European Journal of Clinical Nutrition (1999) 53, Suppl 1, S148±S165
ß 1999 Stockton Press. All rights reserved 0954±3007/99 $12.00
http://www.stockton-press.co.uk/ejcn
High and low carbohydrate and fat intakes: limits imposed by
appetite and palatability and their implications for energy
balance
JE Blundell1* and RJ Stubbs2
1
BioPsychology 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
this paper
In Western countries there has been renewed media, consumer and government concern during the 1990s regarding
the in¯uence that levels of dietary fats and=or CHOs can
exert on human health and well-being (WHO, 1990;
Department of Health 1992, 1994, 1995). Throughout this
time, the alarming rise in the proportion of overweight and
obese adults in Western society has led to considerable
debate regarding the underlying causes of these secular
trends. The two major factors now cited as being conducive
to weight gain in Western populations are reduced levels of
physical activity, which decrease total energy expenditure
(EE), and the ingestion of a high-fat (HF), energy-dense
diet, which appears to facilitate excess energy intakes (EIs)
(Swinburn & Ravussin, 1993; Prentice et al, 1989; Prentice
& Jebb 1995; Department of Health, 1995). These recommendations have led to a near fat-phobia amongst some
Western consumers. Ironically, it has been recognised for
more than 50 y that it is dif®cult to change habitual forms
of behaviour (Gorder et al, 1986; Buzzard et al, 1990;
*Correspondence: Dr JE Blundell, BioPsychology Group, Psychology
Department, University of Leeds, Leeds LS2 9JT, UK.
Kristal et al, 1992; Mela 1995; Brownell & Cohen 1995).
Therefore it is not surprising that in practice it appears
dif®cult to entice the population to spontaneously reduce
fat intake and increase levels of physical activity. The food
industry has been proli®c in the production of lower fat
foods, in the hope that they will assist in reducing dietary
fat (and possibly EIs), while maintaining suf®cient sensory
appeal that consumers will choose and ingest them
(Leveille & Finley 1997; International Food Information
Council, 1997).
One major feature in understanding the role of appetite
in this context is the recognition that fat and CHO intakes
are determined by forms of behaviour. This behaviour is
not solely under biological control. Indeed, feeding behaviour (FB) forms part of an interaction between biology
(physiological mechanisms involved in food processing by
the organism and energy balance [EB]) and the environment (nature of the food supply, composition of foods,
culturally de®ned patterns of eating etc.). This intimate
relationship can be referred to as a transaction.
Therefore, eating is in¯uenced by events in the biological
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
frequency and the selection of particular foods. The processes
of satiation and satiety (acting conjointly) determine, in large
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
part, the size and frequency of eating episodes. In considering
intakes of CHOs and fats, the question can be posed: `how do
fats and CHOs in¯uence the size, frequency and composition
of eating episodes (and therefore total EI), and what are the
mechanisms responsible?'
From a physiological or metabolic standpoint fats and
CHOs can be regarded as types of fuel to be used in
physiological processes. Some problems of EB can be
reformulated as problems of fuel balance. However, in
considering the role of appetite, an extension of this
thinking is required. Eating behaviour is the way by
which fats and CHOs are transported into the body. Once
fats and CHOs are associated with behaviour, their effects
can be generated by features of food other than the value of
the nutrient or fuel. Indeed FB should be considered as the
consumption of `foods' not `fuel'. The nutrient itself can
contribute to the taste, texture, viscosity, weight and bulk of
the food, all of which characteristics can help to determine
when and how much of a food is consumed. When considering EB per se, it may not matter very much whether
CHO enters the body as orange juice or bread. But, in
considering appetite control and palatability, the sensory
features and form of the food would be extremely important, often, perhaps of overriding importance.
For the purposes of this review appetite control may be
de®ned as the sum of the processes which determine
patterns of FB. What are the particular processes, which
limit the amounts of fats, and CHOs that people consume?
Are the limits set by internal physiological signalling, the
composition of foods in the environment or the salience of
cues which in¯uence feeding?
To gain a clearer understanding of the effect that fats
and CHOs exert on appetite and EB, it is important to
examine several issues concerning the effects of dietary fats
and 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 FB and body
weight; (ii) the distribution and density 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; and
(iv) the known effects that fats, CHOs and dietary energy
density (ED) exert on appetite and EB. From these considerations we will discuss: (1) proposed nutrient-based,
physiological models of appetite control and their likely
relevance to observed patterns of FB and macronutrient
intakes; and (2) the potential role of sensory factors in
promoting or limiting fat, CHO and EI in modern human
populations.
Throughout this paper we hope to emphasise the need
for increased semantic precision in the area of appetite
control, FB and EB. Greater semantic precision is likely to
avoid confusion over important issues pertinent to diet
composition and FB. For instance, whether HF or high
ED diets promote excess EI. It is perhaps also timely to
consider replacing the `traditional' obese-lean dichotomy in
describing appetite control and FB with the concept of
phenotypes which describe the likely behavioural and=or
physiological responses of certain groups of people to
dietary factors believed to affect their disposition towards
weight gain (Drewnowski, 1995; Cooling & Blundell,
1998). It is also important to consider the generalisability
of results found in the laboratory to people living their
normal lives in the real world (Blundell & Macdiarmid,
1997).
Physiological drives and learned behaviour as
determinants of feeding
The nature of feeding behaviour and its physiological
determinants
Mammalian feeding occurs regularly and intermittently and
despite a general lack of conscious nutritional knowledge
on the part of the individual, usually appears to match
energy and nutrient intakes with requirements. How is this
achieved? The common explanation is that appetite, EI, FB
or EB are regulated to ensure that physiological requirements are met. However, there is an embarrassing lack of
direct evidence for this regulation (Caterson et al, 1996). It
may be that neither FB, nor appetite are regulated in a
strictly physiological sense since: (i) neither are held
constant within certain narrow limits; and (ii) FB is not
an inevitable outcome which is determined by an altered
physiological signal or need (physiological determinism).
FB is responsive to a number of induced states such as
pregnancy, cold exposure, growth and development, and
weight loss. These responses have often been cited as
evidence of a system (appetite and FB) that is regulated.
It may be that aspects of body size and composition are
regulated and that changes in FB are functionally coupled
to those regulatory processes. Indeed, FB might be said to
be adaptive rather than regulated since quantitative and
qualitative food intake (FI) is ¯exible, responsive and
anticipatory, sometimes enabling the animal to adapt to
changes in the state of the internal and external environment. Eating behaviour connects the phenotype (the biological system of appetite control) to the nutritional
component of the environment. Inasmuch, eating behaviour
is subject to both interoceptive and exteroceptive conditioning. It would appear that under normal ad libitum
feeding conditions encountered in Western society, dayto-day FB is not determined by powerful unconditioned
physiological signals but by learned behaviour in response
to a range of in¯uences, which include physiological
processes associated with ingestion, absorption, storage
and metabolism of nutrients. Other in¯uences include
salient social and cultural variables. It can be appreciated
that as energy imbalances accrue, the in¯uence of additional physiological signals (for example, depletion of fat
mass or lean tissue mass) on FB will escalate. It therefore
appears that there is a margin of EB (that typi®es the
majority of Western adults) within which a large number of
factors in¯uence appetite and EI. Within this zone changes
in energy and nutrient balance do not induce large detectable sensations that lead to corrective changes in FB.
Outside of this range (which may vary among different
individuals) physiological signals may exert more potent
restorative in¯uences on appetite and EB. These in¯uences
appear to be greater in response to energy de®cits and so
appetite control in humans appears skewed towards a
positive EB and defence against negative EBs, since
positive EBs appear more comfortably tolerated than
energy de®cits. Physiological signals may affect FB
either directly or through perceptible changes in functional
integrity (for example, feeling weak and tired during
energy restriction), which can act as learning cues for
feeding. If this argument is correct, it may be that studies
which have examined the impact of covert dietary manipulations on appetite and EB actually assess the extremes
required for physiological signals to in¯uence compensatory changes in FB (Van Stratum et al, 1978; Lissner et al,
S149
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,
1995a, b, 1996, 1997a).
Hunger and satiety often have a large learned, anticipatory (entrained) component rather than being the direct
consequences of unconditioned physiological signals per se
(Booth et al, 1976, 1982, Booth 1977), such as reduced
gastrointestinal content. Such physiological events can act
as important cues for feeding but they do not necessarily
directly determine that behaviour. This has important
implications for the use of substances and technologies
which mimic the sensory attributes of fats and CHOs, since
they will affect the processes whereby humans learn to
associate the sensory characteristics of foods with the
energy and nutrients they contain (Booth et al, 1982;
Booth, 1992). These considerations are important because
they allow us to account for a number of observations
which cannot otherwise be explained: (i) over half of the
adult population of several Western countries are collectively overweight and obese. Models based on pure physiological determinism would have to postulate an
epidemic of physiological defects to account for such a
prevalence of `energy dysregulation'; (ii) few, if any,
exclusively physiological models of appetite control accurately predict a large proportion of the variance in human
FB; (iii) certain conditions such as transient periods of
intense physical activity or the use of covertly manipulated,
unfamiliar foods appear to result in a very poor coupling of
EI with EE; and (iv) while a large number of studies of
human feeding show varying degrees of compensation for a
number of experimental interventions very few have
recorded clear evidence of EB regulation. This has important implications for the manner and extent to which
humans regulate their body weight.
