European Journal of Clinical Nutrition (1997) 51, 846±855
ß 1997 Stockton Press. All rights reserved 0954±3007/97 $12.00
Food intake, energy balance and body weight control
E Doucet and A Tremblay
Physical Activity Sciences Laboratory, PEPS, Laval University, Ste-Foy, QueÂbec, Canada, G1K 7P4
Obesity is a multifactorial and complex affectation that is characterized by a long-term excess energy intake (EI)
above energy expenditure (EE). Since fat oxidation seems to be dependent on SNS activation and also seems to
remain acutely unaffected by fat intake, this macronutrient is certainly partly responsible for this situation. In
addition, high-fat intake does not induce as potent satiety signals or a compensation effect on subsequent EI as do
diets rich in carbohydrates or proteins. Moreover, since alcohol intake acutely inhibits fat oxidation and does not
promote subsequent compensation for its energy content, it should consequently be regarded as a substrate which
can induce a positive energy balance under free-living conditions. Thus, in a weight reducing context, each
energy substrate should be manipulated while taking into account its speci®c characteristics. Obesity has also
often been associated to a decreased sympathetic nervous system (SNS) activity, hence sympathomimetic agents
have been proposed as a possible way to partially correct this situation. Two of these agents are the widely
consumed caffeine (CAF) and the pungent principle of hot red pepper, capsaicin (CAP), which acutely increase
EE and reduce EI under some circumstances. Furthermore, other factors like dietary ®bers, that have been shown
to increase satiety and fullness, and reduce EI in some cases, should also be considered.
Descriptors: obesity; energy balance; macronutrients; alcohol; sympathomimetic agents; dietary ®bers
Introduction
The prevalence of obesity in af¯uent societies is reaching
epidemiological proportions and even if our understanding
and knowledge of the causes leading to obesity are ever
increasing, health professionals cannot seem to reverse this
situation. Obesity is being characterized as a long term
energy imbalance, that is energy intake (EI) being greater
than energy expenditure (EE). Many studies have shown
that nutritional and food-related non-nutritional factors
in¯uence the adjustment of EI to EE. The main objective
of this report is to describe the effects of some of these
factors with the intent to propose strategies that would
enable health professionals to further improve their intervention in obese individuals.
Fat
The ever increasing pool of data concerning the speci®city
of the characteristics of each macronutrient urges the
clinician wishing weight reduction or maintenance to no
longer address EI without also looking into macronutrient
composition (Table 1). In that respect, fat intake seems to
have the most impact on energy balance. Indeed, population studies have, on numerous occasions, shown a positive
association between fat intake and adiposity (Dreon et al,
1988; Romieu et al, 1988; Tremblay et al, 1989; Colditz et
al, 1990; Miller et al, 1990; Klesges et al, 1992; Tucker &
Kano, 1992). Furthermore, industrialized countries, like the
United States where dietary fat intake provides from 31.9±
36.9% of total daily EI for adults of both sexes and all
major ethnic groups (NHANES, 1988±1991), are generally
Correspondence: Dr A Tremblay.
Received 3 June 1997; revised 19 June 1997; accepted 13 August 1997
characterized by a positive fat balance which more often
than not leads to body weight gain. Thus the reduction of EI
as dietary fat is being increasingly targeted as a possible
way to reduce or better control one's body weight. Consequently, it has been repeatedly proposed that lowering fat
intake might be bene®cial to a weight maintenance program (Lissner et al, 1987; Flatt, 1991; Kendall et al, 1991;
Thomas et al, 1992; Westerterp, 1993; Astrup et al, 1994a).
This phenomenon has led the food industry into the era of
low-fat products.
The association between high-fat diets and obesity is
also frequently observed in both animal and human studies.
The animal models have clearly established that high-fat
diets have a profound effect on body weight and composition (Hill et al, 1991; Racefas et al, 1992), even under
isocaloric conditions (Boozer et al, 1993). In humans, the
failure of fat intake to acutely promote fat oxidation (Flatt
et al, 1985; Flatt, 1988; Schutz et al, 1989; Bennett et al,
1992; Jebb et al, 1996) and the fact that fat oxidation seems
to be dependent on SNS stimulation (Acheson et al, 1988a;
Tremblay et al, 1992) could be factors explaining why
high-fat foods favor a positive fat and energy balance.
Furthermore, it was demonstrated that the post-obese state
might be characterized, to an even greater extent, by a
decrease in lipid oxidation under high-fat diet conditions
(Astrup et al, 1994a; Raben et al, 1994a; Ballor et al,
1996). However, it was also demonstrated that obese
women have a greater fat oxidation than the non-obese,
and that this condition might be the result of an adaptation
to high-fat diets to promote long-term fat balance and body
weight stability (Schutz et al, 1992; Astrup et al, 1994b).
