Influences on Child Eating and Weight Development from
a Behavioral Genetics Perspective
Tanja V. E. Kral,1 PHD, and Myles S. Faith,1,2 PHD
1
University of Pennsylvania and 2The Children’s Hospital of Philadelphia
Childhood obesity is a strong risk factor for associated comorbidities such as type 2 diabetes, cardiovascular
disease, and orthopedic abnormalities in youth and its increasing incidents thus represents a major public
health concern. The following review provides evidence for a familial association between parental and child
weight status, eating behaviors, and food preferences. It further draws the link between environmental
influences, such as parent feeding practices, and the development of child eating behaviors and thereby
elucidates how genetic and nongenetic influences can contribute to the familial transmission of obesity.
We use eating in the absence of hunger, an eating trait which refers to children’s susceptibility to eating in
response to the presence of palatable foods in the absence of hunger, as an example to illustrate these
associations. The review concludes with an outlook on possibilities for future research efforts in the field.
Key words
behavior genetics; childhood obesity; eating in the absence of hunger; eating traits.
Introduction
The prevalence of overweight among children has more
than tripled since the early 1960s (Ogden, Flegal, Carroll,
& Johnson, 2002; Ogden et al., 1997; Strauss & Pollack,
2001). The most recent data from the National Health and
Nutrition Examination Survey (NHANES) (2003–2004)
indicate that approximately 14% of children 2–5 years and
19% of children 6–11 years are overweight, which
represents a 25–35% increase since the beginning of this
decade alone (Ogden et al., 2006). Children from certain
ethnic subgroups are disproportionately affected by this
increase in body weight. For example, among Mexican
American and non-Hispanic Black youth the prevalence of
overweight ranges from 10% to as high as 27% across
different age and gender subgroups (Ogden et al., 2006).
Childhood overweight is a critical risk factor for
associated comorbidities such as type 2 diabetes (T2D),
cardiovascular disease, and orthopedic abnormalities
(Berenson et al., 1998; Daniels et al., 1995; Hardy,
Harrell, & Bell, 2004; Rosenbloom, Joe, Young, & Winter,
1999). There is currently great concern about the development of T2D in youth, which also is increasing in
prevalence (Bloomgarden, 2004; Fagot-Campagna, 2000).
As Cruz and colleagues noted, obesity and family history
of T2D are two of the strongest risk factors for the
development of the disease in youth (Cruz et al., 2005).
Dietary factors have been shown to affect insulin dynamics
and b-cell (i.e., cells which produce and release insulin)
function in children. For example, in overweight Latino
children, ages 10–17 years, total sugar intake (g/day) was
found to be positively correlated with children’s body
mass index (BMI), BMI z-scores and total fat mass and
negatively correlated with insulin sensitivity and disposition index (i.e., index of b-cell function) (Davis et al.,
2007). These associations underscore the relationship
between diet and disease risk and the need for dietary
interventions to promote healthy eating habits in children,
especially those who are at high risk for the development of
T2D. The question of how children develop eating
patterns, food preferences, and the ability to regulate
energy intake during growth is fundamental to understanding the development of childhood obesity and its
complications, including T2D.
Obesity-promoting dietary environments are thought
to encourage excessive energy intake among children by
offering convenient access to large portions of palatable,
energy-dense foods. At the same time, genetic predispositions determine how individuals will respond to the
All correspondence concerning this article should be addressed to Tanja V. E. Kral, PhD, Center for Weight and
Eating Disorders, University of Pennsylvania School of Medicine, 3535 Market Street – 3rd Floor, Philadelphia,
PA 19104, USA. E-mail: [email protected]
Journal of Pediatric Psychology 34(6) pp. 596–605, 2009
doi:10.1093/jpepsy/jsn037
Advance Access publication April 10, 2008
Journal of Pediatric Psychology vol. 34 no. 6 ß The Author 2008. Published by Oxford University Press on behalf of the Society of Pediatric Psychology.
