The Brain-Gut-Skin Connection Series: Evidence

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In the previous post, we learned about the brain-gut-skin theory proposed by two dermatologists, John Stokes and Donald Pillsbury, in 1930s.  Here is the gist of the theory: stress produces stress hormones, which leads to low acid production in your stomach, which leads to the changes in your gut microbiota population, which leads to local and systemic inflammation, which leads to skin breakouts.

Here are some evidences that support the brain-gut-skin theory:

Brain-gut connection

Several months before Stokes and Pillsbury completed their theory on the “emotional linkage” between the brain, gut and skin, a study published in the Journal of Mental Sciences reported low stool levels of L. acidophilus in 53 patients with a variety of mental health disorders  (Shera G, J Mental Sci 1930, 76:56-65)

The research has confirmed that low stomach acid production is a significant risk factor for small intestinal bacterial over growth (SIBO).   In 1993, Toskes reported that the excessive small intestinal bacteria compete for nutrients, produce toxic metabolites, and cause direct injury to enterocytes in the small intestine (Toskes PP, Adv Intem Med1993, 38:387-407).   In 2010, just as Stokes and Pillsbury had proposed, a research showed that excess bacteria in SIBO caused increased intestinal permeability and that antimicrobial treatment of SIBO helped to restore the normal intestinal barrier (Lauritano EC et. al. Scand J Gastroenterol 2010, 45:1131-2)

In the mean time, SIBO has been reported to be prevalent in functional syndromes such as fibromyalgia and chronic fatigue syndrome.  In 2005, Wang et al. reported that psychological stress stagnates normal small intestinal transit time, encourages overgrowth of bacteria, and compromises the intestinal barrier (Wang SX et al., World J Gastroenerol 2005, 11:2016-21).  Also, two separate studies observed the strong association between SIBO and depression and anxiety and that the eradication of SIBO improves emotional symptoms (Addolorato G. et al., Int J Clin Pract 2008, 62:1063-9; Pimentel M., et al., Gastroenterology 2000, 118:A414).

A series of experimental and human studies spanning from 2003 to 2008 has shown that a variety of psychological and physiological stressors – confinement, extremes of temperature, crowding, acoustic, academic examination – can impair normal intestinal microflora (Logan AC et al., Med Hypotheses 2005, 64:533-8; Logan AC et al., Med Hypotheses2003, 60:915-23; and Knowles SR et al., Biol Psychol 2008, 77:132-7).  Most notable in these studies are the stress-induced reductions in Lactobacillus and Bifidobacteria species.

Gut-skin Connection

Although the frequency of SIBO in acne vulgaris has not yet been investigated, a recent report indicates that SIBO is 10 times more prevalent in those with acne rosacea vs. healthy controls. Correction of SIBO leads to marked clinical improvement in patients with rosacea (Parodi A. et al., Clin Gastroenterol Hepatol 2008, 6:759-64).

As for intestinal permeability in acne vulgaris, there have been hints that the intestinal lining may be compromised.  As early as in 1916, Strickler et al. observed that approximately 66% of the 57 patients with acne showed positive reactivity to stool-isolated coliforms, this compared to none of the control patients without active skin disease (Strickler A. et al., J. Cutaneous Dis 1916, 34:166-78).  In 1983, a study involving 40 acne patients showed both the presence of, and high reactivity to, lipopolysaccharide (LPS) endotoxins in the blood.  In this study, none of the matched healthy controls reacted to the E. coli lipopolysaccharide endotoxin (E. coli LPS), while 65% of the acne patients had a positive reaction (Juhlin L., et al., Acta Derm Venereol 1983, 63:538-40). The inference of these results is that circulating endotoxins derived from gut microbes is a common feature of acne vulgaris and that intestinal permeability is an issue for acne patients.

In summary, up to date researches seem to show that patients with distress or anxiety and patients suffering from skin diseases tend to have a gut microbiota population low in “good” bacteria; the researches further show that an impaired gut microbiota causes an increase in gut permeability, which allows the leaking of E. coli endotoxin into the blood, and that the E. coli endotoxin in blood is a common presence in the acne patients.  The modern research is still ongoing providing more clues about Stokes and Pillsbury’s Brain-gut-skin theory.  Based on what have been reported so far, the theory is standing solid.

Thanks for reading!

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