High and Low Carbohydrate and Fat Intakes: Limits Imposed by Appetite and Palatability and Their Implications for Energy Balance

Home , Olestra

High and low carbohydrate and fat intakes: limits imposed by appetite and palatability and their implications for energy balance

JE Blundell1* and RJ Stubbs2

1BioPsychology Group, Psychology Department, University of Leeds, Leeds LS2 9JT, UK; and 2The Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB21 9SB, UK

This report examines several issues concerning the effects of dietary fats and carbohydrates (CHOs) on body weight and the limits set on the intake of these nutrients by factors in¯uencing appetite control: (i) the physiological relationship between feeding behaviour (FB) and body weight; (ii) the distribution of nutrients in Western foods and the implications this may have for FB; (iii) the contribution of nutrients in the diet, to total EI under both extreme and typical Western conditions; (iv) the known effects that fats, CHOs and dietary energy density (ED) exert on appetite and energy balance (EB); (v) the potential role of sensory factors in promoting or limiting fat, CHO and energy intakes (EI) in modern human populations Population studies and large surveys have identi®ed individuals with wide ranges of fat and CHO intakes. Intakes of fat can vary from an average of 180 g=day to 25 g=day in a representative sample. But on individual days fat intake can rise to well over 200 g according to a selection of high fat foods. In a single meal, people can consume an amount of fat greater than the population daily average. From this analysis it can be deduced that the appetite control mechanism will permit the consumption of large amounts of fat (if an abundance of high fat foods exist in the food supply). Except for speci®c physiological circumstances (e.g. endurance explorers) where there is an urgent need for EIs, in the face of decreasing body weight, it is unlikely that the body will generate a speci®c drive for fat. Because CHO foods have a lower ED than fat foods (on average) and because of their greater satiating capacity, the free intake of high CHO foods is likely to be self-limiting (at lower EIs than those generated by fatty foods). This does not mean that excess EIs are impossible when people feed ad libitum on high CHO diets.

General introduction: Background and objectives of Kristal et al, 1992; Mela 1995; Brownell & Cohen 1995). this paper Therefore it is not surprising that in practice it appears dif®cult to entice the population to spontaneously reduce In Western countries there has been renewed media, con- fat intake and increase levels of physical activity. The food sumer and government concern during the 1990s regarding industry has been proli®c in the production of lower fat the in¯uence that levels of dietary fats and=or CHOs can foods, in the hope that they will assist in reducing dietary exert on human health and well-being (WHO, 1990; fat (and possibly EIs), while maintaining suf®cient sensory Department of Health 1992, 1994, 1995). Throughout this appeal that consumers will choose and ingest them time, the alarming rise in the proportion of overweight and (Leveille & Finley 1997; International Food Information obese adults in Western society has led to considerable Council, 1997). debate regarding the underlying causes of these secular One major feature in understanding the role of appetite trends. The two major factors now cited as being conducive in this context is the recognition that fat and CHO intakes to weight gain in Western populations are reduced levels of are determined by forms of behaviour. This behaviour is physical activity, which decrease total energy expenditure not solely under biological control. Indeed, feeding beha- (EE), and the ingestion of a high-fat (HF), energy-dense viour (FB) forms part of an interaction between biology diet, which appears to facilitate excess energy intakes (EIs) (physiological mechanisms involved in food processing by (Swinburn & Ravussin, 1993; Prentice et al, 1989; Prentice the organism and energy balance [EB]) and the environ- & Jebb 1995; Department of Health, 1995). These recom- ment (nature of the food supply, composition of foods, mendations have led to a near fat-phobia amongst some culturally de®ned patterns of eating etc.). This intimate Western consumers. Ironically, it has been recognised for relationship can be referred to as a transaction. more than 50 y that it is dif®cult to change habitual forms Therefore, eating is in¯uenced by events in the biological of behaviour (Gorder et al, 1986; Buzzard et al, 1990; domain and in the environment. Since eating in humans is an episodic activity, the limits set by mechanisms of appetite control are those which limit the size of eating episodes, their *Correspondence: Dr JE Blundell, BioPsychology Group, Psychology frequency and the selection of particular foods. The processes Department, University of Leeds, Leeds LS2 9JT, UK. of satiation and satiety (acting conjointly) determine, in large High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S149 part, the size and frequency of eating episodes. In considering Physiological drives and learned behaviour as intakes of CHOs and fats, the question can be posed: `how do determinants of feeding fats and CHOs in¯uence the size, frequency and composition of eating episodes (and therefore total EI), and what are the The nature of feeding behaviour and its physiological mechanisms responsible?' determinants From a physiological or metabolic standpoint fats and Mammalian feeding occurs regularly and intermittently and CHOs can be regarded as types of fuel to be used in despite a general lack of conscious nutritional knowledge physiological processes. Some problems of EB can be on the part of the individual, usually appears to match reformulated as problems of fuel balance. However, in energy and nutrient intakes with requirements. How is this considering the role of appetite, an extension of this achieved? The common explanation is that appetite, EI, FB thinking is required. Eating behaviour is the way by or EB are regulated to ensure that physiological require- which fats and CHOs are transported into the body. Once ments are met. However, there is an embarrassing lack of fats and CHOs are associated with behaviour, their effects direct evidence for this regulation (Caterson et al, 1996). It can be generated by features of food other than the value of may be that neither FB, nor appetite are regulated in a the nutrient or fuel. Indeed FB should be considered as the strictly physiological sense since: (i) neither are held consumption of `foods' not `fuel'. The nutrient itself can constant within certain narrow limits; and (ii) FB is not contribute to the taste, texture, viscosity, weight and bulk of an inevitable outcome which is determined by an altered the food, all of which characteristics can help to determine physiological signal or need (physiological determinism). when and how much of a food is consumed. When con- FB is responsive to a number of induced states such as sidering EB per se, it may not matter very much whether pregnancy, cold exposure, growth and development, and CHO enters the body as orange juice or bread. But, in weight loss. These responses have often been cited as considering appetite control and palatability, the sensory evidence of a system (appetite and FB) that is regulated. features and form of the food would be extremely impor- It may be that aspects of body size and composition are tant, often, perhaps of overriding importance. regulated and that changes in FB are functionally coupled For the purposes of this review appetite control may be to those regulatory processes. Indeed, FB might be said to de®ned as the sum of the processes which determine be adaptive rather than regulated since quantitative and patterns of FB. What are the particular processes, which qualitative food intake (FI) is ¯exible, responsive and limit the amounts of fats, and CHOs that people consume? anticipatory, sometimes enabling the animal to adapt to Are the limits set by internal physiological signalling, the changes in the state of the internal and external environ- composition of foods in the environment or the salience of ment. Eating behaviour connects the phenotype (the biolo- cues which in¯uence feeding? gical system of appetite control) to the nutritional To gain a clearer understanding of the effect that fats component of the environment. Inasmuch, eating behaviour and CHOs exert on appetite and EB, it is important to is subject to both interoceptive and exteroceptive condi- examine several issues concerning the effects of dietary fats tioning. It would appear that under normal ad libitum and CHOs on body weight and the limits set on the intake feeding conditions encountered in Western society, day- of these nutrients by factors in¯uencing appetite control: (i) to-day FB is not determined by powerful unconditioned the physiological relationship between FB and body physiological signals but by learned behaviour in response weight; (ii) the distribution and density of nutrients in to a range of in¯uences, which include physiological Western foods and the implications this may have for FB; processes associated with ingestion, absorption, storage (iii) the contribution of nutrients in the diet, to total EI and metabolism of nutrients. Other in¯uences include under both extreme and typical Western conditions; and salient social and cultural variables. It can be appreciated (iv) the known effects that fats, CHOs and dietary energy that as energy imbalances accrue, the in¯uence of addi- density (ED) exert on appetite and EB. From these con- tional physiological signals (for example, depletion of fat siderations we will discuss: (1) proposed nutrient-based, mass or lean tissue mass) on FB will escalate. It therefore physiological models of appetite control and their likely appears that there is a margin of EB (that typi®es the relevance to observed patterns of FB and macronutrient majority of Western adults) within which a large number of intakes; and (2) the potential role of sensory factors in factors in¯uence appetite and EI. Within this zone changes promoting or limiting fat, CHO and EI in modern human in energy and nutrient balance do not induce large detect- populations. able sensations that lead to corrective changes in FB. Throughout this paper we hope to emphasise the need Outside of this range (which may vary among different for increased semantic precision in the area of appetite individuals) physiological signals may exert more potent control, FB and EB. Greater semantic precision is likely to restorative in¯uences on appetite and EB. These in¯uences avoid confusion over important issues pertinent to diet appear to be greater in response to energy de®cits and so composition and FB. For instance, whether HF or high appetite control in humans appears skewed towards a ED diets promote excess EI. It is perhaps also timely to positive EB and defence against negative EBs, since consider replacing the `traditional' obese-lean dichotomy in positive EBs appear more comfortably tolerated than describing appetite control and FB with the concept of energy de®cits. Physiological signals may affect FB phenotypes which describe the likely behavioural and=or either directly or through perceptible changes in functional physiological responses of certain groups of people to integrity (for example, feeling weak and tired during dietary factors believed to affect their disposition towards energy restriction), which can act as learning cues for weight gain (Drewnowski, 1995; Cooling & Blundell, feeding. If this argument is correct, it may be that studies 1998). It is also important to consider the generalisability which have examined the