All rights reserved. For permissions, please e-mail: [email protected]
Familial Influences on Child Eating and Obesity
environment. One behavioral eating trait which has been
shown to be influenced by both genetic and environmental
factors is eating in the absence of hunger (EAH). EAH,
which refers to children’s susceptibility to eating in
response to the presence of palatable foods in the absence
of hunger, has been shown to be a stable eating trait in
young girls (Birch & Fisher, 2000; Birch, Fisher, &
Davison, 2003; Fisher & Birch, 2002) and to be correlated
with children’s weight status during middle childhood
(Birch & Fisher, 2000; Faith et al., 2006).
The aim of this review is to illustrate how factors
relating to children’s familial predisposition to obesity and
to their home environment can act together to influence
children’s eating and weight development. Specifically, the
first two sections of the paper highlight the extent to which
parental weight status and (eating) behaviors and food
preferences can impact children’s weight status and their
eating behaviors and food preferences. Next, using EAH as
an example of an eating trait which promotes increased
caloric intake in susceptible children, we illustrate how
genetic and nongenetic factors can shape this trait. We
present competing conceptual models which can be used
to test these influences and their impact on EAH. We
conclude the current review with a discussion of possible
gaps in the literature on the study of child eating phenotypes and present an outlook on possibilities for future
collaborations in the field. We note that this review focuses
on ‘‘unmeasured genotype’’ studies (also referred to as
behavioral genetics or quantitative genetics studies) that
did not test specific genes, rather than molecular genetics
studies that test specific genes. These latter studies will be
critically important to future developments in the field,
and merit their own review.
Parental Obesity Status Predicts Child
Overweight Status: The Familial Association
‘‘Obesity in one or both parents probably influences the
risk of obesity in their offspring because of shared genes or
environmental factors within families’’ (Whitaker, Wright,
Pepe, Seidel, & Dietz, 1997). The notion that ‘‘obesity
runs in families’’ has been supported by cross sectional
and longitudinal studies (Gibson et al., 2007; Maffeis,
Talamini, & Tato, 1998; Schaefer-Graf et al., 2005; Wang,
Patterson, & Hills, 2002; Whitaker et al., 1997). These
studies provided evidence that parental overweight
(defined as a BMI 25 kg/m2) and obesity (defined as a
BMI 30 kg/m2) are significant risk factors for overweight
in their offspring. Data from two cross sectional studies
showed that parental overweight or obesity was an
independent risk factor for childhood obesity (Wang
et al., 2002) and that maternal BMI, in particular, was a
significant predictor of BMI z-scores in children ages 6–13
years (Gibson et al., 2007). Data from several longitudinal
studies confirmed these findings and showed that children
of obese parents were at increased risk for developing
obesity later in their life (Maffeis et al., 1998; Schaefer-Graf
et al., 2005; Whitaker et al., 1997). For example, Whitaker
and colleagues (1997) showed that after 6 years of age, the
probability of a child becoming an obese adult exceeded
50% for obese children, as compared with 10% for
nonobese children. In addition, results showed that the
risk of adult obesity was significantly greater if either the
child’s mother or father was obese (Table I). That is,
Table I. Odds Ratios for Obesity in Young Adulthood According to the
Child’s Age and the Obesity Status of the Child and the Parents
No. of subjects obese as
adults/Total No. (%)
Odds ratio (95% CI)*
Subject’s age and mother’s obesity status
1–2 years
Mother not obese
Mother obese
3–5 years
Mother not obese
73/575 (13)
29/85 (34)
1.0
3.6 (2.1–5.9)
77/597 (13)
1.0
36/104 (35)
3.6 (2.2–5.7)
Mother not obese
76/611 (12)
1.0
Mother obese
42/131 (32)
3.3 (2.2–5.1)
73/594 (12)
1.0
53/177 (30)
3.1 (2.0–4.6)
Mother not obese
65/549 (12)
1.0
Mother obese
64/233 (27)
2.8 (1.9–4.1)
Mother obese
6–9 years
10–14 years
Mother not obese
Mother obese
15–17 years
Subject’s age and father’s obesity status
1–2 years
Father not obese
Father obese
55/455 (12)
28/98 (29)
1.0
2.9 (1.7–4.9)
3–5 years
Father not obese
56/475 (12)
1.0
Father obese
34/123 (28)
2.9 (1.8–4.6)
60/497 (12)
40/149 (27)
1.0
2.7 (1.7–4.2)
Father not obese
62/505 (12)
1.0
Father obese
46/184 (25)
2.4 (1.6–3.7)
Father not obese
54/491 (11)
1.0
Father obese
56/221 (25)
2.7 (1.8–4.1)
6–9 years
Father not obese
Father obese
10–14 years
15–17 years
Adapted from Whitaker et al., 1997; Copyright ß 1997 Massachusetts Medical
Society. All rights reserved.
