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      The role of immune abnormality in depression and cardiovascular disease

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          Abstract

          Depression and cardiovascular disease (CVD) are both highly prevalent disorders, and some evidence shows that there is a ‘vicious cycle’ linking major depression and CVD. There is also growing evidence that immune abnormalities underpin the common pathophysiology of both CVD and major depression. The abnormalities include the following: abnormal levels of inflammatory markers, such as interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α) and interleukin-12 (IL-12); increased acute phase proteins, such as C-reactive protein, fibrinogen and haptoglobin; and abnormal complement factors. The findings show that major depression and CVD patients have greater immune abnormalities, which may increase depressive symptoms and cardiovascular pathological changes, and that there may be a bidirectional relationship, therefore more prospective studies are needed to draw conclusions.

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          The effects of acute psychological stress on circulating inflammatory factors in humans: a review and meta-analysis.

          Andrew Steptoe, Mark Hamer, Yoichi Chida (2007)
          Stress influences circulating inflammatory markers, and these effects may mediate the influence of psychosocial factors on cardiovascular risk and other conditions such as psoriasis and rheumatoid arthritis. Inflammatory responses can be investigated under controlled experimental conditions in humans, and evidence is beginning to emerge showing that circulating inflammatory factors respond to acute psychological stress under laboratory conditions. However, research published to date has varied greatly in the composition of study groups, the timing of samples, assay methods, and the type of challenge imposed. The purpose of this review is to synthesize existing data using meta-analytic techniques. Thirty studies met inclusion criteria. Results showed robust effects for increased levels of circulating IL-6 (r=0.19, p=0.001) and IL-1beta (r=0.58, p<0.001) following acute stress, and marginal effects for CRP (r=0.12, p=0.088). The effects of stress on stimulated cytokine production were less consistent. Significant variation in the inflammatory response was also related to the health status of participants and the timing of post-stress samples. A number of psychobiological mechanisms may underlie responses, including stress-induced reductions in plasma volume, upregulation of synthesis, or enlargement of the cell pool contributing to synthesis. The acute stress-induced inflammatory response may have implications for future health, and has become an important topic of psychoneuroimmunological research.
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            The prevalence and distribution of major depression in a national community sample: the National Comorbidity Survey.

            D. Blazer, R C Kessler, K McGonagle … (1994)
            Major depression is a frequent and disabling psychiatric disorder in the United States. This report examines the prevalence and risk factor profile of both pure and comorbid major depression according to data from the National Comorbidity Survey. To estimate the prevalence of psychiatric comorbidity in the United States, a national sample of 8,098 persons 15-54 years of age from the 48 conterminous states was surveyed with a modified version of the Composite International Diagnostic Interview. From the survey data the prevalence of current (30-day) major depression was estimated to be 4.9%, with a relatively higher prevalence in females, young adults, and persons with less than a college education. The prevalence estimate for lifetime major depression was 17.1%, with a similar demographic distribution. Both 30-day and lifetime prevalence estimates were higher than estimates from the earlier Epidemiologic Catchment Area study. When pure major depression was compared with major depression co-occurring with other psychiatric disorders, the risk factor profiles exhibited clear differences. These findings suggest a greater burden of major depression in community-dwelling persons than has been estimated from previous community samples. The risk factor profile showed significant differences between persons with pure and combined major depression.
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              Is depression an inflammatory disorder?

              Charles L. Raison, Andrew Miller (2011)
              Studies consistently report that groups of individuals with major depressive disorder (MDD) demonstrate increased levels of a variety of peripheral inflammatory biomarkers when compared with groups of nondepressed individuals. These findings are often interpreted as meaning that MDD, even in medically healthy individuals, may be an inflammatory condition. In this article, we examine evidence for and against this idea by looking more closely into what the actual patterns of inflammatory findings indicate in terms of the relationship between MDD and the immune system. Data are presented in support of the idea that inflammation only contributes to depression in a subset of patients versus the possibility that the depressogenic effect of inflammatory activation is more widespread and varies depending on the degree of vulnerability any given individual evinces in interconnected physiologic systems known to be implicated in the etiology of MDD. Finally, the treatment implications of these various possibilities are discussed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Geriatr Cardiol
                Journal ID (iso-abbrev): J Geriatr Cardiol
                Journal ID (publisher-id): JGC
                Title: Journal of Geriatric Cardiology : JGC
                Publisher: Science Press
                ISSN (Print): 1671-5411
                Publication date (Print): November 2017
                Volume: 14
                Issue: 11
                Pages: 703-710
                Affiliations
                [1 ]Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China
                [2 ]Department of Hematology, Tongji Hospital, Tongji University School of Medicine; Shanghai, China
                [3 ]Department of Stomatology, Huashan Hospital, Fudan University, Shanghai, China
                Author notes
                [*]

                The first two authors contributed equally to this manuscript.

                Correspondence to: Wen–Lin MA, MD, Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China; Shang–Feng LIU, PhD, Department of Stomatology, Huashan Hospital, Fudan University, 12 Urumqi Road, Shanghai, 200040, China. E-mails: mawenlin@ 123456tongji.edu.cn (MA WL) & shangfengliufudan@ 123456163.com (LIU SF)
                Article
                Publisher ID: jgc-14-11-703
                DOI: 10.11909/j.issn.1671-5411.2017.11.006
                PMC ID: 5756744
                PubMed ID: 29321801
                SO-VID: f2ffbe75-fb22-41fd-a148-5265e755420b
                Copyright © Institute of Geriatric Cardiology
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License, which allows readers to alter, transform, or build upon the article and then distribute the resulting work under the same or similar license to this one. The work must be attributed back to the original author and commercial use is not permitted without specific permission.

                History
                Date received : 20 July 2017
                Date revision received : 8 September 2017
                Date accepted : 8 September 2017
                Categories
                Subject: Review

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: cardiovascular disease,depression,immune abnormality
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: cardiovascular disease, depression, immune abnormality

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