Manufacturing the “Magic Powder”

 Serotonin Robbers. (Cont. #4)

How do we know that tryptophan is essential to the manufacture of serotonin or that robbers are involved?

Tryptophan depletion studies confirm that it is required for serotonin production. How would one find out how to deplete someone of a nutrient? Well, strangely enough, it was discovered in the same way the Tatin’s sister created the famous “Tarte Tatin,” by accident. Patients who were fighting chronic viral infections became depressed after taking a specific drug.

Interferon-α-based immunotherapy was intended to help patients fight infections, but it also affected the cytokine network, inhibiting the creation of serotonin and consequently causing anxiety or depression. This treatment caused tryptophan to be converted to kynurenine rather than serotonin.

These studies confirmed the connection between tryptophan and serotonin, but also exposed a new theory. It isn’t a far reach to extrapolate from this study that as we age, our bodies experience similar inflammation for various reasons. Our bones and joints are deteriorating, and eventually these chronic low-grade issues result in crankiness or even depression. According to a study published by the NCBI, systemic inflammation can be caused by aging changes in adipose tissue that results in increase production of the cytokines, the robbers.(Ref. 8) Therefore, this discovery points to the importance of preventing these anti-inflammatory cytokines from causing further damage.

In other words, while they may not result in pain, secret agents are still affecting the proper manufacture of serotonin. A significant factor in this otherwise healthy immune response is that it does cross the blood-brain barrier, a tightly controlled membrane between the majority of your body and the central nervous system. In doing so, the secret agents access the enzymes essential to converting tryptophan to serotonin. All of this explains why one can feel a bit morose during a head cold. But also, as we age, have joint inflammations, hips or knee that may need attention, we are more likely to experience tryptophan depletion caused by the chronic inflammation and, consequently, low serotonin. These were the exact circumstances I was experiencing, causing the drastic change in my mood. I had been ignoring a failing hip. According to Simon Young, Professor of Behavioral Science at McGill University in Montreal, four factors seem to influence serotonin levels in the brain: 1) therapy, 2) light, 3) exercise, and 4) tryptophan.(Ref. 1)

Addressing any primary challenges to one’s immune system is a priority.

So, what is the solution to decrease these adverse effects?

Discussing problems such as joint pain or any other source of chronic pain with your physician early on is crucial.

Would a regular intake of an anti-inflammatory work to reduce the level of these anti-inflammatory cytokines?

I undertook a small experiment at home. I took two antiinflammatory a day and gave one to my husband, who is not fond of taking pills. After a few days, I observed a significant difference: improved performance in my work, activities and a good mood. I regained some of my sense of well-being, as did my husband. I had not seen him so content and active in a long while. Effective ways to fight these cytokine agents are also under study. (Ref. 2,3,4,5,6)

Later, I found that my hypothesis was further supported by research done by doctors at Emory University department of psychiatry. They wrote an article describing how cytokines target the brain, impacting neurotransmitters and neuro-circuits to cause depression and anxiety.(Ref. 7)

Remember also that sufficient light, exercise, and eating chickpeas (high in tryptophan) may contribute to the positive effects of taking an anti-inflammatory. However, addressing the primary source of inflammation is key.

In conclusion, apart from the search for my missing sparks on that one occasion, the issue of treating depression is an important public health concern. Depression affects so many aspects of daily living and disrupts the hearty fabric of families. We may not realize the significant consequences and how far-reaching the long-term repercussions are. For example, a hostile personality creates a higher risk of heart attack and social isolation, whereas an agreeable personality offers significant protection against premature mortality.(Ref. 1) Simply put: happiness determines how long we live and how strong our families are. Addressing any roadblocks to the healthy production of the magic powder, serotonin, is essential for health and well-being.

About the author: Nicolette Francey Asselin, M.D.has contributed to many publications over the years and enjoys writing about prevention of illnesses.

Followthis author on Mediumpublication or on WordPress at ReFlex-Ions.

References:

(1) Simon N. Young, PhD, “How to increase serotonin in the human brain without drugs, Journal of Psychiatry Neuroscience32, no. 6 (December 2007): 394–399.

(2) Steven M. Opal, MD, and Vera A. DePalo, MD, “Anti-Inflammatory Cytokines,” Chest117, no. 4 (April 2000): 1162–1172.

(3) Ronald S. Smith, “Chapter 7: Immunological Evidence Supporting The Immune-Cytokine Model of Depression,” Cytokines and Depression, http://www.cytokines-and-depression.com/chapter7.html.

(4) Jennifer C. Felger and Francis E. Lotrich, “Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications.Neuroscience 246 (August 2013): 199–229.

(5) Charles A. Dinarello, “Historical Review of Cytokines,” Eur J Immunol37 (July 2007): S34–S45.

(6) Yiquan Chen and Gilles J. Guillemin, “Kynurenine Pathway Metabolites in Humans: Disease and Healthy States” Int J Tryptophan Res2 (January 2009): 1–19.

(7) Andrew H. Miller, MD, Ebrahim Haroon, MD, Charles L. Raison, MD, and Jennifer C. Felger, PhD, “Cytokine Targets in the Brain: Impact of Neurotransmitters and Neurocircuits,” Depress Anxiety 30, no. 4 (April 2013): 297–306.

(8) Meredith A. Greene and Richard F. Loeser, M.D. “Aging-related inflammation in Osteoarthritis,” Osteoarthritis Cartilage. 2015 No; 23(11):1966–1971.

This article is part of a series:

 

Copyright 2019 Corpwell Media

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