Body weight as a set-point or a dynamic equilibrium
The above arguments suggest that body weight is determined not by a set-point mechanism (Keesey et al, 1976;
Bernardis et al, 1988) which operates through powerful,
physiological negative feedback signals, correcting FB in
line with EB in the short-to-medium term. Rather, it would
appear that body weight exists as a dynamic equilibrium
with a tendency to drift upwards. That is, both lean and
overweight subjects may well be in a relatively steady state
or equilibrium for much of the time as regards increases in
body weight. These periods of equilibrium may be punctuated by short, discrete but signi®cant increases in body
mass. Once stabilised, weight may be defended at the new
higher level (the so-called ratchet model of weight gain). If
this is so then factors, which produce episodic gains in
body weight, would have signi®cance for long-term weight
control. Such a system would be consistent with the vast
body of experimental data that has found remarkably little
differences in the reported eating behaviour of lean and
obese subjects (Spitzer & Rodin, 1981). Indeed some
studies have noted remarkable similarities in the responses
of lean and obese subjects to nutrient manipulations (Hill &
Blundell, 1990; Thomas et al, 1992). An important exception to this is the case of mis-reported dietary intakes which
tends to increase with increasing BMI (Black et al, 1991;
Schoeller 1990).
Recent analysis of average weight changes over time
suggests that US adults appear to gain weight at a steady
rate of 1 ± 2 kg per annum (Burmaster & Crouch 1997).
This population trend may actually mask a series of
hyperphagic events which punctuate the more common
state of weight equilibrium. However, the nature, rate and
extent of weight change in the population are insuf®ciently
documented at present to discern exactly how people tend
to gain weight.
Physiological requirements for fat and CHO in relation to
levels available in the environment
If changes in nutrient balance are important cues for or
stimulators of FB, it is reasonable to suppose that the
greater the physiological requirements for these nutrients,
the stronger the drive to ingest them. The requirements for
lipids in adult humans are largely met by all but except
perhaps the most extreme diets. Even during total starvation it has been estimated that on average, adult adipose
tissue mass will provide around 2 kg of essential fatty acids
(Newsholme & Leach, 1992). The requirements of growing
children are however greater.
As regards CHO requirements, it is unclear what, in the
strictly physiological sense, is the absolute requirement for
dietary CHO (Newsholme & Leach, 1992). Populations
subsisting on virtually CHO free-diets usually consume
large amounts of protein which can be used for gluconeogenesis. It therefore appears that part of human adaptation
to variations in the environmental supply of fats and CHOs
consists of considerable physiological plasticity, in meeting
our requirements for speci®c metabolic fuels. This does not
mean that altered physiological levels or utilisation of fat
and CHO do not act as cues which drive FB towards altered
energy and nutrient intakes. However these cues do not
appear to be heavily weighted or deterministic.
In¯uence of sensory stimulation on appetite
In considering the capacity for EI to rise above EE the
weakness of inhibitory factors has to be set against the
potency of facilitatory processes. The palatability of food is
clearly one feature which could exert a positive in¯uence
over behaviour. The logical status of palatability is that of a
construct (it is not an objective feature such as protein
content or blood glucose) (Ramirez, 1990; Rogers, 1990).
The relative palatability of a food can be determined by
choice tests or taste tests relative to other standard ingestants (for example, a 5% sugar solution) (Le Magnen,
1992). However, there has been much more controversy
over the actual de®nition of palatability. The reader is
referred to a recent debate regarding these de®nitions
(Ramirez, 1990). In general the palatability of a food can
be thought of as the sensory capacity to stimulate ingestion
of that food. This de®nition takes account of the fact that
the palatability of the food is jointly determined by the
nature of the food (smell, taste, texture and state), the
sensory capabilities and metabolic state of the subject,
and the environment in which the food and subject interact.
Palatability is therefore not stable; indeed the palatability of
a food typically declines as its own ingestion proceeds.
This process is believed to mediate the phenomenon of
sensory speci®c satiety (Rolls et al, 1981, 1982, 1983,
1988; Rolls 1985, 1986). Work on military personnel
suggests that the decline in preference for highly preferred
foods (for example, chocolate) is greater than that for staple
foods such as bread, which exhibit more stable preference
pro®les (Meiselman & Waterman, 1978). Palatability can
be dissociated from sensory intensity since sensory intensity increases with the concentration of the compound or
food being tasted; palatability generally shows a parabolic
n-shaped curve when plotted against sensory intensity of
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
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 cumulative 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,
1982, 1985, 1986, 1988).
It may be hypothesised that palatability would exert a
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
pleasure from food on the initiation and maintenance of
eating? Although many would agree that palatability exerts
a powerful in¯uence on eating behaviour there is no
systematic body of data to explain the strength or the
limits of the effect (Ramirez et al, 1989).
The nutritional composition of foods can also in¯uence
FB. The fats and CHOs contained in foods can affect both
the palatability of those foods and the density of energy and
nutrients within those foods. Certain CHOs will in¯uence
the digestibility of foods which may limit subsequent
feeding. It is important to consider the extent to which
the ED and total amount of fats and CHOs that are
contained in foods in¯uences the willingness of individuals
to ingest those foods. How do the nutritional properties of
foods (and their sensory attributes) in¯uence or limit the
voluntary food, energy and nutrient intake of individuals,
both in the laboratory and under more naturalistic conditions? Although the effects of fats, CHOs and proteins on
eating has been investigated intensively for some years,
only recently have their effects been considered both as
nutrients in themselves (that is, when ED is controlled and
comparisons are made at the same level of ED, and in terms
of their contribution to overall dietary ED (Stubbs et al,
1995b, 1996, 1997a; O'Reilly et al, 1997; Blundell &
Stubbs, 1997a).
Figure 1 Relationship between percentage weight (expressed in grams)
from dietary macronutrients and water (predictor variables) and energy
density of 1032 ready to eat foods, taken from the British food composition
tables (Holand et al, 1991).
S151
Figure 2 Relationship between percentage of energy (expressed in kJ)
from dietary macronutrients and water (expressed in grams) (predictor
variables) and energy density of 1032 ready to eat foods, taken from the
British food composition tables (Holand et al, 1991).
Energy and nutrient relationships within foods
The contribution of fat, carbohydrate, protein and water to
dietary energy density
We have recently conducted a preliminary analysis of the
relationship between nutrient and water content and ED in
1032 ready to eat foods from the British food composition
tables (Holand et al, 1991) (excluding supplements). When
water and nutrients are plotted in g=100 g of food, as
predictors of dietary ED all nutrients contribute positively
to ED, and water content contributes negatively (Figure 1).
However, only fat (ED ˆ 462.6 ‡ 35.46fat R 2 ˆ 75.0)
and water (ED ˆ 2034 7 21.26 water, R 2 ˆ 66.7) have a
large R2 value, those for protein and CHO indicating a
generally poor relationship. When the relationship between
nutrient composition (expressed as a percentage of total
food energy) and ED was examined, fat again correlates
positively with ED, while protein and CHO show a weak
negative relationship to ED. The relationship for fat under
these conditions is relatively weak (ED ˆ 320.1 ‡ 16.36
fat, R 2 ˆ 35) (Figure 2). Therefore while dietary fat elevates ED, HF foods (expressed as a percentage of energy
from fat) are by no means inevitably high in ED. Furthermore, the major determinants of the ED of a food are the fat
and water content. In this analysis there appears to be a
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
interacts with the food matrix in the gut (Mela, personal
communication). These issues prompt a consideration of
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
issues is incomplete. In addition, the effect of dietary
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.
Energy density as a limiting factor for EI
It is well known that the available energy content of the diet
is crucial in allowing growth and development to proceed
along genetically pre-set levels. In this context ED can refer
to the total energy per gram of food ingested. It can also
refer to the metabolisable energy available from that diet
(Livesey, 1991). It is clear that low dietary ED can limit EI
and produce sub-optimal levels of EB. The extent to which
humans can adequately adapt to low levels of dietary ED is
unclear. Problems with obtaining accurate dietary intake
measures (Black et al, 1991; Schoeller, 1990) and lack of
knowledge of the relationship between ¯uid and FI preclude conclusive statements. While the impact of altering
dietary ED using differing nutrients, on EI and EB is
beginning to emerge in laboratory studies lasting up to
two weeks (Lissner et al, 1987; Kendall et al, 1991;
Thomas et al, 1992; Stubbs et al, 1995a, 1996, 1997a;
O'Reilly et al, 1997), the extent to which humans adapt FB
to changes in the dietary ED over longer periods is
unknown. The few longer-term interventions that have
altered the nutrient density of certain foods have shown
relatively good compensation over periods of a few months
(Aaron et al, 1999; Gatenby et al, 1995; Zimmermans et al,
undated).
