Download Control of Food Intake in the Obese

Control of Food Intake in the Obese
John E. Blundell* and Angela Gillett†
Abstract
BLUNDELL, JOHN E., AND ANGELA GILLETT.
Control of food intake in the obese. Obes Res. 2001;9:
263S–270S.
Food intake (eating) is a form of behavior that is subject to
conscious control. In practice, many obese and weightgaining individuals claim that their eating is out of (their)
control. Mechanistic models describe the interplay of biological and environmental forces that control food intake.
However, because human food intake is characterized by
individuals intervening to adjust their own patterns of behavior, food intake should reflect interactions among biology, environment, and attempted self-imposed control of
behavior. In general, humans display a system of weight
regulation that is asymmetrical—a reduction in body weight
is strongly defended but weight gain is not. The body seems
to tolerate a positive energy balance. There is no mechanism
that can detect a positive energy balance per se or that can
implement a sufficiently strong correction to behavior to
maintain body weight in an environment that promotes
consumption. The evolutionary process has favored biological traits associated with preferences for high energy density (sweet and/or fatty) energy-yielding foods. The control
of food intake in obese or weight-gaining individuals may
display various risk factors that favor an increase in energy.
These include the preference for high energy-dense over
low energy-dense foods, weak postprandial inhibitory signaling, strong hunger traits associated with low leptin levels
after weight loss, and the consumption of fatty foods. In
addition, many individuals (up to 47% of some samples)
display binge eating patterns, whereas ⬃16% show either
night eating or nocturnal eating. Because energy expenditure is only loosely coupled to energy intake, sedentariness
does not down-regulate food intake.
Key words: food intake, appetite, eating, weight regulation, hunger
*Department of Psychobiology, University of Leeds, Leeds and the †Department of Psychology, Kissileff Laboratory, Liverpool, UK.
Address correspondence to Dr. John E. Blundell, Department of Psychobiology, University
of Leeds, Leeds LS2 9JT, UK.
E-mail: [email protected]
Copyright © 2001 NAASO
Introduction
Obese subjects acting under protocol (experiment or clinical trial) do not display typical free-running behavior.
However, real-life food intake is extremely difficult to measure. In some national surveys as many as 70% of obese
subjects reported physiologically implausible levels of food
intake. It can be concluded that obese or weight-gaining
individuals possess a variety of traits that promote eating,
and this food intake is much greater than normally assumed
to be. The pattern of eating is frequently irregular and/or
disorganized. Management will depend on empowering
people to introduce some degree of systematic organization
into the pattern of eating behavior.
There are clear logical reasons for believing that the
control of food intake—reflected in the pattern of eating and
overall energy intake (EI)—makes a huge contribution to
the maintenance of a healthy weight. It follows that poor
regulation can lead to weight gain and obesity. In addition,
gaining control over food intake remains at the heart of the
majority of treatments for obesity—pharmacological, surgical, and behavioral. Evidence from successful weight losers
(1) illustrates that control over the pattern of food intake and
food items selected, together with the conscious recognition
of these features (through self-monitoring), contribute significantly to weight reduction and its maintenance. It can be
argued that food intake in obese or weight-gaining individuals displays features that favor the rise of EI over energy
expenditure (EE; a positive energy balance) and the maintenance of a high intake. In the absence of any detection of
a positive energy balance and in the absence of strong
corrective mechanisms, body weight will rise incrementally
or, in some cases, abruptly. It follows that the lack of tight
control over food intake makes the regulation of body
weight problematic.
The description of a single defective control mechanism
for food intake in the obese is not an attainable goal. In our
opinion, there are many routes to obesity—sometimes arising from habitual diets and lifestyles (2) and sometimes
from metabolic risk factors (3). Moreover, people who are
obese from infancy or childhood are likely to have qualitatively and quantitatively different forms of regulation from
those individuals who reach obesity more gradually over
many years. Some individuals surge to obesity during parOBESITY RESEARCH Vol. 9 Suppl. 4 November 2001
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Control of Food Intake in the Obese, Blundell and Gillett
ticular critical epochs in their lives. In addition, there is not
likely to be a clear distinction between the regulatory processes of those people who are obese (body mass index
[BMI ], ⬎30 kg/m2), and those with BMIs of 27 to 29
kg/m2. Because the prevalence of obesity is increasing
worldwide together with the average BMI in most societies,
obese individuals are in the process of becoming more
obese, while the nearly obese are likely to become obese in
the future. The problem, therefore, is to describe a system of
food intake control that allows weight gain to occur in the
majority of individuals in our societies (at different rates),
while permitting weight stability in a small minority.