The observation that fat intake fails to stimulate fat oxidation when given as a supplement to a basal meal does not
seem to explain differences in daily EE observed when this
macronutrient is isoenergetically substituted by carbohydrates. Accordingly, it was reported that the substitution of
complex carbohydrate by dietary fat has no effect on EE
Food intake and body weight
E Doucet and A Tremblay
Table 1
847
Energy substrate characteristics
Characteristics
Alcohol
Fat
Carbohydrates
Proteins
In¯uence on subjective
feelings of hunger and satiety
No
Tremblay 96
No effect
Poppitt 96
Lesser effects than
proteins or CHO
Lawton 93
Blundell 93
Rolls 94
Stubbs 95
Compared to fat: Greater
Rolls 88
Blundell 93
Lower
Rolls 91
Foltin 90
Better than other substrates
Yes
Hill 90
van Wyk 95
No
de Graaf 92
Potential to exert compensatory
effect on EI
No
Tremblay 96
Poppitt 96
Partial
Foltin 93
Lesser effects than
proteins or CHO
Lissner 87
Tremblay 89, 91
Rolls 94, 95
Stubbs 95
Compared to fat:
Greater
Rolls 94
Stubbs 95
Same as fat
Rolls 91
Foltin 90, 92
Better than other substrates
Yes
High
Shelmet 88
Weststrate 90
Prentice 92
Suter 92
Low
Flatt 85, 88
Schutz 89
Bennett 92
Jebb 96
High
Flatt 78
Acheson 84
Lean 88
Schutz 89
Astrup 92
High
Nair 83
Dauncey 83
Energy density
High
High
Low
Low
Intake associated with increased
risk of weight gain
Yes
Kroumhout 83
Suter 92
Tremblay 95
Cigolini 96
Yes
Dreon 88
Romieu 88
Tremblay 89
Colditz 90
Miller 90
Klesges 92
Tucker 92
No
Toubro 97
Jeffry 95
Lyon 95
Yes
Buemann 95
No
DeCastro 88
Bingham 94
No changes
Acheson 88
Tremblay 92
Decrease
Acheson 88
Tremblay 92
No changes
Acheson 88
Ability to promote its oxidation
No
Fisher 85
Coldtiz 91
Sonko 94
Liu 94
Effect of b-adrenergic blockade
on oxidation
NA
Hill 86
DeCastro 88
Barkeling 90
Bingham 94
CHO ˆ carbohydrates.
NA ˆ data not available.
even if there was a change in substrate oxidation (Roust et
al, 1994). Furthermore, a high-fat low-carbohydrate weight
maintenance diet did not reduce 24 h EE compared to its
isoenergetic high-carbohydrate low-fat diet counterpart
(Abbott et al, 1990).
There is also a growing body of evidence concerning the
effects of fat on food intake and its ability to induce satiety.
Indeed, it has been demonstrated that high-fat diets give
way to overconsumption (Lissner et al, 1987; Tremblay et
al, 1989; Tremblay et al, 1991; Stubbs et al, 1995) because
fat seems to have a lesser effect on satiety than do other
macronutrients (Blundell et al, 1993; Lawton et al, 1993).
In addition, dietary fat seems to have a lesser potential to
exert negative feedback on subsequent EI than do carbohydrates (Rolls et al, 1994; Stubbs et al, 1995) or proteins
(Stubbs et al, 1995). High-fat preloads even seem to exert a
lesser effect on subsequent EI of obese compared to
normal-weight individuals (Rolls & Hammer, 1995).
Another factor which can further potentiate weight gain is
the increased preference for fat in obese and post-obese
individuals (Drewnowski & Greenwood, 1983; Drewnowski et al, 1992).
The reduced capacity of fat to acutely promote its
oxidation, its decreased satiating power and the observation
that obese and post-obese seemingly have a more pro-
nounced preference for this macronutrient are factors that
can potentiate weight gain under high-fat conditions. There
is also growing evidence that dietary fatty acid composition
might play a role in this matter. Results from animal studies
have shown that rats fed a saf¯ower oil (78.6% polyunsaturated fat (PUFA), 11.4% monounsaturated fat (MUFA)
and 9% saturated fat (SFA)) diet as opposed to a beef
tallow (2.1% PUFA, 47.4% MUFA and 48.9% SFA) diet,
accumulated less body fat, had lower respiratory quotient,
demonstrated higher DIT (Shimomura et al, 1990), and
higher SNS activity in brown adipose tissue (Takeuchi et
al, 1994). Moreover, the higher body fat accumulation
under the beef tallow condition seems to be due to a
decreased SNS activity in rats (Matsuo et al, 1995). In
humans, it has been reported that the proportion of saturated to unsaturated fat possibly affects the net contribution
of fat to EE (Jones et al, 1985), and it was demonstrated
that DIT was greater for the high-PUFA to SFA ratio (1.25)
than for the low-PUFA to SFA ratio (0.25) diets (Jones &
Schoeller, 1988). It was also shown that the increase of
dietary PUFA results in an increase of the oxidation of
medium and long-chain fatty cids (Clandinin et al, 1995).
Furthermore, it was reported that the isoenergetic substitution of long-chain triglycerides by medium-chain triglycerides (MCT) had an inhibitory effect on food and EI (Stubbs
Food intake and body weight
E Doucet and A Tremblay
848
& Harbron, 1996) and that incorporation of MCT into the
diet stimulated thermogenesis (Seaton et al, 1986; Hill et
al, 1989; Scal® et al, 1991).
Carbohydrates
It is generally well recognized that populations who consume a greater proportion of energy in the form of
carbohydrates are leaner than those who do otherwise.
