A Brief Explanation of my Serotonin-Autoimmunity Research

On the off chance that anyone out there besides me is reading these studies I am posting, and wondering where it's all leading, I wanted to write up a little explanation.

I started this blog not long after I learned that I suffer from esophageal motility dysfunction. I also have mild Raynaud's Phenomenon, Hashimoto's Thyroiditis and an elevated ANA. For the past 18 months (just about) I have been pursuing treatment in the effort to prevent further progression of autoimmune disease... toward Lupus, RA or Scleroderma.

I follow the antibiotic protocol developed by Dr. Thomas McPherson Brown who believed that mycoplasma infection underlay arthritis and rheumatic disease.

My feeling has been that even if they have not yet proved the infectious theory, it doesn't matter - I just want to get well. I haven't really cared about the mechanism for *why* the antibiotic at low doses work... I am just so grateful that they have helped me to get so much of my life and strength back.

Recently I stumbled across a study that proved serotonin as the link between vascular disease and fibrosis. This was a real eye opener to me.

Scleroderma patients suffer from the following problems:

Reduced motility of the esophagus (reduced or no peristalsis in the lower 2/3 of the esophagus)
Raynaud's Phenomenon
Telangiectasias
Calcinosis
Sclerodactyly
Pulmonary Fibrosis
Cardiac Problems
Kidney Fibrosis

Could serotonin be the common link that connects the vascular disease (Raynaud's) that proceeds onset of scleroderma to the process of fibrosis?

Even more importantly, the study I read stated that it was possible to REVERSE and even prevent fibrosis:

"Dermal fibrosis was reduced in 5-HT2B mice using both inducible and genetic models of fibrosis. Pharmacologic inactivation of 5-HT2B also effectively prevented the onset of experimental fibrosis and ameliorated established fibrosis. Moreover, inhibition of platelet activation prevented fibrosis in different models of skin fibrosis."

This is pretty incredible stuff.

If fibrosis can be reversed by the inactivation of the 5-HT2B serotonin neurotransmitter, it might save the lives of people I now know and care about... people who live courageously with scleroderma every day.

Heck, it might save me too!

And that would be more wonderful than I can say. I have three small children and I don't want to miss a minute with any of them.

That's the thing about autoimmunity - it seems to mainly strike women in our reproductive years. I have a lot of friends now, all somewhere near my age, with kids... who suffer from Lupus, RA, Sjogrens and scleroderma.

This is a very personal research story then... I want to figure this thing out and save us all.

Unfortunately, I am not a scientist!

I was an English major in college and then an elementary and middle school teacher for 10 years. I scurried away from math and science just as quickly as my feet could carry me back in the day before my health went south.

So grappling with the language in these studies is really tough for me. I feel like I need a science dictionary just to wade through the different terms.

My husband, bless his heart, was a biology major and he understands much of this stuff a lot better than I do. I've been turning to him then, frequently, to ask what the scientific jargon means.

What I'm trying to do here in this blog is aggregate all of the articles I can find that show the relationship between the serotonin receptor function and development of autoimmune disease.

I'm hoping that if I can read enough articles, maybe I'll finally understand the "big idea" - the relationship between genetics, pathogens, tryptophan, serotonin and the development of autoimmune problems that I and countless others face.

Here's the catch:

I can't tell yet whether I have too much or too little serotonin in my system!

I can't tell yet what the feedback loops are between serotonin in the brain and serotonin in the rest of the body.

I haven't been able to figure out whether I need MORE serotonin (possible to achieve through supplementation, exercise and diet) or LESS serotonin, possible to achieve with medications and reduction in the amount of tryptophan I consume.

The whole thing is still a mystery to me.

What I do know is that taking doxycycline has helped me vastly with inflammation. I also learned in the last few days that doxycycline actually increases the thickness of serotonin receptors... which could explain how it helps to modulate the amount of serotonin released. This may explain why doxycycline and minocycline have shown themselves to be very helpful in the management of collagen vascular diseases.

In time when I have collected enough research I want very badly to share it with medical researchers who can understand it all... who might be able to have that "Aha!" moment where they put 2 and 2 together and come up with an actual cure or treatment for these devastating chronic diseases.

