Food intake, energy balance and body weight control - Nature

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 toremain acutely unaffected by fat intake, this macronutrient is certainly partly responsible for this situation. Inaddition, high-fat intake does not induce as potent satiety signals or a compensation effect on subsequent EI as dodiets rich in carbohydrates or proteins. Moreover, since alcohol intake acutely inhibits fat oxidation and does notpromote subsequent compensation for its energy content, it should consequently be regarded as a substrate whichcan induce a positive energy balance under free-living conditions. Thus, in a weight reducing context, eachenergy substrate should be manipulated while taking into account its speci®c characteristics. Obesity has alsooften been associated to a decreased sympathetic nervous system (SNS) activity, hence sympathomimetic agentshave been proposed as a possible way to partially correct this situation. Two of these agents are the widelyconsumed caffeine (CAF) and the pungent principle of hot red pepper, capsaicin (CAP), which acutely increaseEE and reduce EI under some circumstances. Furthermore, other factors like dietary ®bers, that have been shownto 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 reachingepidemiological proportions and even if our understandingand knowledge of the causes leading to obesity are everincreasing, health professionals cannot seem to reverse thissituation. Obesity is being characterized as a long termenergy imbalance, that is energy intake (EI) being greaterthan energy expenditure (EE). Many studies have shownthat nutritional and food-related non-nutritional factorsin¯uence the adjustment of EI to EE. The main objectiveof this report is to describe the effects of some of thesefactors with the intent to propose strategies that wouldenable health professionals to further improve their inter-vention in obese individuals.

Fat

The ever increasing pool of data concerning the speci®cityof the characteristics of each macronutrient urges theclinician wishing weight reduction or maintenance to nolonger address EI without also looking into macronutrientcomposition (Table 1). In that respect, fat intake seems tohave the most impact on energy balance. Indeed, popula-tion studies have, on numerous occasions, shown a positiveassociation between fat intake and adiposity (Dreon et al,1988; Romieu et al, 1988; Tremblay et al, 1989; Colditz etal, 1990; Miller et al, 1990; Klesges et al, 1992; Tucker &Kano, 1992). Furthermore, industrialized countries, like theUnited States where dietary fat intake provides from 31.9±36.9% of total daily EI for adults of both sexes and allmajor ethnic groups (NHANES, 1988±1991), are generally

characterized by a positive fat balance which more oftenthan not leads to body weight gain. Thus the reduction of EIas dietary fat is being increasingly targeted as a possibleway to reduce or better control one's body weight. Conse-quently, it has been repeatedly proposed that lowering fatintake might be bene®cial to a weight maintenance pro-gram (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 oflow-fat products.

The association between high-fat diets and obesity isalso frequently observed in both animal and human studies.The animal models have clearly established that high-fatdiets have a profound effect on body weight and composi-tion (Hill et al, 1991; Racefas et al, 1992), even underisocaloric conditions (Boozer et al, 1993). In humans, thefailure of fat intake to acutely promote fat oxidation (Flattet al, 1985; Flatt, 1988; Schutz et al, 1989; Bennett et al,1992; Jebb et al, 1996) and the fact that fat oxidation seemsto be dependent on SNS stimulation (Acheson et al, 1988a;Tremblay et al, 1992) could be factors explaining whyhigh-fat foods favor a positive fat and energy balance.Furthermore, it was demonstrated that the post-obese statemight be characterized, to an even greater extent, by adecrease 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 obesewomen have a greater fat oxidation than the non-obese,and that this condition might be the result of an adaptationto high-fat diets to promote long-term fat balance and bodyweight stability (Schutz et al, 1992; Astrup et al, 1994b).The observation that fat intake fails to stimulate fat oxida-tion when given as a supplement to a basal meal does notseem to explain differences in daily EE observed when thismacronutrient is isoenergetically substituted by carbohy-drates. Accordingly, it was reported that the substitution ofcomplex carbohydrate by dietary fat has no effect on EE

Correspondence: Dr A Tremblay.Received 3 June 1997; revised 19 June 1997; accepted 13 August 1997

European Journal of Clinical Nutrition (1997) 51, 846±855ß 1997 Stockton Press. All rights reserved 0954±3007/97 $12.00

even if there was a change in substrate oxidation (Roust etal, 1994). Furthermore, a high-fat low-carbohydrate weightmaintenance diet did not reduce 24 h EE compared to itsisoenergetic high-carbohydrate low-fat diet counterpart(Abbott et al, 1990).

There is also a growing body of evidence concerning theeffects of fat on food intake and its ability to induce satiety.Indeed, it has been demonstrated that high-fat diets giveway to overconsumption (Lissner et al, 1987; Tremblay etal, 1989; Tremblay et al, 1991; Stubbs et al, 1995) becausefat seems to have a lesser effect on satiety than do othermacronutrients (Blundell et al, 1993; Lawton et al, 1993).In addition, dietary fat seems to have a lesser potential toexert negative feedback on subsequent EI than do carbohy-drates (Rolls et al, 1994; Stubbs et al, 1995) or proteins(Stubbs et al, 1995). High-fat preloads even seem to exert alesser effect on subsequent EI of obese compared tonormal-weight individuals (Rolls & Hammer, 1995).Another factor which can further potentiate weight gain isthe increased preference for fat in obese and post-obeseindividuals (Drewnowski & Greenwood, 1983; Drew-nowski et al, 1992).

The reduced capacity of fat to acutely promote itsoxidation, its decreased satiating power and the observationthat obese and post-obese seemingly have a more pro-

nounced preference for this macronutrient are factors thatcan potentiate weight gain under high-fat conditions. Thereis also growing evidence that dietary fatty acid compositionmight play a role in this matter. Results from animal studieshave shown that rats fed a saf¯ower oil (78.6% polyunsa-turated fat (PUFA), 11.4% monounsaturated fat (MUFA)and 9% saturated fat (SFA)) diet as opposed to a beeftallow (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), andhigher SNS activity in brown adipose tissue (Takeuchi etal, 1994). Moreover, the higher body fat accumulationunder the beef tallow condition seems to be due to adecreased SNS activity in rats (Matsuo et al, 1995). Inhumans, it has been reported that the proportion of satu-rated to unsaturated fat possibly affects the net contributionof fat to EE (Jones et al, 1985), and it was demonstratedthat 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 ofdietary PUFA results in an increase of the oxidation ofmedium and long-chain fatty cids (Clandinin et al, 1995).Furthermore, it was reported that the isoenergetic substitu-tion of long-chain triglycerides by medium-chain triglycer-ides (MCT) had an inhibitory effect on food and EI (Stubbs

Table 1 Energy substrate characteristics

Characteristics Alcohol Fat Carbohydrates Proteins

In¯uence on subjectivefeelings of hunger and satiety

NoTremblay 96

Lesser effects thanproteins or CHO

Compared to fat: GreaterRolls 88

Better than other substratesYes

No effect Lawton 93 Blundell 93 Hill 90Poppitt 96 Blundell 93 Lower van Wyk 95

Rolls 94 Rolls 91 NoStubbs 95 Foltin 90 de Graaf 92

Potential to exert compensatoryeffect on EI

NoTremblay 96Poppitt 96

Lesser effects thanproteins or CHO

Lissner 87

Compared to fat:Greater

Rolls 94

Better than other substratesYes

Partial Tremblay 89, 91 Stubbs 95 Hill 86Foltin 93 Rolls 94, 95 Same as fat DeCastro 88

Stubbs 95 Rolls 91 Barkeling 90Foltin 90, 92 Bingham 94

Ability to promote its oxidation High Low High HighShelmet 88 Flatt 85, 88 Flatt 78 Nair 83Weststrate 90 Schutz 89 Acheson 84 Dauncey 83Prentice 92 Bennett 92 Lean 88Suter 92 Jebb 96 Schutz 89

Astrup 92

Energy density High High Low Low

Intake associated with increasedrisk of weight gain

YesKroumhout 83

YesDreon 88

NoToubro 97

YesBuemann 95

Suter 92 Romieu 88 Jeffry 95 NoTremblay 95 Tremblay 89 Lyon 95 DeCastro 88Cigolini 96 Colditz 90 Bingham 94

Miller 90No Klesges 92

Fisher 85 Tucker 92Coldtiz 91Sonko 94Liu 94

Effect of b-adrenergic blockadeon oxidation

NA No changesAcheson 88

DecreaseAcheson 88

No changesAcheson 88

Tremblay 92 Tremblay 92

CHO� carbohydrates.NA� data not available.

Food intake and body weightE Doucet and A Tremblay

847

& Harbron, 1996) and that incorporation of MCT into thediet stimulated thermogenesis (Seaton et al, 1986; Hill etal, 1989; Scal® et al, 1991).