This might be partly due to the fact that a high amount
of energy in the form of carbohydrates for a few days is
needed to induce de novo lipogenesis (Acheson et al,
1988b) compared to the impact of a high-fat intake which
seems to produce an immediate positive fat balance (Flatt
et al, 1985). Another interesting observation is that people
who had been vegetarians for a long period of time had a
resting metabolic rate that was 11% higher than their
omnivorous counterparts, although this difference disappeared when controlling for carbohydrate, and fat intake
and norepinephrine (Toth & Poehlman, 1994). In previous
studies by the same group, it was demonstrated that male
vegetarians also had a tendency toward higher resting
metabolic rate (RMR) than the typical north-american
dieter (Poehlman et al, 1988; Oberlin et al, 1990). This is
an interesting observation since it has been documented
that carbohydrate intake seems to stimulate SNS activity
(Acheson et al, 1984a). The greater SNS activity under
high-carbohydrate intake condition might be partly responsible for the greater RMR and the effects of carbohydrates
on thermogenesis.
In this regard, it has been reported that DIT of carbohydrates is equivalent to approximately 10% of EI (Flatt,
1978) and that during carbohydrate overfeeding studies,
24 h EE increased from 10±40%. In a recent review, a lowfat high-carbohydrate diet was proposed to lead to a greater
EE than its high-fat, low-carbohydrate counterpart (Westerterp, 1993). Indeed, it would seem that carbohydrates
have a greater potential to increase thermogenesis possibly
due to the obligatory cost of glycogen storage (Acheson et
al, 1984b). It was later demonstrated that carbohydrate
intake promotes carbohydrate oxidation (Schutz et al,
1989), that a high-carbohydrate-containing diet produced
greater DIT than the high-fat diet (Lean & James, 1988)
and that a high-carbohydrate diet administered to postobese women caused an increase in 24 h EE that was
entirely generated by an increase in carbohydrate oxidation
(Astrup et al, 1992).
Carbohydrates exert a stimulating effect on thermogenesis whereas its effects on satiety and food intake do not
yield as clear a trend. A recent study showed that when
comparing the effects of equicaloric preloads (1.2 MJ) of
either carbohydrates, proteins or fat in ten normal-weight
women, carbohydrates and proteins had a greater satiating
power than did fat (Rolls et al, 1988). The latter results are
in accordance with those of Blundell et al (1993) who
demonstrated that in lean subjects a high-carbohydrate
breakfast ( 87% of 3.36 MJ) suppressed hunger ratings
and energy intake signi®cantly more than the equicaloric
high-fat one ( 57% of 3.36 MJ) in a mid-morning snack
served 90 min after the preload whilst no signi®cant
differences were found between conditions at lunch time
which was served 270 min after the preload (Blundell et al,
1993). Moreover a high-carbohydrate preload ( 80% of
1.5 MJ) had a greater suppression power over subsequent
food intake than did the high-fat preload ( 70% of
1.5 MJ) in normal weight restrained males and females,
normal weight unrestrained females and obese restrained
and unrestrained females as rated by the Cognitive
Restraint Scale of the Stunkard Eating Inventory even if
normal weight unrestrained males showed a quite accurate
compensation for energy content of the different preloads
(Rolls et al, 1994). Accordingly, a recent experiment
mimicking free-living conditions in which three different
diets varying in macronutrient composition (20, 67 and
13%; 40, 47 and 13%, and 60, 27 and 13% for fat,
carbohydrates and proteins respectively) showed that carbohydrates and proteins seem to have a greater potential to
exert negative feedback on EI than does fat (Stubbs et al,
1995). However, there is also a considerable body of
evidence that does not support the above proposed effects
of carbohydrates on food intake. In that respect, it has been
demonstrated that either low or high-carbohydrate (1.8 vs
3.5 MJ), or low or high-fat (1.8 vs 3.5 MJ) preloads at
lunch have the same satiating power. Moreover, this study
also demonstrated that subsequent EI over the remainder of
the day was not signi®cantly affected by either manipulation of macronutrient or energy content (Foltin et al, 1990).
These results are in agreement with those of Rolls et al
(1991) who failed to show any signi®cant differences
between responses in food intake following ingestion of a
high-carbohydrate (81% of 0.9 MJ) or a high-fat (65% of
0.9 MJ) preload (Rolls et al, 1991). Furthermore, it was
shown that there is clear evidence for subsequent caloric
compensation when energy content was manipulated, but
equicaloric manipulations of macronutrient, namely carbohydrate and fat content, failed to show differences in
subsequent EI (Foltin et al, 1992).
Even if the data concerning the effects of carbohydrates
on satiety and hunger and also on thermogenesis are quite
abundant, those surrounding the impact of an ad libitum
high-carbohydrate low-fat diet on body weight loss or
maintenance are scanty. However, in a very recent study
from Toubro & Astrup (1997), it was shown that after an
initial weight loss ( 12.6 kg) induced by energy restricted
diets and sympathomimetic agents, subjects who were
given free access to a high-carbohydrate low-fat diet over
a period of one year maintained more of the initial weight
loss (8.0 kg vs 2.5 kg) than did the group who were given a
®xed energy intake ( 7.8 MJ/d). These results are in
accordance with those of Jeffry et al (1995) who found
that under low-fat high-carbohydrate conditions, subjects
lost 2.5 kg vs 0.5 kg for the calorie-counting group after an
intervention period of 12 months. Furthermore, it was
demonstrated that adherence to a low-fat high-carbohydrate
diet was strongly correlated to body fat loss (Lyon et al,
1995). Conversely, it was reported that a ®xed energy
intake was better at producing weight loss (10 kg vs
6 kg) than what was observed under ad libitum low-fat
diet conditions (Schlundt et al, 1993).