Currently, several comprehensive accounts of the mechanisms of food intake exist (4 – 6). All of these describe the
processes that influence feeding activities and provide models for understanding the relationship between biological
and environmental factors. However, this mechanistic approach to the regulation of food intake does not seem to
provide a complete description or understanding of food
intake in obese people.
Food Intake Is Behavior
At the outset, it is worth recognizing that food intake
(eating) is a form of behavior that can be defined according
to its structure (frequency and size of eating episodes). This
pattern of behavior and the nutrient content and energy
density of food determine the energy ingested. In principle,
this behavior operates through the skeletal musculature and
is subject to conscious control. Therefore, people should be
able to volitionally decide when and how to express their
own eating. In practice, people find it extremely difficult to
exert control and many obese (and some non-obese) claim
that their eating is out of (their) control. One methodological
issue concerns the validity of food intake data collected
from obese individuals.
Investigations into human feeding can be conducted under laboratory conditions within closed environments or
under free-running conditions in the natural environment.
Data from the first situation are high in precision and low in
naturalness, whereas data from free-living studies score
higher on naturalness but lack precision (7). Subjects in
laboratory environments or clinical trials who are eating
under strict protocols can be expected to behave differently
from those occasions when they are free to do what they
want. Consequently, it is very difficult to obtain hard quantitative data on the true food intake behavior of obese (and
non-obese) people. Accordingly, the processes of regulation
described on the basis of well-controlled investigations
should be set against clinical accounts and qualitative descriptions of people in natural situations. It is proposed here
that habitual food intake in obese individuals is greater
than it is normally assumed to be and is often erratic and
apparently dysregulated.
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This situation arises, it is argued, because control
of eating behavior is subject to influences from the
following sources:
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Biological processes that reflect the drive for food (urges
to eat) and inhibitory processes from food ingestion and
adipose tissue stores.
Environmental processes that constrain the timing and
distribution of eating episodes and influence the energy
consumed by means of the palatability and nutrient content of foods.
Self-imposed modulations (achieved and attempted) of
the pattern of behavior that arise from the interaction
between biological and environmental processes.
Attempted self-control of behavior is frequently unreliable because it tends to oppose biological tendencies and
environmental pressures.
Food Intake Regulation in the Light of
Body-Weight Increase
In our opinion, a description of the regulation of food
intake in the obese should be based on the recognition that
body weight is increasing in the vast majority of individuals
exposed to an adequate supply of food. This description,
therefore, involves the following processes:
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Body weight is not strictly regulated. The system of
weight regulation in humans can be proposed to be asymmetrical. That is, the system tolerates or permits positive
energy balances leading to weight gain but defends
strongly against negative energy balances that threaten to
cause weight loss.
The body does not seem to possess a mechanism that
senses a positive energy balance per se and that would
potentially form part of a negative feedback loop to
control intake. The body does, however, contain inhibitory feedback signaling from postingestive processes and
energy stores. These serve to oppose a potential positive
energy balance but they are clearly not strong enough to
achieve this effectively.
The evolutionary process has favored the development of
biological traits associated with preferences for high energy-dense (sweet and/or fatty), energy-yielding foods (as
well as with a thrifty metabolism). These dispositions,
therefore, favor eating behavior most likely to lead to a
positive energy balance. These traits can be termed biological risk factors.
There is a loose coupling between EI and EE (8). In many
cases EI is able to be controlled independently of the level
of EE. This means that low levels of physical activity
(sedentary) do not drag down food consumption to a
lower level to match the lower EE. Indeed, some authors
have argued that appetite (eating behavior) operates less
appropriately at low levels of EE (9).
Control of Food Intake in the Obese, Blundell and Gillett
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The environment exerts a powerful influence on the pattern of eating behavior and the nature of foods consumed.
Through the abundance and availability of foods, aggressive marketing (in some societies), the energy density of
foods—particularly the fat content and their high hedonic
value (palatability), the nutritional environment encourages eating behavior leading to a positive energy balance.
These features can be termed environmental risk factors.
The environment has been termed toxic, pathological
(10), or obesigenic (11).
Some individuals (either already obese or those destined
to become obese) carry strong biological traits that make
them more vulnerable than lean individuals to environmental risk factors and less able to deal with the consequences of overconsumption (positive energy balance.).
