The Gut-Brain-Skin Axis
By Debbie Dickson
As crucial interface organs, the gut and skin have much in common. The gut and the skin have an intimate bidirectional connection and can communicate with each other. The absorption of nutrients has a direct effect on your skin health, as do hormonal changes that influence your skin on a physiological level. A healthy gut will even synthesize extra vitamins and minerals that benefit your skin, such as vitamin K, the B vitamins thiamine and riboflavin.
The gut contains a collection of trillions of strains of bacteria and microbes, called the gut microbiome. Essential to skin homeostasis, the gut microbiome impacts integumentary health. Intestinal microbiota exert their influence on skin homeostasis, through the signalling pathways that coordinate this process. Recent advances in metagenomics and the advent of high-throughput DNA-sequencing technology has enhanced our understanding of the microbiome and its dynamic influence on human health and pathology.
Certain gut microbes, metabolites and bacteria promote the accumulation of regulatory T cells, lymphocytes which facilitate anti-inflammatory responses. A healthy skin has more T cells circulating. Segmented filamentous bacteria, alternatively, promote the accumulation of pro-inflammatory Th17 and Th1 cells. SCFAs, particularly butyrate, suppress immune responses by inhibiting inflammatory cells’ proliferation, migration, adhesion, and cytokine production. Psoriasis has an upregulation of Th17 cells.
There is new evidence that the intestinal microbiome may impact cutaneous physiology, pathology, and immune response more directly, through the metastasis of gut microbiota and their metabolites to the skin. https://pubmed.ncbi.nlm.nih.gov/27554239/
If your skin is irritated, inflamed or congested, chances are high that there may be an imbalance in your gut. An imbalance means that there are too many bad bacterial cells or not enough good bacterial cells, basically if you have a gut problem you will have a skin problem. In some ways, your gut and your skin play similar roles. Both defend your body against pathogens, and both are covered in beneficial bacteria when in a healthy state.
Western diets, medications, environmental toxins stress and emotional factors can all imbalance the gut microbiome, leading to bacterial overload, fungal overload in the gut and parasites, leading to leaky gut. Over 70 years have passed since dermatologists John H. Stokes and Donald M. Pillsbury first proposed a gastrointestinal mechanism for the overlap between depression, anxiety and skin conditions such as acne, it is well documented that a period of insulin resistance occurs during puberty, one coinciding with the development of acne, depression and/or anxiety.Stokes and Pillsbury hypothesized that emotional states might alter the normal intestinal microflora, increase intestinal permeability, and contribute to systemic inflammation.
When we have an overload of bad bacteria in the gut, gram negative bacteria, as they die the outer lining produces these endotoxins or lipopolysaccharides, these enter the blood stream and are a big contributor to acne, eczema, psoriasis and rosacea. A study involving 40 acne patients showed both the presence of, and high reactivity to, lipopolysaccharide (LPS) endotoxins in the blood.
Acne vulgaris is frequently associated with depression, anxiety and other psychological sequelae. Considering that 90% of your serotonin is produced in the gut, it makes perfect sense that acne and depression and anxiety would be associated with gastrointestinal disorders and skin problems. Psychological stress stagnates normal small intestinal transit time, encourages overgrowth of bacteria, and compromises the intestinal barrier.
Acne patients are at a higher risk for gastrointestinal distress. For example, one study involving over 13,000 adolescents showed that those with acne were more likely to experience gastrointestinal symptoms such as constipation, halitosis, and gastric reflux. In particular, abdominal bloating was 37% more likely to be associated with acne and other seborrheic diseases. These authors connected emotional states - depression, worry and anxiety - to altered gastrointestinal tract function, changes that cause alterations to the microbial flora, which they theorized, in turn promotes local and systemic inflammation. They wrote, 'an important linkage of emotion with cutaneous outbreaks of erythema, urticaria and dermatitis by way of the physiology and bacteriology of the gastrointestinal tract'.
Research showing that as many as 40% of those with acne have hypochlorhydria. Stokes and Pillsbury hypothesized that less than adequate stomach acid would set the stage for migration of bacteria from the colon towards the distal portions of the small intestine, as well as an alteration of normal intestinal microflora. Furthermore, Stokes and Pillsbury suggested that stress-induced alterations to microbial flora could increase the likelihood of intestinal permeability, which in turn sets the stage for systemic and local skin inflammation. Burden of inflammation and oxidative stress is increased, substance P is elevated, insulin sensitivity is decreased due to endotoxemia. In those genetically susceptible to acne vulgaris, this cascade increases the likelihood of excess sebum production, exacerbations in acne and additional psychological distress
Rosacea patients have an increased incidence of SIBO (small intestinal bacterial overload). Researchers found that 46% of rosacea patients tested positive for SIBO, and that patients with rosacea were nine times more likely to have SIBO than patients without rosacea. Hypochlorhydria is a significant risk factor for small intestinal bacterial overgrowth (SIBO). SIBO damages gut lining, causing leaky gut which leads to the release of pro-inflammatory cytokines (regulators of host immune responses that promote inflammatory reactions) resulting in skin inflammation. SIBO presents itself in a wide variety between being asymptomatic and, at its extreme, a severe malabsorption syndrome. For many, there may be very mild gastrointestinal symptoms, including bloating, diarrhea, abdominal pain, and constipation. It is also reported to be prevalent in functional syndromes such as fibromyalgia and chronic fatigue syndrome. SIBO can compromise proper absorption of proteins, fats, carbohydrates, B vitamins, and other micronutrients due to bacterial interference. Excess bacteria can successfully compete for nutrients, produce toxic metabolites, and cause direct injury to enterocytes in the small intestine.
Several studies suggest that people with psoriasis are more likely to have Candida colonize in their bodies.
Psoriasis is a chronic autoimmune disease that causes skin cells to turn over too quickly and has a strong connection with leaky gut where undigested proteins can pass from the digestive tract into other organs and tissues, triggering an immune response.
Recent evidences have suggested that H. pylori infection plays a role in the pathogenesis of a variety of skin diseases, including psoriasis and rosacea. H. pylori may be one of the organisms capable of triggering the inflammatory response in psoriasis. IBD and psoriasis also share a connection with obesity. Fat tissue seems to make chemicals that change how the body works, including the immune system. Having a lot of extra weight raises your odds of having psoriasis, Crohn's, and UC. People with celiac disease alsohave a higher incidence of psoriasis.
I think its clear to have a healthy skin we need to make sure our insides are healthy first and also reduce the destructive effects of stress. The brain affects the gut and the gut affect the brain and these affect the skin.
When the skin is functioning optimally, it works hard to protect us. When it is compromised, the skin’sability to work as an affective barrier is impaired.
To truly have healthy skin we must look beyond the surface. Healthy skin is in perfect balance, “homeostasis”.
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https://gutpathogens.biomedcentral.com/articles/10.1186/1757-4749-3-1
https://www.webmd.com/skin-problems-and-treatments/psoriasis/psoriasis-digestive-disorders
(Boyle et al., 2011; Moore-Connors et al., 2016).