Gut health has a huge impact on the health of the skin, and clincial evidence supports that skin dysfunction is likely indicative (at least in part) of dysfunction deeper in the gastrointestinal tract.
Dermatologists John H. Stokes and Donald M. Pillsbury first proposed in 1930 a gastrointestinal mechanism for the overlap between depression, anxiety and skin conditions such as acne. They hypothesised that emotional states might alter the normal intestinal microflora, increase intestinal permeability and contribute to systemic inflammation.[1] Among the remedies advocated by Stokes and Pillsbury were L. acidophilus cultures. We now also understand that aberrations in intestinal flora and increased intestinal permeability directly impact our emotional state.[2,3]
Researcher Whitney Bowe[4] has done much of this articulation in recent times with her research further exploring the link between gut health and both the brain and skin. She suggests the ability of the gut microbiota and oral probiotics to influence systemic inflammation, oxidative stress, glycaemic control, tissue lipid content and even mood itself, may have important implications in acne - and that the intestinal microflora may also provide a twist to the developing diet and acne research.
Of course, compromised gastrointestinal integrity can manifest in any number of ways and not everyone with gastrointestinal tract issues will have that manifest as a skin disorder. There are certainly other antecedents, lifestyle and genetic factors that make a skin disorder a more likely outcome in some than others. However, irrespective of the name and presentation of any chronic skin disorder, optimising gastrointestinal structure and function will have a profoundly positive influence on treatment outcomes.
An issue with any of the three critical elements at the gastrointestinal-immune system interface, as well as corollary organs such as the liver, will result in compromised nutrient absorption, cellular detoxification and immune dysregulation - and, in turn, skin issues.
Research shows there is a statistically significant difference in the prevalence of gastrointestinal symptoms (halitosis; gastric reflux; abdominal bloating; constipation) between patients with and without sebaceous gland diseases.[5] Other risk factors identified include excessive axillary, body (especially periareolar) and facial hair. For women this certainly points to PCOS but even this condition may be connected to a disturbance in the gastrointestinal system.[6,7] An increase in the passage of lipopolysaccaride (LPS) from gram-negative colonic bacteria into the systemic circulation activates an inflammatory immune system which interferes with insulin receptor function. This, in turn, drives up serum insulin levels, which then increases the ovaries production of androgens and thus interferes with normal follicle development.
Beauty is, therefore, not only skin-deep and incorporating support from a naturopath, herbalist and/or nutritionist could be an advantageous compliment to any beauty or dermatalogical therapy.
References
- Stokes JH, Pillsbury DH. The effect on the skin of emotional and nervous states: theoretical and practical consideration of a gastrointestinal mechanism. Arch Dermatol Syphilol. 1930;22:962–93.
- Rook GA, Raison CL, Lowry CA. Microbiota, immunoregulatory old friends and psychiatric disorders Adv Exp Med Biol. 2014;817:319-56. [Abstract]
- Borre YE, Moloney RD, Clarke G, et al The impact of microbiota on brain and behavior: mechanisms & therapeutic potential Adv Exp Med Biol. 2014;817:373-403 [Abstract]
- Zhang H, Liao W, Chao W, et al Risk factors for sebaceous gland diseases and their relationship to gastrointestinal dysfunction in Han adolescents J Dermatol. 2008;35(9):555-61. [Abstract]
- Tremellen K, Pearce K. Dysbiosis of Gut Microbiota (DOGMA)--a novel theory for the development of Polycystic Ovarian Syndrome Med Hypotheses. 2012 Jul;79(1):104-12. [Abstract]
- Guo Y1, Qi Y1, Yang X1, et al Association between Polycystic Ovary Syndrome and Gut Microbiota PLoS One. 2016;11(4):e0153196. [Full Text]
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