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      Factors Associated with the Risk of Developing Coronary Artery Disease in Medicated Patients with Major Depressive Disorder

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          Abstract

          Background: The aim of this study was to identify factors associated with high Framingham Risk Score (FRS) in medicated patients with major depressive disorder (MDD). Methods: We examined 61 medicated patients with MDD (mean age 37.77 ± 7.67, 90.2% women) and 43 non-depressed controls (mean age 38.26 ± 9.20, 90.7% women). We administered the Hamilton Depression Rating Scale (HAM-D) and measured systolic blood pressure (SBP), diastolic BP (DBP), mean arterial BP (MAP), pulse wave velocity (PWV), intima-media thickness (IMT), interleukin-6 (IL-6) and triglycerides. Results: We found that medicated patients with MDD had significantly higher levels of HAM-D score ( p < 0.01), SBP ( p = 0.015), MAP ( p = 0.037), IL−6 level ( p = 0.007), as compared with controls. Medicated patients who remained moderately to severely depressed showed significantly higher SBP ( p = 0.049), DBP ( p = 0.009), MAP ( p = 0.024), IL−6 level ( p = 0.019), left PWV ( p = 0.004) and average PWV ( p = 0.026) than those with mild depression. Multivariate regression showed that the interaction effect between HAM-D score and triglyceride level ( p = 0.018) was significantly associated with FRS in medicated patients with MDD. Conclusions: This study highlights that the interaction effect of the severity of depression and the triglyceride level, was a modifiable factor positively associated with high FRS.

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          Interleukin (IL)-6, tumour necrosis factor alpha (TNF-α) and soluble interleukin-2 receptors (sIL-2R) are elevated in patients with major depressive disorder: a meta-analysis and meta-regression.

          Many studies have explored the association between soluble interleukin-2 receptor (sIL-2R), cytokines and major depressive disorder (MDD). However, the results of these studies were not consistent. The aim of our study is to compare the levels of sIL-2R and cytokines in the blood between MDD patients and controls by a meta-analysis and to identify moderators accounting for potential heterogeneity in the levels of sIL-2R and cytokines in MDD patients versus controls by meta-regression analyses. A comprehensive literature search was performed to identify studies comparing the levels of sIL-2R and cytokines between MDD patients and controls. We pooled the effect sizes for standardized mean differences (SMD) of the levels of sIL-2R and cytokines. We also performed meta-regression and sensitivity analyses to investigate the roles of age, gender, sample type, ethnic origin and selected studies' quality in explaining potential heterogeneity and differences in results respectively. Twenty-nine studies were selected for this analysis. The levels of sIL-2R, TNF-α and IL-6 in MDD patients were significantly higher than those of healthy controls (SMD=0.555, p<0.001, SMD=0.567, p=0.010; SMD=0.680, p<0.001). Mean age of all subjects was a significant moderator to explain the high heterogeneity of IL-6. Sensitivity analysis found that European but not non-European subjects have higher levels difference of sIL-2R, TNF-α and IL-1β between MDD patients and controls. The severity of MDD was not considered. The blood levels of sIL-2R, TNF-α and IL-6 were significantly higher in MDD patients than controls. Age, samples source and ethnic origins may play a potential role in heterogeneity. Copyright © 2011 Elsevier B.V. All rights reserved.
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            Exploring the association between childhood and adolescent obesity and depression: a meta-analysis.

            This meta-analysis aimed to evaluate the association between childhood and adolescent obesity and depression. We systematically searched PubMed, PsycInfo, EMBASE and Science Direct for studies that compared prevalence of depression and depressive symptoms in normal weight and obese children and adolescents. Observational studies were included if they reported body mass index and assessed depression by validated instruments or diagnostic interviews. Quality assessment was performed using the Newcastle-Ottawa scale. We used the random-effect model to calculate the pooled odds ratios, standard mean differences (SMDs) and subgroup analysis. Findings for a total of 51,272 participants were pooled across 18 studies and examined. Our analyses demonstrated a positive association between childhood and adolescent obesity and depression (pooled odds ratio = 1.34, 95% confidence interval [CI]: 1.1-1.64, p = 0.005) and more severe depressive symptoms (SMD = 0.23, 95% CI: 0.025-0.44, p = 0.028) in the obese groups. Overweight subjects were not more likely to have either depression (pooled odds ratio = 1.16, 95% CI: 0.93-1.44, p = 0.19) or depressive symptoms (SMD = 0, 95% CI: -0.101 to 0.102, p = 0.997). Non-Western and female obese subjects were significantly more likely to have depression and severe depressive symptoms (p < 0.05). In conclusion, obese children and adolescents are more likely to suffer from depression and depressive symptoms, with women and non-Western people at higher risk.
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              Evidence for low-grade systemic proinflammatory activity in patients with posttraumatic stress disorder.

