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As young omnivores, children make the transition from the exclusive milk diet of infancy to consuming a variety of foods. They must learn to accept a set of the foods available in their environmental niche, and they 'come equipped' with a set of predispositions that facilitate the development of food acceptance patterns, constrained by predisposition and limited by what is offered to them. While children are predisposed to like sweet or salty foods and to avoid sour or bitter foods, their preferences for the majority of foods are shaped by repeated experience. The predispositions that shape food acceptance patterns also include neophobia and the predisposition to learn to prefer and accept new foods when they are offered repeatedly. In addition, the predisposition for associative conditioning affects children's developing food acceptance patterns, resulting in preferences for foods offered in positive contexts, while foods presented in negative contexts will become more disliked via the learning of associations with the social and environmental contexts. Children also learn to prefer energy-dense foods when consumption of those foods is followed by positive post-ingestive consequences, such as those produced when high-energy-density foods are eaten when hungry. Although children are predisposed to be responsive to the energy content of foods in controlling their intake, they are also responsive to parents' control attempts. We have seen that these parental control attempts can refocus the child away from responsiveness to internal cues of hunger and satiety and towards external factors such as the presence of palatable foods. This analysis suggests that taking a closer look at what children are learning about food and eating may provide clues regarding the formation of children's food acceptance patterns, and that this approach also suggests potential causative factors implicated in the aetiology of obesity and the emergence of weight concerns. Current data, although limited, suggest that child-feeding practices play a causal role in the development of individual difference in the controls of food intake, and perhaps in the aetiology of problems of energy balance, especially childhood obesity. These relationships should be pursued in future research.
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PMID:Development of food acceptance patterns in the first years of life. 1009 25

We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. High densities of MC4-R occurred in the ventromedial (VMH) and arcuate (ARC) nuclei, median eminence (ME), and medial habenular nucleus (MHb), with lower densities in the dorsomedial hypothalamus (DMH) and forebrain regions. MC3-R were confined to the VMH, ARC, and MHb. After 10-days of food restriction (14% weight loss), density of MC4-R was significantly increased by 20-65% in the VMH, ARC, ME, and DMH, with no changes elsewhere. Similarly, obese (fa/fa) Zucker rats showed 43-98% increases in MC4-R in the same regions. By contrast, rats with diet-induced obesity (18% heavier than controls) showed significantly decreased binding to MC4-R, especially in the VMH, ARC, and ME. MC3-R showed no significant alterations in any model. We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. MC3-R are not apparently involved in regulating feeding.
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PMID:Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding. 1033

An individual's eating behaviour is shaped by factors ranging from economic conditions and cultural practices to biological influences. The physiological system controlling appetite appears to be adapted to solving the problem of an unevenness of food supply across time, and is fairly permissive in its response to undereating and overeating. Consequently, when food is abundant, the diet is energy dense and energy expenditure is low, there is a strong tendency to become obese (i.e. obesity is better viewed as due to a 'toxic' environment than to faulty physiological control of appetite). Under such conditions the most common method of avoiding obesity is through the cognitive control of eating. However, dietary restraint and dieting are demanding tasks, and are associated with psychological costs, including significant impairment of cognitive performance. Restraint is also prone to disinhibition, with the result that it can sometimes undermine eating control, even leading to the development of highly disordered eating patterns. In part, these difficulties are due to the self-perpetuating nature of dietary habits: for example, hunger tends to be diminished during strict unbroken dieting, but increased in individuals having a highly variable eating pattern (such as occurs when eating is frequently disinhibited). These features of appetite control provide both barriers and opportunities for changing behaviour. Accordingly, there is a need for future research to focus on the psycho-social factors and the dieting practices predicting successful eating and weight control, with the objective of identifying the actual cognitive and behavioural strategies used by the many dieters and restrained eaters who are able to achieve weight loss and maintain long-term weight stability.
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PMID:Eating habits and appetite control: a psychobiological perspective. 1034 41

Leptin is a 16-kDa cytokine secreted in humans primarily but not exclusively by adipose tissues. Its concentration in blood is usually proportional to body fat mass, but is higher in women than in men not only because of a different distribution of and greater fat mass in women, but also because testosterone reduces its level in men. Leptin features in different ways during the life span. It is synthesized in the ovary, transported in the oocyte, and made by both fetus and placenta, particularly during the last month of gestation. It is made by the lactating mammary gland and ingested by the newborn infant in its milk. The prime importance of leptin is realized at puberty when it is necessary for progression to a normal adult reproductive status in females. Fasting and chronic undernutrition result in a lower level of leptin in the blood. Lack of leptin results in hunger, ensuring that the individual eat to survive, and also inhibition of reproduction, until such time as food and fat stores are adequate to supply energy for pregnancy and lactation. Thus, leptin is important for survival of the individual and survival of the species. Although an extremely rare genetic absence of leptin induces hyperphagia and obesity in humans, as it does in mice, there appears to be little role for leptin in humans in ensuring that fat stores are not in excess of adequate, that is, in preventing obesity. The mouse differs from humans in many respects, in particular in the far more drastic ways it conserves energy when it very rapidly adapts to lack of food. These include not only suppression of reproduction but also lowering of its body temperature (torpor), suppressing its thyroid function, suppressing its growth, and increasing secretion of stress hormones (from the adrenal). This review concentrates on roles of leptin in human physiology and pathophysiology but also discusses why some observations on actions of leptin in mice are not applicable to humans.
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PMID:Physiological roles of the leptin endocrine system: differences between mice and humans. 1065 40