Another important issue related to the impact of highcarbohydrate intake pertains to the enhancing effect of this
macronutrient on its own utilization. It might be argued that
the increase of carbohydrate oxidation observed under highcarbohydrate diet conditions is also responsible for the
inhibition of fat oxidation observed under such conditions
which could be detrimental to weight stability. This is
somewhat unlikely because of the relatively low amount of
fat consumed under high-carbohydrate conditions and also
because of the effects of carbohydrates on thermogenesis.
Moreover, satiety seems to be reached with a lesser amount
of calories under high-carbohydrate conditions which is
probably the most likely explanation for the inability of
Food intake and body weight
E Doucet and A Tremblay
high-carbohydrate diets to induce lipogenesis and ultimately
body weight gain under free-living conditions even if this
type of regimen does to a certain extent inhibit fat oxidation.
Proteins
The effects of proteins on EI and EE, and ultimately on
body weight control are probably the lesser considered of
all macronutrients, but there is an increasing pool of data
concerning this issue. DeCastro & Elemore (1988) demonstrated that in subjects self-reporting their food intake for
7 d, proteins were the most ef®cient macronutrient at
suppressing food intake independently of their contribution
to EI. Accordingly, it was reported, via a 16 d weighed
dietary record by post-menopausal women, that proteins
were the only substrate that was negatively correlated to
food intake (Bingham et al, 1994). However, these results
are not supported by another observational study in which
protein intake seemed to be signi®cantly associated with
more adiposity (Buemann et al, 1995).
Experimental data also suggest an existing relation
between the protein content of diet and food or energy
intake. Different preloads of proteins (0.4, 1 and 1.7 MJ)
had no signi®cant effect on subsequent food intake, nor did
different preloads of carbohydrates or fat (deGraaf et al,
1992). However, there is a considerable number of studies
that provide discordant results. In this context, obese as
well as normal-weight individuals have been shown to
signi®cantly decrease their subsequent EI by 19 and 22%,
respectively, when the effects of a high-protein meal (54%
of 2 MJ) were compared to that of an isoenergetic highcarbohydrate meal (63% of 2 MJ) (Hill & Blundell, 1986).
Accordingly, it was demonstrated by the same authors that
a high-protein meal produced greater subjective feelings of
fullness and a greater decrease in the desire to eat than did
an isoenergetic high-carbohydrate meal (Hill & Blundell,
1990). It was also shown that high-protein and highcarbohydrate isoenergetic lunches produced a reduction
of EI at dinner that was 12% greater under the high-protein
lunch condition than for the high-carbohydrate condition
(Barkeling et al, 1990). Accordingly, ingestion of a breakfast (energy equivalent to 75% of basal metabolic rate)
composed of either 3.1 MJ of protein, carbohydrate or fat
resulted in a signi®cantly greater decrease in hunger sensation between breakfast and lunch for the carbohydrates and
proteins when compared to the fat condition (van Wyk et
al, 1995). Furthermore, this study also showed that the
protein breakfast was better at suppressing hunger over a
24 h period in a calorimeter.
It is generally well recognized that protein stores
represent a precisely regulated compartment. It was
reported that amino acid oxidation changes rapidly in
response to changes in amino acid intake in the way
that substrate availability seems to be the primary determinant of substrate oxidation. Thus, the net effect of this
mechanism is a conservation of nitrogen when protein
intake is low and in contrast, a high protein intake leads
to loss of amino acid, nitrogen and carbon (Young &
Marchini, 1990).
The effects of proteins on EE are in agreement with the
idea that protein balance is precisely regulated. Indeed, DIT
of proteins has been shown to be greater than for its
isoenergetic substitution by carbohydrates or fat (Nair et
al, 1983). Accordingly, the isoenergetic substitution of a
high-carbohydrate diet by a high-protein diet resulted in a
12% increase in EE (Dauncey & Bingham, 1983).
Weight loss is normally associated with a decrease in
RMR which can be partly attributable to the decrease in fat
free mass (FFM). However, weight loss under high-protein,
very low-calorie diet (VLCD) has been shown to produce a
decrease in FFM (17%) that is lesser (Barrows & Snook,
1987) than what would be expected under a typical VLCD
(1/3 decrease in FFM and more) (Holloszy, 1974). It was
reported that a severe hypoenergetic diet (2.1 MJ) can
produce signi®cantly more weight loss than a hypoenergetic regimen (4.2 MJ) without the expected decrease in
RMR when isonitrogenous conditions are preserved for
both diets (Stanko et al, 1992). In addition, maintaining
protein intake to its usual level during energy restriction has
been shown to signi®cantly reduce the fall in sleeping
metabolic rate and 24 h EE (Whitehead et al, 1996).
