Disease relevance of Eating Disorders

• Conversely, estrogen directly stimulates the CRH gene promoter and the central noradrenergic system, which may explain adult women's slight hypercortisolism; preponderance of affective, anxiety, and eating disorders; and mood cycles and vulnerability to autoimmune and inflammatory disease, both of which follow estradiol fluctuations [1].
• It is proposed that impaired synaptic transmission in functionally distinct serotonin pathways may result in concurrent or sequential periods of binge eating, behavioral impulsivity, and depression in patients with eating disorders [2].
• It is also not yet clear whether glucagon contributes to some forms of obesity or has potential use as a therapeutic tool in the control of eating disorders [3].
• The changes of serum SHBG concentrations in patients with anorexia nervosa during weight gain make SHBG determination a reliable index of nutritional status in this type of eating disorder [4].
• In a study of serotonin (5-HT) function in patients with eating disorders and healthy control subjects, severe headaches with features of common migraine occurred unexpectedly in 28 of 52 subjects (54%) 8 to 12 hours after receiving a single oral dose of the 5-HT receptor agonist m-chlorophenylpiperazine (m-CPP), 0.5 mg/kg [5].

Psychiatry related information on Eating Disorders

• Further lack of association between the 5-HT2A gene promoter polymorphism and susceptibility to eating disorders and a meta-analysis pertaining to anorexia nervosa [6].
• These findings suggest that abnormal feeding behavior in the patients with eating disorders may reduce circulating adiponectin level, and weight recovery can restore it [7].
• We review SERT imaging studies in patients with depression, anxiety disorders, eating disorders and patients with neurological diseases [8].
• Endogenous depression, which has confounded prior studies of melatonin profiles in women with eating disorders, was excluded in all subjects [9].
• OBJECTIVE--To assess attitudinal and behavioral symptoms of eating disorders in preadolescent and adolescent girls with IDDM and a matched sample of nondiabetic subjects, and to explore the relationship between the perceived impact of IDDM and eating disorder symptoms [10].

High impact information on Eating Disorders

• Eating disorder and epilepsy in mice lacking 5-HT2c serotonin receptors [11].
• Cocaine abuse and eating disorders [12].
• Abnormal signaling at corticotropin-releasing factor CRF1 and CRF2 receptors might contribute to the pathophysiology of stress-related disorders such as anxiety, depression and eating disorders, in addition to cardiac and inflammatory disorders [13].
• The 5-HT neurotransmission system is targeted by drugs useful in many behavioural disorders, including anxiety, depression, psychosis and eating disorders [14].
• Our findings support suggestions that chronic depletion of plasma tryptophan may be one of the mechanisms whereby persistent dieting can lead to the development of eating disorders in vulnerable individuals [15].

Chemical compound and disease context of Eating Disorders

• Changes in melatonin levels but not cortisol levels are associated with depression in patients with eating disorders [16].
• In contrast, levels of autoAbs reacting with adrenocorticotropic hormone, OT, or VP had only few altered correlations with the Eating Disorder Inventory-2 subscale dimensions in AN and BN patients [17].
• Low plasma GABA is also found in a subset of patients with alcohol dependence, but not in schizophrenia, anxiety, or eating disorders, suggesting some diagnostic specificity [18].
• OBJECTIVE: An interesting candidate gene for eating disorders is the gene for insulin-like growth factor 2 (IGF2) [19].
• Naltrexone improves blood glucose control in type 1 diabetic women with severe and chronic eating disorders [20].

Biological context of Eating Disorders

• METHOD: The authors tested nonclinical subjects from 376 families for three IGF2 SNPs and for eating disorders, as reflected in scores on the 26-item Eating Attitudes Test, a self-report questionnaire widely used as a screening instrument [19].
• The intimate relationship between serotonin and the hypothalamic-pituitary-adrenal axis is of great importance in normal physiology such as circadian rhythm and stress, as well as pathophysiological disorders such as depression, anxiety, eating disorders, and chronic fatigue [21].
• Association between 5HT2A receptor gene promoter region polymorphism and eating disorders in Japanese patients [22].
• Among female plebes, there was no evidence of the female athlete triad (eating disorders, menstrual dysfunction, or low bone density) [23].
• Such nutritional modulations may have implications for the treatment of eating disorders and, in normal circumstances, tyrosine may improve exercise tolerance and delay fatigue [24].

Anatomical context of Eating Disorders

• Cerebrospinal fluid levels of kynurenine pathway metabolites in patients with eating disorders: relation to clinical and biochemical variable [25].
• In patients with eating disorder, logarithmic values for leptin were significantly correlated with the body fat mass (r = .828, P < .001), eating behavior score (r = .777, P < .001), and LH (r = .465, P < .001), FSH (r = .440, P < .001), T3 (r = .572, P < .001), insulin (r = .410, P < .001), and cortisol (r = -.389, P < .001) levels [26].
• The future of brain stimulation will depend on new technologies (new circuits, electrodes, web based programmers), waveforms (alternatives to square waves, random distribution), targets (hypothalamic nuclei, locus coeruleus) and indications (dystonia, epilepsy, eating disorders [27].
• Thus, clinical studies have evaluated the possibility that CNS neuropeptide alterations may contribute to dysregulated secretion of the gonadal hormones, cortisol, thyroid hormones and growth hormone in the eating disorders [28].

Gene context of Eating Disorders

• Recently novel non-peptidic antagonists directed against CRH-R1 or CRH-R2 have been proposed as promising agents in the treatment of depression, anxiety and eating disorder [29].
• Preclinical data indicate that corticotropin-releasing hormone (CRH) has anxiogenic properties and a dysregulation in CRH systems has been suggested to play a role in a variety of stress-related psychiatric disorders, such as anxiety, depression, and eating disorders [30].
• The present study therefore investigated the ability of CRH to inhibit the GH response to GHRH in eight young women with anorexia nervosa (AN) and in seven young women with eating disorders which were not otherwise specified (NOS) [31].
• Recently, we found that serum levels of BDNF in patients with eating disorders are significantly decreased compared with normal controls [32].
• We found no association between p.V66M or the additionally genotyped variant c.-46C > T and obesity, ADHD or eating disorders [33].

Analytical, diagnostic and therapeutic context of Eating Disorders

• Twenty-one patients with anorexia nervosa and 35 normal-weight patients with bulimia underwent a series of CSF studies involving measurement of CSF dynorphin A 1-8 immunoreactivity during hospitalization in an eating-disorder treatment and research program [34].
• Since 5-HT1A receptors are implicated in the pathogenesis of anxiety, depression, hallucinogenic behaviour, motion sickness and eating disorders, they are an important target for drug therapy [35].
• RESULTS: Inositol was significantly better than placebo on the Global Clinical Impression, the Visual Analogue Scale, and the Eating Disorders Inventory [36].
• Brain glucose metabolism in eating disorders assessed by positron emission tomography [37].
• Urinary steroid components were measured after enzyme hydrolysis and methoxym-silyl derivatization by capillary gas chromatography in young women with eating disorders [38].

References