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parental obesity more than doubled the risk for children,
obese or nonobese, to become obese adults. This risk
especially applied to children who were under 10 years of
age. The authors note that among nonobese 1- and
2-year-olds, those with at least one obese parent had a
greater chance of being obese as adults compared to those
without an obese parent (28% vs. 10%). Among obese 3to 5-year-olds, the chance of developing adult obesity
increased from 24% if neither parent was obese to 62% if
at least one parent was obese (Whitaker et al., 1997).
Parent (Eating) Behaviors and Food
Preferences Predict Child Eating Behaviors
and Food Preferences: The Familial
Association
The home food environment also plays a crucial role in
forming children’s food preferences and eating traits.
Parents can influence the development of food acceptance
patterns by structuring children’s early eating environments (Birch, 2002). They decide the types and amounts
of food that are served to their children, determine the
timing of children’s meals and snacks, and provide the
social context in which eating occurs.
Parents influence their children’s eating by exerting
feeding practices which may either be conducive or
hindering to the development of healthy eating and
growth patterns. For example, data have shown that
those children whose parents exert much control over their
eating or restrict certain desired foods from them, tend to
show a weaker intake regulation (Birch, McPhee, Shoba,
Steinberg, & Krehbiel, 1987) and more pronounced EAH
(Birch et al., 2003; Francis & Birch, 2005), an eating trait
which will be discussed further below. It should be noted
that these feeding relationships are often bidirectional in
that parents also respond to children’s requests for
particular foods. On the other hand, restrictive feeding
practices may be the result rather than the cause of
increased BMI in children.
Parental feeding practices can also modify genetic
predispositions for likes and dislikes of foods and help
shape food preferences in children. Data from a recent
study (Breen, Plomin, & Wardle, 2006) with monozygotic
(MZ) and dizygotic (DZ) twins suggest that variations in
food preferences are heritable when aggregated across
certain groupings of foods. Specifically, the investigators
found a modest heritability for fruits (heritability,
h2 ¼ 51%), vegetables (37%), and desserts (20%) and a
high heritability for liking of protein foods such as meat
and fish (78%). There also exist data on family correlations
which provide further evidence for a familial transmission
of food preferences. Across studies, the relationship
between child and parent food preferences appears to be
statistically significant but small in magnitude (Faith,
2005). A meta-analysis by Borah-Giddens and Falciglia
(1993) indicated mean parent–child correlations of r ¼ .19
for mother–child pairings and r ¼ .14 for father–child
pairings.
Genetic predispositions for food preferences can be
modified by home environmental factors such as parent
feeding practices. For example, children are born with a
genetic predisposition to neophobia which refers to the
hesitancy to eat novel foods (Barnett, 1963). Neophobia
can impede children’s acceptance of new foods such as
fruits and vegetables. Studies have shown that repeated
exposure to novel foods can significantly reduce neophobia
in children (Birch & Marlin, 1982; Sullivan & Birch,
1994). In support of these findings are results from studies
which have shown that simply making certain types of
foods available and easily accessible to children can impact
their eating habits. For example, Cullen and colleagues
(Cullen et al., 2003) showed that the availability and
accessibility of fruits and vegetables in the home accounted
for 35% of the variance in reported consumption of those
foods. Thus, early exposure to foods can shape children’s
liking of these foods not only for ones that parents desire
their children to consume (e.g., fruits and vegetables),
but also for energy-dense snack foods, which may facilitate
the overconsumption of calories.
