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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 263S 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. 264S OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001 This situation arises, it is argued, because control of eating behavior is subject to influences from the following sources: ● ● ● ● 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: ● ● ● ● 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 ● ● ● 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. OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001 265S Control of Food Intake in the Obese, Blundell and Gillett 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. 266S OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001 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 OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001 267S Control of Food Intake in the Obese, Blundell and Gillett 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 268S OBESITY RESEARCH Vol. 9 Suppl. 4 November 2001 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. 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