In summary, protein intake seems to have a comparable
effect, if not more potent, on the subjective feelings of
hunger and satiety as does carbohydrate intake. The same
can be said about its in¯uence on subsequent EI and
thermogenesis. Furthermore, the preservation of FFM
during weight loss when a high-protein intake is maintained
is another factor that urges clinicians to look at the protein
component with more scrutiny, especially in a weight
reduction context.
Alcohol
In the recent past, the contribution of alcohol to the average
american diet was approximately 5.6% of the total EI
(Block et al, 1985). This represents a contribution to EI
which is not trivial and whose role in the regulation of
energy balance is still a matter of controversy.
In an early study, Gruchow et al (1985) demonstrated
that the calories from alcohol were additive in the diets of
light to moderate drinkers. However, in the same study,
alcohol energy was also shown to replace the calories from
other macronutrients in the diets of heavy drinkers. Other
studies have also demonstrated that alcohol derived calories
were additive, thus not replacing energy from other substrates (Jones et al, 1982; DeCastro & Orozco, 1990;
Tremblay et al, 1995b).
The observation that alcohol energy seems to be additive
to the EI from other energy substrates is in agreement with
the fact that alcohol intake may exert a poor inhibitory
effect on subsequent food and energy intake. Accordingly,
it was shown that a high-fat and alcohol appetizer was
followed by an increased ad libitum EI even after their
high-energy density was controlled (Tremblay & St-Pierre,
1996). Alcohol consumption also seems to have no effect
on satiety and fullness when taken concomitantly with a
high-fat meal. In addition, no compensatory effect of the
excess energy associated to alcohol intake was observed for
the subsequent meal (Tremblay & St-Pierre, 1996), which
is in accordance with a recent study that demonstrated that
the consumption of an alcoholic beverage taken before a
meal had no compensatory effect on the energy content of
the following meal (Poppitt et al, 1996). These results are
consistent with those from an earlier study which showed
that an alcoholic beverage taken at four different times
during the day resulted in a weak compensatory effect
(37%) of its own energy content (Foltin et al, 1993).
Many studies have investigated the role of alcohol in
relation to energy metabolism. In an early study, Rosenberg
& Durnin (1978) demonstrated that alcohol ingestion had
the same effect on resting metabolic rate as did other
energy substrates, and that variations in RMR were prob-
849
Food intake and body weight
E Doucet and A Tremblay
850
ably more closely related to EI than to macronutrient
composition of the diet. These results are in agreement
with those of more recent studies that showed that DIT of
alcohol is almost the same as it is for carbohydrates
(Shelmet et al, 1988; Weststrate et al, 1990; Prentice et
al, 1992). However, more recent results have shown that
DIT of alcohol is equivalent to approximately 20% of its
energy content (Suter et al, 1994) which is substantially
more than that of carbohydrates (Flatt, 1978). Even if the
DIT of alcohol does not characterize it as an adipogenic
substrate, its effects on the oxidation of other substrates
might. Indeed, alcohol acutely suppresses the oxidation of
other substrates (Shelmet et al, 1988) and to a greater
extent fat oxidation (Shelmet et al, 1988; Suter et al, 1992;
Sonko et al, 1994; Murgatroyd et al, 1996). This suppression might be due to the fact that alcohol calories become
the primary source of metabolic fuel as a mode of detoxi®cation which might acutely inhibit the oxidation of other
fuel sources.
Another interesting feature of alcohol is the fact that it
cannot be bodily stored. Despite this characteristic, numerous studies have tried to establish if alcohol intake could be
involved in the mechanisms leading to weight gain. The
results concerning this issue are surrounded by con¯ictual
reports. It was suggested that the habitual consumption of
alcohol in a moderate fashion in excess of energy needs
might lead to a condition which favors lipid storage and
that could consequently lead to weight gain over time
(Suter et al, 1992). It was also reported in an epidemiological study that of all energy substrates, alcohol was the
only one positively correlated with body fatness and it was
thus concluded that alcohol consumption might be an
important factor in body weight gain (Kromhout, 1983).
Furthermore, the combination of alcohol and high-fat diets
favors weight gain in the form of central subcutaneous fat
(Tremblay et al, 1995a). The latter study is in agreement
with recent results that have demonstrated that the increase
of daily energy taken in the form of alcohol is positively
correlated to waist circumference, waist to hip ratio and
probably visceral fat (Cigolini et al, 1996). In contrast,
numerous studies have led to the conclusion that alcohol
intake does not promote body fat storage (Fisher & Gordon,
1985; Colditz et al, 1991; Liu et al, 1994; Sonko et al,
1994) and that it does not, to an even greater extent, in
women (Colditz et al, 1991; Liu et al, 1994). Moreover,
individuals who drink alcohol consume more total daily
energy than those who are non-drinkers, but tend to weigh
less which is possibly due to the inef®cacy in the utilization
of alcohol calories (Fisher et al, 1985).
The idea of an inef®cacy in the disposal of alcohol
calories might be related to the hypothesis of a futile cycle
as described by Lands & Zakhari (1991). This concept
suggests that the futile cycle employs an irreversible
oxidation of alcohol to acetaldehyde and a reduction of
acetaldehyde to alcohol which can dissipate six ATP per
cycle thus eliminating any net gain of alcohol calories after
two or three cycles.
