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Psychobiology of eating disorders
Published in Stephen Wonderlich, James E Mitchell, Martina de Zwaan, Howard Steiger, Annual Review of Eating Disorders Part 2 – 2006, 2018
David C Jimerson, Barbara E Wolfe
There has been considerable interest in studies comparing long-term weight recovered patients with healthy controls matched for body mass index (BMI). Results have shown elevated levels of CSF 5-HIAA (Kaye et al. 1991) and diminished sensitivity to the behavioral effects of fenfluramine (Ward et al. 1998), although neuroendocrine responses are not different from healthy controls (O’Dwyer et al. 1996). Moreover, acute tryptophan depletion resulted in a decrease in symptoms of anxiety in long-term recovered individuals (Kaye et al. 2003). Persistent alteration of serotonin function following remission is reflected in the finding that regional 5-HT2A receptor binding is decreased in individuals who have recovered from the binge-eating/purging subtype of AN (Bailer et al. 2004).
Studies on the Neurobiology of Depression
Published in Siegfried Kasper, Johan A. den Boer, J. M. Ad Sitsen, Handbook of Depression and Anxiety, 2003
Carlos A. Zarate, Dennis S. Charney
Pretreatment plasma tryptophan has been reported to be lower in depressed patients than in healthy controls and to differentiate certain subgroups of depression [187,219]. Depressed patients exhibit reduced plasma concentrations of 5-hydroxytryptophan after ingestion of test doses of oral L-tryptophan [82]. Other studies report that, in normal control subjects, lowering of plasma tryptophan via dietary manipulation produces a depressed mood [89]. The occurrence of depression following acute tryptophan depletion has been reported to occur more commonly in healthy subjects with first-degree relatives with affective disorders than in healthy subjects with no family history of a mood disorder [33,109]. Lower pretreatment plasma tryptophan has been reported to predict antidepressant treatment [181,227]. The depletion of dietary L-tryptophan has also been reported to induce relapse in recently remitted depressed patients [89,239]. In contrast to these findings, several studies have recently found that the effect may be less consistent than previously reported. Moore and colleagues [228] observed no effect on mood in fully remitted patients medicated with selective serotonin reuptake inhibitors (SSRIs). Leyton and colleagues [177] also reported that acute tryptophan depletion did not induce relapse or change in mood in fully remitted, medication-free, former patients with major depression. In another study [1] of patients who had responded to treatment with citalopram, only 5 of 12 patients relapsed, and the effect seemed to be clinically significant in only 1 patient. While depletion of dietary L-tryptophan has been reported to induce relapse in recently remitted depressed patients, Cassidy and colleagues [63] did not find that depletion of L-tryptophan results in relapse in patients who had successful treatment with ECT. These previous studies suggest that acute tryptophan depletion reflects a reversal of mechanisms involved in the therapeutic effects of antidepressants but not of ECT. Depletion of plasma tryptophan has been reported to cause dysphoria in the first-degree relatives of patients with depression.
Almond intake during pregnancy in rats improved the cognitive performance of adult male offspring
Published in Nutritional Neuroscience, 2023
Zahra Bahaeddin, Fariba Khodagholi, Forough Foolad, Fatemeh Emadi, Fatemeh Alijaniha, Shima Zareh Shahamati, Romina Tavassoli Yousef Abadi, Mohsen Naseri
On the other hand, Haider and colleagues revealed an increase in the brain tryptophan and serotonergic turnover of rat’s brains following oral intake of almonds leading to memory improvement in rats [45]. Enhanced serotonin activity of the brain has been shown to improve cognitive performance in both animals and human studies, whereas decreased serotonergic levels by acute tryptophan depletion would impair cognition [46,47]. The role of the serotonergic system in neuroplasticity has been explored, which is critical during brain development [48]. Serotonin acts as a growth factor during embryogenesis and is involved in brain structural changes. The serotonergic system interacts with chemical messengers of the GABAergic, glutamatergic, and dopaminergic neurotransmitters [49]. Given the above-mentioned data, tryptophan can be considered an effective part of almond in improving the memory of adult offspring rats.
Evaluation of dietary intake in children and college students with and without attention-deficit/hyperactivity disorder
Published in Nutritional Neuroscience, 2019
Kathleen F. Holton, Jeanette M. Johnstone, Elizabeth T. Brandley, Joel T. Nigg
Finally, the observation that college students who have higher intakes of tryptophan have a lower likelihood of having ADHD, is consistent with the fact that depression, which has been strongly associated with decreased serotonin levels, is highly comorbid with ADHD.83 Furthermore, research has also suggested that altered levels of 5-HT (serotonin) may be associated with hyperactive and impulsive components of the disorder.42 Acute tryptophan depletion has also been associated with aggression84,85 and attentional performance49 in ADHD. However, Berwerff et al. failed to show differences in blood spot or urine concentrations of tryptophan among children age 6–13 with and without ADHD.56 Thus, more research is needed to determine the potential role of serotonin (mediated by tryptophan intake) on ADHD symptoms.
Inhibition of hormonal and behavioral effects of stress by tryptophan in rats
Published in Nutritional Neuroscience, 2019
Sumera Gul, Darakhshan Saleem, Muhammad A. Haleem, Darakhshan Jabeen Haleem
Previous investigation on the effects of tryptophan on anxiety and depression-like behavior are not very consistent. Low dietary tryptophan produces anxiogenic-like effects in the elevated plus maze test and depressant-like effects in forced swim test in rats.31 Mice fed on tryptophan-limited diet for one month displayed normal levels of anxiety but enhanced emotional responsiveness to stress.32 Acute tryptophan depletion in human subjects also lowered mood and increased irritability or aggression.33 Long-term oral tryptophan administration at a dose of 50 mg/kg did not alter anxiety-like behavior in the elevated plus maze test but elicited depression-like behavior in forced swim test.34 The present study shows that acute administration of tryptophan at a dose of 300 mg/kg not only attenuated immobilization-induced anorexia (Fig. 2), but the effects of immobilization on anxiety-like behavior in the elevated plus maze test (Fig. 3) were also inhibited.