impact of covert dietary manip- of results found in the laboratory to people living their ulations on appetite and EB actually assess the extremes normal lives in the real world (Blundell & Macdiarmid, required for physiological signals to in¯uence compensa- 1997). tory changes in FB (Van Stratum et al, 1978; Lissner et al, High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S150 1987; Kendall et al, 1991; Cotton et al, 1994; Stubbs et al, state of weight equilibrium. However, the nature, rate and 1995a, b, 1996, 1997a). extent of weight change in the population are insuf®ciently Hunger and satiety often have a large learned, antici- documented at present to discern exactly how people tend patory (entrained) component rather than being the direct to gain weight. consequences of unconditioned physiological signals per se (Booth et al, 1976, 1982, Booth 1977), such as reduced Physiological requirements for fat and CHO in relation to gastrointestinal content. Such physiological events can act levels available in the environment as important cues for feeding but they do not necessarily If changes in nutrient balance are important cues for or directly determine that behaviour. This has important stimulators of FB, it is reasonable to suppose that the implications for the use of substances and technologies greater the physiological requirements for these nutrients, which mimic the sensory attributes of fats and CHOs, since the stronger the drive to ingest them. The requirements for they will affect the processes whereby humans learn to lipids in adult humans are largely met by all but except associate the sensory characteristics of foods with the perhaps the most extreme diets. Even during total starva- energy and nutrients they contain (Booth et al, 1982; tion it has been estimated that on average, adult adipose Booth, 1992). These considerations are important because tissue mass will provide around 2 kg of essential fatty acids they allow us to account for a number of observations (Newsholme & Leach, 1992). The requirements of growing which cannot otherwise be explained: (i) over half of the children are however greater. adult population of several Western countries are collec- As regards CHO requirements, it is unclear what, in the tively overweight and obese. Models based on pure phy- strictly physiological sense, is the absolute requirement for siological determinism would have to postulate an dietary CHO (Newsholme & Leach, 1992). Populations epidemic of physiological defects to account for such a subsisting on virtually CHO free-diets usually consume prevalence of `energy dysregulation'; (ii) few, if any, large amounts of protein which can be used for gluconeo- exclusively physiological models of appetite control accu- genesis. It therefore appears that part of human adaptation rately predict a large proportion of the variance in human to variations in the environmental supply of fats and CHOs FB; (iii) certain conditions such as transient periods of consists of considerable physiological plasticity, in meeting intense physical activity or the use of covertly manipulated, our requirements for speci®c metabolic fuels. This does not unfamiliar foods appear to result in a very poor coupling of mean that altered physiological levels or utilisation of fat EI with EE; and (iv) while a large number of studies of and CHO do not act as cues which drive FB towards altered human feeding show varying degrees of compensation for a energy and nutrient intakes. However these cues do not number of experimental interventions very few have appear to be heavily weighted or deterministic. recorded clear evidence of EB regulation. This has important implications for the manner and extent to which In¯uence of sensory stimulation on appetite humans regulate their body weight. In considering the capacity for EI to rise above EE the weakness of inhibitory factors has to be set against the Body weight as a set-point or a dynamic equilibrium potency of facilitatory processes. The palatability of food is The above arguments suggest that body weight is deter- clearly one feature which could exert a positive in¯uence mined not by a set-point mechanism (Keesey et al, 1976; over behaviour. The logical status of palatability is that of a Bernardis et al, 1988) which operates through powerful, construct (it is not an objective feature such as protein physiological negative feedback signals, correcting FB in content or blood glucose) (Ramirez, 1990; Rogers, 1990). line with EB in the short-to-medium term. Rather, it would The relative palatability of a food can be determined by appear that body weight exists as a dynamic equilibrium choice tests or taste tests relative to other standard inge- with a tendency to drift upwards. That is, both lean and stants (for example, a 5% sugar solution) (Le Magnen, overweight subjects may well be in a relatively steady state 1992). However, there has been much more controversy or equilibrium for much of the time as regards increases in over the actual de®nition of palatability. The reader is body weight. These periods of equilibrium may be punc- referred to a recent debate regarding these de®nitions tuated by short, discrete but signi®cant increases in body (Ramirez, 1990). In general the palatability of a food can mass. Once stabilised, weight may be defended at the new be thought of as the sensory capacity to stimulate ingestion higher level (the so-called ratchet model of weight gain). If of that food. This de®nition takes account of the fact that this is so then factors, which produce episodic gains in the palatability of the food is jointly determined by the body weight, would have signi®cance for long-term weight nature of the food (smell, taste, texture and state), the control. Such a system would be consistent with the vast sensory capabilities and metabolic state of the subject, body of experimental data that has found remarkably little and the environment in which the food and subject interact. differences in the reported eating behaviour of lean and Palatability is therefore not stable; indeed the palatability of obese subjects (Spitzer & Rodin, 1981). Indeed some a food typically declines as its own ingestion proceeds. studies have noted remarkable similarities in the responses This process is believed to mediate the phenomenon of of lean and obese subjects to nutrient manipulations (Hill & sensory speci®c satiety (Rolls et al, 1981, 1982, 1983, Blundell, 1990; Thomas et al, 1992). An important excep- 1988; Rolls 1985, 1986). Work on military personnel tion to this is the case of mis-reported dietary intakes which suggests that the decline in preference for highly preferred tends to increase with increasing BMI (Black et al, 1991; foods (for example, chocolate) is greater than that for staple Schoeller 1990). foods such as bread, which exhibit more stable preference Recent analysis of average weight changes over time pro®les (Meiselman & Waterman, 1978). Palatability can suggests that US adults appear to gain weight at a steady be dissociated from sensory intensity since sensory inten- rate of 1 ± 2 kg per annum (Burmaster & Crouch 1997). sity increases with the concentration of the compound or This population trend may actually mask a series of food being tasted; palatability generally shows a parabolic hyperphagic events which punctuate the more common n-shaped curve when plotted against sensory intensity of High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S151 the food. Palatability can be in¯uenced by a number of factors including environmental cues and the physiological state of the organism. The independent index of palatability is usually considered to be the subjective appreciation of pleasantness. This subjective sensation is quanti®ed by expressing it on an objective scale according to standard psychophysical procedures (Hill & Blundell, 1982). This sensation is often taken to re¯ect the hedonic dimension of food. The nature of the relationship between palatability, food consumption and EB has never been systematically determined although palatability does in¯uence the cumu- lative intake curve, and palatability has been invoked as a mediating principle to account for the prolongation of ingestion from a variety of foods due to sensory speci®c satiety operating in short-term studies (Rolls et al, 1981, Figure 2 Relationship between percentage of energy (expressed in kJ) 1982, 1985, 1986, 1988). from dietary macronutrients and water (expressed in grams) (predictor variables) and energy density of 1032 ready to eat foods, taken from the It may be hypothesised that palatability would exert a British food composition tables (Holand et al, 1991). powerful effect on intra-meal satiety (whilst food was being consumed), but is post-ingestive satiety also affected? In addition what is the effect of the expectation of getting Energy and nutrient relationships within foods pleasure from food on the initiation and maintenance of eating? Although many would agree that palatability exerts The contribution of fat, carbohydrate, protein and water to a powerful in¯uence on eating behaviour there is no dietary energy density systematic body of data to explain the strength or the We have recently conducted a preliminary analysis of the limits of the effect (Ramirez et al, 1989). relationship between nutrient and water content and ED in The nutritional composition of foods can also in¯uence 1032 ready to eat foods from the British food composition FB. The fats and CHOs contained in foods can affect both tables (Holand et al, 1991) (excluding supplements). When the palatability of those foods and the density of energy and water and nutrients are plotted in g=100 g of food, as nutrients within those foods. Certain CHOs will in¯uence predictors of dietary ED all nutrients contribute positively the digestibility of foods which may limit subsequent to ED, and water content contributes negatively (Figure 1). 2 feeding. It is important to consider the extent to which However, only fat (ED 462.6 35.46fat R 75.0) 2 the ED and total amount of fats and CHOs that are and water (ED 2034 7 21.26 water, R 66.7) have a 2 contained in foods in¯uences the willingness of individuals large R value, those for protein and CHO indicating a to ingest those foods. How do the nutritional properties of generally poor relationship. When the relationship between foods (and their sensory attributes) in¯uence or limit the nutrient composition (expressed as a percentage of total voluntary food, energy and nutrient intake of individuals, food energy) and ED was examined, fat again correlates both in the laboratory and under more naturalistic condi- positively with ED, while protein and CHO show a weak tions? Although the effects of fats, CHOs and proteins on negative relationship to ED. The relationship for fat under eating has been investigated intensively for some years, these conditions is relatively weak (ED 320.1 16.36 2 only recently have their effects been considered both as fat, R 35) (Figure 2). Therefore while dietary fat ele- nutrients in themselves (that is, when ED is controlled and vates ED, HF foods (expressed as a percentage of energy comparisons are made at the same level of ED, and in terms from fat) are by no means inevitably high in ED. Further- of their contribution to overall dietary ED (Stubbs et al, more, the major determinants of the ED of a food are the fat 1995b, 1996, 1997a; O'Reilly et al, 1997; Blundell & and water content. In this analysis there appears to be a Stubbs, 1997a). relatively weak fat-CHO seesaw expressed as grams vs grams, a strong (and obvious) negative correlation (or seesaw) when expressed as percentage energy but a robust fat-water seesaw which determines dietary ED (when fat is expressed in grams, as percent energy or in absolute kJ).