Carbohydrates

It is generally well recognized that populations who con-sume a greater proportion of energy in the form ofcarbohydrates are leaner than those who do otherwise.This might be partly due to the fact that a high amountof energy in the form of carbohydrates for a few days isneeded to induce de novo lipogenesis (Acheson et al,1988b) compared to the impact of a high-fat intake whichseems to produce an immediate positive fat balance (Flattet al, 1985). Another interesting observation is that peoplewho had been vegetarians for a long period of time had aresting metabolic rate that was 11% higher than theiromnivorous counterparts, although this difference disap-peared when controlling for carbohydrate, and fat intakeand norepinephrine (Toth & Poehlman, 1994). In previousstudies by the same group, it was demonstrated that malevegetarians also had a tendency toward higher restingmetabolic rate (RMR) than the typical north-americandieter (Poehlman et al, 1988; Oberlin et al, 1990). This isan interesting observation since it has been documentedthat carbohydrate intake seems to stimulate SNS activity(Acheson et al, 1984a). The greater SNS activity underhigh-carbohydrate intake condition might be partly respon-sible for the greater RMR and the effects of carbohydrateson thermogenesis.

In this regard, it has been reported that DIT of carbohy-drates 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 low-fat high-carbohydrate diet was proposed to lead to a greaterEE than its high-fat, low-carbohydrate counterpart (Wes-terterp, 1993). Indeed, it would seem that carbohydrateshave a greater potential to increase thermogenesis possiblydue to the obligatory cost of glycogen storage (Acheson etal, 1984b). It was later demonstrated that carbohydrateintake promotes carbohydrate oxidation (Schutz et al,1989), that a high-carbohydrate-containing diet producedgreater DIT than the high-fat diet (Lean & James, 1988)and that a high-carbohydrate diet administered to post-obese women caused an increase in 24 h EE that wasentirely generated by an increase in carbohydrate oxidation(Astrup et al, 1992).

Carbohydrates exert a stimulating effect on thermogen-esis whereas its effects on satiety and food intake do notyield as clear a trend. A recent study showed that whencomparing the effects of equicaloric preloads (1.2 MJ) ofeither carbohydrates, proteins or fat in ten normal-weightwomen, carbohydrates and proteins had a greater satiatingpower than did fat (Rolls et al, 1988). The latter results arein accordance with those of Blundell et al (1993) whodemonstrated that in lean subjects a high-carbohydratebreakfast (� 87% of 3.36 MJ) suppressed hunger ratingsand energy intake signi®cantly more than the equicalorichigh-fat one (� 57% of 3.36 MJ) in a mid-morning snackserved 90 min after the preload whilst no signi®cantdifferences were found between conditions at lunch timewhich was served 270 min after the preload (Blundell et al,1993). Moreover a high-carbohydrate preload (� 80% of1.5 MJ) had a greater suppression power over subsequentfood intake than did the high-fat preload (� 70% of1.5 MJ) in normal weight restrained males and females,

normal weight unrestrained females and obese restrainedand unrestrained females as rated by the CognitiveRestraint Scale of the Stunkard Eating Inventory even ifnormal weight unrestrained males showed a quite accuratecompensation for energy content of the different preloads(Rolls et al, 1994). Accordingly, a recent experimentmimicking free-living conditions in which three differentdiets varying in macronutrient composition (20, 67 and13%; 40, 47 and 13%, and 60, 27 and 13% for fat,carbohydrates and proteins respectively) showed that car-bohydrates and proteins seem to have a greater potential toexert negative feedback on EI than does fat (Stubbs et al,1995). However, there is also a considerable body ofevidence that does not support the above proposed effectsof carbohydrates on food intake. In that respect, it has beendemonstrated that either low or high-carbohydrate (1.8 vs3.5 MJ), or low or high-fat (1.8 vs 3.5 MJ) preloads atlunch have the same satiating power. Moreover, this studyalso demonstrated that subsequent EI over the remainder ofthe day was not signi®cantly affected by either manipula-tion 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 differencesbetween responses in food intake following ingestion of ahigh-carbohydrate (81% of 0.9 MJ) or a high-fat (65% of0.9 MJ) preload (Rolls et al, 1991). Furthermore, it wasshown that there is clear evidence for subsequent caloriccompensation when energy content was manipulated, butequicaloric manipulations of macronutrient, namely carbo-hydrate and fat content, failed to show differences insubsequent EI (Foltin et al, 1992).

Even if the data concerning the effects of carbohydrateson satiety and hunger and also on thermogenesis are quiteabundant, those surrounding the impact of an ad libitumhigh-carbohydrate low-fat diet on body weight loss ormaintenance are scanty. However, in a very recent studyfrom Toubro & Astrup (1997), it was shown that after aninitial weight loss (� 12.6 kg) induced by energy restricteddiets and sympathomimetic agents, subjects who weregiven free access to a high-carbohydrate low-fat diet overa period of one year maintained more of the initial weightloss (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 inaccordance with those of Jeffry et al (1995) who foundthat under low-fat high-carbohydrate conditions, subjectslost 2.5 kg vs 0.5 kg for the calorie-counting group after anintervention period of 12 months. Furthermore, it wasdemonstrated that adherence to a low-fat high-carbohydratediet was strongly correlated to body fat loss (Lyon et al,1995). Conversely, it was reported that a ®xed energyintake was better at producing weight loss (10 kg vs6 kg) than what was observed under ad libitum low-fatdiet conditions (Schlundt et al, 1993).

Another important issue related to the impact of high-carbohydrate intake pertains to the enhancing effect of thismacronutrient on its own utilization. It might be argued thatthe increase of carbohydrate oxidation observed under high-carbohydrate diet conditions is also responsible for theinhibition of fat oxidation observed under such conditionswhich could be detrimental to weight stability. This issomewhat unlikely because of the relatively low amount offat consumed under high-carbohydrate conditions and alsobecause of the effects of carbohydrates on thermogenesis.Moreover, satiety seems to be reached with a lesser amountof calories under high-carbohydrate conditions which isprobably the most likely explanation for the inability of


848

high-carbohydrate diets to induce lipogenesis and ultimatelybody weight gain under free-living conditions even if thistype of regimen does to a certain extent inhibit fat oxidation.

Proteins

The effects of proteins on EI and EE, and ultimately onbody weight control are probably the lesser considered ofall macronutrients, but there is an increasing pool of dataconcerning this issue. DeCastro & Elemore (1988) demon-strated that in subjects self-reporting their food intake for7 d, proteins were the most ef®cient macronutrient atsuppressing food intake independently of their contributionto EI. Accordingly, it was reported, via a 16 d weigheddietary record by post-menopausal women, that proteinswere the only substrate that was negatively correlated tofood intake (Bingham et al, 1994). However, these resultsare not supported by another observational study in whichprotein intake seemed to be signi®cantly associated withmore adiposity (Buemann et al, 1995).

Experimental data also suggest an existing relationbetween the protein content of diet and food or energyintake. Different preloads of proteins (0.4, 1 and 1.7 MJ)had no signi®cant effect on subsequent food intake, nor diddifferent preloads of carbohydrates or fat (deGraaf et al,1992). However, there is a considerable number of studiesthat provide discordant results. In this context, obese aswell as normal-weight individuals have been shown tosigni®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 high-carbohydrate meal (63% of 2 MJ) (Hill & Blundell, 1986).Accordingly, it was demonstrated by the same authors thata high-protein meal produced greater subjective feelings offullness and a greater decrease in the desire to eat than didan isoenergetic high-carbohydrate meal (Hill & Blundell,1990). It was also shown that high-protein and high-carbohydrate isoenergetic lunches produced a reductionof EI at dinner that was 12% greater under the high-proteinlunch condition than for the high-carbohydrate condition(Barkeling et al, 1990). Accordingly, ingestion of a break-fast (energy equivalent to 75% of basal metabolic rate)composed of either 3.1 MJ of protein, carbohydrate or fatresulted in a signi®cantly greater decrease in hunger sensa-tion between breakfast and lunch for the carbohydrates andproteins when compared to the fat condition (van Wyk etal, 1995). Furthermore, this study also showed that theprotein breakfast was better at suppressing hunger over a24 h period in a calorimeter.

It is generally well recognized that protein storesrepresent a precisely regulated compartment. It wasreported that amino acid oxidation changes rapidly inresponse to changes in amino acid intake in the waythat substrate availability seems to be the primary determi-nant of substrate oxidation. Thus, the net effect of thismechanism is a conservation of nitrogen when proteinintake is low and in contrast, a high protein intake leadsto loss of amino acid, nitrogen and carbon (Young &Marchini, 1990).

