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Wednesday, September 14, 2011

Re-Post by Dr. Shawn Talbott

Back in April, I wrote on my blog about a new study in the highly-respected scientific journal, Proceedings of the National Academy of Sciences (PNAS) that showed how common painkillers such as aspirin and ibuprofen (Advil, Motrin) can interfere with the effects of antidepressant medications called SSRIs (selective serotonin reuptake inhibitors) such as Prozac, Zoloft, Paxil, Celexa, Lexapro, Luvox, and many others.



I've received so many followup questions about the links between stress (and depression) and inflammation (and pain), that I thought I would update that original blog article and send the update out to the TALBOTT TIMES Newsletter.



You can read the abstract of the PNAS study here = http://www.pnas.org/content/early/2011/04/20/1104836108.abstract



The new research showed that the anti-depression benefits of SSRI drugs were "cancelled out" when taken along with painkillers (called NSAIDs for non-steroidal anti-inflammatory drugs). NSAIDs cancel out SSRIs - sounds like a lot of alphabet soup - but millions and millions of people take BOTH types of drugs everyday - so this is important research.



We've known for a long time that depression and chronic pain are closely related in many ways. Both conditions share some of the same underlying biochemistry (related to stress hormones such as cortisol and inflammatory compounds such as cytokines) and people with depression tend to experience more episodes of chronic pain (and vice versa). Indeed, physical pain can undoubtedly make psychological pain (depression) worse - likely due to the finding that inflammation is known to worsen and perhaps even cause depression in many people. You might find it interesting to know that cytokines (inflammatory hormone-like chemicals produced in the body)



Conventional wisdom would suggest that controlling depression might also help to control pain - and that reducing pain would help to alleviate depression. However, the research findings in the PNAS article suggest that painkiller drugs may actually interfere with the activity of antidepressant drugs - potentially making depression worse.



I have written about the numerous problems with antidepressant drugs HERE and HERE as well as the problems associated with painkillers HERE - and now we have new evidence of further problems when they are used together.



I also cover the links between inflammation and stress in some detail (full chapters on each) in my upcoming book, The Secret of Vigor - How to Overcome Burnout, Restore Metabolic Balance, and Reclaim Your Natural Energy - which will be released on 11/11/11. You can pre-order a copy from Amazon.com here.



In the new PNAS study, researchers at Rockefeller University in New York City suggested that the widespread use of NSAIDs to control pain may be an important factor underlying the fact that SSRIs have such a poor response rate (they tend to work for only about half of people who try them). Consider that antidepressant drugs accounted for over 250 million prescriptions and nearly $12 billion in sales last year in the United States, while painkillers sales reached nearly 500 million units (between prescription and over-the-counter sales) and over $30 billion - and you can get some idea for how many millions of people are potentially affected when the drugs they rely on to get through the day are actually canceling each other out. No wonder we don't feel good!



Could there be a better way?

Yes - by naturally restoring the body's Inflammatory Balance (reducing cytokines) while simultaneously restoring Stress Hormone Balance (reducing cortisol), we can alleviate depression and improve vigor/wellness. These results have been presented at scientific conferences including the American College of Nutrition (October 2010 at the New York Academy of Medicine in New York City) and at Experimental Biology (April 2010 in Anaheim, CA).



These presentations explore the the synergy between balancing inflammation and stress hormone exposure to improve vigor (better and faster than balancing either aspect of metabolism alone). The data show the synergistic effects of Xango Juice (in balancing healthy levels of inflammation) with Eleviv (in balancing healthy levels of stress hormones) - and how the combined effects significantly improve Vigor (mental/physical energy levels) in moderately stressed subjects (who also tend to be at higher risk for stress-induced pain, depression, fatigue, and burnout).



These results suggest that forcing neurotransmitters (with synthetic antidepressant drugs) and forcing inflammatory cytokines (with synthetic painkillers) is a "bad" approach - whereas restoring inflammatory balance and restoring stress hormone balance with natural approaches delivers meaningful synergistic benefits for both mental and physical health.



As mentioned above, the upcoming Secret of Vigor book goes into some detail about how balancing the Four Pillars of Health (two of which are inflammation and stress) can reduce depression, alleviate fatigue, sharpen mental focus, and simply help you feel good again (trading burnout for a renewed sense of vigor) - I hope that you'll check it out at this link on Amazon.com



Thanks for reading,



Shawn
http://www.ShawnTalbott.com
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Shawn M. Talbott, PhD, LDN, FACSM

www.ShawnTalbott.com

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Antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) are attenuated by antiinflammatory drugs in mice and humans

Jennifer L. Warner-Schmidt, Kimberly E. Vanover, Emily Y. Chen, John J. Marshall, and Paul Greengard

Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10065; and Intra-Cellular Therapies, New York, NY 10032



Abstract

Antiinflammatory drugs achieve their therapeutic actions at least in part by regulation of cytokine formation. A "cytokine hypothesis" of depression is supported by the observation that depressed individuals have elevated plasma levels of certain cytokines compared with healthy controls. Here we investigated a possible interaction between antidepressant agents and antiinflammatory agents on antidepressant-induced behaviors and on p11, a biochemical marker of depressive-like states and antidepressant responses. We found that widely used antiinflammatory drugs antagonize both biochemical and behavioral responses to selective serotonin reuptake inhibitors (SSRIs). In contrast to the levels detected in serum, we found that frontal cortical levels of certain cytokines (e.g., TNFα and IFNγ) were increased by serotonergic antidepressants and that these effects were inhibited by antiinflammatory agents. The antagonistic effect of antiinflammatory agents on antidepressant-induced behaviors was confirmed by analysis of a dataset from a large-scale real-world human study, "sequenced treatment alternatives to relieve depression" (STAR*D), underscoring the clinical significance of our findings. Our data indicate that clinicians should carefully balance the therapeutic benefits of antiinflammatory agents versus the potentially negative consequences of antagonizing the therapeutic efficacy of antidepressant agents in patients suffering from depression.

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