A decline in inflammation is associated with less depressive symptoms after a dietary intervention in metabolic syndrome patients: a longitudinal study.

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.

Lifestyle medicine

Fundamental Clinical Imbalances : Neurological ; Immune and inflammation
Patient Centred Factors : Mediators/CRP
Environmental Inputs : Diet
Personal Lifestyle Factors : Nutrition ; Psychological
Functional Laboratory Testing : Blood
Bioactive Substances : CRP ; Leptin

Methodological quality

Allocation concealment : Not applicable

Metadata

Nutrition Evidence keywords : CRP ; Leptin