking, increases the risk of a break down of the inhibition, and thus to more disinhibition or
impulsive behaviour. Unfortunately, intent to die was not assessed in the current study, but previous
studies report that attempted suicide in AN differs from that in bulimia nervosa by a relatively more
marked intent to die. Moreover, as both attempted suicide and completed suicide appear to be, at least in
part, under genetic control, further study is needed with regard to genetic influences on the occurrence
of suicidal behaviour in eating-disordered patients.
The last part of this thesis described the extent to which personality dimensions are associated
with specific eating-disordered cognitive and behavioural characteristics, using data on the total study
population (n = 800). The findings were in keeping with those as reported in papers 7 and 8, which
were based on a smaller population. When compared to healthy volunteers, ED patients were cautious,
nervous, timid, doubtful, discouraged, insecure, passive, and negativistic, even in situations that do not
worry other people, which reflects their high HA. This important predisposing factor was combined
with difficulties in pursuing self-chosen goals and values, and by a tendency to consider other people and
situations responsible for frustrations due to a reduced self-directedness. ED patients showed a greater
tendency to intolerance, criticism, and opportunism than controls. Due to their clinical perfectionism,
they lack the needed flexibility and showed maladaptive perseveration. When differences between the
ED categories RAN, BPAN, BP were studied, BP patients were less organized, methodical and
systematic, with higher frustration in uncertain situations and less satisfaction with what they have when
compared to AN patients. Differences in traits were most marked between the RAN and the BP group,
as the previously described differences were more outspoken, with an additional by a higher persistence
(P) in the RAN group. These differences were not due to age, duration of illness or age at onset of the
eating disorder. The findings confirmed the hypothesized association between Novelty Seeking and
BMI, HBMI, LBMI, bulimia, external and emotional eating and vomiting and/or laxative abuse. The
negative correlation between drive for thinness and NS, and the lack of a correlation between body
dissatisfaction and NS were unexpected. The hypothesized negative correlation between Persistence and
BMI, HBMI, LBMI, external and emotional eating, and bulimia was also confirmed. The positive
relation between Persistence and restrained eating (p<0.01) and the absence of a (negative) correlation
with drive for thinness was unexpected. Of interest was also the positive correlation between excessive
exercise (mostly seen in the RAN group) and Persistence.
With regard to the three key features of eating disorders i.e. body dissatisfaction, perfectionism
and interpersonal distrust, following correlations were found.
A correlation between body
dissatisfaction and HA (+) and SD (-) was found in all three diagnostic groups (RAN, BPAN and BN).
Perfectionism correlated especially positively with HA and P, and negatively with NS and SD.
Interpersonal distrust correlated positively with HA and negatively with NS, RD and SD.
Body
dissatisfaction thus appears to play a central role in the basic spectrum of all three ED’s, whereas
perfectionism seems to play a more important role in the RAN type and interpersonal distrust correlated
with all personality dimensions in the BP group. The BPAN group has features of the RAN and the BP
group.
Only positive correlations between the eating pathology-related cognitive and behavioural
characteristics were found. Levels of Body dissatisfaction correlated with scores on all eating-disordered
behaviours, except for excessive exercise, and both ‘Perfectionism’ and ‘Interpersonal Distrust’
correlated with restrained eating and laxative abuse.
The outspoken emotion-driven rigidity in RAN patients may interfere with successful cognitive
behaviour therapy, and these patients may thus benefit from psychopharmacological treatment.
Although the mechanism of neurotransmitter action is not yet clear, a genetically determined
vulnerability may be expressed via the central serotonergic system. Functional brain imaging with PET
and SPECT has shown diminished metabolic activity and perfusion in frontal and parietal cortices, and
demonstrated disturbed central serotonergic function in AN patients. Also in our study, patients with
AN, when compared to healthy volunteers, had a significantly reduced 5-HT2a receptor binding index
(BI) in the left frontal cortex, bilateral parietal and occipital cortex. A significant left-right asymmetry
was noted in the frontal cortex (left < right). Neuropsychological studies in AN patients found
cognitive deficits reflecting frontal and parietal dysfunctions. The disturbed body image perception and
deficits in digit symbol test, visual-spatial construction and mental arithmetic can be attributed to
changes in parietal cortical functioning.
