Friday, August 15, 2014

Social causes of Lyme, Parkinson's and depression?

I find this study to be quite interesting and a nuanced conception of how an individual's work, social standing and self image could affect his/her immune system health and potentially create a cascade effect leading to clinical depression and even neurological degeneration. I have read over the years that, for example, the experience of humiliation is one of the most difficult life circumstances to navigate and recover from. In some cultures, public humiliation is tantamount to death, or worse. Historically speaking and cross-culturally, exile and excommunication have often been seen as more deeply punitive than being condemned to death. 


Psychol Bulletin. Author manuscript; available in PMC May 1, 2014.
Published in final edited form as:
Published online Jan 13, 2014. doi:  10.1037/a0035302
PMCID: PMC4006295

From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression

University of California, Los Angeles
Correspondence concerning this article should be addressed to George M. Slavich, Cousins Center for Psychoneuroimmunology, University of California, Los Angeles, UCLA Medical Plaza 300, Room 3156, Los Angeles, CA 90095-7076. Email: ude.alcu.tendem@hcivalsg
George M. Slavich and Michael R. Irwin, Cousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles.
The publisher's final edited version of this article is available at Psychol Bull


Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation.

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