Mood disorders and inflammation: Inflammatory conditions and treatment (Part 3 of 4)

A number of inflammatory conditions coincide with mood disorders. Women with chronic health issues who pursue diagnosis are commonly labeled as having anxiety and the physical symptoms as a result of that. However, there is a significant body of evidence pointing to mood disorders as being organic symptoms of the inflammation rather than the psychological reaction to the changes that come with chronic illness. What we often frame as behavioral or psychiatric symptoms are perceived by some researchers as “sickness behavior” that promotes healing. Low energy, appetite and mood, along with sleeping more, redirect energy from less important functions to immune defense or wound repair.

Patients with autoimmune disease, diabetes, metabolic syndrome, asthma and allergies all experience mood disorders. Psoriasis dramatically increases the frequency of depressive symptoms. Cardiovascular disease patients are more likely to have major depressive disorder or bipolar disorder than the general population. Major depressive disorder increases risk of coronary artery and poorer prognosis with cardiovascular disease.

In one study with ISM and CM patients, 75% reported symptoms of depression. In a different study, 60% reported depressive symptoms and anxiety. Asthma and wheezing are independently associated with major depressive episodes in a massive study with almost 250,000 people from 57 countries.

Depression patients who have attempted suicide show increased TNF and IL-6, along with low IL-2, compared to depression patients who have not attempted suicide. Elevated CRP is also associated with depression. Alexithymia, in which the patient feels no emotions, affects 39-46% of patients with major depressive disorder. These patients also demonstrate very high CRP levels which can decrease cognitive functions.

Treatment of chronic illnesses can also improve associated mood disorders. Aspirin is currently being trialed as a treatment for bipolar disorder. Use of aspirin with an SSRI produced better response than just the SSRI.  Use of COX-2 inhibitors like celecoxib with antidepressants improves symptoms and decreases levels of IL-6 and IL-1b. NSAIDs, which also interfere with COX-2, reduce depression when compared to placebo.

Omega-3 polyunsaturated fatty acids have been found to be potent antidepressants. These molecules also decrease the production of prostaglandins and cytokines. Omega-3 polyunsaturated fatty acids interfere with the COX-2 enzyme that produces prostaglandins.  Curcumin also decreases cytokine production, as well as normalizing activity from the HPA axis and improving mood.

References:

Furtado M, Katzman MA. Examining the role of neuroinflammation in major depression. Psychiatry Research 2015: 229, 27-36.

Rosenblat JD, et al. Inflamed moods: a review of the interactions between inflammation and mood disorders. Progress in Neuro-Psychopharmacology & Biological Psychiatry 2014; 53, 23-34.

2 Responses

  1. cityrose June 27, 2016 / 9:17 am

    Lisa, Thanks for the great information! Fish oil is the first thing that comes to mind when one thinks of trying to lower inflammation…Your research indicates that it also has the potential to lower prostaglandin and cytokine production (My IL-1s are 88 fold over normal which, in turn, produce high PGEs for me). Would FISH OIL be considered generally safe for those with MCAS or mastocytosis or is it too high in histamine? I’d like to give it a try.

  2. Mark June 28, 2016 / 10:53 pm

    Important matter compellingly addressed as usual, Lisa!

    I hardly discount sexism. I’m baffled, though, if anyone imagines men never get blown off/misdiagnosed with fabricated psychic defects. “Somatoform disorder”, etc. are no less bogus when the bogus diagnosis is flung on men.

    I long marshaled medical publications reporting the adverse brain impacts mediators, other physical/physiological stimuli can have. Much, without my comments, can be found at this Mastopedia link: https://mastopedia.wordpress.com/?s=brain

    I would say pathologies, manifest or not, CAN have adverse impacts on mood, other brain functioning. And carefully specify that the cardiovascular disease links with depression are associations, not established factors increasing risks –as discussed in my letter below.

    See also, e.g., http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909644/?tool=pubmed

    http://www.nytimes.com/2011/01/25/opinion/25sloan.html

    http://www.nytimes.com/2012/05/15/health/that-unbearable-itch-1-letter.html?module=Search&mabReward=relbias%3Ar

    http://www.nytimes.com/2002/03/12/opinion/l-better-help-for-the-mentally-ill-027952.html?pagewanted=print&src=pm

    Published letter critiquing a frequent, unfounded leap insisting impaired mood causes illness rather than resulting therefrom [no longer to be found on journal’s website] — by

    Don’t worry, be happy: positive affect and reduced 10-year incident coronary heart disease: The Canadian Nova Scotia Health Survey, Eur Heart J first published online February 17, 2010

    http://eurheartj.oxfordjournals.org/content/early/2010/02/17/eurheartj.ehp603.full

    http://eurheartj.oxfordjournals.org/content/early/2010/02/17/eurheartj.ehp603.full.pdf+html

    and my eletter critique, published w/ the authors’ reply/acknowledgement

    http://eurheartj.oxfordjournals.org/content/early/2010/02/17/eurheartj.ehp603.abstract/reply#ehj_el_279

    Untested hypothesis
    Mark J. Headley, disabled
    New York, NY 10024
    The authors aptly acknowledge in conclusion:
    “Whether increasing positive affect would decrease the risk for CHD is an exciting, but as of yet untested hypothesis, remaining to be addressed.”
    So why does the abstract baselessly assert — in a passage echoed by other parts of the article and misleadingly picked up in many media reports:
    “[P]ositive affect was protective against” coronary heart disease”?
    And why does the accompanying editorial remark:
    “The apparent failure of current antidepressive therapy with SSRIs and TCAs to break the link between depression and CVD emphasizes the importance of new approaches such as those proposed by Davidson et al.”?
    Doesn’t this failure instead suggest that the asserted hypothesis is wrong — that antidepressive therapy doesn’t decrease the enhanced risk of cardiovascular disease in depressed patients because mood is not the cause, but rather an associated manifestation of an underlying disorder or whatever in fact underlies the increased risk of cardiovascular disease in depressed patients, or in patients without “positive affect”?
    Might we just as well, or better, hypothesize that being at increased risk for cardiovascular disease “causes” depression and/or “negative affect”, or decreases positive affect?
    Might we just as well, or better, hypothesize that being at lessened risk for cardiovascular disease is “protective” against negative affect?

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