Deficits in attention and problem-solving abilities can be
related to diminished frontal cortical activity. Confounding factors as estrogen and protein reduction
and physical hyperactivity could explain the described reduction in 5-HT2a BI, but the clear sparing of
the left and right temporal cortex does not support this explanation. Functional imaging study of the 5HT2a receptor in depressed or attempted-suicide patients showed no reduction in parietal BI, nor a
frontal asymmetry. Although the effect of serotonergic pharmacological therapy was demonstrated in
depressed patients, similar research in eating disorders yielded contradictory results. A comparison of
the cortical 5-HT2a receptor binding between 10 normal-weight BP patients with 11 healthy volunteers
demonstrated no significant differences. These biological findings could support our psychological
results, suggesting that divergent mechanisms are involved in patients with different types of eating
disorders. Enhancing self-directedness and treating the comorbidity in terms of comorbid depression by
serotonergic drugs, may nevertheless enhance the effective treatment of bulimic patients.
The implications for treatment and prevention are an important impetus for the study of
personality characteristics in eating disordered patients. According to Cloninger’s psychobiological
model, and thus assuming that character and temperament involve concept-based and percept-driven
memory, stable personality change requires habit modification by conceptual insights, perhaps facilitated
by combined pharmacotherapy. The normalization of eating patterns, and an increase in self-esteem and
in social skills by promoting conflict-handling and problemsolving capacities, are the most important
therapeutic goals. This means that the cognitive behavioural treatment of eating disorders has to include
perceptual (i.e. temperamental) and conceptual (i.e. character-based) learning processes in which classical
and operant conditioning procedures have their place.
Cue exposure to binge food, systematic
desensitisation with forbidden food, and approach behaviour to reinforcing social situations are effective
components by increasing predictability and efficacy. Combined pharmacotherapy could well have a
facilitating effect on such learning procedures since anxiety and rigidity induce and maintain avoidance
and escape behaviour.
The role of drugs targeting the dopaminergic system in the treatment of eating disorders, and
particularly their effect on cognitive and behavioural characteristics as identified in this study is yet to be
established. The role of the low score on Novelty Seeking in anorectic patients and the link with the
dopaminergic system will be the target of further research.
In addition, neuropsychological
investigations are needed to explore deficits in cognitive functioning in the ED groups and to possibly
differentiate between ED and other psychiatric categories.
Nederlandse samenvatting
Eetstoornissen zijn complexe psychiatrische aandoeningen die vooral voorkomen bij meisjes in
de adolescentie. De incidentie van typische eetstoornissen neemt de laatste jaren niet echt toe, maar
deze vaak chronische stoornissen kunnen bijzonder ernstige gevolgen hebben op het vlak van
morbiditeit en mortaliteit. Er is evidentie voor de effectiviteit van de cognitief-gedragstherapeutische
behandeling bij bulimia nervosa, maar zeker in het geval van anorexia nervosa, ontbreekt duidelijkheid
over de causaliteit van eetstoornissen. Gangbare etiologische modellen situeren zich op het continuüm
nature-nurture. Het stress-diathese model vertrekt van de hypothese dat gebeurtenissen bij een
kwetsbaar (genetisch bepaald) persoon op zo’n manier gepercipiëerd, geïnterpreteerd en onthouden
worden dat ze aanleiding kunnen geven tot ziektegedrag dat resulteert in een ziektetoestand. Afhankelijk
van de mate (zowel in verscheidenheid als intensiteit) van de kwetsbaarheid kunnen meerdere
toestandsbeelden zich voordoen of kan de ziekte evolueren naar een chronische toestand.
Dit doctoraatsproefschrift handelt over persoonlijkheidstrekken bij patiënten met eetstoornissen
(ED’s) en hun relatie met de aan de ziekte gebonden cognitieve karaktertistieken en gedragsvariabelen.
Hierbij wordt gebruik gemaakt van een psychobiologisch persoonlijkheidsmodel dat zich het inzicht in
het neurobiologisch functioneren van de informatieverwerking tot doel stelt. Bij ernstige eetstoornissen
kan op basis van een valide biopsychologisch model worden verondersteld dat een combinatie van
psychologische interventies met farmacologische ondersteuning de effectiviteit en de efficiëntie van de
behandeling verbeteren. Op vlak van de individuele patiënt wordt beoogd dat het dagelijks (sociaal)
functioneren meer gecontroleerd en voorspelbaar wordt gemaakt met een groter welbevinden als doel.