The potential importance of considering the effects of diet composition on ¯uid and food intake relationships: implications for EB The `fat-water seesaw' in foods may have important implications for FB. This is because as fat content of foods increases the water content tends to decrease. Fat exerts a weaker osmotic load than CHO and this may effect FB (Ramirez et al, 1989). This implies that ingestion of a high CHO or a high protein diet will induce a higher level of water ingestion, which may in¯uence subsequent FI. The strength of this effect would depend on how that water Figure 1 Relationship between percentage weight (expressed in grams) from dietary macronutrients and water (predictor variables) and energy interacts with the food matrix in the gut (Mela, personal density of 1032 ready to eat foods, taken from the British food composition communication). These issues prompt a consideration of tables (Holand et al, 1991). how diet composition may affect the relationship between High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S152 food and ¯uid intake. At present our understanding of these Energy and nutrient relationships within foods ingested issues is incomplete. In addition, the effect of dietary by human populations nutrient composition on the relationship between solid food and ¯uid intake and the implications this has for EB is, to the best of our knowledge, a neglected area of research in diet-surveys. Recorded extremes of energy intake, extremes of fat and CHO intake As noted above, human populations have been known to subsist for quite prolonged periods on extreme ranges of Energy density as a limiting factor for EI diet composition. For example the Inuit have been reported It is well known that the available energy content of the diet as subsisting for months on diets almost entirely comprised is crucial in allowing growth and development to proceed of animal matter and virtually devoid of all CHOs (Mowatt, along genetically pre-set levels. In this context ED can refer 1975). These diets were therefore high in protein and fat. to the total energy per gram of food ingested. It can also This produces diarrhoea and general malaise during lean refer to the metabolisable energy available from that diet months when the energy to protein ratio of the diet falls too (Livesey, 1991). It is clear that low dietary ED can limit EI low. Similarly, the traditional Japanese diet has been and produce sub-optimal levels of EB. The extent to which reported to provide some 8% of EI as dietary fat, in extreme humans can adequately adapt to low levels of dietary ED is cases. It appears clear from these accounts that human unclear. Problems with obtaining accurate dietary intake populations are capable of adapting, (through their physio- measures (Black et al, 1991; Schoeller, 1990) and lack of logical plasticity) to meet their physiological requirements knowledge of the relationship between ¯uid and FI pre- from a wide range of macronutrient ratios in the diet. The clude conclusive statements. While the impact of altering overall effects of such extreme nutrient intakes have been dietary ED using differing nutrients, on EI and EB is discussed in detail in other papers. beginning to emerge in laboratory studies lasting up to Extremes of EI have been recorded during overfeeding two weeks (Lissner et al, 1987; Kendall et al, 1991; studies (Norgen & Durnin, 1980; Ravussin et al, 1985; Thomas et al, 1992; Stubbs et al, 1995a, 1996, 1997a; Diaz et al, 1992), during ceremonial overfeeding (Pasquet O'Reilly et al, 1997), the extent to which humans adapt FB et al, 1992), underfeeding studies (Keys et al, 1955) and to changes in the dietary ED over longer periods is from EI records derived from famine and concentration unknown. The few longer-term interventions that have camp victims during the second world war. These cases altered the nutrient density of certain foods have shown represent states of accommodation to extreme environmen- relatively good compensation over periods of a few months tal conditions, rather than voluntarily FB. Compensatory (Aaron et al, 1999; Gatenby et al, 1995; Zimmermans et al, responses subsequent to such induced extremes of EB can undated). be spectacular, especially in relation to energy de®cits. During rehabilitation from severe malnutrition, famine and concentration camp victims (with body weights below 55 kg) were recorded as spontaneously ingesting 29 ± 33 MJ=d. These spectacular levels of EI ceased as body How should we de®ne dietary energy density in relation to mass and composition were restored. In healthy subjects, feeding behaviour? such high levels of EI have only been recorded under The importance of dietary ED in altering EB through its conditions of extreme physical activity such as the tour effects on EI have begun to receive renewed attention as de France (Saris et al, 1989), or polar expeditions (Stroud et the effects of dietary fat are being viewed by some as al, 1993). Under these conditions levels of EE were so high exclusively a property of dietary ED. We suggest that some that subjects often remained in some degree of energy caution should be exercised in describing the ED of the diet de®cit. These examples have little to do with the general and its determinants. It is likely that the ED, (as kJ=g wet population at large, rather they illustrate the extremes to weight of food) is not perceived as such by the human which FB can adapt to intense physiological demands body, since the body reacts to the mixture of foods con- imposed by very high levels of physical activity (Saris, tained in a meal rather than the individual components of 1989) or severe malnutrition. Despite these recorded that meal. For instance the Western diet appears to consist extremes of energy and nutrient intake Mela (1995) of a relatively small percentage of EI in the form of points out that Western populations who have economic extremely energy dense foods (that is, > 1.8 kJ=100 g), a and market access to diets of very similar ranges of large number of moderately ED foods (0.4 ± 1.7 MJ=100 g) composition appear to consume, on average, around 37 ± and a variable number of low energy dense foods 42% of their food energy as fat. As the Western diet ( < 0.4 kJ=100 g). Overweight people may preferentially becomes increasingly imposed on, or adopted by, a select from the food categories with a higher ED (Wester- number of less developed nations, obesity and non insulin terp-Plantenga et al, 1996). How does ¯uid intake con- dependent diabetes mellitus approach epidemic proportions tribute to the total ED of the diet? Exactly how does dietary (WHO, 1990). It is however, unclear whether people ED affect human FB? How does the composition of the diet choose to select a Western dietary composition over tradi- in¯uence the relationship between ¯uid and food intake and tional foods or whether secular increases in fat and sugar hence the overall ED of the diet. We have found that as the intake are foisted on communities and individuals by dry matter content of mixed diets increased, so does water economic or other incentives. It has been argued that the intake. Does the ED of a food correlate with its palatabil- sensory appeal of fats, re®ned CHOs and especially mix- ity? Since salt ingestion increases thirst, will adding salt to tures of the two are a major factor facilitating the ready food effectively lower dietary ED? adoption of Western-style foods (Drewnowski, 1997). High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S153 Relationships between diet composition and energy intake in adults consuming their normal (Western) diet Studies by DeCastro (1987) and DeCastro & Elmore (1988) have shown that in free-living subjects, self-recording their FIs by using food diaries for seven days at a time, fat was the least effective of the macronutrients in suppressing subsequent EI. These studies suggest that high EIs on fat- rich diets can be brought about not only because of the energy contributed by fat itself, but also by the weak effect that fat exerts in suppressing EI in general. This is consistent with other laboratory-based short-term studies. Con- versely protein was the most effective at suppressing EI, independent of its contribution to total calories. In a recent study, the food and EIs of 160 post menopausal women living at home in the Cambridge area were measured on four consecutive days in each of the four seasons. This approach produced 16 d of weighed intakes per subject kept over 1 y (Bingham et al, 1994). The proportion of EI from fat correlated positively with total EI (r 0:18), whereas CHO did not correlate at all with total EI (r 0.0) and protein correlated negatively with total EI (r 0:45). In these studies of free-living people the grams of fat ingested contribute 2.2 ± 2.3 times more energy than the grams of protein or CHO ingested. Increasing the percentage of energy from fat therefore usually elevates the ED of the diet. These relationships are of broadly similar direction but somewhat different magnitude to those described above for the relationship between food composition and ED described above. It is crucial to point out that because of the probable extent and prevalence of mis-reporting of dietary intakes (Black et al, 1991; Macdiarmid et al, 1996) that relationships between diet composition and EI are, in isolation, potentially limited. The major effect is that reported EIs are often too low to plausibly maintain EB and the composition of the underreported component is currently unknown. It is nevertheless reassuring in this context that dietary macronutrients appear to exert similar effects on appetite and EI in the laboratory (Stubbs 1995; Blundell & Stubbs, 1997; Blundell & Macdiarmid, 1997).

Variation in fat consumption in the general population While the average protein, CHO and fat intake amongst Figure 3 Frequency distributions of body mass index (BMI) among low-fat (upper panel) and high-fat (lower panel) consumers. Groups are populations exposed to Western diets appears, on average, de®ned by the amount (weight in grams) of fat consumed. The ordinate to be relatively constant, HF and LF consumers have been shows the percentage of each sample. identi®ed within these populations. It has recently been shown that populations of HF consumers (identi®ed by self- recorded intakes) have a BMI distribution skewed towards higher BMIs compared to LF consumers (Figure 3). How- possibility of individual differences in both the willingness ever, comparing the distribution of HF and LF consumers to select fat-containing or CHO-containing foods, and also shows that HF consumers are by no means exclusively fat in the response to such foods. As an example, data from the (Macdiarmid et al, 1996). This means there are a signi®cant Leeds High Fat Study has identi®ed both individual differ- number of HF consumers who manage to maintain a stable ences and large day-to-day variation in fat intake of both body weight, at or below a BMI of 25. It is currently high and low consumers. Consumption of more than 200 g unclear how such HF consumers (ranked by percentage EI fat in one day for a high fat consumer, or in excess of 150 g and absolute intake of fat) manage to avoid the weight per day for a low fat consumer was not uncommon (Figure promoting properties of dietary fat. They may be protected 4). The implications of this daily variation for fat balance by physiological or behavioural mechanisms (or both) have yet to be de®ned. In turn this could disclose informa- which allow them to maintain EB. Nevertheless it does tion about the variability in appetite control mechanism, seem that there is considerable scope in some individuals to which either promote fat intake or limit its consumption. It accommodate a HF diet, low levels of EE or perhaps even has already been reported that high and low fat phenotypes both, without there being an inevitable rise in body weight display different forms of appetite control (Blundell & (Blundell & Macdiarmid, 1997). Macdiarmid, 1997; Cooling & Blundell, 1998). The impli- One of the interesting features of analysing natural cation of the existence of distinct phenotypes Ð with dif- ¯uctuations in fat consumption Ð rather than average fering behavioural and physiological responses to nutrient intake across a whole population Ð is that it raises the challenges Ð is that measures of the `average' responses of High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S154 often correlated negatively with EI in the same studies. While it can be accepted from validation studies (Black et al, 1991; Schoeller, 1990) that the obese appear to systematically underreport EI, it is not clear what the composition of the underreported component is. Lissner & Heitmann (1995) have recently scrutinised the epidemiological evidence in relation to dietary fat and obesity and note that ecological studies describing dietary fat intake and obesity at the population level give mixed results. Indeed, the extensive cross-European MONICA study showed negative correlation between fat and EI (FAO=ICS (1986); Lissner & Heitmann review, 1995). They point out that because of the problems inherent in ecological studies these mixed results are likely to be biased `by both confounding and unknown data quality factors that differ systematically across the populations studied' (Lissner & Heitmann, 1995). However, they note that most cross-sectional studies are generally in agreement that the percentage of fat in the diet correlates positively with EI. Prospective studies yield mixed results, probably because of the public attention that dietary fat has received and the fact that subjects will often change their behaviour in relation to expectation when they are aware that they are being studied. In other words, the fact of being studied may make the subjects more health conscious. Therefore when Colditz et al (1990) used a combined retrospective and prospective design, they found that fat intake was positively associated with previous but not subsequent weight changes. In combination with the work of de Castro (1987) and DeCastro & Elmore (1988) these studies all suggest that under naturalistic conditions (where dietary fat contributes 2.2 ± 2.3 times the energy per gram as protein or CHO), Joule for Joule, fat appears to be less satiating than CHO or protein. This argument is supported by laboratory studies (see below).