How should we de®ne dietary energy density in relation to
feeding behaviour?
The importance of dietary ED in altering EB through its
effects on EI have begun to receive renewed attention as
the effects of dietary fat are being viewed by some as
exclusively a property of dietary ED. We suggest that some
caution should be exercised in describing the ED of the diet
and its determinants. It is likely that the ED, (as kJ=g wet
weight of food) is not perceived as such by the human
body, since the body reacts to the mixture of foods contained in a meal rather than the individual components of
that meal. For instance the Western diet appears to consist
of a relatively small percentage of EI in the form of
extremely energy dense foods (that is, > 1.8 kJ=100 g), a
large number of moderately ED foods (0.4 ± 1.7 MJ=100 g)
and a variable number of low energy dense foods
( < 0.4 kJ=100 g). Overweight people may preferentially
select from the food categories with a higher ED (Westerterp-Plantenga et al, 1996). How does ¯uid intake contribute to the total ED of the diet? Exactly how does dietary
ED affect human FB? How does the composition of the diet
in¯uence the relationship between ¯uid and food intake and
hence the overall ED of the diet. We have found that as the
dry matter content of mixed diets increased, so does water
intake. Does the ED of a food correlate with its palatability? Since salt ingestion increases thirst, will adding salt to
food effectively lower dietary ED?
Energy and nutrient relationships within foods ingested
by human populations
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
diet composition. For example the Inuit have been reported
as subsisting for months on diets almost entirely comprised
of animal matter and virtually devoid of all CHOs (Mowatt,
1975). These diets were therefore high in protein and fat.
This produces diarrhoea and general malaise during lean
months when the energy to protein ratio of the diet falls too
low. Similarly, the traditional Japanese diet has been
reported to provide some 8% of EI as dietary fat, in extreme
cases. It appears clear from these accounts that human
populations are capable of adapting, (through their physiological plasticity) to meet their physiological requirements
from a wide range of macronutrient ratios in the diet. The
overall effects of such extreme nutrient intakes have been
discussed in detail in other papers.
Extremes of EI have been recorded during overfeeding
studies (Norgen & Durnin, 1980; Ravussin et al, 1985;
Diaz et al, 1992), during ceremonial overfeeding (Pasquet
et al, 1992), underfeeding studies (Keys et al, 1955) and
from EI records derived from famine and concentration
camp victims during the second world war. These cases
represent states of accommodation to extreme environmental conditions, rather than voluntarily FB. Compensatory
responses subsequent to such induced extremes of EB can
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
mass and composition were restored. In healthy subjects,
such high levels of EI have only been recorded under
conditions of extreme physical activity such as the tour
de France (Saris et al, 1989), or polar expeditions (Stroud et
al, 1993). Under these conditions levels of EE were so high
that subjects often remained in some degree of energy
de®cit. These examples have little to do with the general
population at large, rather they illustrate the extremes to
which FB can adapt to intense physiological demands
imposed by very high levels of physical activity (Saris,
1989) or severe malnutrition. Despite these recorded
extremes of energy and nutrient intake Mela (1995)
points out that Western populations who have economic
and market access to diets of very similar ranges of
composition appear to consume, on average, around 37 ±
42% of their food energy as fat. As the Western diet
becomes increasingly imposed on, or adopted by, a
number of less developed nations, obesity and non insulin
dependent diabetes mellitus approach epidemic proportions
(WHO, 1990). It is however, unclear whether people
choose to select a Western dietary composition over traditional foods or whether secular increases in fat and sugar
intake are foisted on communities and individuals by
economic or other incentives. It has been argued that the
sensory appeal of fats, re®ned CHOs and especially mixtures of the two are a major factor facilitating the ready
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 fatrich 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. Conversely 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 ˆ 0:18), whereas
CHO did not correlate at all with total EI (r ˆ 0.0) and
protein correlated negatively with total EI (r ˆ ÿ0:45). 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
populations exposed to Western diets appears, on average,
to be relatively constant, HF and LF consumers have been
identi®ed within these populations. It has recently been
shown that populations of HF consumers (identi®ed by selfrecorded intakes) have a BMI distribution skewed towards
higher BMIs compared to LF consumers (Figure 3). However, comparing the distribution of HF and LF consumers
shows that HF consumers are by no means exclusively fat
(Macdiarmid et al, 1996). This means there are a signi®cant
number of HF consumers who manage to maintain a stable
body weight, at or below a BMI of 25. It is currently
unclear how such HF consumers (ranked by percentage EI
and absolute intake of fat) manage to avoid the weight
promoting properties of dietary fat. They may be protected
by physiological or behavioural mechanisms (or both)
which allow them to maintain EB. Nevertheless it does
seem that there is considerable scope in some individuals to
accommodate a HF diet, low levels of EE or perhaps even
both, without there being an inevitable rise in body weight
(Blundell & Macdiarmid, 1997).
One of the interesting features of analysing natural
¯uctuations in fat consumption Ð rather than average
intake across a whole population Ð is that it raises the
Figure 3 Frequency distributions of body mass index (BMI) among
low-fat (upper panel) and high-fat (lower panel) consumers. Groups are
de®ned by the amount (weight in grams) of fat consumed. The ordinate
shows the percentage of each sample.
possibility of individual differences in both the willingness
to select fat-containing or CHO-containing foods, and also
in the response to such foods. As an example, data from the
Leeds High Fat Study has identi®ed both individual differences and large day-to-day variation in fat intake of both
high and low consumers. Consumption of more than 200 g
fat in one day for a high fat consumer, or in excess of 150 g
per day for a low fat consumer was not uncommon (Figure
4). The implications of this daily variation for fat balance
have yet to be de®ned. In turn this could disclose information about the variability in appetite control mechanism,
which either promote fat intake or limit its consumption. It
has already been reported that high and low fat phenotypes
display different forms of appetite control (Blundell &
Macdiarmid, 1997; Cooling & Blundell, 1998). The implication of the existence of distinct phenotypes Ð with differing behavioural and physiological responses to nutrient
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).
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
intake and the occasional very-high-fat intakes that can be reached even by
a low-fat eater with a lower average daily intake.
a heterogeneous sample may provide a very misleading
picture of the variety of individual patterns of responses.
Fat carbohydrates and energy density as determinants
of total energy intake
How does fat affect appetite and energy balance?
Evidence from dietary surveys. There is now a growing
body of evidence derived from most of the recent epidemiological studies (with some notable exceptions) on diet
and body weight suggesting that macronutrients do exert
different effects on EB. A number of studies suggest that
fatter people appear to consume a higher proportion of their
EI from fat rather than from CHO (Lissner & Heitmann,
review, 1995). It is generally assumed that this implicates
HF diets in the promotion of excess EIs. However BMI is
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.
This effect is more pronounced in studies where subjects
are given ad libitum access to covertly manipulated diets
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 longerterm studies these changes are paralleled by changes in
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
(LED) diets (Kendall et al, 1991), which is perhaps not
surprising given the tendency of the appetite system to
defend against energetic decrements rather than increments. The tendency for high fat foods to promote high
EIs (when people are eating to comfortable fullness) has
been termed `passive overconsumption' by Blundell
(1995), since there is little evidence of increased drive to
eat and no intention of voluntarily overeating.
It has been shown that systematically increasing dietary
ED using fat has led to excess EI, weight gain and a
positive fat and EB (Stubbs et al, 1995a). Two studies
have shown that when subjects have ad libitum access to
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
systematically manipulated diets of constant energy and
protein density but differing fat to CHO ratios, subjects ate
a similar amount of food and energy (van Stratum et al,
1978; Stubbs et al, 1996). These observations have raised
the issue of whether the effects of dietary fat on appetite
and EB are entirely attributable to the higher ED (HED) of
dietary fat, or whether fat has unique weight-promoting
properties that are independent of its contribution to overall
dietary ED.
Does fat exert any effects on food and energy intake
independent of its contribution to dietary energy density?
There are a number of examples which show that fat exerts
detectable albeit relatively modest effects on appetite and
EB which are independent of its contribution to dietary ED.
CHO appears to exert a more acute effect on satiety than fat
(Cotton et al, 1994), and three other studies have found this
relatively subtle effect to be independent of ED (Rolls et al,
1994; Johnstone et al, 1996; Stubbs et al, 1997a). In one of
these studies, the low satiating ef®ciency of fat in the short
term appeared to be related to its low osmotic load, as
indicated by the subjective thirst of the subjects (Stubbs et
al, 1997b). Pronounced differences in the satiating ef®ciency of intravenously infused fat and CHO have been
recorded by Gil et al, (1991). In this study equal energy
loads and volumes of infusate were used. These data are
supported by an analysis of the relationship between
change in net macronutrient stores and subsequent EI,
which suggested that increments in protein and CHO
stores negatively predict subsequent EI, while fat stores
did not (Stubbs et al, 1995a).