In enkele voorbereidende studies (Part I) werd bij een aantal kwetsbare groepen (obese vrouwen,
adolescente schoolmeisjes en mode modellen) het risico op het ontwikkelen van gestoord eetgedrag
bestudeerd. In het eerste artikel wordt aangetoond dat obese vrouwen vijf jaar na een multidisciplinaire
behandeling voor hun overgewicht meer eetbuien vertonen als zij in hun therapie een strenger dieet
volgden (‘very low calorie diet’ versus ‘low calorie diet’). Eetbuien kwamen ook voor bij vrouwen bij wie
de behandeling succesvol was (BMI ≤ 30), maar ze waren minder frequent en beperkter qua
hoeveelheid. Uit de tweede en derde studie bleek dat veel meisjes, ongeacht hun gewicht, willen
vermageren met het oog op een ideaal gewicht dat onder de medische standaard ligt.
Dit geeft
aanleiding tot een wijdverspreid lijngedrag en, in mindere mate, braken, gebruiken van laxeermiddelen,
tellen van calorieën en overslaan van maaltijden. Dit lijngedrag komt vaak samen voor met eetbuien.
Gestoord eetgedrag werd nog vaker gerapporteerd door modellen wiens eetstijl veel gelijkenissen
vertoont met die van meisjes met eetstoornissen, zij het in minder extreme mate. Bij meisjes met
eetstoornissen wordt echter vaker een premorbied overgewicht vastgesteld. Jongens, daarentegen, willen
bijkomen in gewicht en het voorkomen van gestoord eetgedrag nam bij hen af met de leeftijd.
Het tweede deel van dit proefschrift (Part II) bestaat uit vijf artikels, waarin een specifiek
persoonlijkheidsprofiel bij vrouwen met eetstoornissen wordt beschreven.
Bovendien blijken
nuanceringen in dit profiel al naargelang de diagnostische categorieën, vooral met betrekking tot
restrictieve anorectische vrouwen (RAN) en purgerende bulemische vrouwen (BP).
Om dit te
onderzoeken werden ED’s vergeleken met een vrouwelijke controlepopulatie (CW) en werden
diagnostische categorieën onderling vergeleken. In de studiepopulatie (n = 800 ED’s en n = 326 CW’s)
werden ED patiënten gekenmerkt door een relatief hoge ‘harm avoidance’ (HA) en lage ‘selfdirectedness’ (SD), gecombineerd met een hogere score voor ‘persistentie’ (P) en een lagere score voor
‘reward dependence’ (RD) en ‘cooperativeness’ (C) in vergelijking met gezonde vrouwen. Dat betekent
dat ED patiënten relatief angstig zijn, moeite hebben om zich te hechten, perfectionistisch zijn in
combinatie met verminderde capaciteiten om hun emoties te sturen of om coöperatief te zijn.
Bij de onderlinge vergelijking werden enkel typische eetstoornissen (anorexia en bulimia
nervosa) betrokken. De niet-purgerende bulemische groep (B-NP) werd apart bestudeerd wegens de
grote gelijkenis met een subcategorie van de aspecifieke eetstoornissen, met name de eetbuienstoornis
(BED). Naast het feit dat patiënten met BED eetbuien niet compenseren en ouder zijn, hebben zij, zelfs
na een correctie voor leeftijd, een hoger premorbid gewicht en een lagere persistentie. Vermoedelijk
maakt dit lijnen voor hen extra moeilijk. Bij de vergelijking van de andere typische eetstoornissen wordt
bij de restrictieve anorectische groep een lagere NS, hogere P en hogere SD gevonden in vergelijking
met de purgerende bulemische groep.
Dit kan worden vertaald in een emotioneel doorgedreven
rigiditeit, die ook klinisch zo herkenbaar is bij deze RAN groep. Deze verschillen konden niet
toegeschreven worden aan leeftijd, ziekteduur of aanvangsleeftijd van de ziekte. Bulemische patiënten
tonen zich sneller gefrustreerd en ontevreden en leggen de verantwoordelijkheid eerder buiten zichzelf.
Naast de categoriale verschillen in persoonlijkheidsdimensies, kon deze differentiatie
geassociëerd worden met de diagnostisch beschreven specificiteit in cognitieve aspecten en
gedragskenmerken. De gemeten persoonlijkheidsverschillen tussen de RAN en de PB group correleren
effectief met meetbaar gedrag en waargenomen cognitieve factoren. Op die manier kon de hypothese
bevestigd worden dat, in combinatie met een lage SD, hoe hoger de NS was, hoe hoger de ‘body mass
index’ (BMI), de hoogste BMI ooit gehad (HBMI), extern en emotioneel eten, zelf-opgewekt braken
en/of misbruik van laxeermiddelen en ‘bulimia’ was. Dit zijn eigenschappen die, zoals diagnostisch
verondersteld en in deze studie gemeten, meer voorkomen bij de BP groep. In tegenstelling tot onze
veronderstelling, konden we geen negatieve correlatie tussen ‘drive for thinnes’ en NS weerhouden noch
een positieve correlatie tussen ‘body dissatisfaction’ en NS.