The effects of proteins on EE are in agreement with theidea that protein balance is precisely regulated. Indeed, DITof proteins has been shown to be greater than for itsisoenergetic substitution by carbohydrates or fat (Nair etal, 1983). Accordingly, the isoenergetic substitution of ahigh-carbohydrate diet by a high-protein diet resulted in a12% increase in EE (Dauncey & Bingham, 1983).

Weight loss is normally associated with a decrease inRMR which can be partly attributable to the decrease in fatfree mass (FFM). However, weight loss under high-protein,very low-calorie diet (VLCD) has been shown to produce adecrease 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 wasreported that a severe hypoenergetic diet (2.1 MJ) canproduce signi®cantly more weight loss than a hypoener-getic regimen (4.2 MJ) without the expected decrease inRMR when isonitrogenous conditions are preserved forboth diets (Stanko et al, 1992). In addition, maintainingprotein intake to its usual level during energy restriction hasbeen shown to signi®cantly reduce the fall in sleepingmetabolic rate and 24 h EE (Whitehead et al, 1996).

In summary, protein intake seems to have a comparableeffect, if not more potent, on the subjective feelings ofhunger and satiety as does carbohydrate intake. The samecan be said about its in¯uence on subsequent EI andthermogenesis. Furthermore, the preservation of FFMduring weight loss when a high-protein intake is maintainedis another factor that urges clinicians to look at the proteincomponent with more scrutiny, especially in a weightreduction context.

Alcohol

In the recent past, the contribution of alcohol to the averageamerican diet was approximately 5.6% of the total EI(Block et al, 1985). This represents a contribution to EIwhich is not trivial and whose role in the regulation ofenergy balance is still a matter of controversy.

In an early study, Gruchow et al (1985) demonstratedthat the calories from alcohol were additive in the diets oflight to moderate drinkers. However, in the same study,alcohol energy was also shown to replace the calories fromother macronutrients in the diets of heavy drinkers. Otherstudies have also demonstrated that alcohol derived calorieswere additive, thus not replacing energy from other sub-strates (Jones et al, 1982; DeCastro & Orozco, 1990;Tremblay et al, 1995b).

The observation that alcohol energy seems to be additiveto the EI from other energy substrates is in agreement withthe fact that alcohol intake may exert a poor inhibitoryeffect on subsequent food and energy intake. Accordingly,it was shown that a high-fat and alcohol appetizer wasfollowed by an increased ad libitum EI even after theirhigh-energy density was controlled (Tremblay & St-Pierre,1996). Alcohol consumption also seems to have no effecton satiety and fullness when taken concomitantly with ahigh-fat meal. In addition, no compensatory effect of theexcess energy associated to alcohol intake was observed forthe subsequent meal (Tremblay & St-Pierre, 1996), whichis in accordance with a recent study that demonstrated thatthe consumption of an alcoholic beverage taken before ameal had no compensatory effect on the energy content ofthe following meal (Poppitt et al, 1996). These results areconsistent with those from an earlier study which showedthat an alcoholic beverage taken at four different timesduring 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 inrelation to energy metabolism. In an early study, Rosenberg& Durnin (1978) demonstrated that alcohol ingestion hadthe same effect on resting metabolic rate as did otherenergy substrates, and that variations in RMR were prob-


849

ably more closely related to EI than to macronutrientcomposition of the diet. These results are in agreementwith those of more recent studies that showed that DIT ofalcohol is almost the same as it is for carbohydrates(Shelmet et al, 1988; Weststrate et al, 1990; Prentice etal, 1992). However, more recent results have shown thatDIT of alcohol is equivalent to approximately 20% of itsenergy content (Suter et al, 1994) which is substantiallymore than that of carbohydrates (Flatt, 1978). Even if theDIT of alcohol does not characterize it as an adipogenicsubstrate, its effects on the oxidation of other substratesmight. Indeed, alcohol acutely suppresses the oxidation ofother substrates (Shelmet et al, 1988) and to a greaterextent fat oxidation (Shelmet et al, 1988; Suter et al, 1992;Sonko et al, 1994; Murgatroyd et al, 1996). This suppres-sion might be due to the fact that alcohol calories becomethe primary source of metabolic fuel as a mode of detox-i®cation which might acutely inhibit the oxidation of otherfuel sources.

Another interesting feature of alcohol is the fact that itcannot be bodily stored. Despite this characteristic, numer-ous studies have tried to establish if alcohol intake could beinvolved in the mechanisms leading to weight gain. Theresults concerning this issue are surrounded by con¯ictualreports. It was suggested that the habitual consumption ofalcohol in a moderate fashion in excess of energy needsmight lead to a condition which favors lipid storage andthat could consequently lead to weight gain over time(Suter et al, 1992). It was also reported in an epidemiolo-gical study that of all energy substrates, alcohol was theonly one positively correlated with body fatness and it wasthus concluded that alcohol consumption might be animportant factor in body weight gain (Kromhout, 1983).Furthermore, the combination of alcohol and high-fat dietsfavors weight gain in the form of central subcutaneous fat(Tremblay et al, 1995a). The latter study is in agreementwith recent results that have demonstrated that the increaseof daily energy taken in the form of alcohol is positivelycorrelated to waist circumference, waist to hip ratio andprobably visceral fat (Cigolini et al, 1996). In contrast,numerous studies have led to the conclusion that alcoholintake 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, inwomen (Colditz et al, 1991; Liu et al, 1994). Moreover,individuals who drink alcohol consume more total dailyenergy than those who are non-drinkers, but tend to weighless which is possibly due to the inef®cacy in the utilizationof alcohol calories (Fisher et al, 1985).

The idea of an inef®cacy in the disposal of alcoholcalories might be related to the hypothesis of a futile cycleas described by Lands & Zakhari (1991). This conceptsuggests that the futile cycle employs an irreversibleoxidation of alcohol to acetaldehyde and a reduction ofacetaldehyde to alcohol which can dissipate six ATP percycle thus eliminating any net gain of alcohol calories aftertwo or three cycles.

It is as of yet unclear how long term alcohol intakeaffects bodily fat stores. It should however be taken intoaccount that discordances observed between different crosssectional studies could be due to the fact that other lifestylefactors might contaminate the results. For instance, it ispossible that the inverse relation observed between alcoholintake and adiposity in women might be partly explainableby better compensatory skills of this group under suchconditions. This is likely the case since experimental

evidence supports that alcohol seems to have a poor orno capacity to in¯uence subjective feelings of hunger andsatiety, and also little in¯uence to promote compensation insubsequent EI (Foltin et al, 1993; Poppitt et al, 1996;Tremblay et al, 1996). Furthermore, alcohol intake seemsto favor alcohol oxidation at the expense of other energysubstrates, 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 Americaare regular coffee drinkers and that it is not uncommon foran individual to consume 200±250 mg (the equivalent ofapproximately 2±3 cups of coffee) of caffeine (CAF) perday (Sawynok, 1995).

Evidence suggests that CAF has the potential to increasemetabolic rate of lean individuals for up to three hours afteringestion (Acheson et al, 1980; Hollands et al, 1981;Dulloo & Geissler, 1989; Astrup et al, 1990; Yoshida etal, 1994; Bracco et al, 1995) and during the ®rst 12 h of a24 h stay in a metabolic ward after which no residual effectof CAF is detected (Dulloo et al, 1989). Moreover, it wouldseem that women have a lesser acute thermogenic responseto CAF than do men (Perkins et al, 1994).

The ability of CAF to alter substrate oxidation is also ofmajor interest. Accordingly, it would seem that CAFingestion produces an increase in lipid oxidation and inthe availability of free fatty acids for energy production(Astrup et al, 1990; Bracco et al, 1995). Furthermore, CAFseems to directly stimulate in vivo lipolysis (Van Soeren etal, 1996).

Some differences have been observed between leansubjects and their obese counterparts with respect to CAFresponsiveness. It has been demonstrated that CAF does notincrease metabolic rate in obese individuals as it does inlean (Astrup et al, 1990; Bracco et al, 1995), and that thereare variations in CAF response among the obese population(Yoshida et al, 1994). Moreover, it was shown that thethermogenic effects of CAF can be prolonged over night inlean subjects but not in the obese, and that this effect isachieved with a normal CAF consumption (Bracco et al,1995). However, it was reported that even if obese indivi-duals have a lesser response to CAF, their lipid oxidationwas nevertheless signi®cantly increased by ingestion of thiscompound (Bracco et al, 1995). In contrast, another studydemonstrated that obese persons have the same sensitivityto CAF than do lean individuals when it is taken alone inthe fasted state, but they rather seem to have a de®cientdietary-induced thermogenesis (DIT) which can be partlycorrected by addition of CAF to meals (Dulloo et al, 1989).