Isoenergetic changes in the fat to CHO ratio of the diet
do not appear to exert important effects on EI in subjects
feeding ad libitum on systematically manipulated diets of
differing composition (van Stratum et al, 1978; Stubbs et
al, 1996). However, in one study isoenergetic, isoenergetically dense, weight-reducing diets were given to women
(4.18 MJ=d), who were also given snacks of a constant
composition to ingest if they felt the need to eat more. Only
on the HF treatment were snack EIs signi®cantly, albeit
marginally, higher than the HP or HC treatments (Johnstone et al, 1997).
Fat also exerts sensory in¯uences on the diet by adding
moisture and mouth-feel to food as well as acting as a
vehicle for a large number of fat-soluble volatile substances. These effects may also be ED independent.
Furthermore, there is evidence that the oro-sensory qualities of dietary fat and sugars may interact to in¯uence the
sensory stimulation to eat. Mela & Sacchetti have reported
that fat preferences increase with increased BMI (Mela &
Sacchetti, 1991). Drewnowski has repeatedly shown that
sugar=fat mixtures appear to exert a synergistic effect on
the sensory pleasure response of human subjects, relative to
fats or sugars alone (Drewnowski, 1997). A comparison of
the effects of HC-sweet, HC-savoury, HF-sweet and HFsavoury snacks on short-term intake has recently been
made. Ingestion of HF-sweet snacks exerted a far greater
effect on EI, which was independent of ED, since EIs were
around twice that on any other treatment despite the fact
that the ED of the HF-savoury snacks was higher (Green &
Blundell, 1996).
In summing up there are a number of individually rather
subtle effects that dietary fat exerts on appetite and EB
which are independent of the contribution of dietary fat to
overall ED. These effects may be additive, synergistic or
cancel each other out under real-life conditions. At the
present time there is insuf®cient data to derive a model,
which articulates the aggregate signi®cance of these effects
in human subjects. Nevertheless, the results of these studies
suggest that dietary fat exerts effects on EI and appetite
control that are independent of its contribution to dietary
ED. However, it should be borne in mind that to some
extent the ED vs macronutrient (per se) issue is a special
argument because in many foods there is a reasonably good
correlation between fat content and ED.
Does type of fat in¯uence appetite and EB?
The majority of studies that have examined the effects of
dietary fat on appetite and EI in humans do not discriminate
between the types of dietary fat used, and these studies tend
to use mixed fats in their dietary preparations. Fats can vary
in structure in terms of (i) chain length, (ii) degree of
saturation; and (iii) number and composition of fatty acids
esteri®ed to the glycerol backbone.
There is evidence that the chain length of fat may
in¯uence EI. In general the shorter the chain length of a
fat the more immediate its oxidation. In this context it is of
note that there is evidence that fat metabolites (including
ketones) may exert potent effects on satiety in rodents
(Carpenter & Grossman, 1983a=b; Rich et al, 1988).
There is also data in rats (Furuse et al, 1992) and humans
(Stubbs & Harbron, 1996) which shows isoenergetic substitution of MCT for LCT at high levels, in HF energy
dense diets limits the excess EIs and weight gains that
frequently appear when subjects feed ad libitum on such
diets. In short-term studies it has been reported that MCT
exerts a stronger effect on satiety than LCT (Rolls et al,
1988a). Incorporation of more moderate amounts of MCT
into the diet is unlikely to be of use in promoting spontaneous weight loss in rodents (Hill et al, 1993) or humans
(Martin et al, 1997).
It has recently been shown that when 20 subjects were
each fed isoenergetic lunches rich in polyunsaturates,
monounsaturates and saturates, monounsaturates signi®cantly suppressed short-term intake less than either polyunsaturates or saturates (Lawton et al, 1997).
The effects of large doses of 1-monoglyceride on appetite and EI have recently been examined both within day
(Ryan et al, 1997) and between days (Johnstone et al,
1997a). Together these studies found that large isoenergetic
doses of dietary monoglyceride or triglyceride did not exert
differential effects on subjective motivation to eat, or
nutrient oxidation or FI. Therefore while the degree of
saturation (Lawton et al, 1997) and chain length of orallyingested dietary fat (Stubbs & Harbron, 1996) can have
signi®cant effects on appetite and EI, these data suggest
that orally ingested 1-monacyl glycerols did not differentially in¯uence appetite and EI relative to triacylglycerols.
It is possible that 2-monacyl glycerols may exert a greater
appetite suppressing effect since these molecules are more
readily absorbed across the gut wall (Bistrian, 1997). The
effects of varying the fatty acid composition of triglycerides (structured lipids) is currently unknown.
In summary it appears that fats and fat derivatives which
tend to be more readily absorbed and=or metabolised exert
a greater suppressive effect on appetite and EI than less
readily utilised fats. The magnitude of these effects under
experimental conditions appears to be signi®cant but
modest (not exceeding 1 MJ=d differentials in EB). Their
signi®cance in the population at large is currently unclear.
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High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
S156
The fat paradox: site and mechanism of action
HF hyperphagia has been shown to occur both in the
laboratory and free-living setting. Conversely, there is
evidence that fat generates potent satiety signals at the
level of the gut. So why does overconsumption occur when
fat generates potent satiety signals? This phenomenon has
been termed the `fat paradox' (Blundell, 1995). One factor
determining the feedback from fat seems to be the site of
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
small intestine have a potent effect on satiety, presumably
by activation of gastrointestinal peptides, CCK and other
receptors (Forbes 1995). Conversely, infusions made intravenously, by-passing the gut, exerted no effect on gastric
emptying or measures of appetite. A study by Gil et al
(1991) found that lipid infusions at around 80% of resting
EE (REE), over 3 d, produced only partial compensation
(43%) of EI. On the other hand, infusions of mixed
nutrients produced good compensation of 103% and with
glucose, 86%. Similar experiments carried out in rats found
intra-duodenal infusions inhibited FI while intravenous
infusions did not (Greenberg et al, 1989). These ®ndings
suggest that after the ingestion of fat, potent fat-induced
satiety signals are generated by pre-absorptive (oro-sensory, stomach and small intestine receptors) rather than
post-absorptive physiological responses. The post-absorptive action (nutrient absorption, substrate utilisation and
oxidation) of fats is weaker than that of other macronutrients (Gil et al, 1991; Stubbs et al, 1995b). Another
possibility is that the fat satiety signals are not initiated
when fat is eaten, only when fat is directly infused into the
intestine. It is most likely that these differential effects of
site of fat administration can probably be explained by
infused lipid producing supraphysiological saturation of the
small-intestine receptors with emulsi®ed fat. This effect
may be diluted by other food constituents and limited by
gastric emptying when fat is fed in the diet, reducing its
capacity to suppress appetite. The essence of the fat
paradox is that very large amounts of fat can be ingested
in the face of potent fat-induced satiety signal. However,
measuring the weight (mass) of food consumed in addition
to EI, indicates that subjects can reduce the weight of foods
eaten slightly (but still consume excess energy). This effect
is most likely to be due to the combination of ED and the
very potent oro-sensory facilitation of EI by fatty foods
which together engender a high intake of fat before inhibitory mechanisms (to terminate eating) can come into
action. The rate of ingestion loads fat into the system
before satiation operates.
How does carbohydrate affect appetite and energy
balance?
CHOs appear to be ef®cient inhibitors of appetite in the
short term. Acute CHO de®cits act as cues that stimulate
intake since 2-deoxy-D-glucose administration actually
increases hunger when given to human subjects (Thompson
& Campbell, 1977). The effectiveness of CHO includes the
effects of sugars and longer chain oligosaccharides such as
maltodextrin and polysaccharides. One interesting issue
here is the relationship between the post-ingestive satiety
effect of CHO and their action upon plasma pro®les of
glucose and insulin. It appears intuitively probable that
tissue uptake and utilisation of glucose is important in its
post-ingestive satiety effect. This probably explains the
relationship between expressed satiety and the integral
(area under the curve) for insulin which has been found
in some studies (Holt et al, 1992). However there is also
evidence that satiety after CHOs may also be mediated by
gastrointestinal (pre absorptive) mechanisms (Read et al,
1994).
Does carbohydrate type affect appetite and EB?
A number of studies have compared the satiating effects of
preloads containing different hexoses and found relatively
few differences between them in terms of appetite
responses. However, it is unclear whether this uniform
response relates to the constraints of the preloading
method or whether the monosaccharides simply have
similar satiating ef®ciencies. There is some evidence that
starches produce a more blunted, yet prolonged in¯uence
on satiety than do mono- and disaccharides (Leathwood &
Pollet 1988), or may help limit EIs (Raben et al, 1997; Kirk
et al, 1997). However, these effects seem relatively modest
and to date there is little published data to suggest that
sugars and starches exert large differential effects on
intake. Interestingly the effect on post-ingestive satiety is
also in¯uenced by the structure of starch as indicated by the
difference between high amylose and amylo-pectin foods
(Van Amelsvoort & Westrate, 1992).
