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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adaptation to long-term starvation is different in men and women. To evaluate whether there are also sex differences during short-term fasting (< 24 hours), we studied glucose metabolism after 16 and again after 22 hours of starvation in healthy subjects: six men, six women in both the follicular and luteal phases of their menstrual cycle, and six women on oral contraceptives ([OCC] day 12 of cycle). Glucose oxidation was measured by indirect calorimetry, and hepatic glucose output by infusion of 3-3H-glucose. There were no differences in hepatic glucose output between men and women during short-term fasting. The basal (16 hours) plasma glucose concentration was lower in women on OCC than in men (P < .05). Prolongation of the postabsorptive state induced a similar decline in plasma glucose concentrations in all groups. Basal (16 hours) glucose oxidation was lower in women on OCC than in men (P < .05). Prolongation of the postabsorptive state by 6 hours caused a significant decrease in glucose oxidation only in men. After 22 hours of fasting, glucose oxidation was lower in women on OCC than in women with normal menstrual cycles. In conclusion, the metabolic adaptation to the postabsorptive state (< 24 hours of fasting) is regulated differently in women on OCC as compared with women with normal menstrual cycles and men. These differences preclude inclusion of women on OCC in studies of glucose metabolism in the postabsorptive state.
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PMID:Sex differences in the adaptation of glucose metabolism to short-term fasting: effects of oral contraceptives. 799 Jul 3

An association between obsessive compulsive disorder and eating disorders has often been reported in the literature. It has been suggested that the association may be accounted for by depression, starvation or family factors but the literature remains inconclusive. In this study self-report scales were used to measure eating attitudes, obsessional symptoms, depressive symptoms and family functioning in an eating disordered group, a psychiatric control group and in the parents of both groups. The eating disordered group scored significantly higher than controls on the Maudsley Obsessive Compulsive Inventory and the Leyton Obsessional Inventory but not on the Childhood Depression Inventory. The differences were not correlated with Quetelet's Body Mass Index. Both groups of parents scored within the normal range for all scales. The high obsessional scores in the anorexic group seem to be due to high scoring on items relating to perfectionism. The role of perfectionism as a risk factor for the development of eating disorders and OCD is discussed.
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PMID:Obsessive compulsive symptoms at initial presentation of adolescent eating disorders. 1055 Jul 1

Eating disorders are evolutionarily novel conditions. They lead to some of the highest mortality rates of all psychiatric disorders. Several evolutionary hypotheses have been proposed for eating disorders, but only the intrasexual competition hypothesis is extensively supported by evidence. We present the mismatch hypothesis as a necessary extension to the current theoretical framework of eating disorders. This hypothesis explains the evolutionarily novel adaptive metaproblem that has arisen when mating motives conflict with the large-scale and easy availability of hyper-rewarding but obesogenic foods. This situation is exacerbated particularly in those contemporary environments that are characterized by sedentary lifestyles, ever-present junk foods, caloric surplus and the ubiquity of social comparisons that take place via social media. Our psychoneuroimmunological model connects ultimate-level causation with proximate mechanisms by showing how the adaptive metaproblem between mating motives and food rewards leads to chronic stress and, further, to disordered eating. Chronic stress causes neuroinflammation, which increases susceptibility to OCD-like behaviors that typically co-occur with eating disorders. Chronic stress upregulates the serotonergic system and causes dysphoric mood in anorexia nervosa patients. Dieting, however, reduces serotonin levels and dysphoric mood, leading to a vicious serotonergic-homeostatic stress/starvation cycle whereby cortisol and neuroinflammation increase through stringent dieting. Our psychoneuroimmunological model indicates that between-individual and within-individual variation in eating disorders partially arises from (co)variation in gut microbiota and stress responsivity, which influence neuroinflammation and the serotonergic system. We review the advances that have been made in recent years in understanding how to best treat eating disorders, outlining directions for future clinical research. Current evidence indicates that eating disorder treatments should aim to reduce the chronic stress, neuroinflammation, stress responsivity and gut dysbiosis that fuel the disorders. Connecting ultimate causes with proximate mechanisms and treating biopsychosocial causes rather than manifest symptoms is expected to bring more effective and sophisticated long-term interventions for the millions of people who suffer from eating disorders.
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PMID:Eating Disorders: An Evolutionary Psychoneuroimmunological Approach. 3174 20