CAF also seems to exert an inhibitory effect on foodintake. Indeed, it was demonstrated that CAF has thepotential to reduce EI in men, but failed to produce thesame effect in women (Tremblay et al, 1988). The latterstudy is supported by data which have clearly establishedthat CAF ingestion in rats reduces food intake and hencebody weight gain (Racotta et al, 1994).

Capsaicin

Decreased and/or de®cient SNS activity has been proposedas a possible factor leading to obesity. Thus, the inclusionof sympathomimetic compounds such as capsaicin (CAP)into the diet might partially correct this situation. CAP is apungent principle of hot red pepper that has long been used


850

for enhancing food palatability and medicinally as a coun-terirritant. Early studies with animals have shown that ratsfed high-fat diets with added CAP gained less weight thancontrols, had lower plasma triglyceride levels (Kawada etal, 1986a) and oxidized more lipids (Kawada et al, 1986b).It was also reported that CAP might promote lipid mobi-lization from adipose tissue of rats during exercise, result-ing in a sparing of glycogen (Lim et al, 1995). Accordingly,it was demonstrated that CAP failed to produce changes incarbohydrate or glycogen metabolism at rest or duringexercise in rats (Matsuo et al, 1996). Furthermore, theeffects of CAP administration were subdued by the additionof 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 addedred pepper, DIT is signi®cantly greater than after a controlmeal, 53 vs 28% increase in metabolic rate, respectively.Moreover, it has been demonstrated that a meal with redpepper signi®cantly increased respiratory quotient andproduced a slight (10% over control) but not signi®cantincrease in EE (Lim et al, 1997). In addition, red pepperingestion would seem to increase carbohydrate oxidationmore than it does for fat (Lim et al, 1997).

The fact that CAP seems to stimulate carbohydrateoxidation in humans and fat oxidation in animals is puz-zling, but can probably be explained by methodologicaldifferences. The fact that most animal studies used capwhereas human studies were conducted with red peppermight be partly responsible for the discordant results.Moreover, the fat content of diets used in animal studieswas relatively high compared to the dietary fat intake ofsubjects involved in human studies.

It is very well established that sympathomimetic drugscan stimulate SNS activity in humans and animals. Sinceweight loss has been shown to produce a decrease in theSNS/parasympathetic nervous system (PNS) ratio (Aronneet al, 1995), the manipulation of some environmentalfactors such as capsaicin, caffeine and exercise has, at theleast, the potential to partly compensate for this effect. Asillustrated in Figure 1, it would be useful to favor adapta-tions in SNS/PNS balance which are compatible with aweight maintenance prescription, especially in the post-obese individuals. However, even if sympathomimeticdrugs and exercise both stimulate substrate oxidation andenergy expenditure, the selectivity of the effects of exerciseneeds to be discussed. It has been demonstrated thatpostexercise EE and fat oxidation are mediated by anincrease in SNS activity (Poehlman & Danforth, 1991;Tremblay et al, 1992). This increase in EE and fat oxida-tion might in turn be generated by an increase in b-adrenergic activity in skeletal muscle, such an effect notbeing observed in the heart (Plourde et al, 1991; Plourde etal, 1993). In contrast, sympathomimetic drugs seem toactivate all SNS mediated systems which not only resultsin an increase of EE and fat oxidation, but also of bloodpressure and heart rate. These observations emphasize therelevance of a stimulation targeting skeletal muscles ratherthan a non-speci®c SNS activity which also affects cardiacfunction.

Fibers

Dietary ®bers seem to have the potential to modify foodeating patterns and energy balance for the following rea-sons: fullness might be associated with bulk because high-®ber diets have a greater volume than high-fat diets, which

could lead to a decreased EI; they promote chewing andtherefore require an increased effort to eat; they slowgastric emptying which might trigger satiety; reduce hungerand prolong fullness; they decrease digestive and absorptiveef®ciency which might lead to an increased loss in fecalenergy; they are more satiating than their energy equivalentlow-®ber foods and they might carry nutrients further downthe ileum, which might trigger the ileal break that has beenshown to reduce ad libitum food intake. Accordingly, evi-dence suggests that obesity is much less prevalent in popula-tions who consume ®ber-rich diets as opposed to those whoconsume low-®ber diets and that animals normally eatingdiets 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 ahigh-®ber regimen on long-term energy balance and bodyweight control. In this context, it was found that subjectswho had greater body mass index (BMI) values also haddiets containing the most fat and the least dietary ®bers(Medeiros et al, 1996). In addition, weight-reducing diets towhich a dietary ®ber supplement had been added (5±6 g/d)were shown to produce a greater body weight loss than thecontrol diets (Rossner et al, 1987; Solum et al, 1987).Accordingly, a recent study on dogs showed that arestricted low-fat high-®ber diet produced signi®cantlygreater weight loss than its isoenergetic high-fat low-®bercounterpart (Borne et al, 1996). On the other hand, adietary ®ber supplement (6.5 g/d) administered with a6.7 MJ/d diet, failed to yield any signi®cant bene®ts asfar as weight reduction was concerned when compared tocontrol diet alone (Rossner et al, 1988).

Even if some doubts persist concerning the potential ofan increase dietary ®ber intake to help better control bodyweight, its effects on the subjective ®ndings of satiety,hunger and fullness has been well documented. Indeed, itwas shown that a low-®ber meal (3 g) was not less satiatingthan a high-®ber meal (12 g) (Burley et al, 1987). However

Figure 1 Illustration of the impact of dietary energy restriction on SNS/PNS balance in obese individuals and potential contribution of exerciseand sympathomimetic agents in the follow-up of post-obese subjects.


851

fullness ratings were higher after the high-®ber meal thanwith the low-®ber meal. In a more recent study, fullnessand satiety were found to be signi®cantly greater after ahigh-®ber breakfast and to stay elevated for up to fourhours after consumption in both men and women (Turconiet al, 1995). This is concordant with other studies that havedemonstrated that dietary ®ber supplementation (3.9±23 g)decreased hunger ratings (Rigaud et al, 1987), increasedsatiety as opposed to low-®ber diets (Raben et al, 1995),increased fullness and decreased the desire to eat (Raben etal, 1994b), and increased fecal energy excretion (Rigaud etal, 1987).

The type of dietary ®bers administered might have a roleto play in relation to the mechanisms that might alter appetiteand hunger ratings. Accordingly, it was reported that adlibitum food intake was signi®cantly reduced by psylliumgum (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 wheatbran (23 g) alone (Stevens et al, 1987). In contrast, a high-®ber breakfast (20 g) of either soluble or insoluble ®berssigni®cantly reduced EI of the subsequent meal compared tothe low-®ber breakfast (3 g) despite the fact that total dailyEI intake was not affected by ®ber type or quantity. How-ever, it would seem that insoluble ®bers have the potential toacutely increase feelings of satiety whilst soluble ®berswould seem to produce greater satiety feelings 13.5 h afteringestion of breakfast (Delargy et al, 1995). In a more recentstudy from the same group, it was demonstrated that subjectsconsumed less energy (1.6 kJ vs 2.2 kJ, respectively) in theacute period following a high-insoluble ®ber (22 g) break-fast compared with the high-soluble ®ber (22 g) breakfast.Despite this difference in the acute phase, total daily EI didnot differ when both soluble and insoluble ®ber conditionswere compared, which is in agreement with the previousstudy (Delargy et al, 1997). Another study showed that gel-forming liquid ®bers favor a decrease in hunger, an increasein fullness, and reduce the amount of food people actuallywanted to eat, although it had no effect on food intake(Tomlin, 1995).

Even if dietary ®bers seem to in¯uence the mechanismscontrolling food intake, they do not seem to increase DIT oralter substrate oxidation in any bene®cial way. Indeed, ahigh-®ber meal (26 g) failed to increase postprandial EE asdid a non-supplemented meal test (8 g) (Scal® et al, 1987).These results are in accordance with a more recent study inwhich it was demonstrated that under isoenergetic condi-tions, 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 fatoxidation (Raben et al, 1994b).

Evidence suggests that dietary ®bers have the potentialto exert a suppressive effect on the subjective feelings ofhunger and satiety. However, this effect does not seem tonecessarily translate into a decrease of food and energyintake. Even if the type of dietary ®bers (soluble vsinsoluble) seems to affect the mechanisms leading to satietyin different ways, the impact of dietary ®bers on EI seemsto be more closely related to amount rather than formingested. The fact that dietary ®bers also seem to acutelyinhibit fat oxidation deserves further consideration.