Opnieuw zoals verwacht werd een
negatieve correlatie gevonden tussen ‘Persistence’, BMI, HBMI, laagste BMI na de groeispurt, ‘External’
en ‘Emotional Eating’en ‘bulimia’. Deze eigenschappen scoren ook effectief het laagst bij de RAN
groep. Bovendien werd een positieve correlatie gevonden tussen Persistence en ‘excessieve beweging’;
die klinisch duidelijk meest aanwezig is bij de RAN groep. De positieve correlatie tussen Persistence (P)
en ‘restrained eating’ en de afwezigheid van een negatieve correlatie tussen Persistence en ‘drive for
thinness’ waren dan weer niet verwacht.
In recente toetsbare etiologische modellen zoals deze van Serpell, Vohs, en Fairburn, wordt de
aan het negatieve ‘self-esteem’ onlosmakelijk verbonden ‘body dissatisfaction’ als centraal kenmerk van
eetstoornissen weerhouden.
Deze uitgesproken preoccupatie met lichaamsvorm en uiterlijk kan
beschouwd worden als vemijdingsgedrag in confrontatie met een gepercipiëerde te bedreigende realiteit
en zou uitgelokt en sterk onderhouden worden door perfectionisme (vooral ‘Self-Oriented
Perfectionism’). Mogelijks zou dit vermijdingsgedrag sterk bekrachtigd worden omdat patiënten met
eetstoornissen zich onveilig voelen in sociale situaties (‘interpersonal distrust’).
Deze sociale
overgevoeligheid kan voortvloeien uit het persoonlijkheidskenmerk perfectionisme (vooral ‘Social
Prescribed Perfectionism’), maar kan eveneens het gevolg zijn van een persoonlijkheidsdimensie (te lage
‘Reward Dependence’).
Deze drie basiskenmerken werden dan ook gemeten bij de drie typische
diagnostische categorieën (RAN, BP en BPAN = binge/purger type van anorexia nervosa).
De
veronderstelde correlaties met de persoonlijkheidsdimensies, afhankelijk van het type eetstoornis,
werden bevestigd. Zo werd een duidelijke positieve correlatie tussen HA en ‘body dissatisfaction’ en een
negatieve correlatie tussen SD en ‘body dissatisfaction’ gevonden bij de drie diagnostische categorieën.
Perfectionisme correleerde positief met HA en P en negatief met NS en SD. ‘Interpersonal distrust’
correleerde positief met HA en negatief met NS, RD en SD. Er werd vastgesteld dat perfectionisme
vooral een belangrijke rol speelt bij de RAN groep, terwijl ‘interpersonal distrust’ met alle
persoonlijkheidsdimensies correleerde in de BP groep. De BPAN deelde kenmerken met de RAN én de
BP groep.
De meer uitgesproken temperamentseigenschappen van de RAN groep (lage NS, hoge HA, lage
RD, hoge P) in vergelijking met de BP groep en dus ook in vergelijking met de normaal populatie (de
scores van de BP groep liggen tussen die van de RAN groep en de gezonde controles), sturen en
onderhouden de observeerbare emotioneel gedreven rigiditeit van deze meisjes.
De resulterende
uithongering, al dan niet gecombineerd met excessieve beweging, kan door verschillende motieven
geactiveerd worden. In overeenstemming met de resultaten van historisch en cross-cultureel onderzoek
wees één van de onderzoeksbevindingen er immers op dat niet alle restrictieve anorectische meisjes een
hoge ‘drive for thinness’ hebben. Voor de meisjes zelf heeft de voedselrestrictie vaak de betekenis van
herwonnen controle, puurheid, sublimatie, het zich verheffen boven het materiële, impulsieve en
lichamelijke. Biologisch gezien zou de ‘starvation’ echter vooral kunnen geïnitiëerd worden door de
gedragsinhibitie ten gevolge van de hoge HA (serotonerg) en lage NS (dopaminerg) met als
bekrachtigend effect een reductie van de serotonerge neuronale activiteit wat mogelijks angstreducerend
werkt. Dit zou een verklaring kunnen bieden voor het egosyntone karakter van het ziektebeeld en de
daaruit volgende ziekte-ontkenning en therapieresistentie.