Eating (food intake) is subject to conscious control.
Therefore, given the current social climate surrounding
obesity, body shape, and fitness, many individuals attempt to intervene coercively in the pattern of behavior
engendered by their own biological processes and the
environment. These interventions are effective in a small
percentage of people (the successful weight reducers and
maintainers); in contrast, many well-intended interventions seem to disrupt natural physiological controls and
lead to a disorganized pattern of eating.
These premises provide a perspective against which
some features of a regulatory system for food intake
can be considered.
Food Intake: Control or Regulation?
Although it is frequently written that food intake is regulated, it is argued here that it is more appropriate to speak
of food intake being controlled in the interests of regulation
(of body weight or energy balance). It is now widely accepted that the control of food intake is based on a network
of interactions forming part of a psychobiological system.
The complexity of this system has been well-described in a
number of recent reviews (4,5,12). In simple terms, however, it can be noted that the expression of food intake is
controlled by inhibitory and excitatory signaling systems.
Quick-Acting Inhibitory Signals
Foremost among these are those physiological events that
are triggered as responses to the ingestion of food and that
constitute the inhibitory processes that first stop eating and
then prevent the reoccurrence of eating until another meal is
triggered. Inhibitory signaling pathways carry information
during the process of eating (satiation signals) and in the
postingestive period (satiety signals). Satiation can be regarded as the complex of processes that brings eating to a
halt (causes meal termination), whereas satiety can be regarded as those events that follow eating and serve to
suppress hunger (the urge to eat) and maintain an inhibition
over eating for a particular period. The characteristic form
of an eating pattern (size and number of meals, snacks, etc.),
therefore, is dependent on the coordinated effects of satiation and satiety, which together control the size and frequency of eating episodes. It follows that any weakness or
tardiness in these inhibitory signaling systems would lead to
individuals being vulnerable to overconsumption through an
increase in the meal size or the frequency of eating. The
actual physiological mechanisms that form these signaling
systems have been described elsewhere (4,12), but the gut
peptides, including cholecystokinin, glucogon-like peptide,
enterostatin, insulin, and amylin, are of particular significance. Considerable research has confirmed the status of
cholecystokinin as a hormone that mediates meal termination (satiation) and possibly early phase satiety. This mechanism is currently being developed as a route for a pharmacological reduction of food intake for the treatment of
obesity. Signals from postabsorptive metabolism (e.g., of
glucose or glycogen turnover) may constitute signals for the
initiation or termination of eating.
Food Intake and the Drive to Eat
For years the focus of investigations of appetite control
has centered on the termination of eating. This is because
the termination of an eating episode— being the endpoint of
a behavioral act—was perceived to be an unambiguous
event around which empirical studies could be organized.
Consequently, satiety came to be the concept that formed
the basis for accounts of appetite.
However, some 50 years ago there was an equal emphasis
on the excitatory or drive features of appetite. This was
embodied in the central motive state of Morgan and in the
location of this within the hypothalamus by Stellar (13).
One major issue was to explain what gave animals (and
humans) the energy and direction that motivated the seeking
of food. These questions are just as relevant today but the
lack of research has prevented much innovative thinking. In
the light of knowledge about the physiology of energy
homeostasis and the use of different fuel sources in the
body, it is possible to make some proposals. One source of
the drive for food arises from the energy used to maintain
physiological integrity and behavioral adaptation.
Consequently, there is a drive for food generated by EE.
Approximately 60% of total EE is contributed by the resting
metabolic rate. Thus, the resting metabolic rate provides a
basis for drive and this resonates with the older concept of
needs translated into drives. The actual signals that help to
transmit this energy need into behavior could be reflected in
oxidative pathways of fuel use (14), abrupt changes in the
availability of glucose in the blood (15), and, eventually,
brain neurotransmitters, such as neuropeptide-Y, which
seems to be linked to metabolic processes. Leptin is also
likely to play a role through this system.
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In turn this drive to seek food—arising from a need
generated by metabolic processing—is given direction
through specific sensory systems associated with smell, but
more particularly, with taste. It is logical to propose that
eating behavior will be directed to foods having obvious
energy value. Of particular relevance to the current situation
are the characteristics of sweetness and fattiness of foods. In
general, most humans possess a strong liking for the sweet
taste of foods and for the fatty texture. Both of these
commodities indicate foods that have beneficial (energyyielding) properties.