Clinical implications

Obesity is necessarily the result of a long-term positiveenergy balance and intervention strategies should be aimed

at factors which are most susceptible to reverse thisphenomenon. Reducing fat intake while increasing carbo-hydrate intake would seem to be one of the most ef®cientmethods to allow satiety while reducing EI. The reductionof alcohol intake should also be addressed, since it wouldseem that alcohol has a poor, or no capacity to in¯uencesubjective feelings of satiety and hunger, and also little, orno in¯uence to promote compensation in subsequent EI.Alcohol intake also seems to promote alcohol oxidation atthe expense of other macronutrients, especially fat. There-fore, the effects of alcohol are typical of a substrate whichcan induce a substantial positive energy and lipid balanceunder free-living conditions and should be regarded assuch.

The documented effects of dietary ®bers on the sub-jective feelings of hunger and satiety would seem to pointtoward their potentially interesting implication regardingenergy balance. However, the effects of dietary ®bers onthese variables do not seem to be associated with substan-tial changes in food or energy intake. One cannot overlookthe fact that the amount of dietary ®bers used in moststudies very rarely exceeds 20 g/d. It is possible that inorder to attain the expected decrease in food and energyintake, one would have to increase to an even greater extent®ber consumption. Further research is needed to clarify thisparticular issue.

The fact that dietary fat oxidation seems to be dependenton beta-adrenergic stimulation (Acheson et al, 1988a;Tremblay et al, 1992) is also of potential interest. More-over, it would seem that the post-obese and obesity-proneindividuals are often characterized by a subnormal restingenergy EE (Geissler et al, 1987) and a defective DIT(Dulloo & Miller, 1986). This could probably be due to adecrease in SNS activity which could be partly responsiblefor the resistance to further reduction and/or maintenanceof the adipose tissue mass in post-obese individuals, even ifthese individuals are very often still overweight. In order tocounteract this situation, the manipulation of environmentalfactors such as sympathomimetic drugs and exercise thathave the potential to elevate SNS activity would be useful.

Conclusions

The literature summarized above tends to show that anegative energy balance is favored by factors such aslow-fat/high-carbohydrate ratio, a high-protein and ®berintake, an increase in PUFA intake and the incorporation offood-related sympathomimetic agents. From a quantitativestandpoint, the currently available data also permit toconclude that the impact of some of these factors onenergy balance is more important than others. Figure 2integrates our interpretation of literature regarding thepotential effect of each factor on energy balance. In ouropinion, the manipulation of the fat-carbohydrate contribu-tion to energy intake is the variable which seems to exertthe greatest impact on energy balance. The impact ofprotein, alcohol and PUFA is also perceived important.Since the effect of a high-®ber regimen on EI has not yetbeen clearly demonstrated, its effect on energy balance andbody weight remains uncertain. Finally, even if caffeineand capsaicin can favor a negative energy balance, theirside effects probably limit the relevance of consuming largedoses of these compounds to induce strong changes inenergy balance.


852

References

Abbott WGH, Howard BV, Ruotolo G & E. R (1990): Energy expenditurein humans: effects of dietary fat and carbohydrate. Metabolism 21,E347±E351.

Acheson KJ, Ravussin E, Schoeller DA, Christin L, Bourquin L, BaertschiP, Danforth E & JeÂquier E (1988a): Two-week stimulation or blockadeof the sympathetic nervous system in man: in¯uence on body weight,body composition, and twenty four-hour energy expenditure. Metabo-lism 37, 91±98.

Acheson KJ, Ravussin E, Wahren J & JeÂquier E (1984a): Thermic effect ofglucose in man: obligatory and facultative thermogenesis. J. Clin.Invest. 74, 1572±1580.

Acheson KJ, Schutz Y, Bessard T, Anantharaman K, J.-P. F & JeÂquier EÂ

(1988b): Glycogen storage capacity and de novo lipogenesis duringmassive carbohydrate overfeeding in man. Am. J. Clin. Nutr. 48, 240±247.

Acheson KJ, Schutz Y, Bessard T, Ravussin E, JeÂquier E & Flatt JP(1984b): Nutritional in¯uence on lipogenesis and thermogenesis after acarbohydrate meal. Am. J. Physiol. 246, E62±E70.

Acheson KJ, Zahorska-Markiewicz B, Pittet P, Anantharaman K & JeÂquierEÂ (1980): Caffeine and coffee: their in¯uence on metabolic rate andsubstrate utilization in normal weight and obese individuals. Am. J.Clin. Nutr. 33, 989±997.

Aronne LJ, Mackintosh R, Rosenbaum M, Leibel RL & Hirsch J (1995):Autonomic nervous system activity in weight gain and weight loss.Metabolism 269, R222±R225.

Astrup A, Buemann B, Christensen NJ & Madsen AJ (1992): 24-hourenergy expenditure and sympathetic activity in postobese womenconsuming a high-carbohydrate diet. Am. J. Physiol. 262, E282±E288.

Astrup A, Buemann B, Christensen NJ & Tourbo S (1994a): Failure toincrease lipid oxidation in response to increasing dietary fat content informerly obese women. Am. J. Physiol. 266, E592±E599.

Astrup A, Buemann B, Western P, Tourbo S, Raben A & Christensen NJ(1994b): Obesity as an adaptation to a high-fat diet: evidence from across-sectional study. Am. J. Clin. Nutr. 59, 350±355.

Astrup A, Tourbo S, Cannon S, Hein P, Breum L & Madsen J (1990):Caffeine: a double-blind placebo-controlled study of its thermogenic,metabolic, and cardiovascular effects in healthy volunteers. Am. J. Clin.Nutr. 51, 759±767.

Ballor DL, Harvey-Barino JR, Ades PA, Cryan J & Calles-Escandon J(1996): Decrease in fat oxydation following a meal in weight-reducedindividuals: A possible mechanism for weight recidivism. Metabolism45, 174±178.

Barkeling B, Rossner S & Bjorvell H (1990): Ef®ciency of a high-proteinmeal (meat) and a high-carbohydrate meal (vegetarian) on satietymeasured and by automated computerized monitoring of subsequentfood intake, motivation to eat and food preferences. Int. J. Obes. 14,743±751.

Barrows K & Snook JT (1987): Effect of high-protein, very-low-caloriediet on body composition and anthropometric parameters of obesemiddle-aged women. Am. J. Clin. Nutr. 45, 381±391.

Bennett C, Reed GW, Peters JC, Abumrad NN, Sun M & Hill JO (1992):Short-term effects of dietary-fat ingestion on energy expenditure andnutrient balance. Am. J. Clin. Nutr. 55, 1071±1077.

Bingham SA, Gill C, Welch A, Day K, Cassidy A, Khaw KT, Sneyd MJ,Key TJA, Roe L & Day NE (1994): Comparison of dietary assessmentmethods in nutritional epidemiology: weighed records v. 24h recalls,food-frequency questionnaires and estimated-diet records Br. J. Nutr.72, 619±643.

Block G, Dresser CM, Hartman AM & Carroll MD (1985): Nutrientsources in the American diet: quantitative data from the NHANES IIsurvey. Macronutrients and fats. Am. J. Epidemiol. 122, 27±40.

Blundell JE, Burley VJ, Cotton JR & Lawton CL (1993): Dietary fat andcontrol of energy intake: evaluating the effects of fat on meal size andpostmeal satiety. Am. J. Clin. Nutr. 57 (suppl), 772S±778S.

Boozer CN, Brasseur A & Atkinson RL (1993): Dietary fat affects weightloss and adiposity during energy restriction in rats. Am. J. Clin. Nutr.58, 846±852.

Borne AT, Wolfsheimer KJ, Truett AA, Kiene J, Wojciechowski T,Davenport DJ, Ford RB & West DB (1996): Differential metaboliceffects of energy restriction in dogs using diets varying in fat and ®bercontent. Obes. Res. 4, 337±345.

Bracco D, Ferrarra JM, Arnaud MJ, JeÂquier EÂ & Schutz Y (1995): Effectsof caffeine on energy-metabolism, heart-rate, and methylxanthinemetabolism in lean and obese women. Am. J. Physiol. 32, E671±E678.

Buemann B, Tremblay A & Bouchard C (1995): Social class interacts withthe association between macronutrients intake and subcutaneous fat. Int.J. Obes. 19, 770±775.

Burley VJ, Leeds AR & Blundell JE (1987): The effect of high and low-®bre breakfasts on hunger, satiety and food intake in a subsequent meal.Int. J. Obes. 11, 87±93.

