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Query: UMLS:C0020175 (hunger)
 5,670 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aberrant eating patterns in the eating disorders have been observed across various laboratory-based and clinical studies. It is now clear that problems in experiencing and expressing hunger, appetite, and satiety in anorexia and bulimia nervosa are likely to perpetuate the disorders once established. Whether problems in appetite regulation are primary or secondary to the development of the disorders is unknown. In studies examining indices of appetite regulation after treatment, there still remain significant levels of eating abnormality. This suggests that the main goals of treatment, including restoration of body weight in anorexia nervosa, abstaining from dieting in anorexia or bulimia nervosa, and reducing or abstaining from binge eating, do not correct some features of abnormal eating. The efficacy of nutritional counseling and specific nutritional management programs have been tested, and these seem to produce positive outcomes in improving eating behavior. Direct behavioral interventions to change eating patterns also have been examined, and these too seem to produce benefits that may be incorporated into CBT. Greater collaboration and cooperation between researchers and clinicians in addressing dysfunctional eating in the eating disorders will highlight improvements in treatment for identifiable eating abnormalities and will further the understanding of the human appetite system.
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PMID:Dysfunctional eating in the eating disorders. 1141 24

Hyperbaric oxygen was given to a patient with anorexia nervosa who had developed postoperative ileus, resulting in not only improvement in ileus, but also enhancement of intestinal movement, inducing the feeling of hunger, and thereby increasing food ingestion. Hyperbaric oxygen may be effective as an initial treatment for anorectic patients showing severe bloating and resistance to food ingestion.
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PMID:Hyperbaric oxygen for anorexia nervosa. 1150 6

The significance of weight and body composition with regard to the fertile menstrual cycle has excited much interest. There is global imbalance of resources and problems of widespread chronic malnutrition in many 3rd world countries. This emphasizes the great importance of the possible effects of diet, body weight, and body composition on fecundity (ability to reproduce), fertility (reproductive performance), and pregnancy outcome. Frisch and Revelle suggested that a critical body weight is required for a girl to progress through puberty, menstruate, and finally develop ovulatory cycles. They postulated a direct relationship between weight and menarche and suggested that before menarche will occur at least 17% of the body weight needs to be made up of fat. The Frisch hypothesis is not universally accepted, and it seems highly unlikely that a single age unrelated body weight is always the trigger for menarche. Many of the data used in Frische's original studies were derived rather than directly observed. It seems likely that both body weight and composition are important and that the peripheral conversion of androgens to estrogens in fat plays a role in pubertal development, but the actual signal whcih triggers the hypothalamic events leading eventually through puberty to menstruation and ovulation remains unkown. Acute malnutrition, as seen during famine, is assoicated with a dramatic decrease in fertility. It is usually secondary to amenorrhea and annovulation. In developing countries weight related amenorrhea and delayed menarche are largely the result of nutritonal deprivation and the demands of lactation on women of boderline body weight, but a different pattern is seen in Western countries. The outstanding example of weight reduction resulting in infertility is seen in patients with anorexia nervosa. These women have extreme self imposed weight loss, a distorted perception of their body image, and disturbance in their attitude towards their feelings of hunger and satiety. Self imposed weight loss is the most common single cause of secondary amenorrhea seen in the Western world. While diagnosis of the gross anoretic is perhaps rarely missed, the more subtle degrees of weight loss and their effect on the menstrual cycle are often overlooked. Simple weight loss of more than 30% of body fat will cause menstrual dysfunction and ultimately amenorrhea. There is no clearly defined threshold between infertility and normal reproductive health, and there will always be women who become pregnant despite suboptimal weight. Patients with simple weight loss may be sufficiently motivated to restore their weight to normal levels, with resultant spontaneous resumption of ovulation.
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PMID:Weight reduction, fertility and contraception. 1226 43