In recent years, research has focused on why fat is so readily overconsumed. Although the palatability of many high fat foods can encourage overconsumption, another possibility is that fat is not very satiating. A number of studies have compared the effects of fat and carbohydrate on both satiation (the amount eaten in a meal) and satiety (the effect on subsequent intake), but have found little difference between these macronutrients when the palatability and energy density were similar. On the other hand, the energy density of foods has been demonstrated to have a robust and significant effect on both satiety and satiation, independently of palatability and macronutrient content. It is likely that the high energy density of many high fat foods facilitates the overconsumption of fat. An understanding of the role that the energy density of foods plays in the regulation of food intake should lead to better dietary management of hunger and satiety in conditions associated with both over- and underconsumption of energy, such as obesity and anorexia.
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PMID:The role of energy density in the overconsumption of fat. 1072 85

BACKGROUND: vertical banded gastroplasty (VBG) and gastric bypass Roux-en-Y (GBP) are adjunctive to lifelong commitment to energy restricted diet in the attempt by the severely obese to lose weight and maintain weight loss. METHODS: the outcome of 48 subjects (36 VBG and 12 GBP) is presented. RESULTS: 18 months nutritional counseling and follow-up indicated VBG and GBP to be equally effective in maintaining appreciable weight loss. Achievement of 'functional weight', such as minimum 50% loss of excess body weight for at least 12 months Post-operatively occurred in the majority of patients. Excess weight loss by GBP and VBG was 77% and 54% respectively during the first 6 months, with 7-15% additional loss during the next 12 months. BMI decreased from an average 43 to 27 kg m(2) after 12 months. During the first 3 months, energy intake was approximately 2930 kJ, increasing to;4605 kJ at 6 months, to; 5860 kJ at 12 months and then stabilizing. Intake of;50% of the Recommended Daily Allowance (RDA) for most vitamins and minerals was reached. Hemoglobin, iron, folic acid and thiamin values were in the normal range for the entire 18 months follow-up, while serum vitamin B12 levels decreased to deficiency levels during the same period. The pre-operative moderately elevated triglycerides, cholesterol, glucose and insulin levels returned to normal range, thereby alleviating the need for medication and reducing the risk of obesity-related morbidity. Most subjects were quickly satiated with small amounts of solid foods and did not report hunger feelings for the first 6 months post-operatively. The main significant changes in food preferences in the first 6 months were the decrease in starch-based products and the increase in semi-solid milk products and eggs. CONCLUSION: taken together these observations suggest that the subjects should be strongly advised to partake in structured counseling for an extended period of time.
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PMID:Weight Loss and Food Intake 18 Months following Vertical Banded Gastroplasty or Gastric Bypass for Severe Obesity. 1073 92

Weight loss and psychosocial events have been compared between low calorie conventional diet (n = 11) or following obesity surgery (n = 17). Interviews were >/= 9 months following initiation of treatment. After surgery significantly less hunger was experienced (surgery 76% [13/17] vs diet 18% [2/11] p < 0.01) and less will-power was required to stop eating (surgery 88% [15/17] vs diet 27% [3/11] p < 0.001). More dieters stopped eating because of 'figure and health' (surgery 12 % [2/17] vs diet 64 % [7/11 ] p < 0.01) whereas postoperative patients stopped due to vomit avoidance (surgery 53% [9/17] vs diet 0% [0/11] p </= 0.05). More of the postoperative group were employed (surgery 76% [13/17] vs diet 18% [2/11) p < 0.005). Following surgery there were subjective appearance improvements (surgery 94% [15/16] vs diet 50% [5/10] p < 0.01) and fewer social limitations (surgery 69% [11/16] vs diet 27% [3/11] p </= 0.05). Physical activity improved (surgery 73% [11/15] vs diet 18% [2/11] p < 0.01). Although both groups continue to feel 'fat' at times, more dieters think other people view them as obese (surgery 35% [6/17] vs diet 91% [10/11] p </= 0.05). Satisfaction with weight control method was greater following surgery (surgery 100% [16/16] vs diet 33% [3/9] p < 0.005). Enforced behavior modification (vomit avoidance) is the mechanism of action of gastric restrictive surgery. Physical activity increases, and satisfaction with weight loss method is greater, after surgery. Employment is greater (probably self selection) in the post-surgical group. We found that comparing >/= 9 months following surgery or beginning a conventional diet, the morbidly obese have a more positive response to surgery.
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PMID:Bariatric Surgery vs. Conventional Dieting in the Morbidly Obese. 1074 58