Studies have shown that not only the types of foods
that are available in the home, but also the amount of food
that is being served to children significantly impacts how
much children eat. For example, data from nationally
representative cross sectional studies revealed positive
associations of food portion sizes consumed and daily
energy intake in children ranging from 6 months to 5 years
(McConahy, Smiciklas-Wright, Birch, Mitchell, & Picciano,
2002; McConahy, Smiciklas-Wright, Mitchell, & Picciano,
2004). Specifically, data from the Continuing Survey of
Food Intakes by Individuals (1994–1996, 1998) showed
that portion sizes for the 10 most frequently consumed
foods in the diets of 2- to 5-year-old children accounted for
17–19% of the variability in children’s energy intakes
(McConahy et al., 2004). Similarly, experimental studies
showed that increases in the portion size of a main entrée
resulted in significant increases in intake among young
children (Fisher, 2007; Fisher, Liu, Birch, & Rolls, 2007;
Orlet Fisher, Rolls, & Birch, 2003; Rolls, Engell, & Birch,
2000). Thus, food environments which offer children convenient access to large portions of palatable, energy-dense
Familial Influences on Child Eating and Obesity
foods may contribute to excessive energy intake and
weight gain.
In summary, the early home environment in which
eating occurs is believed to influence, in important ways,
children’s eating regulation and the development of food
preferences. Genes exert their influence through eating
behaviors which in turn are directly affected by the immediate food environment and feeding styles. Therefore, early
experiences with food and eating have the potential to not
only establish healthy eating habits but also to modify
genetic predispositions (e.g., neophobia) which in turn
may lead to better food acceptance patterns.
EAH: A Behavioral Eating Trait
Perhaps the best example of how genetic and environmental factors act in concert to influence a specific eating
trait linked to obesity is the study of ‘‘eating in the absence
of hunger’’ (EAH). EAH refers to children’s tendency to
eat in response to the presence of palatable foods in the
absence of hunger. The trait has been extensively studied
both from a genetic and environmental perspective and
is associated both with hyperphagia (overeating) and
increased weight gain in children.
EAH in children is operationally assessed by the ‘‘free
access procedure’’ which was developed by Birch and
colleagues (Birch et al., 2003; Fisher & Birch, 1999ab).
Following the consumption of a self-selected standard
meal, each child rates his/her perceived hunger and fullness
to ensure they are fully satiated. Each child is then asked to
participate in a rank-order preference assessment of a
variety of snacks with different sensory properties (e.g.,
potato chips, chocolate bars, and frozen yogurt) to provide
him/her with the opportunity to taste each experimental
snack food. Following the preference assessment each child
is given toys and asked to play by him/herself. During this
‘‘play session’’ the child is given access to an array of sweet
and savory snack foods and told that they could eat any of
these foods and as much as they want. EAH refers to the
number of calories the child consumes from the snack
foods despite being fully satiated.
EAH in children shares behavioral characteristics with
the trait of disinhibited eating (or ‘‘disinhibition’’) in adults.
Disinhibition is the loss of self-imposed cognitive control
over eating in response to external or emotional stimuli,
and is the eating pattern that most consistently differentiates obese and nonobese adults (Lindroos et al., 1997).
There is evidence that obese individuals show greater
disinhibition than do nonobese individuals (Carmody,
Brunner, & St Jeor, 1995; Westenhoefer, Stunkard, &
Pudel, 1999) and that the degree of disinhibition is strongly
associated with energy intake (Lawson et al., 1995;
Lindroos et al., 1997), weight status and weight gain
(McGuire, Wing, Klem, Lang, & Hill, 1999; Williamson
et al., 1995), weight fluctuations (Carmody et al., 1995),
binge eating (Howard & Porzelius, 1999), and body fat
(Provencher, Drapeau, Tremblay, Despres, & Lemieux,
2003). Interestingly, maternal disinhibition has been
shown to predict daughters’ overweight and, when both
maternal disinhibition and daughters’ EAH were used to
predict daughters’ overweight, mothers’ disinhibition
showed an independent prediction (Cutting, Fisher,
Grimm-Thomas, & Birch, 1999).
Thus, to the extent that EAH in childhood is a
behavioral precursor to disinhibited eating in adulthood,
these findings further support the importance of EAH as an
early behavioral marker or risk factor for obesity onset.
Indeed, there is evidence that EAH is relatively stable
overtime in childhood (Birch et al., 2003), which suggests
that the trait could extend into adulthood.