I don't need to be a hero and nobody even needs to know my name. I just want to motivate scientists and physicians to look harder at the connection between serotonin and autoimmunity... and to encourage everyone from pharmaceutical companies to Chinese medicine doctors to naturopaths to pursue targeting the 5-HT2B receptor so that millions of us will be freed from our disease conditions and able to pursue worthy, fulfilling, productive lives.

If you are out there reading this and you understand the science that I do not, please continue reading and examine these 57 studies (and counting!) I have put together. I really believe there is something important here.

From the bottom of my heart, I ask you to take a good look and see if there isn't an answer here to a perplexing mystery that has brought strong men to their knees, torn families apart, taken away the freedom and mobility that many of us so cherish... and ended lives too soon.

Thank you!

Serotonin and Scleroderma (Fibrosis)

Platelet-derived serotonin links vascular
disease and tissue fibrosis 2011

Modulation of bleomycin-induced lung fibrosis by serotonin receptor antagonists in mice
A. Fabre 1 , 2 , J. Marchal-Sommé 1 , S. Marchand-Adam 1 , 3 , C. Quesnel 1 , R. Borie 1 , M. Dehoux 1 , 4 , C. Ruffié 1 , J. Callebert 5 , J-M. Launay 5 , D. Hénin 2 , P. Soler 1 and B. Crestani 1 , 3

"Serotonin (5-hydroxytryptamine; 5-HT) is known to increase proliferation and collagen synthesis by fibroblasts. Two receptor subtypes, 5-HT2A and 5-HT2B, have been shown to play the most important roles in the lung. Serotonin antagonists promoted an antifibrotic environment by decreasing the lung mRNA levels of transforming growth factor-β1, connective growth factor and plasminogen activator inhibitor-1 mRNA... Interestingly, the 5-HT2B receptor was strongly expressed by fibroblasts in the fibroblastic foci in human idiopathic pulmonary fibrosis samples."

Treatment of Carcinoid Fibrosis

Positive data from Lexicon LX1032 Phase 2 study on carcinoid syndrome

Potaba ® Potassium P-Aminobenzoate, U.S.P.

Development of a Scleroderma-like Illness during Therapy with L-5-Hydroxytryptophan and Carbidopa

Our data and studies in the literature suggest that two factors may be important in the pathogenesis of some scleroderma-like illness: high plasma serotonin and the abnormality associated with elevated kynurenine. (N Engl J Med. 1980; 303:782–7.)


Depression, osteoporosis, serotonin and cell membrane viscosity between biology and philosophical anthropology


At the time it is shown that the viscosity of the platelet membrane is a general influencing factor for serotonin receptor uptake, a general principle governing the handling of serotonin itself is established with regard to its relations with the depressive disorder. It may also be involved, to a certain extent, in some pathologies that recognise serotonin changes; that is, scleroderma, inflammatory bowel disease, neuroinflammation, multiple sclerosis and osteoporosis.

The high incidence of depression, in these pathological conditions, leads us to consider a general phenomenological rule rather than a specific error in gene expression or loss of enzyme function. The viscosity of the membrane appears to be a concept more plausible than the fact that it is a phenomenon to which changes may contribute more general factors compared to the exclusivity of a gene expression error and/or an abnormality of enzyme function. The serotonin receptors and their subtypes, together with the modification of gene expression of transporters, represent a very complex and intriguing network. We must understand if it is possible to find a general and common rule to explain all the different molecular aspects of the serotonin pathways, tissue connections and responsibilities in its involvement in pathologies.

Raynaud's Phenomenon and Serotonin Reuptake Inhibitors

Treatment of Raynaud's phenomenon with the selective serotonin reuptake inhibitor fluoxetine

Plasma free and intraplatelet serotonin in patients with Raynaud's phenomenon

Management of Vasculopathy in Connective Tissue Disease

Handb Exp Pharmacol. 2007;(178):347-63.
A novel conditional knockout strategy applied to serotonin receptors.

The Serotonin Signaling System: From Basic Understanding To Drug Development for Functional GI Disorders
Michael D. Gershon⁎, , , Jan Tack‡
Department of Pathology & Cell Biology, Columbia University, College of Physicians and Surgeons, New York, New York

Doxycycline and Serotonin

Serotonin 5HT-1A receptor density in the brain of the spontaneously hypertensive rats
After doxycycline treatment, serotonin 5HT-1A extracellular domain receptor density was significantly increased in the treated SHRs (p<0.05). These results suggest that doxycycline can increase extracellular domain receptor density.