bulimia nervosa/tyrosine

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A double-blind placebo-controlled glucose challenge in bulimia nervosa: psychological effects.

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Nineteen bulimic women and 22 age-matched controls were randomly assigned to receive 25 g of glucose or a placebo injection under double-blind conditions. Blood samples of glucose, insulin, and glucagon, and psychometric assessments of mood and food cravings were obtained 10 min before, and 0, 5,

Dissociable hormonal profiles for psychopathology and stress in anorexia and bulimia nervosa

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Background: Anorexia nervosa (AN) and bulimia nervosa (BN) are complex psychiatric conditions, in which both psychological and metabolic factors have been implicated. Critically, the experience of stress can precipitate loss-of-control

The role of BDNF, leptin, and catecholamines in reward learning in bulimia nervosa.

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BACKGROUND A relationship between bulimia nervosa and reward-related behavior is supported by several lines of evidence. The dopaminergic dysfunctions in the processing of reward-related stimuli have been shown to be modulated by the neurotrophin brain derived neurotrophic factor (BDNF) and the

Behavioral responses to catecholamine depletion in unmedicated, remitted subjects with bulimia nervosa and healthy subjects.

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BACKGROUND Bulimia nervosa (BN) has been associated with dysregulation of the central catecholaminergic system. An instructive way to investigate the relationship between catecholaminergic function and psychiatric disorder has involved behavioral responses to experimental catecholamine depletion

Dopamine-related deficit in reward learning after catecholamine depletion in unmedicated, remitted subjects with bulimia nervosa.

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Disturbances in reward processing have been implicated in bulimia nervosa (BN). Abnormalities in processing reward-related stimuli might be linked to dysfunctions of the catecholaminergic neurotransmitter system, but findings have been inconclusive. A powerful way to investigate the relationship

Reduction in total plasma ghrelin levels following catecholamine depletion: relation to bulimic and depressive symptoms.

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There is increasing preclinical and clinical evidence of the important role played by the gastric peptide hormone ghrelin in the pathogenesis of symptoms of depression and eating disorders. To investigate the role of ghrelin and its considered counterpart, peptide tyrosine tyrosine (PYY), in the

Purging disorder: recent advances and future challenges.

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The present review aims to help specialists remain up-to-date on research from the past 2 years on epidemiology, risk factors, biological correlates, treatment, and outcomes for purging disorder, a DSM-5 other specified feeding and eating disorder.Purging

Familial hypothalamic digoxin deficiency syndrome.

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The case report of a family with coexistence of hypotension, recurrent respiratory infection, motor tics, obsessive-compulsive disorder (OCD), major depressive disorder, early onset osteoporosis, low body mass index, bulimia nervosa, and healthy aging with longevity is described. The family members

Contribution of NTRK2 to the genetic susceptibility to anorexia nervosa, harm avoidance and minimum body mass index.

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Anorexia nervosa (AN) and bulimia nervosa (BN) are eating disorders (ED) with complex genetic and environmental components. Genetic studies and animal models support the participation of brain-derived neurotrophic factor (BDNF) in the vulnerability to AN and BN. We investigated the genetic

Acipimox Administration With Exercise Induces a Co-feedback Action of the GH, PP, and PYY on Ghrelin Associated With a Reduction of Peripheral Lipolysis in Bulimic and Healthy-Weight Czech Women: A Randomized Study.

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Objective: Anti-lipolytic drugs and exercise are enhancers of growth hormone (GH) secretion. Decreased circulating free fatty acids (FFA) have been proposed to exert ghrelin-GH feedback loop after administration of an anti-lipolytic longer-acting analog of nicotinic acid, Acipimox (OLB,

Familial hypodigoxinemic membrane Na(+)-K(+) ATPase upregulatory syndrome - relation between digoxin status and cerebral dominance.

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A family with coexistence of hypotension, recurrent respiratory infection, motor tics, obsessive compulsive disorder, major depressive disorder, early onset osteoporosis, low body mass index, bulimia nervosa and healthy aging with longevity is described. The family members had hyposexual behavior,

Hypothalamic digoxin, hemispheric chemical dominance, and eating behavior.

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The isoprenoid pathway produces an endogenous membrane Na+-K+ ATPase inhibitor, digoxin, which can regulate neurotransmitter and amino acid transport. Digoxin synthesis and neurotransmitter patterns were assessed in eating disorders. The patterns were compared in those with right hemispheric and

Migraine prevalence in eating disorders and pathophysiological correlations.

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The eating disorders (ED): anorexia nervosa (AN) and Bulimia nervosa (BN) are severe psychiatric and somatic conditions occurring mainly in young woman. Although the etiology is largely unknown, same evidences suggest that biological and psychological factors play a relevant role in the

Is migraine a risk factor for the occurrence of eating disorders? Prevalence and biochemical evidences.

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The eating disorders (ED), anorexia nervosa (AN) and bulimia nervosa (BN), are severe psychiatric and somatic conditions occurring mainly in young woman. Although the aetiology is largely unknown, same evidences suggest that biological and psychological factors play a relevant role in the

Possible involvement of brain-derived neurotrophic factor in eating disorders.

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Eating disorders (EDs) manifest as abnormal patterns of eating behavior and weight regulation driven by low self-esteem due to weight preoccupation and perceptions toward body weight and shape. Two major groups of such disorders are anorexia nervosa (AN) and bulimia nervosa (BN). The etiology of EDs

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