Zinc Andtryptophan Levels in Anorexianervosa; a Co-Relational Study (original) (raw)
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Improving therapeutics in anorexia nervosa with tryptophan
Life Sciences, 2017
Tryptophan (2-amino-3-(1H-indol-3-yl) propanoic acid) Serotonin (5-hydroxytryptamine) Dopamine (3,4-dihydroxyphenyl ethylamine) Kynurenic acid (4-hydroxyquinoline-2-carboxylic acid) Quinolinic acid (pyridine-2,3-dicarboxylic acid) 5-HIAA (5-hydroxyindole acetic acid) 5-HTP (5-hydroxytryptophan) Valine (2-amino-3-methylbutyric acid) Fluoxetine (N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine GABA (gamma-aminobutyric acid) A growing body of evidence suggests that our diet is an important contributing factor in the development, management and prevention of a number of psychiatric illnesses. Tryptophan, an essential amino acid, is the sole precursor of neurotransmitter 5-hydroxytryptamine (5-HT; serotonin). Administration of tryptophan can boost serotonin neurotransmission to produce therapeutically important effects in serotonin deficiency disorders. Anorexia nervosa (AN) an eating disorder associated with high levels of psychiatric comorbidity including psychosis, hyperactivity, depression and anxiety has highest lethality of all psychiatric illnesses. Evidence suggests that excessive dieting and food restriction can decrease brain tryptophan and serotonin in AN patients to precipitate depression, psychosis and hyperactivity. There are currently no FDA approved pharmacological treatments available for AN patients; antidepressants and antipsychotics, largely used to treat associated psychiatric comorbidities are also not very effective. The aim of this non-systematic review article is to evaluate and document a potential importance of tryptophan supplementation in improving therapeutics in AN patients.
Plasma tryptophan during weight restoration in patients with anorexia nervosa
Biological Psychiatry, 2005
Background: Anorexia nervosa (AN) is a mental disorder characterized by low weight and concerns about body shape and weight. Disturbance in serotonin function has been described as central to the psychobiology of this disorder. Plasma tryptophan (TRP), the essential amino acid needed for serotonin production, is known to be low following acute caloric restriction but has not been measured during the course of refeeding. Methods: Plasma TRP and other large neutral amino acids (LNAA) levels were measured in 26 female patients with AN and 15 control subjects. Patient levels were measured at admission for inpatient treatment, after 1 week of treatment, and upon weight restoration to weight Ն90% ideal body weight (IBW). For 17 patients, an additional assessment was made when weight reached 80% IBW. Plasma levels were obtained on one occasion from healthy control subjects. Results: Plasma TRP and TRP/LNAA ratio increased significantly during refeeding process. Plasma TRP in patients was 46.88 nmol/mL (SD ϭ 19.59) on admission and 55.54 nmol/L/mL (SD ϭ 8.1) at normal weight, p Ͻ .05. The ratio of TRP to LNAA was .11 (SD ϭ .03) on admission and .13 (SD ϭ .02) at normal weight, p Ͻ .05 . Plasma TRP is significantly lower in low-weight patients than in healthy control subjects (TRP ϭ 53.73 [SD ϭ 8.21]), but there was no significant difference between control subjects and normal-weight patients. Conclusions: Plasma TRP normalizes during the course of refeeding, supporting the hypothesis that serotonin function is disturbed in patients with anorexia nervosa.
Zinc status and meat avoidance in anorexia nervosa
International journal of adolescent medicine and health, 2001
The objective was to investigate the prevalence of meat avoidance and the zinc status of anorexia nervosa (AN) patients. Methods: 45 consecutive patients were recruited at admission to an eating disorder outpatient clinic. Acceptance criteria were illness of less than 30 months of duration without previous hospitalization. Intake and nutritional evaluation were routine except for additional questions on meat avoidance. A fasting plasma zinc test was done close to admission. Urinary zinc excretion was determined for eight patients. One hundred and fifty-six healthy subjects matched for age and demographic characteristics served as controls for meat avoidance, and another eight healthy girls were tested for plasma zinc. Ninety-six percent of patients avoided beef, and 75% avoided both beef and poultry. Meat avoidance was 6.5 times more prevalent among patients than controls. Twenty-five of the 45 patients (56%) became vegetarians several years prior to the onset of AN, at the mean age of 11.1 years. Reported reason for meat avoidance was aversion of varying degree. These "early meat avoiders" were compared with the 20 late avoiders and non-avoiders. Plasma zinc was deficient and identical for both groups of patients (56.3 ± 10.2 mcg/dl) and statistically different from controls (p<0.01). Twenty-four-hour urinary zinc excretion of eight patients was in the deficient range (140.3 ± 86.2 mcg/24 hr). At admission all patients were zinc deficient, independent of diet status. We speculate that zinc deficiency may predate the onset of AN, possibly originating during the adolescent growth spurt, and may cause MA through alterations in the sense of taste. Early MA is then likely to perpetuate low zinc status, destabilize normal eating patterns, and facilitate the development of an eating disorder. Vegetarianism in growing girls may be seen as a symptom of zinc deficiency.