Neuroanatomical and functional studies in the eating disorders (ED) are reviewed. Typically, anorexia nervosa (AN) is associated with cerebral spinal fluid spaces enlargement which generally recover as a function of re-feeding. However, specific cortical areas fail to correct in weight restored anorectic patients suggesting trait-related abnormalities. Functional changes in AN associated with starvation reverse with weight recovery, however, reduced 5-HT2A receptor binding may be fundamental to the pathophysiology of AN since this remains after long term weight restoration. Structural studies of bulimia nervosa (BN) provide evidence of brain atrophy, in the absence of significant weight loss but potentially related to chronic dietary restriction. Functional investigations reveal reduced thalamic and hypothalamic serotonin transporter availability in BN which increases with longer illness duration. Thus, BN is associated with substantial structural and functional alterations despite normal weight. Recent advances in neuroimaging techniques and their interpretation are increasing our understanding of normal processes in the control of food intake including neuroanatomical correlates of hunger and satiety. Taken together with the structural and functional changes observed in the ED, neuroimaging provides a powerful platform to identify the underlying trait-related pathophysiological mechanisms in the aetiology and maintenance of AN and BN.
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PMID:Neuroimaging in eating disorders. 1474 36

Leptin is an adipocyte-derived hormone, which is involved predominantly in the long-term regulation of body weight and energy balance by acting as a hunger suppressant signal to the brain. Leptin is also involved in the modulation of reproduction, immune function, physical activity, and some endogenous endocrine axes. Since anorexia nervosa (AN) and bulimia nervosa (BN) are characterized by abnormal eating behaviors, dysregulation of endogenous endocrine axes, alterations of reproductive and immune functions, and increased physical activity, extensive research has been carried out in the last decade in order to ascertain a role of this hormone in the pathophysiology of these syndromes. In this article, we review the available data on leptin physiology in patients with eating disorders. These data support the idea that leptin is not directly involved in the etiology of AN or BN. However, malnutrition-induced alterations in its physiology may contribute to the genesis and/or the maintenance of some clinical manifestations of AN and BN and may have an impact on the prognosis of AN.
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PMID:Leptin functioning in eating disorders. 1520 12

To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. The area under the curve for glucose was similar in obese (OB) and normal-weight control (C) subjects but was 15% lower in anorexic (AN) subjects. The area under the curve for insulin was 47% lower in AN and 87% higher in OB subjects, compared with C subjects. After the meal, PYY increased significantly in C (+41%, P < 0.05) but not in AN or OB adolescents. Ghrelin concentrations were highest in AN subjects and lowest in the OB group, compared with C subjects and fell significantly by 25% in all three groups. GIP concentrations were lower in AN subjects throughout the test and increased in all three groups after the mixed meal. AN adolescents reported being less hungry than OB and C adolescents. There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). In conclusion, the blunted PYY response to a meal in OB adolescents suggests that PYY plays a role in the pathophysiology of obesity. Ghrelin is unlikely to play a causal role in anorexia nervosa or obesity. The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients.
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PMID:Ghrelin, peptide YY, glucose-dependent insulinotropic polypeptide, and hunger responses to a mixed meal in anorexic, obese, and control female adolescents. 1565 73

Neuroimaging studies of visually presented food stimuli in patients with anorexia nervosa have demonstrated decreased activations in inferior parietal and visual occipital areas, and increased frontal activations relative to healthy persons, but so far no inferences could be drawn with respect to the influence of hunger or satiety. Thirteen patients with AN and 10 healthy control subjects (aged 13-21) rated visual food and non-food stimuli for pleasantness during functional magnetic resonance imaging (fMRI) in a hungry and a satiated state. AN patients rated food as less pleasant than controls. When satiated, AN patients showed decreased activation in left inferior parietal cortex relative to controls. When hungry, AN patients displayed weaker activation of the right visual occipital cortex than healthy controls. Food stimuli during satiety compared with hunger were associated with stronger right occipital activation in patients and with stronger activation in left lateral orbitofrontal cortex, the middle portion of the right anterior cingulate, and left middle temporal gyrus in controls. The observed group differences in the fMRI activation to food pictures point to decreased food-related somatosensory processing in AN during satiety and to attentional mechanisms during hunger that might facilitate restricted eating in AN.
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PMID:Hunger and satiety in anorexia nervosa: fMRI during cognitive processing of food pictures. 1691 46