Signals from Adipose Tissue: Leptin and
Food-Intake Control
One of the classical theories of appetite has involved the
notion of a so-called long-term regulation involving a signal
that informs the brain about the state of adipose tissue
stores. The discovery of leptin in 1994 seemed to provide a
mechanism for this type of regulation. In this way leptin
probably acts in a similar manner to insulin, which has both
central and peripheral actions and which is believed to
represent a body-weight signal with the capacity to control
food intake (5). Although the precise relationship between
leptin (ob-protein) and weight regulation or nutritional intake has not been determined, it is known that in both
animals and humans, there is a strong positive correlation
between body fatness and plasma leptin levels (16). Therefore, although leptin is perfectly positioned to act as a signal
from adipose tissue to the brain, high levels of leptin obviously do not prevent obesity or weight gain.
It seems clear that for the majority of obese people, the
ob-protein (leptin) system is not a major cause of rapid or
massive weight gain. However, for certain individuals, very
low levels of leptin (or the absence of leptin) may constitute
a major risk factor. Recently, a small number of individuals
have come to light. For example, two young cousins have
been studied who displayed marked hyperphagia from a
very early age. This hyperphagia took the form of a constant
hunger accompanied by food cravings and a continuous
demand for food (17). The eldest of the two cousins had
reached a body weight of ⬎90 kg by 9 years of age. Her
serum leptin level (like that of her cousin) was very low,
and, subsequently, a mutation in the gene for leptin was
revealed. This finding seems to implicate leptin (ob-protein)
in the control of the drive for food; namely, in the expression of hunger and active food seeking rather than with
satiety or the short-term inhibition over eating. Leptin,
therefore, seems to modulate the tonic signal associated
with the translation of need into drive. When leptin levels
are low or absent, the drive is unleashed and results in
voracious food seeking. The MC4-R receptor is also part of
the same system and the absence of this receptor also
abolishes restraint over appetite leading to hyperphagia.
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This phenomenon is quite different from the removal of a
single satiety signal, which would lead only to an increase
in meal size or a modest increase in meal frequency.
Integration and the Balance between Drive
and Inhibition
The regulation of food intake can be considered a balance
between the excitatory and inhibitory processes. The excitatory processes arise from bodily energy needs and constitute a drive for food (which in humans is reflected in the
subjective experience of hunger). The most obvious inhibitory processes arise from postingestive physiological processing of the consumed food—and these are reflected in
the subjective sensation of fullness and a suppression of the
feeling of hunger. However, the sensitivity of both the
excitatory and inhibitory processes can be modulated by
signals arising from the body’s energy stores. The embodiment of these processes in the central nervous system
circuits is complex and detailed accounts can be found
elsewhere (4,5).
It should be noted that the drive system probably functions to ensure that EI at least matches EE. This has implications for the maintenance of obesity because total EE is
proportional to body mass. This means that the drive for
food may be strong in obese individuals to ensure that a
greater volume of energy is ingested to match the raised
level of expenditure. At the same time, although there is a
process to prevent EI falling below EE, there does not seem
to be a strong process to prevent intake rising above EE.
Consequently, any intrinsic physiological disturbance that
leads to a rise in excitatory (drive) processes or a slight
weakening of inhibitory (satiety) signals would allow consumption to drift upward without generating a compensatory response. For some reason, a positive energy balance
does not generate an error signal that demands correction.
Consequently, the balance between the excitatory and inhibitory processes has implications for body-weight regulation and for the induction of obesity.
System Characteristics in Obese or
Weight-Gaining Individuals
For those individuals whose body weights are stable, it
follows that EI equals EE and there must be an appropriate
interplay between the excitatory and inhibitory signals controlling the pattern of food intake. However, in weightgaining or obese individuals, it can be postulated that certain
characteristics favor the sporadic or persistent increase of EI
over EE either through an alteration of the pattern of eating
(size or frequency of eating episodes) or through the preferential consumption of high-energy-dense foods.
Recently, Ravussin and Gautier (3) drew attention to
metabolic risk factors that characterize either weight-gain-
Control of Food Intake in the Obese, Blundell and Gillett
ing or obese individuals. Similarly, behavioral risk factors
can be identified that bias the regulation of food intake to
promote EI (2). In weight-gaining individuals, any excess
EI does not seem to be compensated by an elevation of
either activity-based thermogenesis (18) or rapid increase in
fat oxidation (19). The following risk factors can be associated with obese or weight-gaining individuals.