It is as of yet unclear how long term alcohol intake
affects bodily fat stores. It should however be taken into
account that discordances observed between different cross
sectional studies could be due to the fact that other lifestyle
factors might contaminate the results. For instance, it is
possible that the inverse relation observed between alcohol
intake and adiposity in women might be partly explainable
by better compensatory skills of this group under such
conditions. This is likely the case since experimental
evidence supports that alcohol seems to have a poor or
no capacity to in¯uence subjective feelings of hunger and
satiety, and also little in¯uence to promote compensation in
subsequent EI (Foltin et al, 1993; Poppitt et al, 1996;
Tremblay et al, 1996). Furthermore, alcohol intake seems
to favor alcohol oxidation at the expense of other energy
substrates, especially fat (Shelmet et al, 1988; Suter et al,
1992; Sonko et al, 1994; Murgatroyd et al, 1996).
Caffeine
It has been estimated that 80% of adults in North America
are regular coffee drinkers and that it is not uncommon for
an individual to consume 200±250 mg (the equivalent of
approximately 2±3 cups of coffee) of caffeine (CAF) per
day (Sawynok, 1995).
Evidence suggests that CAF has the potential to increase
metabolic rate of lean individuals for up to three hours after
ingestion (Acheson et al, 1980; Hollands et al, 1981;
Dulloo & Geissler, 1989; Astrup et al, 1990; Yoshida et
al, 1994; Bracco et al, 1995) and during the ®rst 12 h of a
24 h stay in a metabolic ward after which no residual effect
of CAF is detected (Dulloo et al, 1989). Moreover, it would
seem that women have a lesser acute thermogenic response
to CAF than do men (Perkins et al, 1994).
The ability of CAF to alter substrate oxidation is also of
major interest. Accordingly, it would seem that CAF
ingestion produces an increase in lipid oxidation and in
the availability of free fatty acids for energy production
(Astrup et al, 1990; Bracco et al, 1995). Furthermore, CAF
seems to directly stimulate in vivo lipolysis (Van Soeren et
al, 1996).
Some differences have been observed between lean
subjects and their obese counterparts with respect to CAF
responsiveness. It has been demonstrated that CAF does not
increase metabolic rate in obese individuals as it does in
lean (Astrup et al, 1990; Bracco et al, 1995), and that there
are variations in CAF response among the obese population
(Yoshida et al, 1994). Moreover, it was shown that the
thermogenic effects of CAF can be prolonged over night in
lean subjects but not in the obese, and that this effect is
achieved with a normal CAF consumption (Bracco et al,
1995). However, it was reported that even if obese individuals have a lesser response to CAF, their lipid oxidation
was nevertheless signi®cantly increased by ingestion of this
compound (Bracco et al, 1995). In contrast, another study
demonstrated that obese persons have the same sensitivity
to CAF than do lean individuals when it is taken alone in
the fasted state, but they rather seem to have a de®cient
dietary-induced thermogenesis (DIT) which can be partly
corrected by addition of CAF to meals (Dulloo et al, 1989).
CAF also seems to exert an inhibitory effect on food
intake. Indeed, it was demonstrated that CAF has the
potential to reduce EI in men, but failed to produce the
same effect in women (Tremblay et al, 1988). The latter
study is supported by data which have clearly established
that CAF ingestion in rats reduces food intake and hence
body weight gain (Racotta et al, 1994).
Capsaicin
Decreased and/or de®cient SNS activity has been proposed
as a possible factor leading to obesity. Thus, the inclusion
of sympathomimetic compounds such as capsaicin (CAP)
into the diet might partially correct this situation. CAP is a
pungent principle of hot red pepper that has long been used
Food intake and body weight
E Doucet and A Tremblay
for enhancing food palatability and medicinally as a counterirritant. Early studies with animals have shown that rats
fed high-fat diets with added CAP gained less weight than
controls, had lower plasma triglyceride levels (Kawada et
al, 1986a) and oxidized more lipids (Kawada et al, 1986b).
It was also reported that CAP might promote lipid mobilization from adipose tissue of rats during exercise, resulting in a sparing of glycogen (Lim et al, 1995). Accordingly,
it was demonstrated that CAP failed to produce changes in
carbohydrate or glycogen metabolism at rest or during
exercise in rats (Matsuo et al, 1996). Furthermore, the
effects of CAP administration were subdued by the addition
of a beta-blocking agent (Kawada et al, 1986b).
In an early study with human subjects, Emery & Henry
(1985) reported that when a meal is consumed with added
red pepper, DIT is signi®cantly greater than after a control
meal, 53 vs 28% increase in metabolic rate, respectively.
Moreover, it has been demonstrated that a meal with red
pepper signi®cantly increased respiratory quotient and
produced a slight (10% over control) but not signi®cant
increase in EE (Lim et al, 1997). In addition, red pepper
ingestion would seem to increase carbohydrate oxidation
more than it does for fat (Lim et al, 1997).
The fact that CAP seems to stimulate carbohydrate
oxidation in humans and fat oxidation in animals is puzzling, but can probably be explained by methodological
differences. The fact that most animal studies used cap
whereas human studies were conducted with red pepper
might be partly responsible for the discordant results.