De resultaten uit de vergelijking tussen ED’s met en deze zonder suïcidepoging wijzen eveneens
in de richting van een specifieke diathese bij AN patiënten. Vooreerst waren er meer BN patiënten
(23%) met een voorgeschiedenis van zelfmoordgedrag in vergelijking met de AN (13,5%) en atypische
(EDNOS, 7%) patiënten. Ten tweede waren er meer suïcides in de anorectische groep (n=3; BN: n=0).
Daarbij komt dat comorbiditeit met depressie een hoger risico vormt voor zelfmoordgedrag bij BN
patiënten, terwijl dit niet het geval is bij AN patiënten.
Tenslotte stijgt het risico op een
zelfmoordpoging, wanneer een hoge HA gecombineerd is met een matige tot hoge NS en lage SD.
Zoals we weten komt deze combinatie van persoonlijkheidsdimensies meestal voor bij BN patiënten.
Echter ook bij AN patiënten zien we het risico op een suïcidepoging verhogen, wanneer de NS niet laag
is. In gedragstermen zou dit kunnen betekenen dat het door de hoge HA geïnitieerde ‘avoidancebehaviour’ (inhibitie) doorbroken wordt door een matige tot hoge NS (desinhibitie), waarop ‘escapebehaviour’ (eetbuien, zelf-opgewekt braken, zelfmoordpoging) volgt.
De doelstelling van dit proefschrift was bij eetstoornissen de diagnostisch beschreven cognitieve
factoren en gedragskenmerken te relateren aan een biopsychologisch persoonlijkheidsmodel teneinde de
psychologische concepten neurobiologisch te kunnen meten. Hoewel meerdere studies in voorbereiding
zijn, werden twee reeds gepubliceerde papers in deze thesis opgenomen. Door middel van functionele
beeldvorming vonden we evidentie voor functionele verschillen in cerebrale activiteit tussen AN en BN
patiënten die kunnen correleren met persoonlijkheidskenmerken. In een vergelijking met gezonde
vrijwilligers, werd door middel van SPECT-onderzoek een significant gereduceerde 5-HT2a receptor
binding index (BI) gevonden bij AN patiënten in de links frontale, bilateraal parietale en occipitale
cortex. Deze resultaten kunnen een verklaring bieden voor de disfunctionele informatieverwerking,
meer specifiek voor de gevonden aandachtsstoornissen, vooral met betrekking tot ‘body image’
(parietaal), en de verminderde problem solving capaciteiten (frontaal).
In vergelijking met andere
psychiatrische populaties (depressieve patiënten en suïcidepogers) is de frontale assymetrie en de
verminderde parietale BI wel heel specifiek voor deze groep.
Meer nog, wanneer we dezelfde
vergelijking maken maar met BP patiënten, vinden we geen verschillen in 5-HT2a receptor binding index
tussen de patiëntengroep en gezonde vrijwilligers.
De bekende diagnostische differentiatie tussen anorectische en bulemische meisjes blijkt op die
manier gerelateerd te zijn aan persoonlijkheidsverschillen, die neurobiologisch meetbaar zijn. Uiteraard
heeft dit therapeutische implicaties. Perceptueel gedreven (temperamentsgebonden en impliciete) en
conceptueel gebaseerde (karakteriëel en expliciete) informatieverwerking zal optimaal kunnen beïnvloed
worden wanneer men de psychologische interventies baseert op de verschillende leerparadigma’s
(klassieke en operante conditionering). Deze psychologische interventies dienen gefaciliteerd te worden
door farmacologische ondersteuning indien de temperamentsconstellatie en/of karakterformatie leren
niet of onvoldoende toelaat. Strategieën dienen gericht te worden op objectievere informatieverwerking
met een shift van de lichaamsgerelateerde focus naar sociale interacties en van ‘vermijdingsgedrag’ naar
‘toenaderingsgedrag’ met uitbreiding van sociale competentie. Op basis van deze resultaten dient, zeker
bij de restrictieve anorectische groep, de nadruk gelegd te worden op het ‘Self-oriented’ en ‘Social
Prescribed’ perfectionisme, dat het vermijdingsgedrag onderhoudt en dat de patiënt doet “kiezen” voor
rigiditeit. Bij BN patiënten zou de therapie kunnen gericht worden op het opnemen van meer eigen
verantwoordelijkheid en zelfsturing om een einde te stellen aan het voortdurend ‘ontsnappen’ aan
conflictueuze gevoelens en/of situaties. De rol van psychofarmaca, die het serotonerge systeem kunnen
reguleren, blijkt belangrijk bij de behandeling van eetstoornissen, maar, zoals uit deze studie kan worden
afgeleid, moet de interactie met het dopaminerge en wellicht ook met het noradrenerge (lage RD)
systeem verhelderd worden.
