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Beyond Repair: Gut Dysbiosis, Leaky Gut and Vitiligo

Healing Through Integrated Approaches

Vitiligo is a complex autoimmune disorder characterized by the loss of skin pigment, leading to white patches. While traditionally understood through genetic and autoimmune lenses, emerging research suggests a significant link between gut health and vitiligo. Specifically, gut dysbiosis and leaky gut syndrome may play crucial roles in the pathogenesis of vitiligo. Here’s how these factors contribute to the condition and how addressing them can potentially reverse its effects.

Understanding Gut Dysbiosis and Leaky Gut

Gut Dysbiosis: This term refers to an imbalance in the gut microbiota—the diverse community of microorganisms living in our intestines. A healthy gut microbiome is essential for optimal immune function, digestion, and overall health. However, factors such as poor diet, stress, antibiotics, and infections can disrupt this balance, leading to an overgrowth of harmful bacteria and a decrease in beneficial bacteria (Ott et al., 2004).

Leaky Gut Syndrome: Also known as increased intestinal permeability, leaky gut occurs when the lining of the small intestine becomes damaged. This allows undigested food particles, toxins, and microbes to "leak" through the intestinal wall into the bloodstream, triggering widespread inflammation and an immune response (Fasano, 2012).

The Link Between Gut Health and Vitiligo

1. Autoimmune Trigger: Vitiligo is widely considered an autoimmune disease. The immune system mistakenly targets and destroys melanocytes. This is supported by the presence of antibodies and T-cells that are directed against melanocytes in the skin of individuals with vitiligo (Taieb & Picardo, 2007; van den Boorn et al., 2010). Dysbiosis and leaky gut will eventually lead to systemic inflammation causing autoimmune diseases. The immune system may start attacking the body’s own cells, including melanocytes—the cells responsible for skin pigmentation—in vitiligo (Taieb & Picardo, 2007).

2. Inflammatory Mediators and Oxidative Stress: The local skin environment in vitiligo shows increased levels of inflammatory cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). These cytokines can induce the expression of molecules that contribute to melanocyte apoptosis and inhibit melanocyte function (Klein et al., 2011). An imbalanced gut microbiome can increase the production of pro-inflammatory cytokines. These inflammatory mediators can contribute to the destruction of melanocytes, exacerbating vitiligo (Schallreuter et al., 2008).

Melanocytes in individuals with vitiligo are more susceptible to oxidative stress, which can result from an accumulation of reactive oxygen species (ROS) from chronic inflammation as well as poor mitochondrial health. This oxidative stress can lead to melanocyte damage and death, contributing to the depigmentation seen in vitiligo (Schallreuter et al., 2008).

3. Genetic Expression: Genetic predisposition plays a significant role in the development of vitiligo. Several genes associated with immune function and melanocyte biology have been linked to an increased risk of vitiligo. These include genes involved in the immune response (such as HLA and PTPN22) and melanocyte survival and function (such as TYR and PAX3) (Spritz, 2008). The gut microbiota can influence gene expression through epigenetic mechanisms. Dysbiosis may lead to the expression of genes associated with autoimmunity and inflammation, further promoting vitiligo (Dinwiddie et al., 2013).

At the Med Spa at Clinical Edge we use 3x4 Genetics to find out which pathways are involved and which pathways need to be improved using both nutrigenetics and supplements. Support of the detoxification pathways, inflammation pathways and methylation pathways changes the way genes are expressed, known as epigenetics.

Treating Gut Dysbiosis and Healing the Gut Lining

Probiotics and Prebiotics: Supplementing with probiotics can help restore the balance of beneficial bacteria in the gut. Prebiotics, which are non-digestible fibers that feed beneficial bacteria, can further support a healthy microbiome (Hill et al., 2014).

Anti-inflammatory Diet: Adopting an anti-inflammatory diet rich in fruits, vegetables, whole grains, and healthy fats can help reduce systemic inflammation. Foods such as bone broth, fermented foods, and omega-3 rich fish can support gut healing (Vajro et al., 2013).