Moreover, the fat content of diets used in animal studies
was relatively high compared to the dietary fat intake of
subjects involved in human studies.
It is very well established that sympathomimetic drugs
can stimulate SNS activity in humans and animals. Since
weight loss has been shown to produce a decrease in the
SNS/parasympathetic nervous system (PNS) ratio (Aronne
et al, 1995), the manipulation of some environmental
factors such as capsaicin, caffeine and exercise has, at the
least, the potential to partly compensate for this effect. As
illustrated in Figure 1, it would be useful to favor adaptations in SNS/PNS balance which are compatible with a
weight maintenance prescription, especially in the postobese individuals. However, even if sympathomimetic
drugs and exercise both stimulate substrate oxidation and
energy expenditure, the selectivity of the effects of exercise
needs to be discussed. It has been demonstrated that
postexercise EE and fat oxidation are mediated by an
increase in SNS activity (Poehlman & Danforth, 1991;
Tremblay et al, 1992). This increase in EE and fat oxidation might in turn be generated by an increase in badrenergic activity in skeletal muscle, such an effect not
being observed in the heart (Plourde et al, 1991; Plourde et
al, 1993). In contrast, sympathomimetic drugs seem to
activate all SNS mediated systems which not only results
in an increase of EE and fat oxidation, but also of blood
pressure and heart rate. These observations emphasize the
relevance of a stimulation targeting skeletal muscles rather
than a non-speci®c SNS activity which also affects cardiac
function.
Fibers
Dietary ®bers seem to have the potential to modify food
eating patterns and energy balance for the following reasons: fullness might be associated with bulk because high®ber diets have a greater volume than high-fat diets, which
851
Figure 1 Illustration of the impact of dietary energy restriction on SNS/
PNS balance in obese individuals and potential contribution of exercise
and sympathomimetic agents in the follow-up of post-obese subjects.
could lead to a decreased EI; they promote chewing and
therefore require an increased effort to eat; they slow
gastric emptying which might trigger satiety; reduce hunger
and prolong fullness; they decrease digestive and absorptive
ef®ciency which might lead to an increased loss in fecal
energy; they are more satiating than their energy equivalent
low-®ber foods and they might carry nutrients further down
the ileum, which might trigger the ileal break that has been
shown to reduce ad libitum food intake. Accordingly, evidence suggests that obesity is much less prevalent in populations who consume ®ber-rich diets as opposed to those who
consume low-®ber diets and that animals normally eating
diets rich in dietary ®bers become obese on low-®ber diets
(Van Italie, 1978; Leeds, 1987; Kimm, 1995).
Many studies have tried to determine the impact of a
high-®ber regimen on long-term energy balance and body
weight control. In this context, it was found that subjects
who had greater body mass index (BMI) values also had
diets containing the most fat and the least dietary ®bers
(Medeiros et al, 1996). In addition, weight-reducing diets to
which a dietary ®ber supplement had been added (5±6 g/d)
were shown to produce a greater body weight loss than the
control diets (Rossner et al, 1987; Solum et al, 1987).
Accordingly, a recent study on dogs showed that a
restricted low-fat high-®ber diet produced signi®cantly
greater weight loss than its isoenergetic high-fat low-®ber
counterpart (Borne et al, 1996). On the other hand, a
dietary ®ber supplement (6.5 g/d) administered with a
6.7 MJ/d diet, failed to yield any signi®cant bene®ts as
far as weight reduction was concerned when compared to
control diet alone (Rossner et al, 1988).
Even if some doubts persist concerning the potential of
an increase dietary ®ber intake to help better control body
weight, its effects on the subjective ®ndings of satiety,
hunger and fullness has been well documented. Indeed, it
was shown that a low-®ber meal (3 g) was not less satiating
than a high-®ber meal (12 g) (Burley et al, 1987). However
Food intake and body weight
E Doucet and A Tremblay
852
fullness ratings were higher after the high-®ber meal than
with the low-®ber meal. In a more recent study, fullness
and satiety were found to be signi®cantly greater after a
high-®ber breakfast and to stay elevated for up to four
hours after consumption in both men and women (Turconi
et al, 1995). This is concordant with other studies that have
demonstrated that dietary ®ber supplementation (3.9±23 g)
decreased hunger ratings (Rigaud et al, 1987), increased
satiety as opposed to low-®ber diets (Raben et al, 1995),
increased fullness and decreased the desire to eat (Raben et
al, 1994b), and increased fecal energy excretion (Rigaud et
al, 1987).
The type of dietary ®bers administered might have a role
to play in relation to the mechanisms that might alter appetite
and hunger ratings. Accordingly, it was reported that ad
libitum food intake was signi®cantly reduced by psyllium
gum (23 g) and psyllium gum combined to wheat bran
(23 g) by 640 kJ/d and 481 kJ/d, respectively. However,
this effect was not seen with the supplementation of wheat
bran (23 g) alone (Stevens et al, 1987). In contrast, a high®ber breakfast (20 g) of either soluble or insoluble ®bers
signi®cantly reduced EI of the subsequent meal compared to
the low-®ber breakfast (3 g) despite the fact that total daily
EI intake was not affected by ®ber type or quantity. However, it would seem that insoluble ®bers have the potential to
acutely increase feelings of satiety whilst soluble ®bers
would seem to produce greater satiety feelings 13.5 h after
ingestion of breakfast (Delargy et al, 1995). In a more recent
study from the same group, it was demonstrated that subjects
consumed less energy (1.6 kJ vs 2.2 kJ, respectively) in the
acute period following a high-insoluble ®ber (22 g) breakfast compared with the high-soluble ®ber (22 g) breakfast.