Most work on the effects of different CHOs on EI has
been done with unavailable complex CHOs (UCCs), or
®bre. The time-energy displacement concept has been
invoked to suggest that the addition of UCCs to the diet
enhances satiation and limits meal sizes. This effect is
apparent in some of the studies discussed above and the
phenomenon has been used to limit weight gain in farm
animals with access restricted to single feeds (Forbes,
1995). The post-ingestive effects of ®bre will depend
upon the amount and type delivered in experimental
meals and is likely to be in¯uenced by the proportions of
soluble and insoluble ®bre, which will have different
effects on gastro-intestinal processing. Fermentable CHOs
produce signi®cant quantities of short-chain fatty acids.
The absorption and metabolism of acetate, propionate and
butyrate may themselves exert in¯uences on satiety.
Over 50 studies have been conducted which have
examined the effects of dietary ®bre on FI and body
weight (Levine & Billington, 1994). These have been
extensively covered in four recent reviews, (Levine &
Billington, 1994; Blundell & Burley 1987; Stevens, 1988;
Burley & Blundell, 1990) to which the reader is referred for
a detailed discussion of this issue. In summary, various
loads of UCC or ®bre at one meal have been shown to
decrease both hunger and EI at the next meal, but the
effects are relatively modest. The conclusion seems to be
that supplementing the diet with tolerable levels of
extracted UCC appear to have, at best, modest effects in
decreasing body weight over several months or more.
However, ®bre-rich bulky diets of low ED may have
different effects and the reader should consider the methodological issues detailed in a number of references
(Levine & Billington, 1994; Blundell & Burley 1987;
Stevens 1988; Burley & Blundell, 1990) before drawing
®rm conclusions.
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
Wet and dry carbohydrates: an osmotic brake on excess
intake?
It was stated above that CHOs appear to be ef®cient
inhibitors of appetite whether given in the diet or parenterally. One interesting and important exception to this is the
®nding that calories contained in drinks appear to be poorly
compensated for. In 1955 Fryer supplemented the diet of
college students with a HC drink containing 1.8 MJ. Compensation was incomplete ( 50%) after eight weeks
(Fryer, 1958). Mattes has recently conducted a meta-analysis of feeding responses to either liquid or solid manipulations of the nutrient and energy content of the diet. The
analysis suggests that the physical state of ingested CHO
intake may be important in in¯uencing subsequent caloric
compensation (Mattes, 1996). Speci®cally energy contained in drinks (including CHOs) does not appear to
induce compensatory reductions in food intake as ef®ciently as energy contained in solid foods. The reasons
for this are at present unclear, but may relate to the rate,
timing and density at which the energy is ingested. There
may be a threshold in these parameters, below which
energy is poorly detected. Another factor in¯uencing the
effect of CHOs on intra and intermeal satiety is the osmotic
load that CHOs exert in the small intestine. As starches are
digested water is required to hydrolyse the glycosidic
bonds. This will have the net effect of slowing digestion
(and hence short-term food intake) and increasing thirst. It
is reasonable to hypothesise that these effects would
enhance post-ingestive, preabsorptive satiety. Sweet,
CHO-rich drinks with a water:CHO ratio above 3 : 1
should exert maximal oro-sensory stimulation on intake
and minimal osmotic reduction of intake. While wet CHOs
have been shown to induce hyperphagia in rodents
(Ramirez, 1987), their effect on humans eating less monotonous diets is currently unclear. Rogers & Blundell have
considerable evidence that high CHO drinks (glucose or
sucrose) do suppress short-term intake (1.0 ± 1.5 h later)
(Rogers & Blundell, 1988, 1989), but the longer-term
effects of such manipulations are currently unknown.
When does a high CHO diet produce high levels of EI in
humans?
It has been demonstrated that excess EIs are possible when
normal weight men feed ad libitum on HC diets (Stubbs et
al, 1997a). The sensory attribute primarily associated with
short-chain CHOs (sweetness) is known to stimulate EI,
especially when combined as mixtures with fats (Drewnowski, 1997). Do the sensory attributes of some sweet
foods elevate palatability and hence intake of those foods?
Dissolving short-chain CHOs in solution appears to be an
effective means of supplementing EI. The majority of
snack foods produced tend to be high in CHO and ED
(Stubbs, unpublished). There is evidence that high levels of
physical activity promote high EIs on HC diets. These
considerations suggest that there is considerable scope for
HC foods to promote high levels of EI and in some cases
EB. The exact conditions under which this occurs and in
whom are presently unclear. Currently we are aware of
claims that intake of high CHO foods which are reasonably
energy dense may lead to obesity in the USA. At the
present time we are unaware of clear evidence to support
those claims. There does, however appear to be evidence
that the increase of these foods in both the market and the
diets of consumers has not slowed or reversed current
secular trends in obesity.
How does varying the ED of the diet (using different
compositions) affect appetite and EB?
The majority of studies examining the effects of dietary fat
or fatty foods on appetite, EI or EB have confounded
dietary ED and fat content. However, a series of studies
has recently assessed the effects of altering the ED of the
diet using fat, primarily CHOs or mixed regimes (Stubbs et
al, 1995a, b, 1997b; O'Reilly et al, 1997). Alcohol is
excluded from the present discussion, since it also exerts
pharmacological effects, which may actually stimulate EI
(see Mattes, 1996). In the studies where the ED of the diet
was altered primarily using fat, subjects did not compensate
at all for alterations in dietary ED and HF hyperphagia was
a prominent outcome (Stubbs et al, 1995a, b). Furthermore,
there were no signi®cant differences in subjective hunger
between the diets (Stubbs et al, 1995a). In the study where
the ED of the diet was altered primarily using CHOs there
was no compensation for the ED of the diets but subjects
were signi®cantly (and anecdotally) more hungry on the
LED diet, compared to the HED diet (Stubbs et al, 1995) In
the study where the ED of mixed diets was altered there
were no signi®cant differences in subjective hunger
between the diets but there was a signi®cant diet effect
for prospective consumption (that is, subjects felt they
could eat more food after the low ED meals). Subjects
also showed a highly signi®cant (albeit quantitatively small
20%) compensation of solid food and hence EI on going
from the LED to the HED diet. Therefore subjects
responded more effectively to changes in the ED of the
mixed nutrient manipulations (by active changes in FI) than
the primarily CHO-based manipulations (detectable
changes in hunger) which in turn showed a greater response
than the primarily fat-based manipulations. These ®ndings
again suggest that fat is more weakly sensed by the appetite
control mechanisms than is CHO. These comparisons are
consistent with infusion studies in rodents (Walls & Koopmans, 1992) and humans (Gil et al, 1991) which have
found greater caloric compensation in response to mixed
infusions than glucose-infusions, which in turn produced
greater caloric compensation than lipid infusions. This
suggests that the effects of altered ED on appetite and EB
are partially dependent on the composition of the diet.
Consequently the effects of ED depend upon the nutrients
supplying the energy. Other researchers have also noted
that `Joule for Joule' fat is less satiating than CHO (Rolls et
al, 1994). These ®ndings, in turn, are consistent with the
notion that dietary macronutrients exert hierarchical effects
on satiety, protein having the greatest effect and fat the
least (Stubbs, 1995). Under these conditions the experimental environment may constrain the ¯exibility of subject
response relative to real life, where degree of caloric
compensation may be somewhat greater, especially to
energy de®cits (Blundell & Stubbs, 1997).
Appetite control mechanisms which limit CHO and fat
intakes
Carbohydrate-based models of feeding
Mayer initially suggested that EB regulation occurred
predominantly through short-term `glucostatic' responses
that could be corrected by longer-term `lipostatic' regulation, should short-term regulation be suf®ciently perturbed
(Mayer, 1955). Russek postulated the presence of glucose
receptors in the liver and formulated the hepatostatic theory
of EB regulation (Russek, 1963) Flatt extended these
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High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
S158
models and evolved the glycogenostatic model of appetite
regulation, which is based on the notion that CHO stores
(which are related to CHO intake) exert negative feedback
on EI (Flatt, 1987).