Cigolini M, Targher G, Bergamo Andreis IA, Tonoli M, Filippi F, MuggeoM & De Sandre G (1996): Moderate alcohol consumption and itsrelation to visceral fat and plasma androgens in healthy women. Int. J.Obes. 20, 206±212.

Clandinin MT, Wang LCH, Rajotte RV, French MA, Goh Y & Kielo ES(1995): Increasing the dietary polyunsaturated fat content alters whole-body utilization of 16:0 and 10:0. Am. J. Clin. Nutr. 61, 1052±1057.

Colditz GA, Giovannucci E, Rimm EB, Stampfer MJ, Rosner B, SpeizerFE, Gordis E & Willett WC (1991): Alcohol intake in relation to dietand obesity in women and men. Am. J. Clin. Nutr. 54, 49±55.

Colditz GA, Willett WC, Stampfer MJ, London SJ, Segal MR & SpeizerFE (1990): Patterns of weight change and their relation to diet in acohort of healthy women. Am. J. Clin. Nutr. 51, 1100±1105.

Dauncey MJ & Bingham SA (1983): Dependence of 24-h energy ex-penditure in man on the composition of nutrient intake. Br. J. Nutr. 50,1±13.

DeCastro JM & Orozco S (1990): Moderate alcohol intake on thespontaneous eating patterns of humans: evidence of unregulated sup-plementation. Am. J. Clin. Nutr. 52, 246±253.

DeCastro J & Elmore DK (1988): Subjective hunger relationships withmeal patterns and spontaneous feeding behaviour of humans: evidencefor a causal connection. Physiol. Behav. 43, 159±165.

deGraaf C, Hulshof T, Westrate JA & Jas P (1992): Short-term effects ofdifferent amount of proteins, fats and carbohydrates on satiety. Am. J.Clin. Nutr. 55, 33±38.

Delargy HJ, Burley VJ, O'Sullivan KR, Fletcher RJ & Blundell JE (1995):Effects of different soluble:insoluble ®ber ratios at breakfast on 24-hpattern of dietary and satiety. Eur. J. Clin. Nutr. 49, 754±766.

Delargy HJ, O'Sullivan KR, Fletcher RJ & Blundell JE (1997): Effects ofamount and type of dietary ®ber (soluble and insoluble) on short-termcontrol of appetite. Int. J. Food Sci. Nutr. 48, 67±77.

Dreon DM, Frey-Hewitt B, Ellsworth N, Williams PT, Terry RB & WoodPD (1988): Dietary fat:carbohydrate ratio and obesity in middle-agedmen. Am. J. Clin. Nutr. 47, 995±1000.

Drewnowski A & Greenwood MRC (1983): Cream and sugar: humanpreferences for high-fat foods. Physiol. Behav. 30, 629±633.

Drewnowski A, Kurth C, Holden-Wiltse J & Saari J (1992): Foodpreferences in human obesity: carbohydrates versus fats. Appetite 18,207±221.

Dulloo AG & Geissler CA (1989): Normal caffeine consumption: in¯u-ence on thermogenesis and daily energy expenditure in lean andpostobese human volunteers. Am. J. Clin. Nutr. 49, 44±50.

Figure 2 Identi®cation of factors promoting either negative (a) orpositive energy balance (b). The size of typescript re¯ects proposedrelative quantitative importance on energy balance.


853

Dulloo AG & Miller DS (1986): The thermogenic properties ofephedrine/methylxanthine mixtures: Human studies. Int. J. Obes. 10,467±481.

Fisher M & Gordon T (1985): The relation of drinking and smoking habitsto diet: the Lipid Research Clinics Prevalence Study. Am. J. Clin. Nutr.41, 623±630.

Flatt JP(1978) The biochemistry of energy expenditure. In: RecentAdvances in Obesity Research. (Bray GA ed.) pp 100±116. Wesport:Food and Nutrition Press Inc.

Flatt JP (1988): Importance of nutrient balance in body weight regulation.Diabetes/Metab. Rev. 4, 571±581.

Flatt JP (1991): The RQ/FQ concept and body weight maintenance. NestleFoundation Annual Report 49±71.

Flatt JP, Ravussin E, Acheson KJ & JeÂquier E (1985): Effects of dietary faton post-prandial substrate oxidation and on carbohydrate and fatbalances. J. Clin. Invest. 76, 1119±1124.

Foltin RW, Fischman MW, Moran TH, Rolls BJ & Kelly TH(1990): Caloric compensation for lunches varying in carbohydratecontent by humans in a residential laboratory. Am. J. Clin. Nutr. 52,969±980.

Foltin RW, Kelly TH & Fischman MW (1993): Ethanol as an energysource in humans: comparison with dextrose containing beverages.Appetite 20, 95±110.

Foltin RW, Rolls BJ, Moran TH, Kelly TH, McNelis AL & Fischman MW(1992): Caloric, but not macronutrient, compensation by humans forrequired-eating occasions with meals and snack varying in fat andcarbohydrate. Am. J. Clin. Nutr. 55, 331±342.

Geissler CA, Miller DS & Shaj M (1987): The daily metabolic rate of thepost-obese and the lean. Am. J. Clin. Nutr. 45, 914±920.

Gruchow HW, Sobocinski KA, Barboriak JJ & Scheller JG (1985):Alcohol consumption, nutrient intake and relative weight among USadults. Am. J. Clin. Nutr. 42, 289±295.

Henry CJK & Emery B (1985): Effect of spiced food on metabolic rate.Hum. Nutr.: Clin. Nutr. 40C, 165±168.

Hill AJ & Blundell JE (1986): Macronutrients and satiety: the effects ofhigh-protein or high-carbohydrate meal on subjective motivation to eatand food preferences. Nut. Behav. 3, 133±144.

Hill AJ & Blundell JE (1990): Comparison of the action of macronutrientson the expression of appetite in lean and obese humans. Ann. NY Acad.Sci. 597, 529±531.

Hill JO, Lin D, Yakabu F & Peters JC (1991): Development of dietaryobesity in rats: in¯uence of amount and composition of dietary fat. Int.J. Obes. 16, 321±333.

Hill JO, Peters JC, Yang D, Sharp T, Kaler M, Abumrad NN & Greene HL(1989): Thermogenesis in humans during overfeeding with medium-chain triglycerides. Metabolism 38, 641±648.

Hollands MA, Arch JRS, Phil D & Cawthorne MA (1981): A simpleapparatus for comparative measurements of energy expenditure inhuman subjects: the thermic effect of caffeine. Am. J. Clin. Nutr. 34,2291±2294.

Holloszy JO (1974): The effect of endurance exercise on body composi-tion. In Vague J, & Boyer J. eds. The Regulation of the Adipose TissueMass. (eds) pp 254±258. Amsterdam: Expertica Medica.

Jebb SA, Prentice AM, Goldberg GR, Murgatroyd PR, Black AE &Coward WA (1996): Changes in macronutrient balance during over-and underfeeding assessed by 12-d continuous whole-body calorimetry.Am. J. Clin. Nutr. 64, 259±266.

Jeffry RW, Hellerstedt WL, French SA & Baxter JE (1995): A randomizedtrial of counselling for fat restriction versus calorie restriction in thetreatment of obesity. Int. J. Obes. 19, 132±137.

Jones BR, Barrett-Connor E, Criqui MH & Holbrook MJ (1982): Acommunity study of calorie and nutrient intake in drinkers and non-drinkers of alcohol. Am. J. Clin. Nutr. 35, 135±139.

Jones PJH, Pencharz PB & Clandinin MT (1985): Whole body oxidation ofdietary fatty acids: implications for energy utilization. Am. J. Clin. Nutr.42, 769±777.

Jones PJH & Schoeller DA (1988): Polyunsaturated:saturated ratio of dietfat in¯uences energy substrate utilization in the human. Metabolism 37,145±151.

Kawada T, Hagihara K-I & Iwai K (1986a): Effects of capsaicin on lipidmetabolism in rats fed high fat diet. J. Nutr. 116, 1272±1278.

Kawada T, Watanabe T, Takaishi T, Tanaka T & Iwai K (1986b):Capsaicin-induced b-adrendergic action on energy metabolism in rats:In¯uence of capsaicin on oxygen consumption, respiratory quotient, andsubstrate utilization. Exp. Biol. Med. 183, 250±256.

Kendall A, Levitsky DA, Strupp BJ & Lissner L (1991): Weight loss onlow-fat diet: consequence of the imprecision of the control of foodintake in humans. Am. J. Clin. Nutr. 53, 1124±1129.