Ghrelin is produced mainly in the stomach and is an essential link of the brain-gut axis. Ghrelin stimulates hunger centers in hypothalamus controlling food intake and body mass gain. The aim of the study is to analyze the total ghrelin plasma level in patients suffering from restrictive type of anorexia nervosa (AN-R). According to DSM-IV classification a group of 30 AN-R patients was investigated before and after 3 and 6 months of therapy. Therapy included normocaloric diet and cognitive-behavioral psychotherapy (CBT). The control group consisted of 20 girls without any eating disorders. Before the therapy the total ghrelin plasma level in AN-R patients was significantly higher than in the control group. After 3 and 6 months of treatment the total ghrelin plasma level in AN-R patients was significantly lower than in the control group. In AN-R patients, the total ghrelin plasma level is connected with the pathological feeding behavior.
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PMID:Total ghrelin plasma level in patients with the restrictive type of anorexia nervosa. 1718 77

Ghrelin is produced primarily in the stomach in response to hunger, and circulates in the blood. Plasma ghrelin levels increase during fasting and decrease after ingesting glucose and lipid, but not protein. The efferent vagus nerve contributes to the fasting-induced increase in ghrelin secretion. Ghrelin secreted by the stomach stimulates the afferent vagus nerve and promotes food intake. Ghrelin also stimulates pituitary gland secretion of growth hormone (GH) via the afferent vagus nerve. GH inhibits stomach ghrelin secretion. These findings indicate that the vagal circuit between the central nervous system and stomach has a crucial role in regulating plasma ghrelin levels. Moreover, body mass index modulates plasma ghrelin levels. In a lean state and anorexia nervosa, plasma ghrelin levels are increased, whereas in obesity, except in Prader-Willi syndrome, plasma ghrelin levels are decreased and the feeding- and sleeping-induced decline in plasma ghrelin levels is disrupted. There are two forms of ghrelin: active n-octanoyl-modified ghrelin and des-acyl ghrelin. Fasting increases both ghrelin types compared with the fed state. Hyperphagia and obesity are likely to decrease plasma des-acyl ghrelin, but not n-octanoyl-modified ghrelin levels. Hypothalamic serum and glucocorticoid-inducible kinase-1 and serotonin 5-HT2C/1B receptor gene expression levels are likely to be proportional to plasma des-acyl ghrelin levels during fasting, whereas they are likely to be inversely proportional to plasma des-acyl ghrelin levels in an increased energy storage state such as obesity. Thus, a dysfunction of the ghrelin feedback systems might contribute to the pathophysiology of obesity and eating disorders.
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PMID:Ghrelin and feedback systems. 1798 56

Ghrelin increases hunger sensation and food intake in various patients with appetite loss. Anorexia nervosa (AN) begins with psychological stress-induced anorexia and some patients cannot increase their food intake partly because of malnutrition-induced gastrointestinal dysfunction. The effects of ghrelin on appetite, food intake and nutritional parameters in anorexia nervosa (AN) patients were examined. Five female restricting- type AN patients (age: 14-35 y; body mass index: 10.2-14.6 kg/m(2)) had persistently complained of gastrointestinal symptoms and failed to increase body weight. They were hospitalized for 26 days (6 days' pretreatment, 14 days' ghrelin-treatment, and 6 days' post-treatment) and received an intravenous infusion of 3 microg/kg ghrelin twice a day. Ghrelin infusion improved epigastric discomfort or constipation in 4 patients, whose hunger scores evaluated by visual analogue scale questionnaires also increased significantly after ghrelin infusion. Daily energy intake during ghrelin infusion increased by 12-36 % compared with the pre-treatment period. Serum levels of total protein and triglyceride as nutritional parameters significantly increased after ghrelin treatment. There were no serious adverse effects including psychological symptoms. We found that ghrelin decreases gastrointestinal symptoms and increases hunger sensation and daily energy intake without serious adverse events in AN patients. Although the present study had major limitations of the lack of a randomized, placebo-controlled group, non-blindness of the investigators and the small number of patients recruited, it would contribute to further investigations for therapeutic potential of ghrelin in AN patients.
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PMID:Ghrelin increases hunger and food intake in patients with restricting-type anorexia nervosa: a pilot study. 1975 53


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