Dietary CHOs have also been viewed as being central to
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
(Fernstrom & Wurtman, 1972). Fernstrom (1987) has
reviewed this model and he, with others, has concluded
that the system does not operate as a mechanism for diet
selection, although the importance of the serotonin system
as a central mechanism in¯uencing FB remains undiminished (Blundell, 1990). The remaining CHO-based models
of feeding have recently attracted more interest since they
predict broadly similar effects on FB: (i) CHO stores or
metabolism exert a negative feedback on EI; (ii) because of
this feedback, diets high in fat but low in CHO will
promote excess EIs; (iii) manipulating CHO status, that
is, oxidation or CHO stores, will reciprocally in¯uence EI;
and (iv) excess ad libitum EIs on HC diets should be very
dif®cult to achieve without a conscious effort, due to the
strength of putative negative feedback arising from CHO
status. The key question in relation to these models is
whether they are useful. Is there evidence that glucostatic
or glycogenostatic mechanisms exert a large enough in¯uence on FB to be quantitatively important in the laboratory
and in real life? One recent short-term report suggests that
body glycogen stores play at most a minor role in shortterm food intake control (Snitker et al, 1997). To support
these mechanisms, studies should demonstrate a high
probability that changes in CHO status will exert predictable effects on FB that are consistent with these models.
CHO-based models of EB regulation are intuitively attractive, because the predictions of these models appear to be
consistent with the role of fat as a risk factor for weight
gain (Lissner & Heitmann, 1995), because these predictions
are testable, and because the predictions of these models
offer a potential means of manipulating EB. However, it is
becoming increasingly recognised that FB is not an inevitable outcome of physiological signalling systems. Rather
FB is coupled (to varying degrees) to physiological processes through perception and conditioning (see section 2
above). Their relevance to the FB of real people in real-life
must therefore be considered in this context.
Fat-based models of feeding
Kennedy, 1953 argued for feedback information reaching
the hypothalamus from adipose tissue, which he argued is
closely monitored through the sensitivity of the hypothalamus to the concentration of circulating metabolites. Hervey
in 1969 proposed a mechanism for lipostatic regulation,
based on endogenous measurement of the fat mass by
means of a fat soluble hormone that monitors adipose
tissue mass by the dilution principle (Hervey, 1969).
Experiments in the late 1970s using genetically obese
rodents and parabiotic regimes (Coleman 1978) created
the conceptual context for the studies that have led to the
identi®cation of the protein `Leptin' (Zhang et al, 1994),
which is currently the subject of remarkable scienti®c
scrutiny. At the present time it would appear that the
actions of total circulating leptin may not be entirely
consistent with a potent satiety factor arising from adipose
tissue and exerting negative feedback on body weight, in a
manner consistent with lipostatic correction of glucostatically controlled FB (Mayer, 1955). The leptin system does
however, appear to interact with a number of physiological
signalling systems concerned with control of several physiological functions (Camp®eld et al, 1997).
Integrative macronutrient models of feeding
Set-point theory has evolved out of the EB concept (Mrosovsky & Powley, 1977). The concept of a set-point
assumes that body weight (and hence EB) is in some way
monitored by a basic sensor which purportedly operates to
increase or decrease food and EI, through a straightforward
negative feedback loop that corrects FB to restore energy
imbalances. No such `set-point' controller has ever been
discovered and the above discussions suggest that an
Arthurian quest for one will prove fruitless. The concept
of a dynamic equilibrium has recently been invoked in
relation to models of appetite control or body weight
maintenance. Friedman & Stricker initially proposed that
the body exists in a dynamic equilibrium between oxidation
and storage, and the rate of peripheral fuel utilisation exerts
negative feedback on FB (Friedman & Stricker, 1976).
Therefore factors which skew the oxidation=storage equilibrium towards nutrient storage, remove those nutrients
from the `calorie sensor' and will increase intake; factors
promoting the net release of nutrients from body stores and
their increased oxidation should decrease intake (Friedman
& Tordoff, 1986; Friedman et al, 1990; Ritter & Calingasan, 1994). Langhans & Scharrer have speci®cally suggested that nutrient oxidation rates in the liver leads to
changes in hepatocyte membrane polarity, which acts as a
satiety signal relayed to the brain by sensory vagal afferents
(Langhans & Scharrer, 1992). These models do not specify
how the mechanism, which senses nutrient oxidation,
distinguishes between endogenously and exogenously
derived nutrients. This may be achieved by monitoring in
some way the composition of fuels contributing to EE,
since in starvation fat is the main metabolic fuel, while
protein and CHO oxidation are minimal. In the fed state the
reverse is true. Alternatively preabsorptive signals and
absorptive phase processes may serve such a function.
A number of studies have examined the predictions of
models which propose that CHO status drives FB. Some
have acutely manipulated CHO (but not EB) and found that
CHO stores do not exert a large unconditioned effect on
subsequent EI (Stubbs, 1994; Shetty et al, 1994; Snitker et
al, 1997). Another examined the ongoing day-to-day relationship between nutrient balance and EI in men housed in
an indirect calorimeter for seven consecutive days (Stubbs
et al, 1995a). Increments in protein and CHO balance
exhibited a potentially suppressive effect on subsequent
EI, fat stores did not. While these effects were signi®cant
they only explained a small proportion of the total variance
in EI. Furthermore, a statistical model, which included the
effects of all three macronutrients, accounted for the greatest proportion of the variance in subsequent EI (Stubbs et
al, 1995a). This suggests that all of the dietary macronutrients in¯uence appetite control and EI in some way, but to
differing degrees. The notion that the body is blind to fat
from the perspective of appetite control is therefore erroneous. Macronutrients appear to exert more complex
effects on satiety and FB than can be accounted for by
single nutrient-based models (Stubbs, 1995).
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
Do nutrient-based models of feeding adequately predict
feeding behaviour?
There is a large mass of evidence that suggests that the
dietary macronutrients in¯uence physiological signalling
systems associated with appetite control and FB. At this
point it is necessary to make a distinction between preabsorptive signals and post-absorptive (largely metabolic)
processes. There is direct and indirect evidence that
changes in gastrointestinal responses in¯uence the amount
of food ingested at meals. A number of nutrient speci®c
models are broadly consistent with secular trends in nutrient intake in relation to body weight (WHO, 1990) or
correlations between NB and subsequent FB in rodents
(Flatt, 1987) and humans (Stubbs, 1995). However these
nutrient speci®c models only explain a small proportion of
the variance in EI. While earlier models viewed peripheral
control of feeding as due to one or more simple negative
feedback loops, more recently research has focused on the
multiple signalling systems involved in the maintenance of
energy and NB (Blundell & Stubbs, 1997). Integrative
models that account for the way in which the brain
monitors the ¯ux of peripheral signals related to overall
metabolic fuel status appear to have greater explanatory
power than single nutrient-based models of feeding (Friedman & Tordoff, 1986; Friedman et al, 1990; Ritter &
Calingasan, 1994; Langhans & Scharrer, 1992). As the
complexity of the appetite system unravels, the need for a
conceptual structure to order our understanding of physiological and non-physiological control of feeding becomes
increasingly necessary. The differential in¯uences that
macronutrients exert on satiety and EI appear to operate
via a number of sequential mechanisms, which have been
set out conceptually by Blundell as a `satiety cascade'.
However, to appreciate the probable importance of these
various metabolic signals concerned with feeding, it is
critical to appreciate that physiological signals associated
with nutrient ingestion are loosely linked to FB except in
relatively extreme physiological circumstances. This means
that nutrient-based models of feeding poorly predict FB
because metabolic processing probably exerts a modest
in¯uence on habitual day-to-day FB of Western individuals. Under these conditions metabolism does not appear
to strongly determine behaviour. Metabolic events may
exert far more potent effects on feeding under more
extreme conditions (Saris et al, 1989; Gil et al, 1991).
Sensory determinants of CHO and fat intake
Sensory factors that promote or limit food and energy
intake
In the above sections it has been argued that physiological
signals act as cues for, rather than determinants of, FB.
Sensory attributes of foods also act as cues for identi®cation, selection and ingestion of foods. Sensory stimuli act as
a `gatekeeper of acceptability' for foods, a phenomenon
with which the food industry is familiar. Until recently, the
sensory attributes of a food provided people with reliable
information on the probable nutrient content of foods. Fats
and CHOs have distinct sensory attributes, when ingested
separately or as various mixtures contained in foods.
Children (whose energy requirements are disproportionately high due to growth) develop conditioned preferences
for energy-rich foods (Birch, 1992). Drewnowski has
further argued that sugars act as a vehicle for fat intake
through such sensorially mediated, nutrient-associated
hedonistic drives (Drewnowski, 1997). There is evidence
that this is the case, and that such effects can override
differences in the ED of foods (Green & Blundell, 1996).
However, by the same token it is likely that sugar also acts
as a vehicle for starch intake. Some interventions that have
attempted to bring about a reduction in the fat content of
participants' diets found that sensory factors exerted a
major in¯uence on fat-reduction success rates (Terry et
al, 1991; Kristal et al, 1992). A main reason why women
felt giving up dietary fat was dif®cult related to their
perception that fat enhanced the taste quality of the diet.
Additionally it appeared that women found that dif®culties
in increasing starch intake precluded their ability to reduce
fat intake (Buzzard et al, 1990; Gorder et al, 1986). This
suggests that it is relatively dif®cult to increase starch
intake. The ready to eat breakfast cereal industry uses a
variety of sugar:starch mixtures to improve the sensory
appeal of their products. It is therefore likely that sweetness
acts as a vehicle for both starch and for fat intake. However
the natural differences in ED between CHOs and fats
means that the sugar-fat mixture has a greater potential to
increase EI than the sugar-starch combinations.