Genetic Influences on EAH
‘‘Heritability’’ (h2) refers to the extent to which variability
in a trait is influenced by genetic variations within a
population (Maes, Neale, & Eaves, 1997), such that a trait
with h2 ¼ 0% is completely influenced by environmental
factors while a trait with h2 ¼ 100% is entirely genetically
influenced. Most traits are at least partially genetically
influenced, and so heritability is useful for understanding
the relative influence of genes, or the overall ‘‘genetic
loading’’ of a trait. Heritability is most commonly
estimated from twin studies that compare the phenotypic
similarity of a trait in MZ twins compared to DZ twins,
using ‘‘biometrical’’ statistical methods for heritability
estimation (for details, see Neale & Cardon, 1992). There
are a number of methodological issues, caveats, and
limitations to twin designs. One example is the ‘‘equal
environments assumption’’ (i.e., the assumption that the
extent to which MZ twin pairs are exposed to similar
environments is not different from the extent to which DZ
twin pairs are exposed to similar environments). These
methodological issues have been reviewed extensively by
Maes and colleagues (Maes et al., 1997) and Guo (2001).
Numerous studies show that child weight status is
highly genetically influenced. In a sample of 66 pairs of
3- to 17-year-old twins residing in the New York
metropolitan area, the heritability of BMI and percent
body fat was estimated to be 86% and 76%, respectively
(Faith et al., 1999). Analyses of a population-based sample
of 608 MZ and 1210 DZ twin pairs from the UK estimated
the heritability of weight (corrected for height) to be 64%
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Kral and Faith
for boys and 61% for girls (Koeppen-Schomerus, Spinath,
& Plomin, 2003). In a large national sample of adolescents
from the United States, Jacobson and Rowe found that
total genetic influences on BMI were 67%, 45%, and 81%
for Black females, White females, and all males (i.e., all
ethnic groups combined), respectively (Jacobson & Rowe,
1998). High heritability estimates for child overweight from
twin studies have been shown in the literature, even in
recent publications from relatively current cohorts and
despite the increasing prevalence of pediatric obesity
(Musani, Erickson, & Allison, 2008). Thus, despite secular
changes in childhood obesity prevalence in recent decades,
the prominent role of genes cannot be dismissed.
By contrast, the genetics of child eating patterns is a
relatively understudied field (Faith & Keller, 2004).
Studies which have examined EAH point to the importance
of genetic factors on the trait. Faith and colleagues (Faith
et al., 2006) found that EAH in boys who were born at high
risk for obesity on the basis of maternal prepregnancy body
weight was more than twice that of boys who were born at
low risk for obesity. This investigation, however, could not
tease apart genetic from environmental influences on the
trait. Findings from a study with 801 children from 300
Hispanic families who were part of the Viva la Familia
Study (Fisher, Cai et al., 2007) indicated that EAH was a
highly heritable eating trait (51%).
The notion that EAH is heritable is consistent with
findings from prior studies establishing the heritability of
disinhibition in adults. For example, Steinle and colleagues
(Steinle et al., 2002) showed that among the three eating
behaviors (i.e., cognitive restraint, disinhibition, and
hunger) assessed with the Eating Inventory (Stunkard &
Messick, 1985), disinhibition showed the highest heritability (h2 ¼ 40%) and the strongest association with
obesity traits. Findings from the Quebec Family Study
indicated a heritability estimate for disinhibition of 17.5%
as well as significant parent–offspring and spousal correlations for disinhibited eating (Provencher et al., 2005).
Environmental Influences on EAH
Parental feeding practices have been identified as one
environmental factor which can considerably influence
children’s susceptibility to EAH. Specifically, dietary
restriction, or the tendency of parents to restrict children’s
access to desired, palatable foods (such as snack foods),
has been found to be a significant predictor of EAH. EAH
was predicted by mothers’ reports of using restrictive
feeding practices at age 5 (Birch et al., 2003; Fisher &
Birch, 2002; Francis & Birch, 2005), and was associated
with increased risk of overweight in children (Fisher &
Birch, 2002). Interestingly, the association between
restrictive feeding patterns and child EAH depended
upon maternal overweight status. That is, among daughters
of overweight mothers only, greater use of restrictive
feeding patterns when the children were 5 years of age
predicted greater EAH by daughters when they were 7
(Birch et al., 2003; Fisher & Birch, 2002) and 9 years of
age (Birch et al., 2003; Francis & Birch, 2005). However,
daughters of normal-weight mothers showed significantly
greater EAH only at age 5, but not at ages 7 and 9 years
(Francis & Birch, 2005). In addition, those girls who were
overweight at age 5 and subject to higher levels of
restriction showed the greatest EAH at age 9 (Birch et al.,
2003; Fisher & Birch, 2002).