Evidence from experimental interventions. In recent years it has been repeatedly demonstrated that increasing the fat content and ED of experimental diets or modi®ed foods induces subjects to eat a similar amount of food and hence higher levels of EI as the fat content and dietary ED rise. Figure 4 Pro®les of a low-fat consumer (upper graph) and a high-fat consumer (lower graph) indicating the large day-to-day variation in fat This effect is more pronounced in studies where subjects intake and the occasional very-high-fat intakes that can be reached even by are given ad libitum access to covertly manipulated diets a low-fat eater with a lower average daily intake. than under conditions where speci®c meals or snacks are manipulated and subjects have ad libitum access to a range of familiar food items (Foltin et al, 1990, 1992). In longer- a heterogeneous sample may provide a very misleading term studies these changes are paralleled by changes in picture of the variety of individual patterns of responses. body weight (Lissner et al, 1987; Kendall et al, 1991; Stubbs et al, 1995a, b). Weight losses are typically modest when subject feed ad libitum on LF, low energy density Fat carbohydrates and energy density as determinants (LED) diets (Kendall et al, 1991), which is perhaps not of total energy intake surprising given the tendency of the appetite system to How does fat affect appetite and energy balance? defend against energetic decrements rather than incre- Evidence from dietary surveys. There is now a growing ments. The tendency for high fat foods to promote high body of evidence derived from most of the recent epide- EIs (when people are eating to comfortable fullness) has miological studies (with some notable exceptions) on diet been termed `passive overconsumption' by Blundell and body weight suggesting that macronutrients do exert (1995), since there is little evidence of increased drive to different effects on EB. A number of studies suggest that eat and no intention of voluntarily overeating. fatter people appear to consume a higher proportion of their It has been shown that systematically increasing dietary EI from fat rather than from CHO (Lissner & Heitmann, ED using fat has led to excess EI, weight gain and a review, 1995). It is generally assumed that this implicates positive fat and EB (Stubbs et al, 1995a). Two studies HF diets in the promotion of excess EIs. However BMI is have shown that when subjects have ad libitum access to High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S155 systematically manipulated diets of constant energy and cancel each other out under real-life conditions. At the protein density but differing fat to CHO ratios, subjects ate present time there is insuf®cient data to derive a model, a similar amount of food and energy (van Stratum et al, which articulates the aggregate signi®cance of these effects 1978; Stubbs et al, 1996). These observations have raised in human subjects. Nevertheless, the results of these studies the issue of whether the effects of dietary fat on appetite suggest that dietary fat exerts effects on EI and appetite and EB are entirely attributable to the higher ED (HED) of control that are independent of its contribution to dietary dietary fat, or whether fat has unique weight-promoting ED. However, it should be borne in mind that to some properties that are independent of its contribution to overall extent the ED vs macronutrient (per se) issue is a special dietary ED. argument because in many foods there is a reasonably good correlation between fat content and ED. Does fat exert any effects on food and energy intake independent of its contribution to dietary energy density? Does type of fat in¯uence appetite and EB? There are a number of examples which show that fat exerts The majority of studies that have examined the effects of detectable albeit relatively modest effects on appetite and dietary fat on appetite and EI in humans do not discriminate EB which are independent of its contribution to dietary ED. between the types of dietary fat used, and these studies tend CHO appears to exert a more acute effect on satiety than fat to use mixed fats in their dietary preparations. Fats can vary (Cotton et al, 1994), and three other studies have found this in structure in terms of (i) chain length, (ii) degree of relatively subtle effect to be independent of ED (Rolls et al, saturation; and (iii) number and composition of fatty acids 1994; Johnstone et al, 1996; Stubbs et al, 1997a). In one of esteri®ed to the glycerol backbone. these studies, the low satiating ef®ciency of fat in the short There is evidence that the chain length of fat may term appeared to be related to its low osmotic load, as in¯uence EI. In general the shorter the chain length of a indicated by the subjective thirst of the subjects (Stubbs et fat the more immediate its oxidation. In this context it is of al, 1997b). Pronounced differences in the satiating ef®- note that there is evidence that fat metabolites (including ciency of intravenously infused fat and CHO have been ketones) may exert potent effects on satiety in rodents recorded by Gil et al, (1991). In this study equal energy (Carpenter & Grossman, 1983a=b; Rich et al, 1988). loads and volumes of infusate were used. These data are There is also data in rats (Furuse et al, 1992) and humans supported by an analysis of the relationship between (Stubbs & Harbron, 1996) which shows isoenergetic sub- change in net macronutrient stores and subsequent EI, stitution of MCT for LCT at high levels, in HF energy which suggested that increments in protein and CHO dense diets limits the excess EIs and weight gains that stores negatively predict subsequent EI, while fat stores frequently appear when subjects feed ad libitum on such did not (Stubbs et al, 1995a). diets. In short-term studies it has been reported that MCT Isoenergetic changes in the fat to CHO ratio of the diet exerts a stronger effect on satiety than LCT (Rolls et al, do not appear to exert important effects on EI in subjects 1988a). Incorporation of more moderate amounts of MCT feeding ad libitum on systematically manipulated diets of into the diet is unlikely to be of use in promoting sponta- differing composition (van Stratum et al, 1978; Stubbs et neous weight loss in rodents (Hill et al, 1993) or humans al, 1996). However, in one study isoenergetic, isoenerge- (Martin et al, 1997). tically dense, weight-reducing diets were given to women It has recently been shown that when 20 subjects were (4.18 MJ=d), who were also given snacks of a constant each fed isoenergetic lunches rich in polyunsaturates, composition to ingest if they felt the need to eat more. Only monounsaturates and saturates, monounsaturates signi®- on the HF treatment were snack EIs signi®cantly, albeit cantly suppressed short-term intake less than either poly- marginally, higher than the HP or HC treatments (John- unsaturates or saturates (Lawton et al, 1997). stone et al, 1997). The effects of large doses of 1-monoglyceride on appe- Fat also exerts sensory in¯uences on the diet by adding tite and EI have recently been examined both within day moisture and mouth-feel to food as well as acting as a (Ryan et al, 1997) and between days (Johnstone et al, vehicle for a large number of fat-soluble volatile sub- 1997a). Together these studies found that large isoenergetic stances. These effects may also be ED independent. doses of dietary monoglyceride or triglyceride did not exert Furthermore, there is evidence that the oro-sensory quali- differential effects on subjective motivation to eat, or ties of dietary fat and sugars may interact to in¯uence the nutrient oxidation or FI. Therefore while the degree of sensory stimulation to eat. Mela & Sacchetti have reported saturation (Lawton et al, 1997) and chain length of orally- that fat preferences increase with increased BMI (Mela & ingested dietary fat (Stubbs & Harbron, 1996) can have Sacchetti, 1991). Drewnowski has repeatedly shown that signi®cant effects on appetite and EI, these data suggest sugar=fat mixtures appear to exert a synergistic effect on that orally ingested 1-monacyl glycerols did not differen- the sensory pleasure response of human subjects, relative to tially in¯uence appetite and EI relative to triacylglycerols. fats or sugars alone (Drewnowski, 1997). A comparison of It is possible that 2-monacyl glycerols may exert a greater the effects of HC-sweet, HC-savoury, HF-sweet and HF- appetite suppressing effect since these molecules are more savoury snacks on short-term intake has recently been readily absorbed across the gut wall (Bistrian, 1997). The made. Ingestion of HF-sweet snacks exerted a far greater effects of varying the fatty acid composition of triglycer- effect on EI, which was independent of ED, since EIs were ides (structured lipids) is currently unknown. around twice that on any other treatment despite the fact In summary it appears that fats and fat derivatives which that the ED of the HF-savoury snacks was higher (Green & tend to be more readily absorbed and=or metabolised exert Blundell, 1996). a greater suppressive effect on appetite and EI than less In summing up there are a number of individually rather readily utilised fats. The magnitude of these effects under subtle effects that dietary fat exerts on appetite and EB experimental conditions appears to be signi®cant but which are independent of the contribution of dietary fat to modest (not exceeding 1 MJ=d differentials in EB). Their overall ED. These effects may be additive, synergistic or signi®cance in the population at large is currently unclear. High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S156 The fat paradox: site and mechanism of action tissue uptake and utilisation of glucose is important in its HF hyperphagia has been shown to occur both in the post-ingestive satiety effect. This probably explains the laboratory and free-living setting. Conversely, there is relationship between expressed satiety and the integral evidence that fat generates potent satiety signals at the (area under the curve) for insulin which has been found level of the gut. So why does overconsumption occur when in some studies (Holt et al, 1992). However there is also fat generates potent satiety signals? This phenomenon has evidence that satiety after CHOs may also be mediated by been termed the `fat paradox' (Blundell, 1995). One factor gastrointestinal (pre absorptive) mechanisms (Read et al, determining the feedback from fat seems to be the site of 1994). action. In humans, the infusion of corn oil into the small intestine led to reduced gastric emptying, increased feeling of fullness and reduced intake at a test meal (Welch et al, 1988). Similar effects have been found in pigs (Gregory et al, 1989). Large doses of lipid infused straight into the Does carbohydrate type affect appetite and EB? small intestine have a potent effect on satiety, presumably A number of studies have compared the satiating effects of by activation of gastrointestinal peptides, CCK and other preloads containing different hexoses and found relatively receptors (Forbes 1995). Conversely, infusions made intra- few differences between them in terms of appetite