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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The decision to eat, and to eat particular foods, varies for different individuals and situations. Individual differences in food likes and desires develop throughout life because of differing food experiences and attitudes. There are many internal and external cues, not just stimulation from foods or hunger, which can trigger the immediate desire to eat or orient eating toward certain foods. Food desires and intake are an outcome of interactions between these cues and more stable individual physiological and psychological characteristics. Overweight and obese individuals show a tendency toward greater liking and selection of energy-dense foods, which may contribute to development and maintenance of these conditions. However, although liking (pleasure from eating) is an important part of food choice, it may make only a modest contribution to overall variation in food choice and eating behaviors. Indeed, difficulties of weight control may reflect problems with cues and motivations to eat, rather than with heightened pleasure derived from eating. Paradoxically, individuals highly concerned with food intake and weight control may be particularly susceptible to thoughts, emotions, and situational cues that can prompt overeating and undermine their attempts to restrain eating. Repeat dieting, high day-to-day fluctuations in intakes, and attempts to enforce highly rigid control over eating all seem to be counterproductive to weight control efforts and may disrupt more appropriate food choice behaviors. Longer-term weight maintenance solutions and programs that offer a degree of structuring of the personal food environment, while retaining flexibility in choices, therefore, may be particularly beneficial in weight management.
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PMID:Determinants of food choice: relationships with obesity and weight control. 1170 50

Prader-Willi syndrome (PWS) is a genetic disorder occurring in 1 of 10,000-16,000 live births and is characterized by excessive appetite with progressive massive obesity as well as short stature and mental retardation. Most patients have GH deficiency and hypogonadotropic hypogonadism. The causes of the hyperphagia and abnormal GH secretion are unknown. To determine whether ghrelin, a novel GH secretagogue with orexigenic properties, is elevated in PWS, we measured fasting plasma ghrelin concentration; body composition (dual-energy x-ray absorptiometry); and subjective ratings of hunger (visual analog scale) in seven subjects (6 males and 1 female; age, 26 +/- 7 yr; body fat, 39 +/- 11%, mean +/- SD) with PWS (diagnosis confirmed by genetic test) and 30 healthy subjects (reference population, 15 males and 15 females; age, 32 +/- 7 yr; body fat, 36 +/- 11%) fasted overnight. All subjects were weight stable for at least 6 months before admission to the study. The mean plasma ghrelin concentration was higher in PWS than in the reference population (307 +/- 164 vs. 109 +/- 24 fmol/ml; P < 0.001), and this difference remained significant after adjustment for percentage body fat (P < 0.001). Plasma ghrelin was also higher (P = 0.0004) in PWS than in five healthy subjects fasted for 36 h. A positive correlation was found between plasma ghrelin and subjective ratings of hunger (r = 0.71; P = 0.008). Furthermore, in subjects with PWS, the concentration of the hormone was not different before and after ingestion of 2 ml and a satiating amount of the same liquid meal (ghrelin concentrations: 307 +/- 164 vs. 306 +/- 205 vs. 260 +/- 134 fmol/ml, respectively; ANOVA for repeated measures, P = 0.56). This is the first evidence that ghrelin, a novel orexigenic hormone, is elevated in subjects with PWS. Our finding suggests that ghrelin may be responsible, at least in part, for the hyperphagia observed in PWS.
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PMID:High circulating ghrelin: a potential cause for hyperphagia and obesity in prader-willi syndrome. 1246 37

U.S. adults are now gaining more weight and becoming obese at an earlier age than in previous years. The specific causes of adult weight gain are unknown, but may be attributed to a combination of factors leading to positive energy balance. U.S. food supply data indicate that Americans have had a gradual increase in energy intake since 1970, and that per capita energy intake was 1.42 MJ/d (340 kcal/d) higher in 1994 than that in 1984. In contrast, self-reported physical activity remained constant between 1990 and 1998. Taken together, these data indicate that the increasing trend in U.S. adult weight gain is primarily attributable to overconsumption of energy. Epidemiological and experimental studies in animals and humans provide strong evidence that biobehavioral factors such as dietary variety, liquid (vs. solid) energy, portion size, palatability (taste), snacking patterns, restaurant and other away-from-home food, and dietary restraint and disinhibition influence hunger, satiety and/or voluntary energy intake. When these eating behaviors are consistently experienced either separately or in combination over the long term, they are likely to facilitate overeating. We provide a brief overview of the evidence to date for the role of these biobehavioral factors in contributing to excess energy intake and increases in body weight over time.
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PMID:Biobehavioral influences on energy intake and adult weight gain. 1246 34