Avoiding Triggers: Identifying and eliminating food sensitivities and allergens can help reduce gut inflammation. Common culprits include gluten, A1 dairy, wheat, added sugars and processed foods (Fasano, 2012).

Gut-Healing Supplements: Supplements such as glutamine, zinc, and omega-3 fatty acids can help repair the intestinal lining and reduce inflammation (Marchix et al., 2018).

Epigenetic Modifications

Lifestyle Changes: Implementing lifestyle changes such as regular exercise, stress management, and adequate sleep can positively influence gene expression and overall health (Shanahan, 2010).

Nutrigenomics: Some theories suggest that neurochemical mediators released from nerve endings in the skin may contribute to melanocyte destruction. This neurogenic hypothesis is supported by the observation that vitiligo patches often appear symmetrically and along certain nerve distributions (Yu et al., 2012). Nutrigenomics studies the interaction between nutrition and genes. Consuming nutrient-dense foods rich in vitamins, minerals, and antioxidants can help modulate gene expression and reduce the risk of autoimmune reactions (Afman & Muller, 2012).


At the Med Spa at Clinical Edge we get to the root cause of Vitiligo using, gut biome testing and genetic testing to strategize a personalized approach and treatment plan. We Integrate strategies to treat gut dysbiosis, heal the intestinal lining, and influence gene expression through epigenetics offering a holistic approach to managing and potentially reversing vitiligo. While more research is needed to fully understand these connections, focusing on gut health provides a promising avenue for improving outcomes in vitiligo patients.


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Dinwiddie, D. L., Manickam, K., & Wright, C. A. (2013). Epigenetics, the microbiome and autoimmunity. Clinical Immunology, 149(3), 271-282. Fasano, A. (2012). Leaky gut and autoimmune diseases. Clinical Reviews in Allergy & Immunology, 42(1), 71-78.

Hill, C., Guarner, F., Reid, G., Gibson, G. R., Merenstein, D. J., Pot, B., ... & Sanders, M. E. (2014). Expert consensus document: The International Scientific Association for Probiotics and Prebiotics consensus statement on the scope and appropriate use of the term probiotic. Nature Reviews Gastroenterology & Hepatology, 11(8), 506-514.

Klein, R., Schiffner, R., & Degitz, K. (2011). Vitiligo pathogenesis and treatment. American Journal of Clinical Dermatology, 12(5), 357-370. 

Marchix, J., Godon, C., Vinolo, M. A., Berdeaux, A., & Foretz, M. (2018). Dietary polyamines and gut microbiota: Experimental and human data. Nutrients, 10(12), 1875.

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Schallreuter, K. U., Wood, J. M., & Pittelkow, M. R. (2008). Advances in the understanding of the pathogenesis of vitiligo. Journal of Investigative Dermatology Symposium Proceedings, 13(1), 17-19.

Shanahan, F. (2010). The gut microbiota: A clinical perspective on lessons learned. Nature Reviews Gastroenterology & Hepatology, 9(10), 609-614.

Spritz, R. A. (2008). The genetics of generalized vitiligo. Current Directions in Autoimmunity, 10, 244-257.

Taieb, A., & Picardo, M. (2007). Clinical practice. Vitiligo. New England Journal of Medicine, 356(11), 1148-1156.

van den Boorn, J. G., Konijnenberg, D., Dellemijn, T. A., van der Veen, J. P., Bos, J. D., Melief, C. J., & Luiten, R. M. (2010). Autoimmune destruction of skin melanocytes by perilesional T cells from vitiligo patients. Journal of Investigative Dermatology, 130(8), 2163-2173.

Yu, H. S., Wu, C. S., Yu, C. L., Kao, Y. H., & Chiou, M. H. (2012). Different approaches for treating vitiligo in traditional Chinese medicine. Journal of Autoimmunity, 39(1-2), 3-7.

Vajro, P., Paolella, G., Fasano, A., & Liguoro, I. (2013). Probiotics, gut microbiota and gastrointestinal disease in children. Journal of Pediatric Gastroenterology and Nutrition, 57(3), 293-299.

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