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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In anorexia nervosa, psychopathological features and reduced body weight are inseparable, suggesting a prominent role of behavioral factors in achievement and maintenance of extreme underweight. Due to the considerably higher prevalence of this eating disorder in females, anorexia nervosa contributes to the left end of the distribution of the body mass index, especially in the female sex. By reviewing the relevant literature we examined whether genetic research in anorexia nervosa can profit from considering this disorder as an extreme weight condition. For this purpose we compared genetic studies pertaining to both anorexia nervosa and the heritability of the body mass index. Whereas previous genetic studies in anorexia nervosa have mostly concentrated on the assessment of the familial psychopathology, further studies are warranted that additionally attempt to analyze the complex phenotype body weight in relatives of affected probands. Further insight into pathogenetic mechanisms underlying anorexia nervosa might be gained by contrasting the epidemiological, psychopathological and prognostic factors with those in severe obesity. Thus, epidemiological studies suggest that females are more likely to develop both extreme underweight and extreme obesity. A possible explanation for this phenomenon is that the, on average, higher percentage of total body weight composed of fat mass might predispose females towards the development of both extreme weight conditions.
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PMID:Anorexia nervosa viewed as an extreme weight condition: genetic implications. 781 9

A case of a 7-year-old girl with a remarkable food aversion and excessive weight reduction caused by fear of obesity, which has been demonstrated in pubertal girls with symptoms partly similar to anorexia nervosa, is reported. Although the patient's weight was reduced to the upper limits of the normal range with diet and exercise, she reduced her food intake more strictly and did not at all eat food consisting of carbohydrates. Exercise was performed longer than before. Her weight continued to decrease and height velocity lowered from 6.0 to 4.1 cm/year (mean +/- SD of the age-matched normal girls: 5.5 +/- 0.74 cm/year). Her eating behavior was normalized without specific psychotherapy for anorexia nervosa. It is suggested that food aversion with weight loss and decrease in height gain due to fear of obesity may occur in prepubertal children as well as in adolescent girls.
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PMID:Excessive food aversion, compulsive exercise and decreased height gain due to fear of obesity in a prepubertal girl. 784 64

Plasma atrial natriuretic peptide (ANP) concentrations were determined in basal conditions and after infusion of 1000 ml of 0.9% NaCl in women with anorexia nervosa, in normotensive obese women and in healthy women of the control group. Additionally, in the obese women and in the controls, plasma ANP was measured after iv injection of clonidine. Anorectic patients were investigated in the period of weight loss (mean deficit of body weight was 40%). The mean body mass index (BMI) in the obese women was 36.44 +/- 0.36 kg/m2. Basal plasma ANP concentrations were significantly higher in both anorectic and obese women (p < 0.001 and p < 0.01, respectively). The response of ANP to acute water load was markedly blunted in anorexia nervosa and in obesity (delta % = 232% in control group, 14% in anorexia nervosa and 21% in obesity. A significant increase of ANP was found after iv injection of clonidine in the control group and in obesity (p < 0.001 and p < 0.01, respectively). However, the increase of response (expressed as a percentage change) in obese patients was lower than that in the control group (delta % = 64% and 199%, respectively). The response of ANP to alpha 2-adrenergic stimulation was higher than to hemodynamic stimulus. Our results suggest that the disturbed control of neuropeptides and neurotransmitters as well as changes in peripheral metabolism may explain the impaired responsibility of ANP to hemodynamic stimuli in anorectic and obese patients.
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PMID:Impaired response of atrial natriuretic peptide to acute water load in obesity and in anorexia nervosa. 924 7

Somatostatin concentrations in plasma were measured before and after a standardized fat and protein-rich fluid test meal in patients with anorexia nervosa, weight-recovered anorectic patients, obese women, and healthy controls. Somatostatin was significantly elevated in all four groups after the test meals. Hormone levels remained elevated for up to 100 min after the test meal. The area under the response curve was significantly higher (p < .01) in the anorectic patients as compared with healthy controls and weight-recovered anorectics. Obese women had blunted somatostatin responses. The findings may explain alterations in insulin secretion and in gastric emptying described earlier in patients with eating disorders.
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PMID:Somatostatin in eating disorders. 790 55

With Russell's description of bulimia nervosa in 1979, followed by the DSM-III diagnosis of bulimia, a "new" eating syndrome found its official acceptance in the scientific world. In the two preceding decades clinicians and researchers gradually payed more attention to special forms of overeating. In the 1970s the nosographic conceptualizations of binge eating, bulimia, compulsive eating, or hyperorexia clearly shifted from a symptom level--closely connected to anorexia nervosa and/or obesity--to a syndrome level. Around the same time and independently from one another, clinicians from different countries proposed various descriptive labels for this new diagnostic entity, which, finally, became accepted as bulimia nervosa.
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PMID:Emergence of bulimia nervosa as a separate diagnostic entity: review of the literature from 1960 to 1979. 798 45

This study examined the relationship between characteristics of alexithymia and eating disorders (anorexia nervosa, bulimia nervosa, and obesity) in a nonclinical sample of 308 college women. Scores on the Toronto Alexithymia Scale were mostly unrelated to a weight index, which assessed subjects' deviation from their expected weight, but were correlated with subjects' scores on the Eating Disorders Inventory (EDI). EDI scores were related to the affective deficits of alexithymia (difficulty identifying and communicating feelings), but not to the cognitive disturbance associated with alexithymia.
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PMID:Characteristics of alexithymia and eating disorders in college women. 799 72