Hunger–Satiety-Based Risk Factors
Hunger can exist as a trait or a state (20), and both have
been related to the tendency to eat more or to resist weight
loss. In a weight-loss study using a very-low-calorie diet,
subjects who dropped out had higher hunger trait scores
(21), and following gastrointestinal surgery, high hunger
scores were associated with less weight reduction (22). In
two additional studies, weight loss in obese subjects generated high hunger scores, which were inversely correlated
with the lowered leptin levels (23,24). Subjects whose leptin
levels were most reduced reported stronger feelings of hunger. In another weight-loss study, low leptin was associated
with low feelings of fullness (25). In one case of treatmentinduced leptin deficiency, the patient displayed ravenous
hunger accompanied by a 50% increase in daily food intake
and a body-weight gain of 18 kg (26). Taken together, these
data strongly suggest that the biological disposition of relatively low plasma leptin levels constitutes a risk factor that
acts through a behavioral process. This is likely to be one
way in which food-intake regulation is adjusted in weightgaining or obese individuals. In addition, obese individuals
fail to display the normal hypothalamic inhibitory responses
to glucose infusions (27), suggesting that there is poor
recognition of postprandial satiety signaling. Consequently,
obese individuals may be deprived of important inhibitory
feedback signaling at the end of a meal. It is a long-standing
idea that obese people display weak satiety signals, which
allow the consumption of persistently large meals.
Food-Based Risk Factors
Adjustments to the signaling of hunger and satiety will
affect the pattern of food consumption in weight-gaining or
obese individuals; this will be manifested through an increase in the size or frequency of eating episodes. However,
EI could also be raised through the consumption of high
energy-yielding foods. There is considerable evidence that
high-fat diets lead to positive energy (and fat) balances,
which, in the absence of a capacity for fat oxidation, will
lead to weight gain (28 –30). There is a much greater prevalence of obesity among habitual high-fat than low-fat consumers when the quality of the data are improved by omitting implausible self-reports of food intake (31). In addition,
obese women show a strong preference for sweet high-fat
foods (32), which is matched by high consumption of foods
with a combination of high-sugar and high-fat content (33).
Moreover, in contrast to normal-weight subjects, obese individuals select more high energy dense and fewer low
energy dense foods (34). The proposition that a positive
energy balance is brought about by the energy density of
foods rather than by the fat content is not supported unequivocally by evidence. There is considerable evidence
that people do not maintain a uniform weight of food intake
when the energy density changes (7,30). Moreover, the
highest energy densities can only be achieved by the inclusion of large amounts of fat (the macronutrient with the
highest energy density). There is also evidence that fat itself
may weaken the regulation of food intake. Subjects given a
high-fat diet for 3 weeks demonstrated higher hunger levels
at the end than at the beginning of the period (35). This
finding resonates with the finding that although highercarbohydrate meals raise leptin levels (36), high-fat meals
actually reduce 24-hour plasma leptin concentrations (37).
Consequently, a high-fat intake contributes to a positive
energy balance directly by increasing the amount of energy
consumed (perhaps through passive overconsumption) (29)
and also by increasing the drive to eat through increased
hunger levels. It follows that individuals who possess the
trait of high hunger levels and the trait of high-fat food
preference would possess a considerable risk of achieving a
positive energy balance. It is possible that these traits are
linked through the mediation of leptin.
Environment-Based Risk Factors
The concept of an obesigenic environment (11) suggests
that an environment abundant with risk factors constrains
individuals from adjusting their patterns of intake or the
nature of foods consumed or both. Many factors have been
described but some of the most relevant include foods eaten
outside the home, which are associated with weight gain
(38), the consumption of high-fat foods (39), large portion
sizes, and the encouragement to eat unlimited amounts of
food for a set price. All of these would exploit the capacity
of hunger-based or food-based risk factors to promote the
rise of EI above EE.
Self-Generated Interventions into the
Regulation of Food Intake
Individuals possessing biologically based risk factors associated with hunger–satiety or food selection would be
very likely to achieve a persistent positive energy balance,
particularly in the presence of a plethora of environmentbased risk factors. In the face of tremendous adverse social
pressure surrounding weight gain and obesity, it is clear that
many individuals, particularly women, attempt to impose
some control over their own pattern of eating and food
selection. This is commonly termed dietary restraint, which
has been described as a process to substitute cognitive
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control for natural physiological control (40). The attempt
to exercise volitional self-control over a form of behavior
strongly determined by both biological dispositions (probably with a genetic base) and environmental pressures is
often self-defeating and may lead to a disorderly pattern of
eating or a serious distortion of the structure of behavior.