Eetstoornissen zijn complexe psychiatrische aandoeningen, niet alleen omwille van de
consequenties voor het individu, haar familie en omgeving, haar hulpverlener en de gezondheidszorg,
maar eveneens omwille van de veelheid van de betrokken persoonlijkheidsdimensies. Dit proefschrift
had dan ook als voornaamste doel het leveren van een bijdrage aan het leren begrijpen en respecteren
van deze complexiteit.
BIJLAGE: GEBRUIKTE AFKORTINGEN
5-HIAA: 5-hydroxyindole acetic acid: the major metabolite of serotonin
5-HT: 5-hydroxytryptamine or serotonin
APA: American Psychiatric Association
AS: attempted suicide
BDI-II-NL: Beck Depression Inventory (Beck et al., Swets & Zeitlinger)
BI: binding index
BMI: body mass index (G/L2)
CSF: cerebrospinal fluid
CW: control women
DEBQ: Dutch Eating Behaviour Questionnaire (Van Strien, 1986)
RE: restrained eating
EE: external eating, eating elicited by external stimuli
EME: emotional eating: eating elicited by emotional stimuli,
DSM-IV: 4th Revised editon of the Diagnostic and Statistical Manual of Mental disorders
As I :Clinical disorders (and other conditions that may be a focus of clinical attention
As II : Personality disorders (and mental retardation)
Cluster A: paranoïd, schizoïd, schizotypical PD
Cluster B : antisocial, borderline, histrionic, narcissistic PD
Cluster C: avoidant, dependent, obsessive-compulsive PD
As III: General medical conditions
As IV: Psychosocial and environmental problems
As V:
Global assessment of functioning
ED: eating disorders
AN: anorexia nervosa
RAN anorexia nervosa of the restricting type
BPAN anorexia nervosa of the binge-purging type.
BN: bulimia nervosa
BP: purging type
BNP: non-purging type of bulimia nervosa
EDNOS: eating disorders not otherwise specified (USA) or atypical eating disorders (UK)
BED: binge eating disorder
EDE: Eating Disorder Examination (Fairburn & Cooper, 1993)
EDI: Eating Disorder Inventory (Garner, Olmstead & Polivy, 1983)
DT: drive for thinness (subscale)
FE: Fischer exact test
HBMI: highest lifetime BMI (after 16 years)
ICD-10: international classification of diseases (WHO, 1992)
LBMI: lowest lifetime BMI
LCD: low calorie diet
MWU: Mann-Whitney test
N: number
OCD: obsessive-compulsive disorder
OCPD: obsessive-compulsive personality disorder
PET: positron emission tomography
PSED: partial syndrome of eating disorders
RE: restrained eating, the tendency to eat to lose weight
SCAN: Schedules for Clinical Assessment in Neuropsychiatry
SD: Standard deviation
SMR: standardized mortality ratio
SPECT : single photon emission computerized tomography
TCI: Temperament and Character Inventory; Cloninger et al., 1993
NS: novelty seeking
HA: harm avoidance
RD: reward dependence
P: persistence
SD: self-directedness
C: cooperativeness
ST: self-transcendence
TRP: tryptophan, the precursor of 5-HT
VLCD: very low calorie diet
VOI: volume of interest
Eating disorder (ED): syndrome, in which disturbed eating behaviour is the central and meaningful
characteristic associated with an extreme worry about or preoccupation with body size and body weight
Disturbed eating behaviour: fasting, dieting and/or binge eating, and/or inappropriate compensating
behaviour, including self-induced vomiting or misuse of laxatives, diuretics, or enemas, and excessive
exercise.
Binge eating: eating, in a limited period of time (e.g., within a two-hour period), an amount of food
that is definitely larger than most people would eat during a similar period of time and under similar
circumstances, combined with a sense of lack of control over this eating behaviour.