Despite this difference in the acute phase, total daily EI did
not differ when both soluble and insoluble ®ber conditions
were compared, which is in agreement with the previous
study (Delargy et al, 1997). Another study showed that gelforming liquid ®bers favor a decrease in hunger, an increase
in fullness, and reduce the amount of food people actually
wanted to eat, although it had no effect on food intake
(Tomlin, 1995).
Even if dietary ®bers seem to in¯uence the mechanisms
controlling food intake, they do not seem to increase DIT or
alter substrate oxidation in any bene®cial way. Indeed, a
high-®ber meal (26 g) failed to increase postprandial EE as
did a non-supplemented meal test (8 g) (Scal® et al, 1987).
These results are in accordance with a more recent study in
which it was demonstrated that under isoenergetic conditions, subjects had a reduced DIT after a high-®ber meal
(25.5 g) as opposed to a low-®ber one (9.2 g). In addition,
the high-®ber meal was associated with a decrease in fat
oxidation (Raben et al, 1994b).
Evidence suggests that dietary ®bers have the potential
to exert a suppressive effect on the subjective feelings of
hunger and satiety. However, this effect does not seem to
necessarily translate into a decrease of food and energy
intake. Even if the type of dietary ®bers (soluble vs
insoluble) seems to affect the mechanisms leading to satiety
in different ways, the impact of dietary ®bers on EI seems
to be more closely related to amount rather than form
ingested. The fact that dietary ®bers also seem to acutely
inhibit fat oxidation deserves further consideration.
Clinical implications
Obesity is necessarily the result of a long-term positive
energy balance and intervention strategies should be aimed
at factors which are most susceptible to reverse this
phenomenon. Reducing fat intake while increasing carbohydrate intake would seem to be one of the most ef®cient
methods to allow satiety while reducing EI. The reduction
of alcohol intake should also be addressed, since it would
seem that alcohol has a poor, or no capacity to in¯uence
subjective feelings of satiety and hunger, and also little, or
no in¯uence to promote compensation in subsequent EI.
Alcohol intake also seems to promote alcohol oxidation at
the expense of other macronutrients, especially fat. Therefore, the effects of alcohol are typical of a substrate which
can induce a substantial positive energy and lipid balance
under free-living conditions and should be regarded as
such.
The documented effects of dietary ®bers on the subjective feelings of hunger and satiety would seem to point
toward their potentially interesting implication regarding
energy balance. However, the effects of dietary ®bers on
these variables do not seem to be associated with substantial changes in food or energy intake. One cannot overlook
the fact that the amount of dietary ®bers used in most
studies very rarely exceeds 20 g/d. It is possible that in
order to attain the expected decrease in food and energy
intake, one would have to increase to an even greater extent
®ber consumption. Further research is needed to clarify this
particular issue.
The fact that dietary fat oxidation seems to be dependent
on beta-adrenergic stimulation (Acheson et al, 1988a;
Tremblay et al, 1992) is also of potential interest. Moreover, it would seem that the post-obese and obesity-prone
individuals are often characterized by a subnormal resting
energy EE (Geissler et al, 1987) and a defective DIT
(Dulloo & Miller, 1986). This could probably be due to a
decrease in SNS activity which could be partly responsible
for the resistance to further reduction and/or maintenance
of the adipose tissue mass in post-obese individuals, even if
these individuals are very often still overweight. In order to
counteract this situation, the manipulation of environmental
factors such as sympathomimetic drugs and exercise that
have the potential to elevate SNS activity would be useful.
Conclusions
The literature summarized above tends to show that a
negative energy balance is favored by factors such as
low-fat/high-carbohydrate ratio, a high-protein and ®ber
intake, an increase in PUFA intake and the incorporation of
food-related sympathomimetic agents. From a quantitative
standpoint, the currently available data also permit to
conclude that the impact of some of these factors on
energy balance is more important than others. Figure 2
integrates our interpretation of literature regarding the
potential effect of each factor on energy balance. In our
opinion, the manipulation of the fat-carbohydrate contribution to energy intake is the variable which seems to exert
the greatest impact on energy balance. The impact of
protein, alcohol and PUFA is also perceived important.
Since the effect of a high-®ber regimen on EI has not yet
been clearly demonstrated, its effect on energy balance and
body weight remains uncertain. Finally, even if caffeine
and capsaicin can favor a negative energy balance, their
side effects probably limit the relevance of consuming large
doses of these compounds to induce strong changes in
energy balance.
Food intake and body weight
E Doucet and A Tremblay
Figure 2 Identi®cation of factors promoting either negative (a) or
positive energy balance (b). The size of typescript re¯ects proposed
relative quantitative importance on energy balance.
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