Fasting in mood disorders:neurobiology and effectiveness.A review of the literature (original) (raw)
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Scientific Reports
Major depressive disorder (MDD) is frequently associated with poor response to treatment. Common antidepressants target neurotransmission and neuronal plasticity, which require adequate energy supply. As imaging studies indicate disturbances in central energy metabolism, and caloric restriction improves neuroplasticity and impacts mood and cognition, correction of energy status might increase the effectiveness of antidepressant treatments and reduce the psychopathological symptoms of depression. Metabolic parameters, stress hormones, and brain-derived neurotrophic factor (BDNF) levels were assessed in serum of depressed inpatients (MDD, N = 21) and healthy volunteers (Ctrl, N = 28) before and after a 72 h fasting period during which only water was consumed. Depression severity was assessed by Beck’s Depression Inventory (BDI)-2 sum-score and cognitive-affective and somatic sub-scores. Fasting similarly impacted metabolic parameters and stress systems in both groups. Fasting elevated...
Nutrients
Background. Fasting interventions have shown effectiveness in alleviating stress, anxiety and depressive symptoms. However, no quantitative analysis has been carried out thus far. The objective was to determine the effectiveness of fasting interventions on stress, anxiety and depression and if these interventions were associated with increased or decreased fatigue/energy. Methods. Overall, 11 studies and 1436 participants were included in the quantitative analyses. Results. After limiting analyses to randomized controlled trials with low risk of bias, we found that fasting groups had lower anxiety (b = −0.508, p = 0.038), depression levels (b= −0.281, p = 0.012) and body mass index compared to controls without increased fatigue. There was no publication bias and no heterogeneity for these results. These interventions were safe, even in patients with type 2 diabetes. Conclusions. These results should be taken with a caveat. These results are preliminary and encouraging and fasting ap...
Marcadores biológicos e nível de funcionalidade em pacientes bipolares
2007
Alterations in specific structures of CNS, in particular, fronto-lymbic system, and a reduction of neurons and glial cells appear to be involved in the pathophysiology of bipolar disorder. Glial cells have an important role in the CNS, for example, the production of neurotrophins, especially, Glial Cell Line-derived Neurotrophic Factor (GDNF). In this study, we showed a marked increased in the serum levels of GDNF in depressive (F= 42.31; p=0.004; one-way ANOVA) and manic bipolar patients (F= 42.31; p=0.001; one-way ANOVA), which suggested that GDNF could be involved in the physiopathology of bipolar disorder. On the other hand, alterations in the neurotrophic factors hinder synaptic plasticity mechanisms, may result in cognitive impairment in bipolar patients. In particular, memory difficulties have been reported here, and these difficulties influence occupational and social functioning in these subjects. High rates of functional impairment showed by bipolar patients and a lack of standardization of the instruments available to assess functioning in the studies motivated us to development the scale. The Functioning Assessment Short test (FAST) is a rapid instrument and easy to apply developed to use in psychiatry, especially, bipolar patients. It assesses six specific domains of functioning, such as autonomy, occupational functioning, cognitive functioning, financial issues and leisure time. The validation of FAST was performed by psychometric tests such as internal consistency (Cronbach's alpha: 0.909), concurrent validity compared to the GAF (r=-0.903; p<0.001), validity as a discriminative measure to detect the difference between euthymic (18.55; F=23.59; p<0.001) and acute patients (manic: 38.50; depressive: 42.38; mixed: 43.21), factorial analysis and test-retest reliability (0.953; p<0.01). The FAST scale showed strong psychometric properties and it is now available for use in both clinical practice and investigation settings.
Biology of Mood & Anxiety Disorders, 2013
In March, 2012 we held the first Mideast conference on "Depression and Anxiety Spectrum disorders: from basic science to the clinic and back", at the University of Amman, Jordan. This event brought together both clinical and basic scientists with expertise in depression and anxiety spectrum disorders. The meeting took place in a large lecture hall at the University of Jordan Medical School. The audience included faculty, residents, and students. The Dean of the Medical School opened the meeting, welcoming the guest speakers and participants.