Kimm SYS (1995): The role of dietary ®ber in the development andtreatment of childhood obesity. Pediatrics 96, 1010±1014.

Klesges RC, Klesges LM, Haddock CK & Eck LH (1992): A longitudinalanalysis of the impact of dietary intake and physical activity on weightchange in adults. Am. J. Clin. Nutr. 55, 818±822.

Kromhout D (1983): Energy and macronutrient intake in lean and obesemiddle-aged men (the Zutphen Study). Am. J. Clin. Nutr. 37, 295±299.

Lands WEM & Zakhari S (1991): The case of the missing calories. Am. J.Clin. Nutr. 54, 47±48.

Lawton CL, Burley VJ, Wales JK & Blundell JE (1993): Dietary fat andappetite control in obese subjects; weak effects on satiety. Int. J. Obes.17, 409±416.

Lean MEJ & James WPT (1988): Metabolic effects of isoenergeticnutrient exchange over 24 hours in relation to obesity in women. Int.J. Obes. 8, 641±648.

Leeds AR (1987): Dietary ®bre: mechanisms of action. Int. J. Obes. 11,3±7.

Lim K, Kim K, Suh H, Lee S, Yoshioka M, Saitoh S & Suzuki M (1995):The effect of capsaicin on energy substrates utilization at rest andduring exercise in rats. Kor. J. Phys. Edu. 34, 248±256.

Lim K, Yoshioka M, Kikuzato S, Kiyonaga A, Tanaka H, Shindo M &Suzuki M (1997): Dietary red pepper ingestion increases carbohydrateoxydation at rest and during exercise in runners. Med. Sci. Sports Exerc.29, 355±361.

Lissner L, Levitsky DA, Strupp BJ, Kalkwarf HJ & Roe DA (1987):Dietary fat and the regulation of energy intake in human subjects. Am. J.Clin. Nutr. 46, 886±892.

Liu S, Serdula MK, Williamson DF, Mokdad AH & Byers T (1994): Aprospective study of alcohol intake and change in body weight amongUS adults. Am. J. Epidemiol. 140, 912±920.

Lyon X-H, Di Vetta V, Milon H, Jequier E & Schutz Y (1995):Compliance to dietary advice directed towards increasing the carbohy-drate to fat ratio of the every day diet. Int. J. Obes. 19, 260±269.

Matsuo T, Shimomura Y, Saitoh S, Tokuyama K, Takeuchi H & Suzuki M(1995): Sympathetic activity is lower in rats fed a beef tallow diet thanin rats fed a saf¯ower oil diet. Metabolism 44, 934±939.

Matsuo T, Yoshioka M & Suzuki M (1996): Capsaicin in diet does notaffect glycogen contents in the liver and skeletal muscle of rats beforeand after exercise. J. Nutr. Sci. Vitaminol. 42, 249±256.

Medeiros DM, Auld GW, Bock MA, Bruhn CM, Gabel K, Lauritzen G,Lee YS, Mcnulty J, Newman R, Nitzke S, Ortiz M, Read M, Schutz H& Sheehan ET (1996): Diet fat and ®ber knowledge, beliefs andpractices are minimally in¯uenced by health-status. Nutr. Res. 16,751±758.

Miller WC, Lindeman AK, Wallace J & Niederpruem M (1990): Dietcomposition, energy intake, and exercise in relation to body fat in menand women. Am. J. Clin. Nutr. 52, 426±430.

Murgatroyd PR, Van de Ven MLHM, Goldberg GR & Prentice AM(1996): Alcohol and the regulation of energy balance: overnight effectson diet-induced thermogenesis and fuel storage. Br. J. Nutr. 75, 33±45.

Nair KS, Halliday D & Garrow JS (1983): Thermic response to isoener-getic protein, carbohydrate or fat meals in lean and obese subjects. Clin.Sci. 65, 307±312.

NHANES III (1988±1991): Third report on nutrition monitoring in theUnited States. Volume 1, p. 132.

Oberlin P, Melby CL & Poehlman ET (1990): Resting energy expenditurein young vegetarians and non-vegetarians. Nutr. Res. 10, 39±49.

Perkins KA, Sexton JE, Epstein LH, DiMarco A, Fonte C, Stiller RL,Scierka A & Jacob RG (1994): Acute thermogenic effects of nicotinecombined with caffeine during light physical activity in male andfemale smokers. Am. J. Clin. Nutr. 60, 312±319.

Plourde G, Rousseau Migneron S & Nadeau A (1993): Effect of endurancetraining on beta-adrenergic system in three different skeletal muscle.J. Appl. Physiol. 74, 1641±1646.

Plourde G, Rousseau-Migneron S & Nadeau A (1991): b-Adrenoceptoradenylate cyclase system adaptation to physical training in fat ventri-cular tissue. J. Appl. Physiol. 70, 1633±1638.

Poehlman ET, Arciero PJ, Melby CL & Badylak DMV (1988): Restingmetabolic rate and postprandial thermogenesis in vegetarians and non-vegetarians. Am. J. Clin. Nutr. 48, 209±213.

Poehlman ET & Danforth E (1991): Endurance training increases meta-bolic rate and norepinephrine appearance rate in older individual. Am. J.Physiol. 261, E233±E239.

Poppitt SD, Eckhardt JW, McGonagle J, Murgatroyd PR & Prentice AM(1996): Short-term effects of alcohol consumption on appetite andenergy intake. Physiol. Behav. 60, 1063±1070.

Prentice AM, Sonko BJ, Goldberg GR & Murgatroyd PR (1992): The caseof the missing calories revisited. Am. J. Clin. Nutr. 55, 478±485.

Raben A, Anderson HB, Christensen NJ, Madsen J, Holst JJ & Astrup A(1994a): Evidence for an abnormal postprandial response to a high-fatmeal in women predisposed to obesity. Am. J. Physiol. 267, E549±E559.


854

Raben A, Christensen NJ, Madsen J, Holst JJ & Astrup A (1994b):Decreased postprandial thermogenesis and fat oxidation but increasedfullness after high-®ber meal compared with a low-®ber meal. Am. J.Clin. Nutr. 59, 1386±1394.

Raben A, Due Jensen N, Marckmann P, SanstroÈm B & Astrup A (1995):Spontaneous weight loss during 11 weeks' ad libitum intake of a lowfat/high ®ber diet in young, normal weight subjects. Int. J. Obes. 19,916±923.

Racefas I, Esteve M, Fernandez-Lopez X, Remesar X & Alemany M(1992): Deposition of dietary fatty acids in young Zucker rats fed acafeteria diet. Int. J. Obes. 16, 775±787.

Racotta IS, Leblanc J & Richard D (1994): The effect of caffeine onfood intake in rats: Involvement of corticotropin-releasing factor andthe sympatho-adrenal system. Pharmacol. Biochem. Behav. 48, 887±892.

Rigaud D, Ryttig K, Leeds AR, Bard A & Apfelbaum M (1987): Effects ofmoderate dietary ®bre supplement on hunger rating, energy input andfaecal energy output in young, healthy volunteers. Int. J. Obes. 11, 73±78.

Rolls BJ & Hammer VA (1995): Fat, carbohydrate, and the regulation ofenergy intake. Am. J. Clin. Nutr. 62 (suppl), 1086S±1095S.

Rolls BJ, Hetherington M & Burling VJ (1988): The speci®city of satiety:the in¯uence of foods of different macronutrient content on the devel-opment of satiety. Physiol. Behav. 43, 145±153.

Rolls BJ, Kim S, McNelis AL, Fischman MW, Foltin RW & Moran TH(1991): Time course of effects of preloads high in fat or carbohydrate onfood intake and hunger ratings in humans. Am. J. Physiol. 260, R756±R763.

Rolls BJ, Kim-Harris S, Fischman MW, Foltin RW, Moran TH & StonerSA (1994): Satiety after preloads with different amounts of fat andcarbohydrate: implications for obesity. Am. J. Clin. Nutr. 60, 476±487.

Romieu I, Willett WC, Stampfer MJ, Colditz GA, Sampson L, Rosner B,Hennekens CH & Speizer FE (1988): Energy intake and other determi-nants of relative weight. Am. J. Clin. Nutr. 47, 406±412.

Rosenberg K & Durnin JVGA (1978): The effect of alcohol on restingmetabolic rate. Br. J. Nutr. 40, 293±298.

Rossner S, Anderson IL & Ryttig K (1988): Effects of dietary ®bresupplements to a weight reduction programme on blood pressure.Acta. Med. Scand. 223, 353±357.

Rossner S, Von Zweigberg P, Ohlin A & Ryttig K (1987): Weightreduction with dietary ®bre supplements. Acta. Med. Scand. 222, 83±88.