The obvious human capacity to perceive one’s own public
behavior and to attempt to control it is a factor that must be
included to understand the control of food intake for individuals who are obese or who are gaining weight.
The difficulty of assessing the extent of this attempted
self-control in natural situations means that knowledge of
the free-running regulation of food intake is extremely
difficult to achieve. However, it can be demonstrated that
patterns of eating behavior are often aberrant. For example,
binge eating is widespread, with estimates of the condition
reaching clinically relevant proportions of up to 47% of
obese people seeking treatment. Recently, the occurrence of
binge eating disorder was diagnosed as moderate in 26%
and serious in 19% of a sample of obese patients (41). The
presence of either night eating or nocturnal eating syndrome in 14% of obese patients attending a clinic is
also noteworthy (42).
It cannot be inferred whether these distorted patterns of
eating are the result of attempts to control a perceived
pattern of eating driven by external forces or whether they
arise from underlying patterns of physiological processes.
However, the occurrence of such patterns plus the existence
of critical risk factors place a strain on the control of food
intake in individuals who are prone to weight gain or who
are already helpless in the face of their own obesity.
The Problem of Knowing
Most of the data concerning the control of food consumption have been gathered from controlled investigations in
laboratories or research units or from subjects operating
under protocol in clinical trials. Surveys designed to obtain
food intake data from large samples living naturally all rely
on some form of self-report. It has been repeatedly demonstrated that self-reported estimates of energy and macronutrient intakes (i.e., of foods consumed) are universally prone
to misreporting with the most frequent tendency being under-reporting (43). There is also good evidence of selective
underreporting of fat in general (44) or of specific fatcontaining foods (45).
Underreporting is particularly rife among obese individuals and dieters (i.e., those attempting to impose a control
over their regulatory processes). In some national surveys,
as many as 70% of obese subjects report EIs that are
physiologically implausible (33). This is not surprising in
view of the prevalence of unusual patterns of consumption
involving binge eating, habitual high-fat intakes, nocturnal
and night eating, a high proportion of foods eaten outside of
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the home, and foods consumed generally considered unhealthy or embarrassing (33). Consequently, in obese individuals, it is extremely difficult to discern exactly the pattern of food intake and the amount of food actually being
eaten. However, it can be safely concluded that we underestimate the total amount of energy being consumed by
obese or weight-gaining individuals.
Summary
The many millions of weight-gaining and obese individuals constitute heterogeneous groups of people. There are
many routes, with differing combinations of metabolic and
behavioral variables, through which obesity can be attained
(2). There is not likely to be any single unique pattern of
food intake or regulatory deficit that is common to all.
However, it is possible to define behavioral risk factors
related to the modulation of hunger and satiety or to preferences for (and consumption of) foods or drinks that favor
the rise of EI over EE. These risk factors influence the
structure of the eating pattern and the energy content of the
foods consumed. These risky behaviors are linked to biological states and are held in place by the operation of
incentives, rewards, and contingencies offered by the obesigenic environment. Given the human capacity for conscious action, it is inevitable that people attempt to intervene
coercively in their own patterns of weight-increasing food
habits. This can lead to a disruption of the pattern through
the introduction of binges and nighttime or nocturnal eating.
A number of obese individuals show erratic patterns of food
intake with little or no synchrony between feelings of hunger/fullness and eating. These circumstances make it extremely difficult to obtain true estimates of food intake in
the free-running situation, and as many as 70% of obese
report physiologically implausible levels of EI. The presence of widespread sedentariness does not promote a downregulation of food intake to match a lower level of EE.
Because food provides one of life’s most accessible and
potent forms of pleasure, perhaps we should accept that we
are dealing with behavior governed by hedonism within a
permissive system for energy balance.
Acknowledgment
Dr. Blundell has worked as a consultant and/or received
research grants from food and pharmaceutical companies
whose products are discussed in this article.
References
1. Klem ML, Wing RR, McGuire MT, Seagle HM, Hill JO. A
descriptive study of individuals successful at long-term maintenance of substantial weight loss. Am J Clin Nutr. 1997;66:
239 – 46.