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Oxidative stress in applied basic research and clinical practice, 2015
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2021
There is a strong relationship between a healthy diet and mental well-being. Several foods and food compounds are known to modulate biomarkers and molecular mechanisms involved in the aetiogenesis of several mental disorders, and this can be useful in containing the disease progression, including its prophylaxis. This is an updated systematic review of the literature to justify the inclusion and recognition of nutrition in the management of psychiatric illnesses. Such foods and their compounds include dietary flavanols from fruits and vegetables, notable antioxidant and anti-inflammatory agents, probiotics (fermented foods) known to protect good gut bacteria, foods rich in polyunsaturated fatty acids (e.g., Omega-3), and avoiding diets high in saturated fats and refined sugars among others. While the exact mechanism(s) of mitigation of many nutritional interventions are yet to be fully understood, the evidence-based approach warrants the inclusion and co-recognition of nutrition in ...
Journal of Psychiatry …, 2007
The 30th Annual Meeting of the Canadian College of Neuropsychopharmacology (CCNP) was held in Banff, Alberta, June 15 to June 19, 2007. This report summarizes the 3 CCNP award lectures and 10 symposia. CCNP Heinz Lehmann Award lecture Dr. Hymie Anisman (Carleton University, Ottawa) was the recipient of this year's Heinz Lehmann award, and his talk was entitled "Stress, cytokines and depressive illness." As Dr. Anisman noted, in recent years it has become clear that stressors can affect the immune system. This led to the converse question: can the immune system affect psychological states? Investigations of these associations have benefited from distinguishing between different types of stressors: predictable versus unpredictable, chronic versus intermittent, and processive (e.g., cognitive) versus systemic (e.g., disease activated). Depending on these stressor features, along with intensity and duration, the elicited response can facilitate coping, or it can lead to dysfunction and disease. For example, mild, controllable stressors activate monoamine release and lead to increased synthesis plus an enhanced coping response on subsequent re-exposure. In comparison, severe, uncontrollable stressors deplete monoamine stores, and synthesis rates are unable to compensate adequately. Similarly, monoamine sensitization might simultaneously enhance short-term coping but, in the absence of adequate increases in synthesis, increase vulnerability to the effects of prolonged stressors. The latter change might be related to the progressive acceleration of relapse rates in patients with recurrent major depression. Marked individual and rodent strain differences in these responses are also evident. Recent work by Dr. Anisman's group has identified a neurobiological pathway that could mediate many of these effects: stress-induced activation of immune signalling cytokines. Inflammatory cytokines such as interleukin-1 (IL-1) and interferon-γ (IFN-γ) are present in the brain, and their activation can affect cell death, neurogenesis, and cell metabolism. Patients suffering from severe stress and depression exhibit increased cytokine activity, whereas cytokine immunotherapy (e.g., interferon-α, tumour necrosis factor-α [TNF-α]) can induce antidepressant-reversible depressions. In Dr. Anisman's studies, administration of IL-1, like stress, increases norepinephrine (NE) metabolism and serotonin (5-HT) release. The bacterial endotoxin (LPS) increases dopamine (DA) release in the nucleus accumbens (NAc), whereas chronic stressor regimens can decrease responding for electrical brain stimulation (EBS) reward. Following exposure to a cytokine such as TNF-α, there is an increase in sicklike behavioural responses (e.g., ptosis, ruffled fur, altered body posture), corticosterone release and NE metabolism, and this response becomes greater after repeated exposures followed by extended intertest intervals. These associations have recently been followed up in studies
Biological Psychiatry, 2002
Trials and Translation Workgroup was asked to define priorities for clinical trials in mood disorders and for research on how best to translate the results of such research to clinical practice settings. Through two face-to-face meetings and a series of conference calls, we established priorities based on the literature to date and what was known about research currently in progress in this area. We defined five areas of priority that cut across developmental stages, while noting that research on adult mood disorders was at a more advanced stage in each of these areas than research on child or geriatric disorders. The five areas of priority are: 1) maximizing the effectiveness and cost-effectiveness of initial (acute) treatments for mood disorders already known to be efficacious in selected populations and settings when they are applied across all populations and care settings; 2) learning what further treatments or services are most likely to reduce symptoms and improve functioning when the first treatment is delivered well, but the mood disorder does not remit or show adequate improvement; 3) learning what treatments or services are most cost-effective in preventing recurrence or relapse and maintaining optimal functioning after a patient's mood disorder has remitted or responded maximally to treatment; 4) developing and validating clinical, psychosocial, biological, or other markers that predict: a) which treatments are most effective, b) course of illness, c) risk of adverse events/ tolerability and acceptability for individual patients or well-defined subgroups of patients; 5) developing clinical trial designs and methods that result in lower research costs and greater generalizability earlier in the treatment development and testing process. A rationale for the importance of each of these priorities is provided. Biol Psychiatry 2002;52:631-654