Anxiolytic effects of acute tryptophan depletion in anorexia nervosa
International Journal of Eating Disorders, 2003
Abstract: Objective: Recent studies have raised the question as to whether,a dysregulation of the neurotransmitter,serotonin may,contribute to the alterations in mood,seen in anorexia nervosa (AN). People with AN tend to be anxious, obsessional, perfectionistic, and harm avoidant. These traits are premorbid,and persist after recovery. It has been,suggested,that increased activity of brain serotonin systems could contribute to this pathologic,condition. Dieting in
Physiology & Behavior, 1984
1984.-Anorexia is a major manifestation of zinc deficiency, but the mechanism(s) for this anorexia are not well defined. In this study we investigated the effects of three modulators of feeding response on the food consumption of zinc deficient rats. Zinc deficient rats showed partial resistance to norepinephrine, eating significantly less at the 20/~g dose than the zinc sufficient ad lib controls, and food ingestion could not be induced at the 10/zg dose. Similarly, higher doses of the GABA agonist, muscimol, were requiredto induce feeding in the zinc deficient animals compared to the zinc sufficient controls. The dopamine agonist, bromergocryptine, failed to induce feeding in the zinc deficient animals. These findings are compatible with the concept that zinc deficiency produces a generalized decrease in receptor responsitivity, possibly secondary to alterations in membrane fluidity.
The role of the endogenous opiates in zinc deficiency anorexia
Physiology & Behavior, 1984
The role of the endogenous opiates in zinc deficiency anorexia. PHYSIOL BEHAV 32(3) 475-478, 1984.mAnorexia is a major symptom of zinc deficiency, but the mechanism(s) for this anorexia are poorly defined. Recent studies have suggested an integral role for endogenous opiate peptides in appetite regulation. Dynorphin, a leucine-enkephalin containing opiate peptide, is a potent inducer of spontaneous feeding. In this study we showed that zinc deficient animals were relatively resistant to dynorphin-induced feeding. Measurement of dynorphin levels using a highly sensitive radioimmunoassay showed that zinc deficient animals had lower levels of dynorphin in the hypothalamus than did ad lib fed animals, with weight restricted animals having intermediate values. ['~H]-naioxone binding was significantly increased to isolated brain membranes from zinc deficic.,at animals using I nM unlabeled naloxone when compared to ad lib fed controls with the weight restricted animals again having intermediate values. These data suggest that abnormalities in endogenous opiate regulation of appetite may well play a role in the anorexia of zinc deficiency. The effects of zinc deficiency on endogenous opiate action appear to include alterations in receptor affinity, a post-receptor defect and alterations in the synthesis and/or release of dynorphin.
Zinc deficiency and anorexia in rats: normal feeding patterns and stress induced feeding
Physiology & Behavior, 1984
We report the effects of zinc deficiency on normal feeding behavior in rats and the effects of zinc deficiency on stress-induced eating in rats. Zinc deficient (ZD) rats weighed significantly less than their pair-fed and ad lib controls. Zinc repletion allowed improved growth, but ZD rats never displayed catch-up growth compared to their ad lib controls. ZD rats rapidly developed a depressed food efficiency ratio which normalized with zinc supplementation. Food consumption in ZD rats was approximately one-third that ofad lib controls and water intake was also significantly reduced. Mild tail pinch was able to induce feeding in these normally anorexic ZD rats. We conclude that zinc deficiency represents an interesting model of anorexia which may enhance our understanding of appetite regulation.