              Posttraumatic stress disorder (PTSD) may increase cardiovascular risk but the psychophysiological mechanisms involved are elusive. We hypothesized that proinflammatory activity is elevated in patients with PTSD as diagnosed by the Clinician Administered PTSD Scale (CAPS) interview. Plasma levels of proinflammatory C-reactive protein (CRP), interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, and of anti-inflammatory IL-4 and IL-10 were measured in 14 otherwise healthy PTSD patients and in 14 age- and gender-matched healthy non-PTSD controls. Levels of TNF-alpha (p=0.038; effect size Cohen's d=0.58) and of IL-1beta (p=0.075, d=0.68) were higher in patients than in controls. CRP (d=0.10), IL-6 (d=0.18), IL-4 (d=0.42), and IL-10 (d=0.37) were not significantly different between groups. Controlling for traditional cardiovascular risk factors, mood, and time since trauma revealed lower IL-4 in patients than in controls (p=0.029) and rendered group differences in TNF-alpha and IL-1beta insignificant. In all subjects, TNF-alpha correlated with total (frequency and intensity) PTSD symptom cluster of re-experiencing (r=0.49, p=0.008), avoidance (r=0.37, p=0.050), and hyperarousal (r=0.42, p=0.026), and with PTSD total symptom score (r=0.37, p=0.054). Controlling for time since trauma attenuated these associations. The correlation between IL-1beta and total avoidance symptoms (r=0.42, p=0.028) became insignificant when controlling for anxiety and depression. IL-4 correlated with total hyperarousal symptoms (r=-0.38, p=0.047), and after controlling for systolic blood pressure and smoking status, with PTSD total symptom score (r=-0.41, p=0.035). PTSD patients showed a low-grade systemic proinflammatory state, which, moreover, was related to PTSD symptom levels suggesting one mechanism by which PTSD could contribute to atherosclerotic disease.
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                Author and article information

                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                21 September 2018
                October 2018
                : 15
                : 10
                : 2073
                Affiliations
                [1 ]Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore; annacyz@ 123456gmail.com (A.C.C.); e0157451@ 123456u.nus.edu (S.F.H.)
                [2 ]Biomedical Global Institute of Healthcare Research & Technology (BIGHEART), National University of Singapore, Singapore 119228, Singapore
                [3 ]Center of Excellence in Behavioral Medicine, Nguyen Tat Thanh University, Ho Chi Minh City 70000, Vietnam
                [4 ]Institute for Preventive Medicine and Public Health, Hanoi Medical University, Hanoi 100000, Vietnam; bach.ipmph@ 123456gmail.com
                [5 ]Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 21205, USA
                [6 ]Vietnam Young Physicians’ Association, Hanoi 100000, Vietnam
                [7 ]College of Healthcare Sciences, James Cook University, Singapore 387380, Singapore; carol.choo@ 123456jcu.edu.au
                [8 ]Institute for Global Health Innovations, Duy Tan University, Hanoi 73000, Vietnam; gigi.vugiang@ 123456gmail.com
                [9 ]Institute of Medical Science, University of Toronto, Toronto, ON M5S 1A8, Canada; Roger.McIntyre@ 123456uhn.ca
                [10 ]Mood Disorders Psychopharmacology Unit, University Health Network, Toronto, ON M5G 2C4, Canada
                [11 ]Department of Psychiatry, University of Toronto, Toronto, ON M5T 1R8, Canada
                [12 ]Department of Toxicology and Pharmacology, University of Toronto, Toronto, ON M5S 1A8, Canada
                [13 ]Department of Psychological Medicine, National University Health System, Singapore 119228, Singapore; su_hui_ho@ 123456nuhs.edu.sg
                Author notes
                [* ]Correspondence: pcmrhcm@ 123456nus.edu.sg ; Tel.: +65-6772-4511
                Author information
                https://orcid.org/0000-0001-9629-4493
                https://orcid.org/0000-0001-7827-8449
                https://orcid.org/0000-0001-7868-5757
                Article
                ijerph-15-02073
                10.3390/ijerph15102073
                6210477
                30248896
                4e2608f2-3119-45d9-aef2-741e5fca74d2
                © 2018 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 15 August 2018
                : 20 September 2018
                Categories
                Article

                Public health
                antidepressants,cytokines,depression,framingham risk score,hamilton depression rating scale,pulse wave velocity,triglycerides

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