venously, by-passing the gut, exerted no effect on gastric responses. However, it is unclear whether this uniform emptying or measures of appetite. A study by Gil et al response relates to the constraints of the preloading (1991) found that lipid infusions at around 80% of resting method or whether the monosaccharides simply have EE (REE), over 3 d, produced only partial compensation similar satiating ef®ciencies. There is some evidence that (43%) of EI. On the other hand, infusions of mixed starches produce a more blunted, yet prolonged in¯uence nutrients produced good compensation of 103% and with on satiety than do mono- and disaccharides (Leathwood & glucose, 86%. Similar experiments carried out in rats found Pollet 1988), or may help limit EIs (Raben et al, 1997; Kirk intra-duodenal infusions inhibited FI while intravenous et al, 1997). However, these effects seem relatively modest infusions did not (Greenberg et al, 1989). These ®ndings and to date there is little published data to suggest that suggest that after the ingestion of fat, potent fat-induced sugars and starches exert large differential effects on satiety signals are generated by pre-absorptive (oro-sen- intake. Interestingly the effect on post-ingestive satiety is sory, stomach and small intestine receptors) rather than also in¯uenced by the structure of starch as indicated by the post-absorptive physiological responses. The post-absorp- difference between high amylose and amylo-pectin foods tive action (nutrient absorption, substrate utilisation and (Van Amelsvoort & Westrate, 1992). oxidation) of fats is weaker than that of other macronu- Most work on the effects of different CHOs on EI has trients (Gil et al, 1991; Stubbs et al, 1995b). Another been done with unavailable complex CHOs (UCCs), or possibility is that the fat satiety signals are not initiated ®bre. The time-energy displacement concept has been when fat is eaten, only when fat is directly infused into the invoked to suggest that the addition of UCCs to the diet intestine. It is most likely that these differential effects of enhances satiation and limits meal sizes. This effect is site of fat administration can probably be explained by apparent in some of the studies discussed above and the infused lipid producing supraphysiological saturation of the phenomenon has been used to limit weight gain in farm small-intestine receptors with emulsi®ed fat. This effect animals with access restricted to single feeds (Forbes, may be diluted by other food constituents and limited by 1995). The post-ingestive effects of ®bre will depend gastric emptying when fat is fed in the diet, reducing its upon the amount and type delivered in experimental capacity to suppress appetite. The essence of the fat meals and is likely to be in¯uenced by the proportions of paradox is that very large amounts of fat can be ingested soluble and insoluble ®bre, which will have different in the face of potent fat-induced satiety signal. However, effects on gastro-intestinal processing. Fermentable CHOs measuring the weight (mass) of food consumed in addition produce signi®cant quantities of short-chain fatty acids. to EI, indicates that subjects can reduce the weight of foods The absorption and metabolism of acetate, propionate and eaten slightly (but still consume excess energy). This effect butyrate may themselves exert in¯uences on satiety. is most likely to be due to the combination of ED and the Over 50 studies have been conducted which have very potent oro-sensory facilitation of EI by fatty foods examined the effects of dietary ®bre on FI and body which together engender a high intake of fat before inhi- weight (Levine & Billington, 1994). These have been bitory mechanisms (to terminate eating) can come into extensively covered in four recent reviews, (Levine & action. The rate of ingestion loads fat into the system Billington, 1994; Blundell & Burley 1987; Stevens, 1988; before satiation operates. Burley & Blundell, 1990) to which the reader is referred for a detailed discussion of this issue. In summary, various How does carbohydrate affect appetite and energy loads of UCC or ®bre at one meal have been shown to balance? decrease both hunger and EI at the next meal, but the CHOs appear to be ef®cient inhibitors of appetite in the effects are relatively modest. The conclusion seems to be short term. Acute CHO de®cits act as cues that stimulate that supplementing the diet with tolerable levels of intake since 2-deoxy-D-glucose administration actually extracted UCC appear to have, at best, modest effects in increases hunger when given to human subjects (Thompson decreasing body weight over several months or more. & Campbell, 1977). The effectiveness of CHO includes the However, ®bre-rich bulky diets of low ED may have effects of sugars and longer chain oligosaccharides such as different effects and the reader should consider the meth- maltodextrin and polysaccharides. One interesting issue odological issues detailed in a number of references here is the relationship between the post-ingestive satiety (Levine & Billington, 1994; Blundell & Burley 1987; effect of CHO and their action upon plasma pro®les of Stevens 1988; Burley & Blundell, 1990) before drawing glucose and insulin. It appears intuitively probable that ®rm conclusions. High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S157 Wet and dry carbohydrates: an osmotic brake on excess How does varying the ED of the diet (using different intake? compositions) affect appetite and EB? It was stated above that CHOs appear to be ef®cient The majority of studies examining the effects of dietary fat inhibitors of appetite whether given in the diet or parent- or fatty foods on appetite, EI or EB have confounded erally. One interesting and important exception to this is the dietary ED and fat content. However, a series of studies ®nding that calories contained in drinks appear to be poorly has recently assessed the effects of altering the ED of the compensated for. In 1955 Fryer supplemented the diet of diet using fat, primarily CHOs or mixed regimes (Stubbs et college students with a HC drink containing 1.8 MJ. Com- al, 1995a, b, 1997b; O'Reilly et al, 1997). Alcohol is pensation was incomplete ( 50%) after eight weeks excluded from the present discussion, since it also exerts (Fryer, 1958). Mattes has recently conducted a meta-ana- pharmacological effects, which may actually stimulate EI lysis of feeding responses to either liquid or solid manip- (see Mattes, 1996). In the studies where the ED of the diet ulations of the nutrient and energy content of the diet. The was altered primarily using fat, subjects did not compensate analysis suggests that the physical state of ingested CHO at all for alterations in dietary ED and HF hyperphagia was intake may be important in in¯uencing subsequent caloric a prominent outcome (Stubbs et al, 1995a, b). Furthermore, compensation (Mattes, 1996). Speci®cally energy con- there were no signi®cant differences in subjective hunger tained in drinks (including CHOs) does not appear to between the diets (Stubbs et al, 1995a). In the study where induce compensatory reductions in food intake as ef®- the ED of the diet was altered primarily using CHOs there ciently as energy contained in solid foods. The reasons was no compensation for the ED of the diets but subjects for this are at present unclear, but may relate to the rate, were signi®cantly (and anecdotally) more hungry on the timing and density at which the energy is ingested. There LED diet, compared to the HED diet (Stubbs et al, 1995) In may be a threshold in these parameters, below which the study where the ED of mixed diets was altered there energy is poorly detected. Another factor in¯uencing the were no signi®cant differences in subjective hunger effect of CHOs on intra and intermeal satiety is the osmotic between the diets but there was a signi®cant diet effect load that CHOs exert in the small intestine. As starches are for prospective consumption (that is, subjects felt they digested water is required to hydrolyse the glycosidic could eat more food after the low ED meals). Subjects bonds. This will have the net effect of slowing digestion also showed a highly signi®cant (albeit quantitatively small (and hence short-term food intake) and increasing thirst. It 20%) compensation of solid food and hence EI on going is reasonable to hypothesise that these effects would from the LED to the HED diet. Therefore subjects enhance post-ingestive, preabsorptive satiety. Sweet, responded more effectively to changes in the ED of the CHO-rich drinks with a water:CHO ratio above 3 : 1 mixed nutrient manipulations (by active changes in FI) than should exert maximal oro-sensory stimulation on intake the primarily CHO-based manipulations (detectable and minimal osmotic reduction of intake. While wet CHOs changes in hunger) which in turn showed a greater response have been shown to induce hyperphagia in rodents than the primarily fat-based manipulations. These ®ndings (Ramirez, 1987), their effect on humans eating less mono- again suggest that fat is more weakly sensed by the appetite tonous diets is currently unclear. Rogers & Blundell have control mechanisms than is CHO. These comparisons are considerable evidence that high CHO drinks (glucose or consistent with infusion studies in rodents (Walls & Koop- sucrose) do suppress short-term intake (1.0 ± 1.5 h later) mans, 1992) and humans (Gil et al, 1991) which have (Rogers & Blundell, 1988, 1989), but the longer-term found greater caloric compensation in response to mixed effects of such manipulations are currently unknown. infusions than glucose-infusions, which in turn produced greater caloric compensation than lipid infusions. This When does a high CHO diet produce high levels of EI in suggests that the effects of altered ED on appetite and EB humans? are partially dependent on the composition of the diet. It has been demonstrated that excess EIs are possible when Consequently the effects of ED depend upon the nutrients normal weight men feed ad libitum on HC diets (Stubbs et supplying the energy. Other researchers have also noted al, 1997a). The sensory attribute primarily associated with that `Joule for Joule' fat is less satiating than CHO (Rolls et short-chain CHOs (sweetness) is known to stimulate EI, al, 1994). These ®ndings, in turn, are consistent with the especially when combined as mixtures with fats (Drew- notion that dietary macronutrients exert hierarchical effects nowski, 1997). Do the sensory attributes of some sweet on satiety, protein having the greatest effect and fat the foods elevate palatability and hence intake of those foods? least (Stubbs, 1995). Under these conditions the experi- Dissolving short-chain CHOs in solution appears to be an mental environment may constrain the ¯exibility of subject effective means of supplementing EI. The majority of response relative to real life, where degree of caloric snack foods produced tend to be high in CHO and ED compensation may be somewhat greater, especially to (Stubbs, unpublished). There is evidence that high levels of energy de®cits (Blundell & Stubbs, 1997). physical activity promote high EIs on HC diets. These considerations