Although people with intellectual disabilities are at increased risk for psychiatric disorders, the type and rate of these problems differ between those with different causes for their retardation. In this paper, we review behavioural and psychiatric problems in persons with Prader-Willi syndrome, a disorder caused by a paternally derived deletion at chromosome 15(q11-q13) in about 70% of affected patients, and by maternal uniparental disomy in the majority of the remaining patients. In addition to the syndrome's characteristic hyperphagia and food seeking, individuals with Prader-Willi syndrome also have increased risks of nonfood, compulsive behaviours. These include skin picking, which is highly prevalent, as well as more variable rates of hoarding, redoing and concerns with symmetry, exactness, cleanliness, ordering and arranging. Relative to others with mental retardation, persons with Prader-Willi syndrome are at a marked increased risk for developing full-blown, obsessive-compulsive disorder. In addition, many people with Prader-Willi syndrome show increased rates of tantrums, oppositionality and aggression. Recent findings suggest that they also have an increased risk of psychotic disorder or affective illness with a psychotic component, especially young adult patients and those with the maternal uniparental disomy as opposed to paternal deletion. Dietary approaches include a reduced-calorie diet and increased physical activity, as well as close supervision around food and keeping food locked away. To date, neither CNS stimulants nor anorectic agents have been effective in treating hyperphagia, in part because hyperphagia in Prader-Willi syndrome is attributed to decreased satiation as opposed to increased hunger. Treatment for compulsivity and maladaptive behaviours include: behavioural programming; a structured, predictable routine; extra help with transitions; family support; and pharmacotherapy. Although formal drug studies have yet to be conducted, SSRIs have been effective in reducing skin picking, compulsivity and aggressive episodes in some individuals with Prader-Willi syndrome. Atypical antipsychotics have also proven helpful in persons with psychotic features or extreme aggression and impulsivity. Largely on the basis of case studies, the risks and benefits of these and other drugs in Prader-Willi syndrome are reviewed. Drug trials that move beyond case studies and that assess the relative efficacy of behavioural treatments alone or in combination with pharmacotherapy are sorely needed.
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PMID:Psychiatric disorders in Prader-Willi syndrome: epidemiology and management. 1261 96

In order to evaluate the effectiveness of a cognitive behavioural group therapy programme for the treatment of obesity in clinical practice, 122 patients from 14 general practices (n = 70) were randomised into either a treatment or a control arm with a ratio of 3 to 2. The group treatment programme was also assessed in a clinical centre (n = 52; University Hospital Basel). Before therapy, a clinical interview and a mental disorder examination were carried out on all patients. The instructors of the programme (practitioners; clinic physicians) were trained during two afternoon meetings to supervise the group sessions. The treatment programme consisted of 16 group sessions of 90 min each, and contained psycho-educational elements concerning a balanced diet, instruction for the integration of more activity in everyday life (lifestyle activity), problemsolving strategies, and the cognitive restructuring of dysfunctional cognition regarding the own body. All the patients who were treated in the various settings demonstrated a benefit from therapy. Compared to the control groups which received usual medical care, they were able to reduce their starting weight by around 5% (p <0.001 for the group treated by practitioners) at the end of treatment and stabilise it until follow up after one year. In regard to psychological factors the treatment groups showed an increased sense of control over eating behaviour, and feelings of distractibility and hunger were reduced after treatment and at follow up (p <0.05). All treatment groups showed statistically relevant increases in feelings of attractiveness regarding their body and shape (p <0.05). These results support the effectiveness of the integrated cognitive behavioural treatment programme in clinical practice over a duration of 12 months.
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PMID:Evaluation of a lifestyle change programme for the treatment of obesity in general practice. 1270 42

Obesity is predominantly caused by overeating, an abnormal behaviour for which there is no unequivocal neurophysiological explanation. Functional neuroimaging techniques, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), have recently emerged as new tools to search for regions of the brain that are involved in the regulation of eating behaviours and those that are involved in the pathophysiology of obesity. Using these techniques, a limited number of studies have provided the first in vivo images of the human hypothalamic response to nutritional stimuli and revealed the complexity of the human brain response to hunger, taste, and satiation. Selective differences have been reported in the functional architecture of the brain of obese and lean individuals. We discuss current use and possible future developments of functional neuroimaging applied to obesity research. We conclude that functional neuroimaging provides an increasingly important tool for investigating how different regions of the brain work in concert to orchestrate normal eating behaviours and how they conspire to produce obesity and other eating disorders.
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PMID:Functional neuroimaging: a new generation of human brain studies in obesity research. 1464 73