Roust LR, Hammel KD & Jensen MD (1994): Effects of isoenergetic, low-fat diets on energy metabolism in lean and obese women. Am. J. Clin.Nutr. 60, 470±475.

Sawynok J (1995): Pharmalogical rationale for the clinical use of caffeine.Drugs 49, 37±46.

Scal® L, Coltorti A & Contaldo F (1991): Postprandial thermogenesis inlean and obese subjects after meals supplemented with medium-chainand long-chain triglycerides. Am. J. Clin. Nutr. 53, 1130±1133.

Scal® L, Coltorti E, D'Arrigo V, Carandente C, Mazzacano M, Dipalo M& Contaldo F (1987): Effect of dietary ®bre on postprandial thermo-genesis. Int. J. Obes. 11, 95±99.

Schlundt DG, Hill JO, Pope-Cordle J, Arnold D, Virts KL & Katahn L(1993): Randomised evaluation of low fat ad libitum high carbohydratediet for weight reduction. Int. J. Obes. 17, 623±629.

Schutz Y, Flatt JP & JeÂquier E (1989): Failure of dietary fat intake topromote fat oxidation: a factor favoring the development of obesity.Am. J. Clin. Nutr. 50, 307±314.

Schutz Y, Tremblay A, Weinsier RL & Nelson KM (1992): Role of fatoxidation in the long-term stabilization of body weight in obese women.Am. J. Clin. Nutr. 55, 670±674.

Seaton TB, Welle SL, Warenko MK & Campbell RG (1986): Thermiceffect of medium-chain and long-chain triglycerides in man. Am. J.Clin. Nutr. 44, 630±634.

Shelmet JJ, Reichard GA, Skutches CL, Hoedtke RD, Owen OE & BodenG (1988): Ethanol causes acute inhibition of carbohydrate, fat, andprotein oxydation and insulin resistance. J. Clin. Invest. 81, 1137±1145.

Shimomura Y, Tamura T & Suzuki M (1990): Less body fat accumulationin rats fed a saf¯ower oil diet than in rats fed a beef tallow diet. J. Nutr.120, 920±925.

Solum TT, Ryttig KR, Solum E & Larsen S (1987): The in¯uence of high-®bre diet on body weight, serum lipids and blood pressure in slightlyoverweight persons. Int. J. Obes. 11, 67±71.

Sonko BJ, Prentice AM, Murgatroyd PR, Goldberg GR, van de VenMLHM & Coward WA (1994): Effect of alcohol on postmeal fatstorage. Am. J. Clin. Nutr. 59, 619±625.

Stanko RT, Tietze DL & Arch JE (1992): Body composition, nitrogenmetabolism, and energy utilization with feeding of mildly restricted(4.2 MJ/d) and severely restricted (2.1 MJ/d) isonitrogenous diets. Am.J. Clin. Nutr. 56, 636±640.

Stevens J, Levitsky DA, VanSoest PJ, Robertson JB, Kalkwarf HJ & RoeDA (1987): Effect of psyllium gum and wheat bran on spontaneousenergy intake. Am. J. Clin. Nutr. 46, 812±817.

Stubbs JR, Harbon GH, Murgatroyd PR & Prentice AM (1995): Covert man-ipulation of dietary fat and energy density: effect on substrate ¯ux andfood intake in men eating ad libitum. Am. J. Clin. Nutr. 62, 316±329.

Stubbs RJ & Harbron CG (1996): Covert manipulation of the ratio ofmedium- to long-chain triglycerides in isoenergetically dense diets:effect on food intake in ad libitum feeding in men. Int. J. Obes. 20, 437±444.

Suter PM, JeÂquier E & Schutz Y (1994): Effect of alcohol on energyexpenditure. Am. J. Physiol. 266, 1204±1212.

Suter PM, Schutz Y & JeÂquier E (1992): The effect of ethanol on fatstorage in healthy subjects. New Engl. J. Med. 326, 983±987.

Takeuchi H, Matsuo T, Tokuyama K, Shimomura Y & Suzuki M (1994):Diet-induced thermogenesis is lower in rats fed a lard diet than in thosefed a high oleic acid saf¯ower diet, a saf¯ower oil diet or a linseed oildiet. J. Nutr. 125, 920±925.

Thomas CD, Peters JC, Reed GW, Abumrad NN, Sun M & Hill JO (1992):Nutrient balance and energy expenditure during ad libitum feeding ofhigh-fat and high-carbohydrate diets in humans. Am. J. Clin. Nutr. 55,934±942.

Tomlin J (1995): The effect of the gel-forming liquid ®bre on feedingbehavior in man. Br. J. Nutr. 74, 427±436.

Toth MJ & Poehlman ET (1994): Sympathetic nervous system activity andresting metabolic rate in vegetarians. Metabolism 43,

Toubro S & Astrup A (1997): Randomised comparison of diets formaintaining obese subjects' weight after major weight loss: ad lib,low fat high carbohydrate v ®xed energy intake. Br. J. Med. 314, 29±34.

Tremblay A, Buemann B, TheÂriault G & Bouchard C (1995a): Bodyfatness in active individuals reporting low-lipid and alcohol intake. Eur.J. Clin. Nutr. 49, 824±831.

Tremblay A, Coveney JP, DespreÂs JP, Nadeau A & Prud`homme D (1992):Increased restoring metabolic rate and lipid oxidation in exercise-trained individuals: evidence for a role of beta adrenergic stimulation.Can. J. Physiol. Pharmacol. 70, 1342±1347.

Tremblay A, LavalleÂe N, AlmeÂras N, Allard L, DespreÂs JP & Bouchard C(1991): Nutritional determinants of the increase in energy intakeassociated with a high fat-diet. Am. J. Clin. Nutr. 53, 1134±1137.

Tremblay A, Masson E, Leduc S, Houde A & DespreÂs J-P (1988): Caffeinereduces spontaneous energy intake in men but not in women. Nutr. Res.8, 553±558.

Tremblay A, Plourde G, DespreÂs JP & Bouchard C (1989): Impact ofdietary fat content and fat oxidation on energy intake in humans. Am. J.Clin. Nutr. 49, 799±805.

Tremblay A & St-Pierre S (1996): The hyperphagic effect of high-fat andalcohol persists after control for energy density. Am. J. Clin. Nutr. 63,479±482.

Tremblay A, Wouters E, Wenker M, St-Pierre S, Bouchard C & DespreÂsJ-P (1995b): Alcohol and high-fat diet: a combination favoring over-feeding. Am. J. Clin. Nutr. 62, 639±644.

Tucker LA & Kano M (1992): Dietary fat and body fat: a multivariatestudy of 205 adult females. Am. J. Clin. Nutr. 56, 616±622.

Turconi G, Bazzano R, Caramella R, Porrini M, Crovetti R & Lanzola E(1995): The effects of high intakes of ®bre ingested at breakfast onsatiety. Eur. J. Clin. Nutr. 49, S281±S285.

Van Italie TB (1978): Dietary ®ber and obesity. Am. J. Clin. Nutr. 31,S43±S52.

Van Soeren MV, Mohr T, Kjaer M & Graham TE (1996): Acute effects ofcaffeine ingestion at rest on humans with impaired epinephrineresponse. Am. J. Physiol. 80, 999±1005.

van Wyk MCW, Stubbs RJ, Johnstone AM & Harbon CG (1995): Break-fasts high in protein, fat and carbohydrate: effect on within-day appetiteand energy balance. Int. J. Obes. 19, P134 Abstr.

Westerterp KR (1993): Food quotient, respiratory quotient and energybalance. Am. J. Clin. Nutr. 53 (suppl), 759S±765S.

Westrate JA, Wunnink I, Deurenberg P & Hautvast JGAJ (1990): Alcoholand its acute effects on resting metabolic rate and diet-induced thermo-genesis. Br. J. Nutr. 64, 413±425.

Whitehead JM, McNeil G & Smith JS (1996): The effect of protein intake on24-henergyexpenditureduringenergyrestriction. Int.J.Obes.20, 727±732.

Yoshida T, Sakane N, Umekawa T & Kondo M (1994): Relationshipbetween basal metabolic rate, thermogenic response to caffeine, andbody weight loss following combined low calorie and exercise treat-ment in obese women. Int. J. Obes. 18, 345±350.

Young VR & Marchini JS (1990): Mechanisms and nutritional signi®canceof metabolic responses to altered intakes of protein and amino acids,with reference to nutritional adaptations in humans. Am. J. Clin. Nutr.51, 270±289.


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Food intake, energy balance and body weight control - Nature

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