2. Blundell JE, Cooling J. Routes to obesity: phenotypes, food
choices and activity. Br J Nutr. 2000;83:S33– 8.
Control of Food Intake in the Obese, Blundell and Gillett
3. Ravussin E, Gautier JF. Metabolic predictors of weight gain.
Int J Obes Relat Metab Disord. 1999;23:37– 41.
4. Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG.
Central nervous system control of food intake. Natl Insight
Obes. 2000;404:661–71.
5. Woods SC, Schwartz MW, Baskin DG, Seeley RJ. Food
intake and the regulation of body weight. Annu Rev Psychol.
2000;51:255–77.
6. Weinsier RL, Hunter GR, Heini AF, Goran MI, Sell SM.
The etiology of obesity: relative contribution of metabolic
factors, diet and physical activity. Am J Med. 1998;105:
145–50.
7. Blundell JE, Stubbs RJ. Diet composition and the control of
food intake in humans. In: Bray GA, Bouchard C, James
WPT, eds. Handbook of Obesity. New York, NY: Marcel
Dekker; 1998, pp. 243–72.
8. Blundell JE, King NA. Effects of exercise on appetite control: loose coupling between energy expenditure and energy
intake. Int J Obes Relat Metab Disord. 1998;22:S22–9.
9. Mayer J, Roy P, Mitra KP. Relation between caloric intake,
body weight and physical work: studies in an industrial male
population in West Bengal. Am J Clin Nutr. 1956;4:169 –75.
10. Ravussin E, Swinburn BA. Pathophysiology of obesity. Lancet. 1992;340:404 – 8.
11. Egger G, Swinburn BA. An ecological approach to the
obesity pandenic. Br Med J. 1997;315:477– 80.
12. Halford JCG, Blundell JE. Pharmacology of appetite suppression. In: Jucker E, ed. Progress in Drug Research. Vol.
54. Basel, Switzerland: Birkhäuer Verlag; 2000, pp. 25–58.
13. Stellar E. The physiology of motivation. Psychol Rev. 1954;
61:5–22.
14. Friedman MI, Rawson NE. Fuel metabolism and appetite
control. In: Ferstrom JD, Miller GD, eds. Appetite and Body
Weight Regulation. Boca Raton, FL: CRC Press; 1994, pp.
63–76.
15. Campfield LA, Brandon P, Smith FJ. On-line continuous
measurement of blood glucose and meal pattern in free feeding rats: the role of glucose in meal initiation. Brain Res Bull.
1985;4:605–16.
16. Maffei M, Halaas J, Ravussin E, et al. Leptin levels in
human and rodent: measurement of plasma leptin and ob RNA
in obese and weight reduced subjects. Nat Med. 1995;1:
1155– 61.
17. Montague CT Farooqi IS, Whitehead JP, et al. Congenital
leptin deficiency is associated with severe early-onset of obesity in humans. Nature. 1997;387:903– 8.
18. Levine JA, Eberhardt NL, Jensen MD. Role of non-exercise
activity thermogenesis in resistance to fat gain in humans.
Science. 1999;283:212– 4.
19. Schrauen P, Van Marken Lichtenbelt WD, Sarin WMH,
Westerterp KR. Changes in fat oxidation in response to a
high fat diet. Am J Clin Nutr. 1997;66:276 – 82.
20. Gillett A, Blundell JE. The role of state and trait hunger in
the morbidly obese. Int J Obes Relat Metab Disord. 2000;
24(suppl 1):S155.
21. Torgerson J, Lissner L, Lindroos AK, Kruijer H, Sjöström
L. VLCD plus dietary and behavioral support versus support
alone in the treatment of severe obesity: a randomized two-
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
year clinical trial. Int J Obes Relat Metab Disord. 1997;21:
987–94.
Karlsson J, Sjöström L, Sullivan M. Swedish obese subjects
(SOS)—an intervention study of obesity: two-year follow-up
of health-related quality of life (HRQL) and eating behavior
after gastric surgery for severe obesity. Int J Obes Relat Metab
Disord. 1998;22:113–26.
Heini AF, Lara-Castro C, Kirk KA, Considine RV, Caro
JF, Weinsier RL. Association of leptin and hunger-satiety
ratings in obese women. Int J Obes Relat Metab Disord.
1988;22:1084 –7.