In another study, Faith et al. (Faith et al., 2004)
showed that maternal use of restrictive feeding patterns
was associated with excess weight gain in children, but
only among children who were born at high risk for obesity
based on elevated maternal prepregnancy body weight.
There was no association between maternal use of
restrictive feeding and excess weight gain among children
born at low risk for obesity. These findings suggest that the
use of restrictive feeding practices by parents may interact
with a child’s genetic predisposition for obesity to promote
excess weight gain, which may occur through greater EAH.
Although Faith and colleagues did not measure EAH per
se, the findings are consistent with those generated by
Francis and Birch (Francis & Birch, 2005).
That being said, maternal obesity as a risk factor for
overweight in their offspring may not necessarily be conferred by ways of maternal feeding practices. A study by
Wardle and colleagues (Wardle, Sanderson, Guthrie,
Rapoport, & Plomin, 2002) found that obese mothers
did not differ from normal-weight mothers in the extent to
which they offered food to deal with emotional distress,
used food as a form of reward, or encouraged children to
eat more than they wanted. With respect to exerting
control over their child’s eating, the results of this study
showed that obese mothers reported significantly less
control over children’s intake than did normal-weight
mothers (Wardle et al., 2002).
Table II depicts key findings from select investigations
which further illustrate EAH’s role as a behavioral eating
trait in the development of childhood obesity.
Competing Conceptual Models of Factors
Influencing EAH
An important area for future research will be to determine
the extent to which the association between EAH and
excess weight gain is mediated by genetic factors,
Familial Influences on Child Eating and Obesity
Table II. Genetic and Non-genetic Factors Affecting EAH
Characteristic
Heritability
Findings
Studies
EAH shown to be a heritable eating trait
Fisher, Cai et al., 2007
EAH shown to be more pronounced in boys born
at high risk for obesity compared to those born
Faith et al., 2006
at low risk for obesity
EAH shown to share similarities to disinhibition in adults,
Cutting et al., 1999; Provencher et al., 2005; Steinle et al., 2002
a trait which has been found to be heritable
Environment
EAH shown to be exacerbated by restrictive feeding
Birch et al., 2003; Fisher & Birch, 1999a; Francis & Birch, 2005
practices and monitoring
Stability
EAH shown to be an eating trait which is stable over time
Fisher & Birch, 2002; Francis & Birch, 2005
Energy intake
Body weight
EAH shown to be associated with increased energy intake
EAH shown to be predictive of increased weight
Fisher & Birch, 1999b, 2000
Birch et al., 2003; Fisher & Birch, 2002; Shunk & Birch, 2004
gain among children
For all odds ratios, the nonobese group served as the reference group. The subject’s obesity status during childhood is based on the mean z-score for the child’s BMI during the
age interval, as follows: not obese, z < 1.036 (corresponding to the 85th percentile for a normal population of the same age and sex); obese, z 1.036 (85th percentile); and very
obese, mean z 1.645 (95th percentile).
environmental factors, or both. That is, research studies
should attempt to discern if EAH and weight gain have
genetic factors in common, environmental factors in
common, or both genetic and environmental factors in
common. Figure 1 illustrates three competing models that
could be tested. Model 1 posits that the relationship
between EAH and excess weight gain is entirely due to
genes that influence both traits, while Model 2 posits that
the association is entirely environmentally mediated.
Model 3 posits that both genetic and environmental
factors are influential. A properly designed study could test
these competing models, as illustrated in a recent study by
Fisher and colleagues (Fisher, Cai et al., 2007).