Carbohydrate related sensory stimuli: sweetness
For the last decade there has been a healthy controversy
raging about the role of sweetness, sucrose and arti®cial
sweeteners (Porikos & Van Itallie, 1984; Booth et al, 1988;
Blundell & Rogers, 1994; Clydesdale 1995; Black &
Anderson, 1994) in maintaining EB. The key issue relates
to what effects sweetness, plus or minus CHO energy, has
on appetite and EB. There are three main hypotheses: (i)
adding sweetness without calories to foods leads to lower
levels of EI than when sweetness with calories are added;
(ii) sweetness without calories leads to an anticipatory
facilitation of eating; and (iii) ingestion of sugars (sweetness with calories) correlates with thinness and lowers fat
intake which is itself the reason for the lower body weight.
These alternatives have probably been interpreted too
rigorously because the effects of these factors on appetite
and EI are likely to be in¯uenced by the conditions under
which they are assessed.
There is little doubt that most animals display a preference for sweetness at a very early age, and that sweetness is a factor favouring the selection and subsequent
ingestion of sweet foods. Conversely, different people
exhibit markedly different preferences for sweetness intensities and so simply adding sweetness to foods will not
stimulate everyone to eat. Assuming that sweetness does in
general stimulate the selection and consumption of these
foods, the next question relates to whether sweetness with
or without calories differentially affects appetite and EI.
Can replacement of sugar by intense sweeteners drive EI
down? Despite the common assumption that replacing
dietary sugars with intense sweeteners will promote a
more negative EB, there is a remarkable paucity of data
to demonstrate this effect. There is certainly little epidemiological evidence to suggest that arti®cial sweetener
consumption correlates with lower BMIs, or that increased
arti®cial sweetener consumption in the population has
contributed to any reduction in EIs or the prevalence of
overweight and obesity. A problem with the majority of
laboratory studies, which examine the effect of sweetness,
sugars and arti®cial sweeteners, is that many are short-term
and therefore do not address the issue of EB. It is also
possible that covert replacement of sugars with arti®cial
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High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
S160
sweeteners is more likely to decrease EI if subjects can
only alter the amount they eat of a diet of ®xed composition
rather than having access to a variety of familiar foods.
Most authors seem to be in agreement that the purely
post-ingestive effects of aspartame do not stimulate intake
(Blundell & Rogers 1994; Clydesdale 1995; Black &
Anderson 1994). Blundell et al initially reported that
arti®cially-sweetened drinks could actually stimulate appetite. They suggested that sweetness without calories provides a sensory cue for CHO calories, which leads to
cephalic-phase physiological changes that anticipate EI
(Blundell & Rogers 1994). Intense sweeteners have only
been found to stimulate intake when a food has been
sweetened with intense sweeteners or when a less sweet
food has been compared with an isoenergetically equivalent
food to which sweetness has been added (their `additive
principle') and not when two foods of differing ED but the
same level of sweetness are compared. This they call the
`substitutive principle'. Again this area is bedevilled by
methodological controversies, such as the appropriate drink
vehicle for the sweetener (water or a familiar soft drink),
the time-course of experiment, and the subjects used.
Blundell & Rogers argue that the strongest experimental
designs contain tests of both the additive and substitutive
principle (Blundell & Rogers 1994). No long-term studies
which address EB have yet achieved this dual testing.
Black & Anderson report that the use of aspartame-sweetened water leads to an acute short-term increase in subjective appetite in lean men, but that aspartame-sweetened
carbonated soft drinks induce a transient suppression of
appetite in similar subjects over a similar time-frame
(Black & Anderson, 1994). The issue is complicated by
the fact that satiety can be transiently conditioned by starch
containing drinks that are paired with a given sensory cue
such as ¯avour (Booth et al, 1988). Once conditioned,
similar levels of satiation can be transiently induced by the
conditioning stimulus alone. Therefore the effects of prior
conditioning could in¯uence the outcome of studies using
vehicles that mimic the sensory properties of familiar
foods.
Dietary restraint may also in¯uence the response of
subjects to sweetness, sugar and arti®cial sweeteners
(Lavin et al, 1997). Again there is a notable lack of
longer-term studies in this area that address EB.
In summary, there is little evidence that arti®cial sweeteners reliably decrease appetite or reduce EI, but they could
perhaps prevent any excess EI which would otherwise
occur when calories were provided as drinks (substitutive
principle). There are conditions where arti®cially-sweetened drinks have been found to stimulate appetite and
less often EI, but there is little evidence to suggest that
sweeteners reduce intake. Understanding the applicability
of these ®ndings to free-living humans is an important
problem yet to be resolved.
Fat-related sensory stimuli
The most commonly used tool to examine the effect of fatrelated sensory stimuli on appetite and EI has been short-tomedium term examinations of the impact of substituting
real fat with the caloric fat replica Olestra. These studies
have been conducted using the Blundell & Rogers' substitutive principle, which is the intended use of food
products containing olestra. The majority of these studies
show that in the short-to-medium term subjects fail to
compensate completely for reductions in the ED of the
diet by replacing fat with olestra (de Graaf et al, 1996;
Hulshof et al, 1995a, b; Bray et al, 1995; Cotton et al,
1994; Johnson et al, 1995; Miller et al, 1995, 1996). As
with products containing intense sweeteners, restrained
subjects may show a greater degree of disinhibition when
they are aware that they are using the reduced fat product
(Miller et al, 1995, 1996) Only one short term study has
examined the effects of olestra on appetite and EI using the
additive principle; it found that the sensory qualities of fat
without its energy content did alter short-term FI (Rolls et
al, unpublished). A number of animal studies report that
oro-sensory stimulation with fat can facilitate appetite
(Tordoff & Reed 1991). To date there have been no
structured comparisons of the effect of fat- and sugarrelated sensory stimuli (with and without the attendant
energy) on appetite control and EB. Furthermore there is
a marked absence of long term studies in this area. It is not
therefore known whether the use of nutrient mimetics
maintains sensory preference for the nutrients concerned.
The effect of including nutrient mimetics in foods on
learned FB is also largely unknown.
Sensory stimulation to eat Ð a fat:sugar seesaw or a fatsugar synergism?
The effects of nutrient-related sensory stimuli on FB appear
to be at odds with the notion of the fat : sugar seesaw, which
has been derived from apparent epidemiological relationships between the amount of fat and sugar (as a percentage
of EI) that people appear to eat (Romeau et al, 1988;
Miller, 1990; Tucker & Kano 1992; Bolton-Smith &
Woodward 1994).
It is now generally accepted that the views of the early
1970s are wrong, that is, sweetness provided in the form of
CHO energy stimulated EI and contributed to increases in
obesity. The epidemiological data suggest that consumption
of sugars, that is, sweetness with CHO, is associated with
thinness. Yet the same studies tend to show that as sugar
intake increases so does EI. This suggests that more
physically active people select more sugars and therefore
does not necessarily imply that increased sugar intake
spontaneously promotes thinness. However, interpretations
arising solely from epidemiological data are hazardous
because of the known unreliability of dietary survey data.
While there is evidence of some reciprocity in the
population between the percentage of energy ingested as
CHO and sugar intake on the one hand and the percentage
of energy ingested as fat on the other, this probably re¯ects
the fact that people eat to defend against energy de®cits,
rather than implying that there is some active process
whereby sugar intake promotes dietary fat avoidance.
Analysis of the relationship between the fat, sugar and
the sensory stimulation to eat suggest that fat and sugar
should synergistically increase EI (Drewnowski, 1997).
Indeed as the number of grams of fat intake increases in
diet surveys, so usually does the number of grams of sugar.
There is little or no evidence that increasing sugar intake
promotes a negative EB and weight loss: the critical
experiments have not been conducted. One approach to
this issue will be to examine the effects on food and
nutrient selection of experimentally titrating fats and
sugars into the diet. Equally important here is the consideration of subgroups that may display fat and sugar
intake quite different from the mean values for the whole
population. There is evidence for gender differences and
for gender differences which vary with BMI.
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
Nutrient selection
Sensory in¯uences of fats and CHOs as determinants of
food selection
There is evidence that sensory factors can re-set the limits
to the intake of fats and CHOs in the short- to medium-term
(Rolls et al, 1981, 1982, 1983; Le Magnen 1992; Green &
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
foods. For instance we have recently shown that increasing
the sensory variety of nutritionally identical diets (with
respect to macronutrient composition) leads to spontaneous
increases in food and EI in lean men over seven days
(Johnstone et al, 1997). It is however unclear what the
longer-term impact of these effects is. It is interesting that a
sensory manipulation in this study led to an increase in FI
(the weight of food eaten), while fat manipulations usually
produce passive overconsumption and FI is not increased.
