To send this article to your account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send this article to your Kindle, first ensure firstname.lastname@example.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Objective: To compare the scientific content of recent general media articles on tryptophan, diet and depression, with recent empirical research into dietary manipulation of tryptophan published in the scientific literature.
Method: A review of the recent empirical research into the role of tryptophan in depression, focusing on dietary methods to influence tryptophan levels. In parallel, a review of recent articles in the general English language media regarding tryptophan and mood.
Results: Empirical evidence for improving mood through dietary manipulation of tryptophan is lacking, and it is difficult to change plasma tryptophan levels through diet alone. Tryptophan supplementation and depletion studies suggest that altering tryptophan levels may only benefit certain groups of patients who have a personal or family history of depression. Scientific studies also focus on elucidating mechanisms in depression, rather than treating depression by changing tryptophan levels. However, general media articles often recommend diets and foods to increase blood tryptophan levels and raise brain serotonin levels. Such recommendations are not supported by scientific studies.
Conclusion: It is very difficult to alter blood tryptophan levels through dietary methods alone, outside of a laboratory or research setting. Only a small number of lay articles provide sound advice, with general media reports on tryptophan often being hyperbolic and misleading. A clinician should be aware of the type of (mis)information a patient may have accessed and have the scientific knowledge to explain the impracticalities of influencing tryptophan levels through diet alone.
Background: Several studies have investigated the association of FKBP5 gene polymorphisms with mood disorders, but findings are not always consistent. The aim of our study was to assess the association of FKBP5 gene polymorphisms with mood disorders using a meta-analysis.
Methods: Data were collected from the following electronic databases: PubMed, Elsevier Science Direct, Cochrane Library, Chinese Biomedical Literature Database, China National Knowledge Infrastructure and Wanfang, with the last report up to March 2010. Meta-analysis was performed in a fixed/random effect model.
Results: We identified six studies using search, and one study was excluded because of unavailable data. One study contained data on two different ethnicities and we treated them independently. Thus, six separate studies (2655 cases and 3593 controls) were included in the meta-analysis. Meta-analysis was performed for three FKBP5 gene polymorphisms (rs1360780, rs3800373 and rs4713916) in overall and Caucasian populations. We did not detect any association of FKBP5 gene rs1360780 and rs3800373 polymorphisms with mood disorders (p > 0.05). However, a significant association of FKBP5 gene rs4713916 polymorphism with mood disorders was found, and the heterozygous individual (GA genotype) was more susceptible to mood disorders in comparison to homozygous analogues (GG or AA genotype) [overall: GA vs. GG: OR (odds ratio) = 1.20, 95% CI (confidence interval) = 1.03–1.40, p = 0.02; GA vs. AA: OR = 1.44, 95% CI = 1.09–1.90, p = 0.009; Caucasian: GA vs. GG: OR = 1.22, 95% CI = 1.04–1.44, p = 0.01; GA vs. AA: OR = 1.43, 95% CI = 1.09–1.89, p = 0.01].
Conclusion: This meta-analysis shows that mood disorders are associated with FKBP5 gene rs4713916 polymorphism, but not with rs1360780 and rs3800373.
Background: The molecular pathogenesis of depression and psychopharmacology of antidepressants remain elusive. Recent hypotheses suggest that changes in neurogenesis and plasticity may underlie the aetiology of depression. The hippocampus is affected by depression and shows neuronal remodelling during adulthood.
Objective: The present study on the adult rat hippocampus, was to evaluate the dose-related effects of chronic venlafaxine on the expression of brain-derived neurotrophic factor (BDNF) and phosphorylated cyclic-AMP response element binding protein (pCREB).
Methods: Sprague-Dawley rats were exposed to a variety of chronic unpredictable stressors (CUSs) to establish a depression model. Rats were treated for either 14 or 28 days with venlafaxine (5 and 10 mg/kg, respectively). The hippocampal expression of pCREB and BDNF mRNA and protein was assessed by using immunohistochemistry, western blotting and reverse transcription polymerase chain reaction (RT-PCR).
Results: Rats subjected to CUS procedure consumed less sucrose solution compared with non-stressed rats. The CUS influenced exploratory activity resulting in a reduction of the motility counts. Chronic low dose (5 mg/kg, 14 and 28 days), but not high dose (10 mg/kg, 14 and 28 days) of venlafaxine treatment increased the expression of pCREB and BDNF mRNA and protein in the CUS rat hippocampus.
Conclusion: Neuronal plasticity-associated proteins such as pCREB and BDNF play an important role both in stress-related depression and in antidepressant effect.
Aim: Investigation of responses of multifocal visual-evoked potentials (mfVEPs) in schizophrenic patients under treatment in whom no abnormality was detected on the conventional perimetry.
Methods: Recordings of mfVEPs were performed in 31 schizophrenic patients and 30 normal subjects using a VERIS Junior Science recording apparatus (Mayo, Aichi, Japan). Responses from eight sites in each subject were divided into four quadrants (superior and inferior temporal quadrants, and superior and inferior nasal quadrants). In each quadrant, two response waves were grouped and averaged, and the latency and amplitude of main waveforms that appeared near 100 ms were evaluated.
Results: The peak latency was about 7–9 ms prolonged and the amplitude was reduced by about 2–5 nV/deg2 in the schizophrenic patient group compared to those in the normal subject group, and significant differences were noted in both parameters in all quadrants.
Conclusion: In schizophrenic patients under treatment with psychotropic agents, prolongation of the latency and amplitude reduction were noted in mfVEPs even though no abnormality was detected on the conventional perimetry.