Inflammation causes Depression, perhaps this is why vitamin D helps with depression – Sept 2013

So depression is an inflammatory disease, but where does the inflammation come from?

BMC Med. 2013 Sep 12;11:200. doi: 10.1186/1741-7015-11-200.
Berk M, Williams LJ, Jacka FN, O'Neil A, Pasco JA, Moylan S, Allen NB, Stuart AL, Hayley AC, Byrne ML, Maes M.
IMPACT Strategic Research Centre, School of Medicine, Deakin University, Geelong, VIC, Australia. mikebe@barwonhealth.org.au.

BACKGROUND: We now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder. The obvious question this poses is 'what is the source of this chronic low-grade inflammation?'

DISCUSSION: This review explores the role of inflammation and oxidative and nitrosative stress as possible mediators of known environmental risk factors in depression, and discusses potential implications of these findings. A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency.

SUMMARY: The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.

Clipped section from PDF which discusses Vitamin D

Vitamin D

Low levels of Vitamin D, particularly 25-hydroxyvitamin D are widespread among Western populations [219], making it the most prevalent deficiency state. Low Vitamin D is linked to a diversity of adverse health outcomes, such as osteoporosis and cancer [220]. Notably, the physiology of vitamin D overlaps with the patho-physiology of depression. Vitamin D receptors are expressed in key brain areas; and vitamin D has a role in circadian rhythms and sleep, affects glucocorticoids and influences neuronal growth, cell proliferation in the developing brain and embryogenesis [221]. There is a growing epidemiological evidence-base linking depressive symptoms to low levels of serum 25-hydroxyvitamin D. These studies include both cross-sectional studies, as well as prospective data suggesting that low levels are associated with increased risk for the development of depression. There are positive trials of the potential anti-depressant effects of vitamin D [222], although there are equally negative trials [223].

Vitamin D has well documented modulatory effects on immunity. It modulates immune responses to infections, such as tuberculosis [224]. In rats given a high fat diet, 1a, 25-dihydroxyvitamin D3 (calcitriol) treatment reduced concentrations of various inflammatory markers, including TNF-a, CRP and IL-6, and protected the liver from inflammatory damage [225]. In human studies, supplementation robustly reduces inflammatory markers in people with cystic fibrosis, including TNF-a and IL-6, but not other cytokines. Curiously, those two cytokines are the most robustly associated with depression in meta-analyses [226]. In multiple sclerosis, vitamin D reduces markers of inflammation and attenuates disease progression [227]. A one-year clinical trial of supplementation with Vitamin D in obese individuals reduced TNF-a levels, but increased hsCRP. The implications of these changes are unclear [225]. Inflammation and oxidative stress are tightly interlinked, and in human studies, vitamin D supplementation additionally reduced oxidative stress markers [228]. Vitamin D is a proxy of sunlight exposure, and it is useful to note that sunlight may suppress immunity via pathways other than via vitamin D. In fact, vitamin D derived from safe sunlight exposure may reduce systemic inflammation. There are additional skin photoreceptors that absorb ultraviolet light, and play a role in immunoregulation, that include DNA and lipids in skin cells and fra#s-urocanic acid found in the stratum corneum [229].

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References in Mercola 2016
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19 University of Maryland Medical Center, Omega-3 Fatty Acids
20 Omega-3 Institute, Differentiation of ALA (plant sources) from DHA + EPA (marine sources) as Dietary Omega-3 Fatty Acids for Human Health
21 NutraIngredients.com April 10, 2006

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