Feeding is a complex process responsive to sensory information related to sight and smell of food, previous feeding experiences, satiety signals elicited by ingestion and hormonal signals related to energy balance. Dopamine released in specific brain regions is associated with pleasurable and rewarding events and may reinforce positive aspects of feeding. Dopamine also influences initiation and coordination of motor activity and is required for sensorimotor functions. Thus, dopamine may facilitate integration of sensory cues related to hunger, initiating the search for food and its consumption. Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens, where they modulate movement and reward. There are projections from the nucleus accumbens to the lateral hypothalamus that regulate feeding. Dopamine-deficient mice (Dbh(Th/+), Th-/-; hereafter DD mice) cannot synthesize dopamine in dopaminergic neurons. They gradually become aphagic and die of starvation. Daily treatment of DD mice with L-3,4-dihydroxyphenylalanine (L-DOPA) transiently restores brain dopamine, locomotion and feeding. Leptin-null (Lep(ob/ob)) mice exhibit obesity, decreased energy expenditure and hyperphagia. As the hypothalamic leptin-melanocortin pathway appears to regulate appetite and metabolism, we generated mice lacking both dopamine and leptin (DD x Lep(ob/ob)) to determine if leptin deficiency overcomes the aphagia of DD mice. DD x Lep(ob/ob) mice became obese when treated daily with L-DOPA, but when L-DOPA treatment was terminated the double mutants were capable of movement, but did not feed. Our data show that dopamine is required for feeding in leptin-null mice.
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PMID:Dopamine is required for hyperphagia in Lep(ob/ob) mice. 1080 66

In order to better understand the factors that may influence and regulate the intake of the macronutrients carbohydrate, fat and protein a 7 d diet diary technique was employed to study eating behaviour in the natural environment of free-living human subjects. In general, factors that promote energy intake tend to promote fat and protein intake to a greater extent than carbohydrate intake. This increased intake occurs as the result of: environmental factors such as social facilitation and the time of day, week or lunar phase; subjective factors such as hunger and elation; individual difference factors such as obesity, restraint and ageing. There are indications that the intake of macronutrients is regulated by negative feedback systems. In the short term, the amount of protein remaining in the stomach at the onset of a meal appears to have a restraining effect on intake, especially protein intake. Over several days, macronutrient intake appears to be affected by a nutrient-specific delayed negative feedback. Protein intake during 1 d is negatively associated with protein intake 2 and 3 d later, while carbohydrate intake is negatively related to later carbohydrate intake, and fat intake to later fat intake; both peaking after a 2 d delay. Studies of the intakes of twins suggested that many aspects of the control of macronutrient intake are influenced by inheritance; these factors include the overall amounts ingested, the before-meal stomach contents and the responsiveness of the subject to the negative impact of the stomach contents. The results indicate that macronutrient intakes are regulated by multiple persistent processes that are to a large extent inherited.
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PMID:What are the major correlates of macronutrient selection in Western populations? 1081 41

For the purpose of enriching the knowledge on the glycaemic (GI) and insulinaemic (InIn) indices of indigenous foods, 3 single foods and 3 realistic high complex carbohydrate meals (bread=100) were studied in 8 healthy subjects. Observed GI (mean+/-SEM) were: beans (B) 19.3+/-3.4, wheat tortilla (WT) 42.5+/-6.9, corn tortilla (CT) 73.8+/-6.5, wheat tortilla beans taco (BWT) 39.9+/-12.8, corn tortilla beans taco (BCT) 56.2+/-8.2 and corn tortilla potato taco (PT) 111.0+/-11.5. The glycaemic index of all foods was lower than white bread (WB) (p<0.01) except for PT. B represented the lowest GI. InIn indices of B (41.7+/-4.5), WT (62.4+/-6.7) and CT (85.5+/-7.8) were lower than WB (p<0.01), whereas PT (171.3+/-11.4) was higher. B InIn was the lowest except for WT, and the highest InIn was for PT. B, WT and CBT might be included in a regular diet for weight maintenance and control of hunger. It is suggested to moderate the ingestion of CT and PT in subjects with obesity and hyperglycaemia complications. It is important to study single and realistic foods with varied composition in diabetic subjects, whose glycaemic responses in reference to their insulinaemic responses might be different to those reported in the present study.
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PMID:Glycaemic and insulinaemic indices of Mexican foods high in complex carbohydrates. 1082 18


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