suggest that there is considerable scope for Appetite control mechanisms which limit CHO and fat HC foods to promote high levels of EI and in some cases intakes EB. The exact conditions under which this occurs and in whom are presently unclear. Currently we are aware of Carbohydrate-based models of feeding claims that intake of high CHO foods which are reasonably Mayer initially suggested that EB regulation occurred energy dense may lead to obesity in the USA. At the predominantly through short-term `glucostatic' responses present time we are unaware of clear evidence to support that could be corrected by longer-term `lipostatic' regula- those claims. There does, however appear to be evidence tion, should short-term regulation be suf®ciently perturbed that the increase of these foods in both the market and the (Mayer, 1955). Russek postulated the presence of glucose diets of consumers has not slowed or reversed current receptors in the liver and formulated the hepatostatic theory secular trends in obesity. of EB regulation (Russek, 1963) Flatt extended these High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S158 models and evolved the glycogenostatic model of appetite manner consistent with lipostatic correction of glucostati- regulation, which is based on the notion that CHO stores cally controlled FB (Mayer, 1955). The leptin system does (which are related to CHO intake) exert negative feedback however, appear to interact with a number of physiological on EI (Flatt, 1987). signalling systems concerned with control of several phy- Dietary CHOs have also been viewed as being central to siological functions (Camp®eld et al, 1997). nutrient selection models through their putative effects on the synthesis of the neurotransmitter, serotonin (5-HT), which purportedly led to a neurochemically mediated oscillation in diet selection between CHO and protein Integrative macronutrient models of feeding (Fernstrom & Wurtman, 1972). Fernstrom (1987) has Set-point theory has evolved out of the EB concept (Mro- reviewed this model and he, with others, has concluded sovsky & Powley, 1977). The concept of a set-point that the system does not operate as a mechanism for diet assumes that body weight (and hence EB) is in some way selection, although the importance of the serotonin system monitored by a basic sensor which purportedly operates to as a central mechanism in¯uencing FB remains undimin- increase or decrease food and EI, through a straightforward ished (Blundell, 1990). The remaining CHO-based models negative feedback loop that corrects FB to restore energy of feeding have recently attracted more interest since they imbalances. No such `set-point' controller has ever been predict broadly similar effects on FB: (i) CHO stores or discovered and the above discussions suggest that an metabolism exert a negative feedback on EI; (ii) because of Arthurian quest for one will prove fruitless. The concept this feedback, diets high in fat but low in CHO will of a dynamic equilibrium has recently been invoked in promote excess EIs; (iii) manipulating CHO status, that relation to models of appetite control or body weight is, oxidation or CHO stores, will reciprocally in¯uence EI; maintenance. Friedman & Stricker initially proposed that and (iv) excess ad libitum EIs on HC diets should be very the body exists in a dynamic equilibrium between oxidation dif®cult to achieve without a conscious effort, due to the and storage, and the rate of peripheral fuel utilisation exerts strength of putative negative feedback arising from CHO negative feedback on FB (Friedman & Stricker, 1976). status. The key question in relation to these models is Therefore factors which skew the oxidation=storage equili- whether they are useful. Is there evidence that glucostatic brium towards nutrient storage, remove those nutrients or glycogenostatic mechanisms exert a large enough in¯u- from the `calorie sensor' and will increase intake; factors ence on FB to be quantitatively important in the laboratory promoting the net release of nutrients from body stores and and in real life? One recent short-term report suggests that their increased oxidation should decrease intake (Friedman body glycogen stores play at most a minor role in short- & Tordoff, 1986; Friedman et al, 1990; Ritter & Calinga- term food intake control (Snitker et al, 1997). To support san, 1994). Langhans & Scharrer have speci®cally sug- these mechanisms, studies should demonstrate a high gested that nutrient oxidation rates in the liver leads to probability that changes in CHO status will exert predict- changes in hepatocyte membrane polarity, which acts as a able effects on FB that are consistent with these models. satiety signal relayed to the brain by sensory vagal afferents CHO-based models of EB regulation are intuitively attrac- (Langhans & Scharrer, 1992). These models do not specify tive, because the predictions of these models appear to be how the mechanism, which senses nutrient oxidation, consistent with the role of fat as a risk factor for weight distinguishes between endogenously and exogenously gain (Lissner & Heitmann, 1995), because these predictions derived nutrients. This may be achieved by monitoring in are testable, and because the predictions of these models some way the composition of fuels contributing to EE, offer a potential means of manipulating EB. However, it is since in starvation fat is the main metabolic fuel, while becoming increasingly recognised that FB is not an inevi- protein and CHO oxidation are minimal. In the fed state the table outcome of physiological signalling systems. Rather reverse is true. Alternatively preabsorptive signals and FB is coupled (to varying degrees) to physiological pro- absorptive phase processes may serve such a function. cesses through perception and conditioning (see section 2 A number of studies have examined the predictions of above). Their relevance to the FB of real people in real-life models which propose that CHO status drives FB. Some must therefore be considered in this context. have acutely manipulated CHO (but not EB) and found that CHO stores do not exert a large unconditioned effect on Fat-based models of feeding subsequent EI (Stubbs, 1994; Shetty et al, 1994; Snitker et Kennedy, 1953 argued for feedback information reaching al, 1997). Another examined the ongoing day-to-day rela- the hypothalamus from adipose tissue, which he argued is tionship between nutrient balance and EI in men housed in closely monitored through the sensitivity of the hypothala- an indirect calorimeter for seven consecutive days (Stubbs mus to the concentration of circulating metabolites. Hervey et al, 1995a). Increments in protein and CHO balance in 1969 proposed a mechanism for lipostatic regulation, exhibited a potentially suppressive effect on subsequent based on endogenous measurement of the fat mass by EI, fat stores did not. While these effects were signi®cant means of a fat soluble hormone that monitors adipose they only explained a small proportion of the total variance tissue mass by the dilution principle (Hervey, 1969). in EI. Furthermore, a statistical model, which included the Experiments in the late 1970s using genetically obese effects of all three macronutrients, accounted for the great- rodents and parabiotic regimes (Coleman 1978) created est proportion of the variance in subsequent EI (Stubbs et the conceptual context for the studies that have led to the al, 1995a). This suggests that all of the dietary macronu- identi®cation of the protein `Leptin' (Zhang et al, 1994), trients in¯uence appetite control and EI in some way, but to which is currently the subject of remarkable scienti®c differing degrees. The notion that the body is blind to fat scrutiny. At the present time it would appear that the from the perspective of appetite control is therefore erro- actions of total circulating leptin may not be entirely neous. Macronutrients appear to exert more complex consistent with a potent satiety factor arising from adipose effects on satiety and FB than can be accounted for by tissue and exerting negative feedback on body weight, in a single nutrient-based models (Stubbs, 1995). High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S159 Do nutrient-based models of feeding adequately predict hedonistic drives (Drewnowski, 1997). There is evidence feeding behaviour? that this is the case, and that such effects can override There is a large mass of evidence that suggests that the differences in the ED of foods (Green & Blundell, 1996). dietary macronutrients in¯uence physiological signalling However, by the same token it is likely that sugar also acts systems associated with appetite control and FB. At this as a vehicle for starch intake. Some interventions that have point it is necessary to make a distinction between pre- attempted to bring about a reduction in the fat content of absorptive signals and post-absorptive (largely metabolic) participants' diets found that sensory factors exerted a processes. There is direct and indirect evidence that major in¯uence on fat-reduction success rates (Terry et changes in gastrointestinal responses in¯uence the amount al, 1991; Kristal et al, 1992). A main reason why women of food ingested at meals. A number of nutrient speci®c felt giving up dietary fat was dif®cult related to their models are broadly consistent with secular trends in nutri- perception that fat enhanced the taste quality of the diet. ent intake in relation to body weight (WHO, 1990) or Additionally it appeared that women found that dif®culties correlations between NB and subsequent FB in rodents in increasing starch intake precluded their ability to reduce (Flatt, 1987) and humans (Stubbs, 1995). However these fat intake (Buzzard et al, 1990; Gorder et al, 1986). This nutrient speci®c models only explain a small proportion of suggests that it is relatively dif®cult to increase starch the variance in EI. While earlier models viewed peripheral intake. The ready to eat breakfast cereal industry uses a control of feeding as due to one or more simple negative variety of sugar:starch mixtures to improve the sensory feedback loops, more recently research has focused on the appeal of their products. It is therefore likely that sweetness multiple signalling systems involved in the maintenance of acts as a vehicle for both starch and for fat intake. However energy and NB (Blundell & Stubbs, 1997). Integrative the natural differences in ED between CHOs and fats models that account for the way in which the brain means that the sugar-fat mixture has a greater potential to monitors the ¯ux of peripheral signals related to overall increase EI than the sugar-starch combinations. metabolic fuel status appear to have greater explanatory power than single nutrient-based models of feeding (Fried- Carbohydrate related sensory stimuli: sweetness man & Tordoff, 1986; Friedman et al, 1990; Ritter & For the last decade there has been a healthy controversy Calingasan, 1994; Langhans & Scharrer, 1992). As the raging about the role of sweetness, sucrose and arti®cial complexity of the appetite system unravels, the need for a sweeteners (Porikos & Van Itallie, 1984; Booth et al, 1988; conceptual