The importance of the central melanocortin system in the regulation of energy balance is highlighted by studies in transgenic animals and humans with defects in this system. Mice that are engineered to be deficient for the melanocortin-4 receptor (MC4R) or pro-opiomelanocortin (POMC) and those that overexpress agouti or agouti-related protein (AgRP) all have a characteristic obese phenotype typified by hyperphagia, increased linear growth, and metabolic defects. Similar attributes are seen in humans with haploinsufficiency of the MC4R. The central melanocortin system modulates energy homeostasis through the actions of the agonist, alpha-melanocyte-stimulating hormone (alpha-MSH), a POMC cleavage product, and the endogenous antagonist AgRP on the MC3R and MC4R. POMC is expressed at only two locations in the brain: the arcuate nucleus of the hypothalamus (ARC) and the nucleus of the tractus solitarius (NTS) of the brainstem. This chapter will discuss these two populations of POMC neurons and their contribution to energy homeostasis. We will examine the involvement of the central melanocortin system in the incorporation of information from the adipostatic hormone leptin and acute hunger and satiety factors such as peptide YY (PYY(3-36)) and ghrelin via a neuronal network involving POMC/cocaine and amphetamine-related transcript (CART) and neuropeptide Y (NPY)/AgRP neurons. We will discuss evidence for the existence of a similar network of neurons in the NTS and propose a model by which this information from the ARC and NTS centers may be integrated directly or via adipostatic centers such as the paraventricular nucleus of the hypothalamus (PVH).
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PMID:The central melanocortin system and the integration of short- and long-term regulators of energy homeostasis. 1474 11

Obesity is among the most pressing health issues affecting developed countries. The etiology of obesity remains unclear despite its associated health risks. We propose a framework for obesity modeled upon overeating as a substance dependence disorder arising from a combination of abnormal cognitive and neuroendocrine processes. While significant work in both of these fields has investigated the body's regulation of satiety signals, fewer studies have focused upon the mechanisms by which these two seemingly disparate systems interact. Although emotional states have been shown to mediate reward processing, the implications for hunger mediating reward have not previously been addressed. We review the interaction between central satiety signals and reward responses to food stimuli and discuss the implications of this research for understanding the causes of obesity.
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PMID:Interaction of satiety and reward response to food stimulation. 1525 42

Obesity is increasing in severity and prevalence in the United States and represents a major public health issue. No effective pharmacologic treatment leading to sustained weight loss currently exists. The growing interest in the regulation of food intake stems from the current drug treatments for obesity, almost all of which interfere with the monoamine system. Our knowledge of potential interactions between the orexigenic and anorexigenic pathways is limited and fragmented, making the development of targeted drug therapy for obesity difficult. The present review of the interaction of neuropeptides and monoamines emphasizes the complexity of the central mechanisms that regulate feeding behavior. Two main systems are implicated in food intake regulation: neuropeptide Y (NPY) and pro-opiomelanocortin. alpha-Melanocyte-stimulating hormone is a tridecapeptide cleaved from pro-opiomelanocortin that acts to inhibit food intake. The predominant NPY orexigenic receptors are NPY-Y1 and NPY-Y5, and the two anorexigenic melanocortin receptors involved in hypothalamic food intake control are MC3-R and MC4-R. Both neuropeptides interact with monoamines in the hypothalamus to control physiologic states such as hunger, satiation, and satiety. Serotonin suppresses food intake and body weight, acting mainly through the serotonin 1B receptor. Dopamine regulates hunger and satiety by acting in specific hypothalamic areas, through the D1 and D2 receptors. Noradrenaline activation of alpha1- and beta2-adrenoceptors decreases food intake, and stimulation of the alpha2-adrenoceptor increases food intake. A better understanding of the detailed mechanisms underlying the pathogenesis of hyperphagia and hypophagia is needed to develop new therapeutic approaches to obesity.
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PMID:Neuropeptide Y, alpha-melanocyte-stimulating hormone, and monoamines in food intake regulation. 1572 58

Leptin deficiency has been associated with extreme obesity and hyperphagia in rodents and humans. A rare genetic disorder in humans yields the absence of the hormone leptin, extreme obesity, and a ravenous appetite. Reports on these rare cases have indicated that therapy using leptin injections can yield significant weight loss and changes in appetite. The aim of this report on acute leptin therapy in three leptin deficient adults was to provide a microanalysis of changes in eating behavior and ratings of hunger and satiety. In addition to substantial weight loss, 15 weeks of leptin therapy was associated with approximately 50% reduction in food intake and substantial changes in ratings of hunger and satiety before most meals. After short-term leptin therapy, the three participants ate until ratings indicated they were satiated, which was comparable to the ratings before leptin therapy. These findings suggest that one of the primary effects of acute leptin therapy may be to reduce the ravenous hunger associated with leptin deficiency, resulting in reduced food intake and significant weight loss. These results are discussed in the context of the scientific literature pertaining to leptin and its effects on appetite and obesity.
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PMID:Microanalysis of eating behavior of three leptin deficient adults treated with leptin therapy. 1594 71


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