Keim NL, Stern JS, Havel PJ. Relation between circulating
leptin concentrations and appetite during a prolonged, moderate energy deficit in women. Am J Clin Nutr. 1998;68:
794 – 801.
Doucet E, Imbeault P, St-Pierre S, et al. Appetite after
weight loss by energy restriction and a low-fat diet-exercise
follow-up. Int J Obes Relat Metab Disord. 2000;24:906 –14.
Leitner GC, Roob JM, Bahadori B, Wallner S, Wascher
TC. Leptin deficiency due to lipid apheresis: a possible reason
for ravenous hunger and weight gain. Int J Obes Relat Metab
Disord. 2000;1900:24:259 – 60.
Matsuda M, Liu Y, Mahankali S, et al. Altered hypothalamic function in response to glucose ingestion in obese humans. Diabetes. 1999;48:1801– 6.
Schrauwen P, Westerterp KR. The role of high-fat diets and
physical activity in the regulation of body weight. Br J Nutr.
2000;84:417–27.
Blundell JE, Macdiarmid JI. Passive overconsumption fat
intake and short-term energy balance. Annu N Y Acad Sci.
1997;827:392– 407.
Blundell JE, Lawton CL, Cotton JR, Macdiarmid J. Control of human appetite: implications for the intake of dietary
fat. Ann Rev Nutr. 1996;16:285–319.
Macdiarmid JL, Cade JE, Blundell JE. High and low fat
consumers, their macronutrient intake, and body mass index:
further analysis of the national diet and nutritional survey of
British adults. Eur J Clin Nutr. 1996;50:505–12.
Drewnowski A, Kurth C, Holden-Wiltse J, Saari J. Food
preferences in human obesity: carbohydrates versus fats. Appetite. 1992;18:207–21.
Macdiarmid JI, Cade JE, Blundell JE. The sugar-fat relationship revisited: differences in consumption between men
and women of varying BMI. Int J Obes Relat Metab Disord.
1998;22:1053– 61.
Westerterp-Plantenga MS, Ijederma MJW, WijckmansDuijsens NEG. The role of macronutrient selection in determining patterns of food intake in obese and non-obese women.
Eur J Clin Nutr. 1996;50:580 –91.
French SJ, Murray B, Rumsay RDE, Fadzlin R, Read NW.
Adaptation to high fat diets; effects on eating behavior and
plasma cholecystokinin. Br J Nutr. 1995;73:179 – 89.
Dirlewanger M, Di Vetta V, Guenat E, et al. Effects of
short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female
subjects. Int J Obes Relat Metab Disord. 2000;24:1413– 8.
Havel PJ, Townsend R, Chaump L, Teff K. High-fat meals
OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001
269S
Control of Food Intake in the Obese, Blundell and Gillett
38.
39.
40.
41.
reduce 24-h circulating leptin concentrations in women. Diabetes. 1999;48:334 – 41.
Crawford D, Jeffrey RW, French SA. Can anyone successfully control their weight? Findings of a three-year community-based study of men and women. Int J Obes Relat Metab
Disord. 2000;24:1107–10.
Sherwood NE, Jeffrey RW, French SA, Hannan PJ, Murray DM. Predictors of weight gain in the Pound of Prevention
Study. Int J Obes Relat Metab Disord. 2000;24:395– 403.
Herman CP, Mack D. Restrained and unrestrained eating. J
Person. 1975;43:647– 60.
D’Armore A, Massignan C, Montera P, Moles A, De
Lorenzo A, Scucchi S. Relationship between obesity-induced
restraint, binge eating, and leptin in obese women. Int J Obes
Relat Metab Disord. 2001;25:373–7.
270S
OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001
42. Cerú-Björk C, Andersson I, Rössner S. Night eating and
nocturnal eating—two different or similar syndromes among
obese patients? Int J Obes Relat Metab Disord. 2001;25:
365–72.
43. Blundell JE. What foods do people habitually eat? A dilemma
for nutrition, an enigma for psychology. Am J Clin Nutr.
2000;71:3–5.
44. Goris AHC, Westerterp-Platenga MS, Westertep KR. Under-eating and under-recording of habitual food intake in
obese men: selective under-reporting of fat intake. Am J Clin
Nutr. 2000;71:130 – 4.
45. MacDiarmid JI, Cade JE, Blundell JE. The sugar-fat relationship revisited: differences in consumption between men
and women of varying BMI. Int J Obes Relat Metab Disord.
1998;22:1053– 61.