structure to order our understanding of physio- Blundell & Rogers, 1994; Clydesdale 1995; Black & logical and non-physiological control of feeding becomes Anderson, 1994) in maintaining EB. The key issue relates increasingly necessary. The differential in¯uences that to what effects sweetness, plus or minus CHO energy, has macronutrients exert on satiety and EI appear to operate on appetite and EB. There are three main hypotheses: (i) via a number of sequential mechanisms, which have been adding sweetness without calories to foods leads to lower set out conceptually by Blundell as a `satiety cascade'. levels of EI than when sweetness with calories are added; However, to appreciate the probable importance of these (ii) sweetness without calories leads to an anticipatory various metabolic signals concerned with feeding, it is facilitation of eating; and (iii) ingestion of sugars (sweet- critical to appreciate that physiological signals associated ness with calories) correlates with thinness and lowers fat with nutrient ingestion are loosely linked to FB except in intake which is itself the reason for the lower body weight. relatively extreme physiological circumstances. This means These alternatives have probably been interpreted too that nutrient-based models of feeding poorly predict FB rigorously because the effects of these factors on appetite because metabolic processing probably exerts a modest and EI are likely to be in¯uenced by the conditions under in¯uence on habitual day-to-day FB of Western indivi- which they are assessed. duals. Under these conditions metabolism does not appear There is little doubt that most animals display a pre- to strongly determine behaviour. Metabolic events may ference for sweetness at a very early age, and that sweet- exert far more potent effects on feeding under more ness is a factor favouring the selection and subsequent extreme conditions (Saris et al, 1989; Gil et al, 1991). ingestion of sweet foods. Conversely, different people exhibit markedly different preferences for sweetness inten- sities and so simply adding sweetness to foods will not Sensory determinants of CHO and fat intake stimulate everyone to eat. Assuming that sweetness does in Sensory factors that promote or limit food and energy general stimulate the selection and consumption of these intake foods, the next question relates to whether sweetness with In the above sections it has been argued that physiological or without calories differentially affects appetite and EI. signals act as cues for, rather than determinants of, FB. Can replacement of sugar by intense sweeteners drive EI Sensory attributes of foods also act as cues for identi®ca- down? Despite the common assumption that replacing tion, selection and ingestion of foods. Sensory stimuli act as dietary sugars with intense sweeteners will promote a a `gatekeeper of acceptability' for foods, a phenomenon more negative EB, there is a remarkable paucity of data with which the food industry is familiar. Until recently, the to demonstrate this effect. There is certainly little epide- sensory attributes of a food provided people with reliable miological evidence to suggest that arti®cial sweetener information on the probable nutrient content of foods. Fats consumption correlates with lower BMIs, or that increased and CHOs have distinct sensory attributes, when ingested arti®cial sweetener consumption in the population has separately or as various mixtures contained in foods. contributed to any reduction in EIs or the prevalence of Children (whose energy requirements are disproportio- overweight and obesity. A problem with the majority of nately high due to growth) develop conditioned preferences laboratory studies, which examine the effect of sweetness, for energy-rich foods (Birch, 1992). Drewnowski has sugars and arti®cial sweeteners, is that many are short-term further argued that sugars act as a vehicle for fat intake and therefore do not address the issue of EB. It is also through such sensorially mediated, nutrient-associated possible that covert replacement of sugars with arti®cial High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S160 sweeteners is more likely to decrease EI if subjects can diet by replacing fat with olestra (de Graaf et al, 1996; only alter the amount they eat of a diet of ®xed composition Hulshof et al, 1995a, b; Bray et al, 1995; Cotton et al, rather than having access to a variety of familiar foods. 1994; Johnson et al, 1995; Miller et al, 1995, 1996). As Most authors seem to be in agreement that the purely with products containing intense sweeteners, restrained post-ingestive effects of aspartame do not stimulate intake subjects may show a greater degree of disinhibition when (Blundell & Rogers 1994; Clydesdale 1995; Black & they are aware that they are using the reduced fat product Anderson 1994). Blundell et al initially reported that (Miller et al, 1995, 1996) Only one short term study has arti®cially-sweetened drinks could actually stimulate appe- examined the effects of olestra on appetite and EI using the tite. They suggested that sweetness without calories pro- additive principle; it found that the sensory qualities of fat vides a sensory cue for CHO calories, which leads to without its energy content did alter short-term FI (Rolls et cephalic-phase physiological changes that anticipate EI al, unpublished). A number of animal studies report that (Blundell & Rogers 1994). Intense sweeteners have only oro-sensory stimulation with fat can facilitate appetite been found to stimulate intake when a food has been (Tordoff & Reed 1991). To date there have been no sweetened with intense sweeteners or when a less sweet structured comparisons of the effect of fat- and sugar- food has been compared with an isoenergetically equivalent related sensory stimuli (with and without the attendant food to which sweetness has been added (their `additive energy) on appetite control and EB. Furthermore there is principle') and not when two foods of differing ED but the a marked absence of long term studies in this area. It is not same level of sweetness are compared. This they call the therefore known whether the use of nutrient mimetics `substitutive principle'. Again this area is bedevilled by maintains sensory preference for the nutrients concerned. methodological controversies, such as the appropriate drink The effect of including nutrient mimetics in foods on vehicle for the sweetener (water or a familiar soft drink), learned FB is also largely unknown. the time-course of experiment, and the subjects used. Blundell & Rogers argue that the strongest experimental Sensory stimulation to eat Ð a fat:sugar seesaw or a fat- designs contain tests of both the additive and substitutive sugar synergism? principle (Blundell & Rogers 1994). No long-term studies The effects of nutrient-related sensory stimuli on FB appear which address EB have yet achieved this dual testing. to be at odds with the notion of the fat : sugar seesaw, which Black & Anderson report that the use of aspartame-swee- has been derived from apparent epidemiological relation- tened water leads to an acute short-term increase in sub- ships between the amount of fat and sugar (as a percentage jective appetite in lean men, but that aspartame-sweetened of EI) that people appear to eat (Romeau et al, 1988; carbonated soft drinks induce a transient suppression of Miller, 1990; Tucker & Kano 1992; Bolton-Smith & appetite in similar subjects over a similar time-frame Woodward 1994). (Black & Anderson, 1994). The issue is complicated by It is now generally accepted that the views of the early the fact that satiety can be transiently conditioned by starch 1970s are wrong, that is, sweetness provided in the form of containing drinks that are paired with a given sensory cue CHO energy stimulated EI and contributed to increases in such as ¯avour (Booth et al, 1988). Once conditioned, obesity. The epidemiological data suggest that consumption similar levels of satiation can be transiently induced by the of sugars, that is, sweetness with CHO, is associated with conditioning stimulus alone. Therefore the effects of prior thinness. Yet the same studies tend to show that as sugar conditioning could in¯uence the outcome of studies using intake increases so does EI. This suggests that more vehicles that mimic the sensory properties of familiar physically active people select more sugars and therefore foods. does not necessarily imply that increased sugar intake Dietary restraint may also in¯uence the response of spontaneously promotes thinness. However, interpretations subjects to sweetness, sugar and arti®cial sweeteners arising solely from epidemiological data are hazardous (Lavin et al, 1997). Again there is a notable lack of because of the known unreliability of dietary survey data. longer-term studies in this area that address EB. While there is evidence of some reciprocity in the In summary, there is little evidence that arti®cial sweet- population between the percentage of energy ingested as eners reliably decrease appetite or reduce EI, but they could CHO and sugar intake on the one hand and the percentage perhaps prevent any excess EI which would otherwise of energy ingested as fat on the other, this probably re¯ects occur when calories were provided as drinks (substitutive the fact that people eat to defend against energy de®cits, principle). There are conditions where arti®cially-swee- rather than implying that there is some active process tened drinks have been found to stimulate appetite and whereby sugar intake promotes dietary fat avoidance. less often EI, but there is little evidence to suggest that Analysis of the relationship between the fat, sugar and sweeteners reduce intake. Understanding the applicability the sensory stimulation to eat suggest that fat and sugar of these ®ndings to free-living humans is an important should synergistically increase EI (Drewnowski, 1997). problem yet to be resolved. Indeed as the number of grams of fat intake increases in diet surveys, so usually does the number of grams of sugar. Fat-related sensory stimuli There is little or no evidence that increasing sugar intake The most commonly used tool to examine the effect of fat- promotes a negative EB and weight loss: the critical related sensory stimuli on appetite and EI has been short-to- experiments have not been conducted. One approach to medium term examinations of the impact of substituting this issue will be to examine the effects on food and real fat with the caloric fat replica Olestra. These studies nutrient selection of experimentally titrating fats and have been conducted using the Blundell & Rogers' sub- sugars into the diet. Equally important here is the con- stitutive principle, which is the intended use of food sideration of subgroups that may display fat and sugar products containing olestra. The majority of these studies intake quite different from the mean values for the whole show that in the short-to-medium term subjects fail to population. There is evidence for gender differences and compensate completely for reductions in the ED of the for gender differences which vary with BMI. High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S161 