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Zinc, Magnesium, Selenium and Depression: A Review of the Evidence, Potential Mechanisms and Implications.
Wang, J, Um, P, Dickerman, BA, Liu, J
Nutrients. 2018;10(5)
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Adequate micronutrient consumption and mental health are of major public health importance. Recent findings suggest micronutrient deficiencies may play a role in the development and progression of depression, yet the findings remain unclear. The aim of this review is to present the recent evidence on the association between several micronutrients and depression and discuss the potential mechanisms and clinical implications. Based on the current literature, evidence shows an association between both zinc and magnesium deficiency and the risk of depression, with stronger evidence supporting zinc. Studies on selenium are limited or inconclusive. According to these findings, the authors support the importance of adequate micronutrient consumption for promoting mental health. They suggest future research should investigate the safety and efficacy of micronutrient supplementation as an adjunct treatment for depression to better inform current prevention and treatment strategies.
Abstract
Micronutrient deficiency and depression are major global health problems. Here, we first review recent empirical evidence of the association between several micronutrients—zinc, magnesium, selenium—and depression. We then present potential mechanisms of action and discuss the clinical implications for each micronutrient. Collectively, empirical evidence most strongly supports a positive association between zinc deficiency and the risk of depression and an inverse association between zinc supplementation and depressive symptoms. Less evidence is available regarding the relationship between magnesium and selenium deficiency and depression, and studies have been inconclusive. Potential mechanisms of action involve the HPA axis, glutamate homeostasis and inflammatory pathways. Findings support the importance of adequate consumption of micronutrients in the promotion of mental health, and the most common dietary sources for zinc and other micronutrients are provided. Future research is needed to prospectively investigate the association between micronutrient levels and depression as well as the safety and efficacy of micronutrient supplementation as an adjunct treatment for depression.
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A decline in inflammation is associated with less depressive symptoms after a dietary intervention in metabolic syndrome patients: a longitudinal study.
Perez-Cornago, A, de la Iglesia, R, Lopez-Legarrea, P, Abete, I, Navas-Carretero, S, Lacunza, CI, Lahortiga, F, Martinez-Gonzalez, MA, Martinez, JA, Zulet, MA
Nutrition journal. 2014;13:36
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Metabolic syndrome (defined as a cluster of cardiovascular risk factors including central obesity, glucose intolerance, hypertension and lipid disorders) is rising rapidly worldwide. Certain features of metabolic syndrome including adiposity, glucose intolerance and lipid disorders have also been linked to depression, another burden on healthcare worldwide. The exact pathways linking these diseases are unclear but appear to be bidirectional and dependent on biological and behaviour factors. This study hypothesises that hypo caloric treatment may have a positive impact on both metabolic syndrome and depression, and explores the possible mechanisms for this effect. The sample included 60 subjects with a BMI of at least 36.1 and aged over 50 years. These were a subsample of the RESMENA-S study which involved a 6 month weight loss intervention (either RESMANA-S or a control both with the same energy restrictions). This study found a reduction in depressive symptoms, alongside a reduction in CRP and leptin following the diet. Previous research has found a relationship between weight loss and reduced depression, but this study specifically found the decrease in CRP and leptin with a reduction of depression. The precise mechanism between CRP and depression remains unclear but the authors suggest that inflammation may be responsible. Theoretically, the association between leptin and depression may be related to its metabolic properties and neurobiological activity (it may relate to mood and cognition).
Abstract
BACKGROUND Metabolic syndrome (MetS) and depression have become two prevalent diseases worldwide, whose interaction needs further investigation. Dietary treatment for weight loss in patients with MetS may improve depressive manifestations, however, the precise interactive pathways remain uncertain. Therefore, the aim of this study was to examine the effects of a hypocaloric diet designed to reduce MetS features on self-perceived depression and the possible underlying factors. METHODS Sixty subjects (Age: 50 ± 1 y; BMI: 36.1 ± 0.6 kg/m(2)) with MetS were selected from the RESMENA study (control and intervention) after they completed the 6-months hypocaloric treatment and rated for depressive symptoms using the Beck Depression Inventory (BDI). Anthropometric and biochemical measurements including leptin, C-reactive protein (CRP) and insulin levels were evaluated. RESULTS Depressive symptoms decreased during the weight loss intervention, with no differences between both dietary groups (control group -4.2 ± 0.8 vs RESMENA group -3.2 ± 0.6, P = 0.490). The number of criteria of the MetS was higher among subjects with more somatic-related depressive symptoms at baseline (B = 1.032, P-trend = 0.017). After six months of dietary treatment, body weight decreased in all subjects (-8.7%; confidence interval (95% CI) = 7.0-9.7) and also self-perceived depression (-37.9%; 95% CI = 2.7-4.9), as well as circulating leptin (-20.1%; 95% CI = 1.8-6.8), CRP (-42.8%; 95% CI = 0.6-3.0) and insulin (-37.7%; 95% CI = 4.1-7.2) concentrations. The decrease in BDI was significantly associated with declines in body fat mass (B = 0.34, 95% CI = 0.11-0.56) and also with the decrease in leptin (B = 0.16, 95% CI = 0.04-0.28) and CRP (B = 0.24, 95% CI = 0.01-0.46) concentrations. CONCLUSIONS The decrease in depressive manifestations after a weight loss intervention was related with adiposity, CRP and leptin in subjects with MetS. TRIAL REGISTRATION ClinicalTrials.gov: NCT01087086.