This review provides a historical background on sleep-related eating disorders, summarizes findings from a series of 38 adults, and presents a current classification. The "night-eating syndrome" was first reported in 1955; only nine reports on this syndrome appeared during the next 36 years, seven being single-case studies and two containing the objective monitoring of sleep, that is, polysomnography. In 1991 our sleep center reported on 19 cases, and in 1993 on 38 cases, diagnosed by polysomnography and clinical evaluations. Mean age was 39 years, mean duration of night-eating was 12 years, 66% were women, 68% had nightly binge eating, and 44% were overweight from night-eating. Sleepwalking was the predominant disorder responsible for night-eating; restless legs syndrome, obstructive sleep apnea, and various other conditions (including two cases of anorexia nervosa) were also identified. Cognitive-behavioral therapies were ineffective, but pharmacotherapy was very effective in controlling night-eating and inducing loss of excess weight, and often consisted of a dopaminergic agent taken with codeine at bedtime. Thus, sleep-related eating can be an occult but often treatable cause of obesity. Further research, utilizing polysomnography, is encouraged.
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PMID:Review of nocturnal sleep-related eating disorders. 803 49

Adipsin, which is identical to complement factor D, is synthesized by fat cells, circulates in the bloodstream and is profoundly deficient in mice with genetic and hypothalamic obesity. With the recent cloning of human adipsin, a quantitative human immunoassay has been developed. In the present study, we measured adipsin blood concentrations in humans with increased and decreased adipose stores as well as adipsin secretion by adipose tissue obtained from lean and obese individuals. The results demonstrate that adipsin is released by human adipose tissue fragments as has previously been shown in mice, and that, in contrast to obese mice, blood adipsin concentrations were not reduced in the obese humans tested in this study. We also observed that blood adipsin concentrations can vary as a function of feeding or adiposity, in that they tend to be mildly elevated in obese individuals or mildly reduced in individuals with total lipo-atrophy, cachexia related to AIDS and anorexia nervosa. Thus, the circulating concentration of adipsin tends to correlate positively with degree of adiposity. Clearly, no deficiency in blood adipsin concentrations or adipsin secretion by adipose tissue was observed in the obese individuals studied.
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PMID:Concentrations of adipsin in blood and rates of adipsin secretion by adipose tissue in humans with normal, elevated and diminished adipose tissue mass. 804 95

Sleep-related eating disorders distinct from daytime eating disorders have recently been shown to be associated with sleepwalking (SW), periodic limb movement (PLM) disorder and triazolam abuse in a series of 19 adults. We now report eight other primary or combined etiologies identified by clinical evaluations and polysomnographic monitoring of 19 additional adults (mean age 40 years; 58% female): i) obstructive sleep apnea (OSA), with eating during apnea-induced confusional arousals (n = 3); ii) OSA-PLM disorder (n = 1); iii) familial SW and sleep-related eating (n = 2); iv) SW-PLM disorder (n = 1); v) SW-irregular sleep/wake pattern disorder (n = 1); vi) familial restless legs syndrome and sleep-related eating (n = 2); vii) anorexia nervosa with nocturnal bulimia (n = 2) and viii) amitriptyline treatment of migraines (n = 1). In our cumulative series of 38 patients (excluding six with simple obesity from daytime overeating), 44% were overweight (i.e. > 20% excess weight) from sleep-related eating. Nightly sleep-related binge eating (without hunger or purging) had occurred in 84% of patients. Onset of sleep-related eating was also closely linked with i) acute stress involving reality-based concerns about the safety of family members or about relationship problems (n = 6), ii) abstinence from alcohol and opiate/cocaine abuse (n = 2) and iii) cessation of cigarette smoking (n = 2). Current treatment data indicate a primary role of dopaminergic agents (carbidopa/L-dopa; bromocriptine), often combined with codeine and clonazepam, in controlling most cases involving SW and/or PLM disorder. Fluoxetine was effective in two of three patients. Nasal continuous positive airway pressure therapy controlled sleep-related eating in two OSA patients.
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PMID:Additional categories of sleep-related eating disorders and the current status of treatment. 810 56

Previously, we have shown that in the opposite extremes of nutritional status, obesity and anorexia nervosa (AN), growth hormone (GH) response to growth hormone-releasing hormone (GH-RH) is not inhibited by the ingestion of a normal 800-cal meal consumed at lunch time (1 PM), which is at variance with results in normal subjects. However, in obese patients the postprandial increase in GH response to GH-RH is inhibited by an infusion of naloxone (NAL). In this study we have tested anorectic patients, performing the following tests at 1 PM: GH-RH test (50 micrograms IV) or, in a different day session, NAL (1.6 mg/h, starting 30 minutes before GH-RH) + GH-RH test (50 micrograms IV). The tests were performed in the following three different experimental conditions: (1) short-term fasting studies (lasting from breakfast), (2) long-term fasting studies (from midnight of the day before) and (3) postprandial studies (after a standard meal consumed 1 hour before the test). In AN, the GH response to GH-RH was not influenced by NAL infusion at 1 PM, in both short- and long-term fasting studies (short-term fasting: peak values after GH-RH alone, 26.5 +/- 6.5 ng/mL, during NAL, 28.0 +/- 3.3 ng/mL; long-term fasting: peak values after GH-RH alone, 32.2 +/- 6.8 ng/mL, during NAL, 30.6 +/- 4.0 ng/mL). A partial NAL-inhibitory effect was instead observed in postprandial studies, as evidenced by the calculation of areas under the curve ([AUCs] 1,662.1 +/- 90.0 after GH-RH alone v 1,090.5 +/- 245.4 ng/mL/h during NAL).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Opioid dysregulation in anorexia nervosa: naloxone effects on preprandial and postprandial growth hormone response to growth hormone-releasing hormone. 812 Dec 92


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