Nutrient selection basis of food rejection or avoidance. Exactly how subtle these effects can be with reference to food selection is not Sensory in¯uences of fats and CHOs as determinants of yet known. Therefore it has recently been claimed from food selection published trials that the aversive side effects of the pan- There is evidence that sensory factors can re-set the limits creatic lipase inhibitor (which inhibits fat digestion) favour to the intake of fats and CHOs in the short- to medium-term selection away from further fat ingestion, in subjects (Rolls et al, 1981, 1982, 1983; Le Magnen 1992; Green & engaged in stage three clinical trials. Blundell, 1996; Johnstone et al, 1998). The main features indicate that EI can be raised by sensory contrasts (the variety effect), and by very potent sensory attributes of Summary: position statement on the role of behaviour foods. For instance we have recently shown that increasing and appetite in determining the limits of fat and CHO the sensory variety of nutritionally identical diets (with intake respect to macronutrient composition) leads to spontaneous increases in food and EI in lean men over seven days Mechanisms that control the amount of food consumed and (Johnstone et al, 1997). It is however unclear what the determine food choices are of paramount importance when longer-term impact of these effects is. It is interesting that a considering the upper and lower limits of fat and CHO sensory manipulation in this study led to an increase in FI intake. Appetite mechanisms exert their greatest in¯uence (the weight of food eaten), while fat manipulations usually over the amount of food and its composition (fat=CHO) produce passive overconsumption and FI is not increased. when there is an abundance of food available and indivi- Sensory factors are likely to interact with diet composition, duals can make choices among distinguishable products. dietary ED or other environmental in¯uences on intake, to It is important to note that the actual consumption of determine overall EB. Such integrative models are a food is a form of behaviour. When behaviour is a scienti®c development for the future. end point it cannot be considered as a variable equivalent to a physiological end point such as the plasma level of metabolite, oxidation rate or change in organ function. Physiological determinants of nutrient selection When behaviour operates naturally (in free living indivi- In rodent models a number of neurochemicals have been duals) and its amount and direction are not restrained, its identi®ed which may be involved in linking information expression is in¯uenced by both biological and environ- regarding peripheral CHO status to FB (Lebowitz 1992; mental in¯uences. The nature of the food supply is a part of Bray, 1992; Langhans, 1996, for reviews). Likewise, cen- the environment. Therefore when free behaviour is seen as tral administration of a number of neuropeptides can the vehicle by which nutrients (fat and CHO) are ingested selectively increase or decrease fat intake in rats with the composition of foods in the food supply can assume access to pure macronutrient sources (Lebowitz, 1992; major importance. Bray, 1992; Langhans, 1996). It is unclear whether these Appetite mechanisms can be said to control the pattern extreme interventions actually drive nutrient selection in of eating behaviour. This pattern is episodic. Food, energy the experimental models used or whether they in¯uence and nutrient intakes are therefore a function of the size of other factors such as the oro-sensory response to the pure eating episodes, the frequency of episodes, and the compo- nutrient sources provided, or actually make some pure sition (F, CHO content) of the foods consumed. nutrient sources aversive. The use of pure nutrient sources The processes of satiation and satiety are convenient in this respect is a limitation of such studies, as are the concepts to describe effects on the size and frequency of supraphysiological manipulations that are often made. At eating episodes. Both satiation and satiety re¯ect the the present time there is very little evidence of environ- integration of signals from inside and outside the body mental or behavioural factors that will directionally in¯u- (biological and environmental). The following representa- ence nutrient selection in humans. tion of events is important: There are a number of extreme situations in animal models where nutrient selection has been demonstrated, as (1) Food consumed generates physiological responses (for a result of changes in peripheral physiology. In some cases example, gastric emptying rates, plasma levels of there may be analogous situations in humans. For example, metabolites and oxidative processes in different tis- streptozotocin-diabetic rats ®nd glucose aversive, since sues), which are regarded as satiety signals. These they have dif®culty in utilising it. They preferentially internally generated satiety signals vary in intensity select a HF diet (Edens & Friedman 1988). It is possible and duration; they therefore have the potential to that some insulin resistant humans show similar effects. In in¯uence the size and frequency of eating episodes. some studies intense exercise stimulates CHO intake in rats (2) Certain proximal satiety signals (close to the process of over a period of weeks (Miller et al, 1994). This is clearly a ingestion) can, in turn be traced to neurochemical conditioning effect since rats are not capable of receiving events in the brain and in some cases, to the activation nutritional wisdom from humans, although a good deal of of speci®c receptors. When the gene for the receptor is information relating to the quality of the diet can be learned known this provides a link between satiety signals and from con-speci®cs (Sclafani 1995, 1997). It is not known genetics, that is the capacity for genotypes to express how much of preferential CHO intake in humans is condi- strong or weak satiety signalling. tioned or taught. In general, changes in the composition of (3) One recently postulated appetite signal linked to a the diet which are noticeably bene®cial to the subject may genotype involves `leptin' (ob-protein) linked to the lead to the acquisition of behaviours favouring selection of ob gene. Another possible signal involves the serotonin those foods. It is therefore possible that the preferential (5-HT)2C receptor. This receptor is involved in satiety, CHO selection that occurs as a response to sustained the gene for the receptor has been cloned, and there is intense exercise is maintained by a conditioned change in an experimental animal `knockout' preparation. The 5- FB. Factors leading to aversive states are likely to form the HT2C knockout displays hyperphagia, hence there High and low carbohydrate and fat intakes JE Blundell and RJ Stubbs S162 exists a potential genetically controlled satiety mechan- expected, in turn, to in¯uence the impact of endogenous ism. However, currently the search for polymorphisms signalling. Because CHO foods have a lower ED than fat of the 5-HT2C receptor linked to obesity or eating foods (on average) and because of their greater satiating disorders has proved inconclusive. capacity, the free intake of high CHO foods is likely to be The question can therefore be posed: to what extent do self-limiting (at lower EIs than those generated by fatty these satiety signals Ð triggered from biological processes foods). This does not mean that excess EIs are impossible by the impact of ingested food Ð control the intake of fat when people feed ad libitum on high CHO diets. and CHO. That is, do these signals help to set the limits for From this analysis it can be deduced that the appetite the amounts of fat and CHO that can be consumed? It is control mechanisms will permit the consumption of large generally agreed that the actions of protein, fat and CHO, amounts of fat (if an abundance of high fat foods exists in once ingested, generate satiety signals of differing strengths the food supply). Except for speci®c physiological circum- and at different physiological points. The rank order of stances (endurance explorers) where there is an urgent need potency is believed to be protein (strongest), CHO and fat for high EIs, in the face of decreasing body weight, it is (weakest), although the differences between CHO and fat at unlikely that the body will generate a speci®c drive for fat. the same level of dietary ED may be rather smaller than It is also possible, that the body will permit the consumption often assumed. of large amounts of CHO (if an abundance of high CHO However, it should be recognised that endogenously foods exists in the food supply). However the intake of such generated satiety signals can be overridden by deliberate high CHO foods should tend to yield a lower intake of conscious action and by the properties of foods themselves. energy than the eating of high fat foods. This is because The features of individual foods which are most potent are high CHO foods tend to be less energy-dense than high fat the oro-sensory attributes (taste, texture, smell, mouth feel) foods. There is good reason (but currently little evidence) to and the energy load of the food. When many foods are suggest that drive to ingest CHOs may be produced by high available for consumption, the variety of the foods (contrast rates of CHO oxidation in exercise. between sensory properties) becomes an important factor, One major implication of an examination of appetite within a given meal. The longer-term consequences might mechanisms Ð and their effects on upper and lower intakes appear intuitively obvious but are not documented by of fat and CHO Ð is that the control of FB is of special empirical data. signi®cance. It is also apparent that the control of eating Foods that are highly palatable can stimulate and pro- behaviour cannot be understood in the absence of an under- mote consumption. The availability of different types of standing of physiology and EE. Equally, it follows that the foods with contrasting sensory properties can allow eating impact of fat and CHO on physiology cannot be fully to be re-stimulated during the course of a meal. This will appreciated until the consequent effects of behaviour are engender a greater meal size. The longer-term effects are understood. Therefore physiologists should pay more atten- unclear. The size of eating episodes (measured by energy tion to the effects of their manipulations on behaviour (via value) can also be increased by the energy load contained in appetite signalling mechanisms), and behaviour-oriented the food. Since fat is the most energy dense nutrient (and researchers should understand the way in which the com- also possesses the weakest effect on satiety) it is likely that position of foods can affect changes in physiological func- high fat foods will exert a strong tendency to enlarge the tion and its behavioural sequelae. energetic content of eating episodes. There is currently considerable interest in the relative roles of the concentration of nutrients per se (protein, fat, References CHO) in foods versus ED in general on EI. 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