It will be important to know the extent to which
response to childhood obesity treatment and prevention
initiatives is determined by genetic and environmental
factors. Behavioral genetics research is expected to
contribute to future research endeavors by, first, continuing
to identify the heritability of child eating phenotypes that
are associated with excess body weight, as well as by
estimating genetic and environmental influences on treatment response. A range of behavioral genetics studies
including twin designs, adoption designs, and (extended)
family designs can address these questions (see Neale &
Cardon, 1992, for details). However, it is implausible that,
for example, the classic twin design, by itself, will be able to
address the full range of research questions concerning the
familial transmission of child eating traits. The various
behavioral genetics designs have their own respective
strengths and limitations that make certain designs more
desirable than others for certain research questions. A more
detailed discussion of these designs is provided elsewhere
(Plomin, DeFries, McClearn, & McGuffin, 2000).
The value of such studies rests in their potential to
resolve the extent to which the association between EAH
and weight gain is due to genetic and environmental
factors, respectively. If the association is primarily
environmentally mediated, this would provide greater
support for the potential of environmental interventions
that could foster healthier eating patterns and weight
trajectories among children. However, because child
weight status is highly heritable, it is conceivable that
obesity-promoting genes also drive increased EAH.
Genetically informative designs are very powerful for
resolving these questions.
Summary and Limitations
EAH is an eating trait which has been widely studied both
from an environmental and a genetic perspective in
children. Despite the many important insights these
studies have generated so far, there still exist large gaps
as to how children’s eating behavior and weight regulation
can be ameliorated. For one, EAH has been studied
primarily in white, middle class girls, although more
recently the eating trait has also been examined in Hispanic
children (Fisher, Cai et al., 2007). The fact that EAH has
been studied primarily in Caucasian girls limits the
generalizability of the findings to a broader population of
children. It will be crucial to further expand these studies
to children from different ethnic groups and of different
socio-economic status (SES) in the future. Second, the
mechanisms which underlie the development and maintenance of EAH in children remain poorly understood and
need further investigation. Furthermore, the systematic
study of children’s eating behavior should be widened to
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Kral and Faith
Genetics
Genetics
EAH
Weight Gain
Environment
Environment
Genetics
Genetics
EAH
Weight Gain
Environment
Environment
Genetics
Genetics
EAH
Weight Gain
Environment
Environment
Figure 1. Model 1: There are genetic and environmental influences on
EAH and weight gain, respectively. The correlation between EAH and
weight gain is due entirely to genetic pathways that impact on both
traits. Model 2: There are genetic and environmental influences on EAH
and weight gain, respectively. The correlation between EAH and weight
gain is due entirely to environmental pathways that impact on both
traits. Model 3: There are genetic and environmental influences on EAH
and weight gain, respectively. The correlation between EAH and weight
gain is due both to genetic and environmental pathways that impact on
both traits.
other eating traits and properties of foods (e.g., energy
density), which may affect children’s eating. These studies
should encompass both short- and long-term investigations. It will also be important to investigate the effects of
parental factors such as SES, education, and income on
child eating behavior. Lastly, self-report instruments need
to be developed for EAH and other eating traits because the
assessment of these traits in the laboratory will not be
feasible for large-scale genetics studies.
The purpose of the current review was to provide an
overview of how genetic and nongenetic factors can affect
children’s eating and weight development. This review
primarily focused on behavior genetics and did not take
into account molecular genetics studies which tested the
effects of specific genes on child eating traits or body
weight. The specific genes influencing EAH currently are
unknown and, in principle, one could speculate about any
of the hundreds of genes that have been associated with
variations in human weight status or adiposity (see the
‘‘Human Obesity Gene Map’’) (Rankinen et al., 2006).
Future research is expected to address the specific genes
influencing child EAH. This review also did not discuss the
influence of physical activity on children’s eating and
weight regulation.
Conclusions
In conclusion, the study of genetic and home environmental influences with respect to children’s eating and
weight development is an important area of research which
presents a great opportunity for collaboration among
scientists from diverse disciplines. The findings from
studies in this area likely will have important implications
for the prevention and treatment of childhood obesity in
both research and clinical settings. As detailed earlier,
children’s response to dietary interventions may depend
on their genotype. Once identified, it is conceivable that
dietary regimens may be tailored to children’s genetic
predisposition to promote healthy growth and eating
patterns. Parents’ involvement in child feeding and the
structuring of the early home food environment will be
crucial components in these interventions.
Conflicts of interest: None declared.
Received December 13, 2007; revisions received and
accepted March 19, 2008
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