Sensory factors are likely to interact with diet composition,
dietary ED or other environmental in¯uences on intake, to
determine overall EB. Such integrative models are a
development for the future.
Physiological determinants of nutrient selection
In rodent models a number of neurochemicals have been
identi®ed which may be involved in linking information
regarding peripheral CHO status to FB (Lebowitz 1992;
Bray, 1992; Langhans, 1996, for reviews). Likewise, central administration of a number of neuropeptides can
selectively increase or decrease fat intake in rats with
access to pure macronutrient sources (Lebowitz, 1992;
Bray, 1992; Langhans, 1996). It is unclear whether these
extreme interventions actually drive nutrient selection in
the experimental models used or whether they in¯uence
other factors such as the oro-sensory response to the pure
nutrient sources provided, or actually make some pure
nutrient sources aversive. The use of pure nutrient sources
in this respect is a limitation of such studies, as are the
supraphysiological manipulations that are often made. At
the present time there is very little evidence of environmental or behavioural factors that will directionally in¯uence nutrient selection in humans.
There are a number of extreme situations in animal
models where nutrient selection has been demonstrated, as
a result of changes in peripheral physiology. In some cases
there may be analogous situations in humans. For example,
streptozotocin-diabetic rats ®nd glucose aversive, since
they have dif®culty in utilising it. They preferentially
select a HF diet (Edens & Friedman 1988). It is possible
that some insulin resistant humans show similar effects. In
some studies intense exercise stimulates CHO intake in rats
over a period of weeks (Miller et al, 1994). This is clearly a
conditioning effect since rats are not capable of receiving
nutritional wisdom from humans, although a good deal of
information relating to the quality of the diet can be learned
from con-speci®cs (Sclafani 1995, 1997). It is not known
how much of preferential CHO intake in humans is conditioned or taught. In general, changes in the composition of
the diet which are noticeably bene®cial to the subject may
lead to the acquisition of behaviours favouring selection of
those foods. It is therefore possible that the preferential
CHO selection that occurs as a response to sustained
intense exercise is maintained by a conditioned change in
FB. Factors leading to aversive states are likely to form the
basis of food rejection or avoidance. Exactly how subtle
these effects can be with reference to food selection is not
yet known. Therefore it has recently been claimed from
published trials that the aversive side effects of the pancreatic lipase inhibitor (which inhibits fat digestion) favour
selection away from further fat ingestion, in subjects
engaged in stage three clinical trials.
Summary: position statement on the role of behaviour
and appetite in determining the limits of fat and CHO
intake
Mechanisms that control the amount of food consumed and
determine food choices are of paramount importance when
considering the upper and lower limits of fat and CHO
intake. Appetite mechanisms exert their greatest in¯uence
over the amount of food and its composition (fat=CHO)
when there is an abundance of food available and individuals can make choices among distinguishable products.
It is important to note that the actual consumption of
food is a form of behaviour. When behaviour is a scienti®c
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.
When behaviour operates naturally (in free living individuals) and its amount and direction are not restrained, its
expression is in¯uenced by both biological and environmental in¯uences. The nature of the food supply is a part of
the environment. Therefore when free behaviour is seen as
the vehicle by which nutrients (fat and CHO) are ingested
the composition of foods in the food supply can assume
major importance.
Appetite mechanisms can be said to control the pattern
of eating behaviour. This pattern is episodic. Food, energy
and nutrient intakes are therefore a function of the size of
eating episodes, the frequency of episodes, and the composition (F, CHO content) of the foods consumed.
The processes of satiation and satiety are convenient
concepts to describe effects on the size and frequency of
eating episodes. Both satiation and satiety re¯ect the
integration of signals from inside and outside the body
(biological and environmental). The following representation of events is important:
(1) Food consumed generates physiological responses (for
example, gastric emptying rates, plasma levels of
metabolites and oxidative processes in different tissues), which are regarded as satiety signals. These
internally generated satiety signals vary in intensity
and duration; they therefore have the potential to
in¯uence the size and frequency of eating episodes.
(2) Certain proximal satiety signals (close to the process of
ingestion) can, in turn be traced to neurochemical
events in the brain and in some cases, to the activation
of speci®c receptors. When the gene for the receptor is
known this provides a link between satiety signals and
genetics, that is the capacity for genotypes to express
strong or weak satiety signalling.
(3) One recently postulated appetite signal linked to a
genotype involves `leptin' (ob-protein) linked to the
ob gene. Another possible signal involves the serotonin
(5-HT)2C receptor. This receptor is involved in satiety,
the gene for the receptor has been cloned, and there is
an experimental animal `knockout' preparation. The 5HT2C knockout displays hyperphagia, hence there
S161
High and low carbohydrate and fat intakes
JE Blundell and RJ Stubbs
S162
exists a potential genetically controlled satiety mechanism. However, currently the search for polymorphisms
of the 5-HT2C receptor linked to obesity or eating
disorders has proved inconclusive.
The question can therefore be posed: to what extent do
these satiety signals Ð triggered from biological processes
by the impact of ingested food Ð control the intake of fat
and CHO. That is, do these signals help to set the limits for
the amounts of fat and CHO that can be consumed? It is
generally agreed that the actions of protein, fat and CHO,
once ingested, generate satiety signals of differing strengths
and at different physiological points. The rank order of
potency is believed to be protein (strongest), CHO and fat
(weakest), although the differences between CHO and fat at
the same level of dietary ED may be rather smaller than
often assumed.
However, it should be recognised that endogenously
generated satiety signals can be overridden by deliberate
conscious action and by the properties of foods themselves.
The features of individual foods which are most potent are
the oro-sensory attributes (taste, texture, smell, mouth feel)
and the energy load of the food. When many foods are
available for consumption, the variety of the foods (contrast
between sensory properties) becomes an important factor,
within a given meal. The longer-term consequences might
appear intuitively obvious but are not documented by
empirical data.
Foods that are highly palatable can stimulate and promote consumption. The availability of different types of
foods with contrasting sensory properties can allow eating
to be re-stimulated during the course of a meal. This will
engender a greater meal size. The longer-term effects are
unclear. The size of eating episodes (measured by energy
value) can also be increased by the energy load contained in
the food. Since fat is the most energy dense nutrient (and
also possesses the weakest effect on satiety) it is likely that
high fat foods will exert a strong tendency to enlarge the
energetic content of eating episodes.
There is currently considerable interest in the relative
roles of the concentration of nutrients per se (protein, fat,
CHO) in foods versus ED in general on EI. Whilst it is
accepted that the effects of fat (in promoting overconsumption) is heavily in¯uenced by its ED, the role of ED as an
independent variable is not clear. The question arises as to
whether the effects of ED can be independent of the
nutrients which provide the energy. Furthermore, changes
in ED may be differentially in¯uenced by the nutrients
contributing to that change.
Population studies and large surveys have identi®ed
individuals with a range of fat and CHO intake. Intakes of
fat can vary from an average of 180 g=d to 25 g=d in a
representative sample. But on individual days fat intake can
rise to well over 200 g by selection of high fat foods. In a
single meal, people can consume an amount of fat greater
than the population daily average. Therefore under natural
circumstances, fatty foods have the capacity to generate
extremely high intakes of fat and energy.
Since it is known that individuals under natural circumstances can self-generate enormous fat intakes leading to
very high overall EIs this means that the appetite mechanisms which are involved must permit this to happen (or may
even facilitate the high intakes). These habitual intakes of
high fat (greater than 45% food energy) may lead to a
number of physiological circumstances which would be
expected, in turn, to in¯uence the impact of endogenous
signalling. 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.
From this analysis it can be deduced that the appetite
control mechanisms will permit the consumption of large
amounts of fat (if an abundance of high fat foods exists in
the food supply). Except for speci®c physiological circumstances (endurance explorers) where there is an urgent need
for high EIs, in the face of decreasing body weight, it is
unlikely that the body will generate a speci®c drive for fat.
It is also possible, that the body will permit the consumption
of large amounts of CHO (if an abundance of high CHO
foods exists in the food supply). However the intake of such
high CHO foods should tend to yield a lower intake of
energy than the eating of high fat foods. This is because
high CHO foods tend to be less energy-dense than high fat
foods. There is good reason (but currently little evidence) to
suggest that drive to ingest CHOs may be produced by high
rates of CHO oxidation in exercise.
One major implication of an examination of appetite
mechanisms Ð and their effects on upper and lower intakes
of fat and CHO Ð is that the control of FB is of special
signi®cance. It is also apparent that the control of eating
behaviour cannot be understood in the absence of an understanding of physiology and EE. Equally, it follows that the
impact of fat and CHO on physiology cannot be fully
appreciated until the consequent effects of behaviour are
understood. Therefore physiologists should pay more attention to the effects of their manipulations on behaviour (via
appetite signalling mechanisms), and behaviour-oriented
researchers should understand the way in which the composition of foods can affect changes in physiological function and its behavioural sequelae.
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