(Updated: 17th Oct 2018)
Vitiligo (also called “leukoma”) is an autoimmune condition where loss of pigment from areas of the skin result in irregular white patches, the texture of which remain normal. Similar with all autoimmune disorders:
i. the body is attacking its own tissue. In the case of vitiligo the body is attacking the melanocytes (the cells responsible for skin colouring).
ii. the triggering cause may vary. I have seen 1 case where it started after a car accident at an early stage of life & another where it developed after a stressful period at late 40s.
iii. the development of the disease is the result of genetic predisposition as well as environmental factors.
iv. there is a higher than normal risk for the simultaneous presence of other autoimmune conditions.
Cease the Fire.
As an autoimmune condition vitiligo has to be treated as an immunological problem and not solely as a skin one. While the symptoms manifest in the skin it is the immune system that is over-reacting. This is the reason why in many cases immunosuppressive drugs are prescribed (Boone B., et al., 2007). Stopping the over-activity of the immune system may not be as straight forward as we wish. Foods, heavy metals, infections have been shown or speculated to be the root cause of this unfavourable behaviour of the immune system (IS).
In order to address each of the above one can:
i. follow an anti-inflammatory diet.
ii. remove any obvious toxic deposits in the body (i.e. mercury fillings, tattoos)
iii. get tested for carrying any of the common viruses associated with autoimmunity (i.e. Epstein Barr virus)
Test for other AI conditions.
While there are 100s of autoimmune conditions, Hashimoto’s & Celiac Disease have been shown to have a higher prevalence among patients of vitiligo. Hashimoto’s can be easily diagnosed through an inexpensive blood test for TPO (Thyroid peroxidase) & TgAB (Thyroglobulin) antibodies. The diagnosis of Celiac Disease requires a biopsy which is why a lot of patients with vitiligo decide to eliminate gluten from their diet without going through the hustle of testing.
If the body is attacking more than one of its own tissue it is best for all autoimmune cases to be supported at the same time.
For the depigmentation is of the “milky” patches the 2 versions of light therapy have been used successfully are: Narrowband UVB & Targeted light therapy (Grimers PE 2005).
Narrowband UV-B involves the use of UV lamps with a peak emission around 311 nm. It induces local immunosuppression while stimulating the production of melanocyte-stimulating hormone, and the increase of melanocyte proliferation and melanogenesis. In a study (Njoo M D et al., 2000) where 51 children with generalised vitiligo were treated with narrowband UV-B:
a) 53% achieved >75% of repigmentation
b) 29% had 26-50% of repigmentation
c) 18% had <25% of repigmentation
The main advantages of narrowband UV-B include:
a) safety for both adults & children
b) lack of systemic adverse effects
Source: Njoo M D et al., 1998
A number of supplements have been shown to help reverse vitiligo. Accompanying light therapy with supplementation is likely to amply its benefits.
NLRP1 is a gene involved in the production of proteins called inflammasomes. Inflammasomes participate in the regulation of the immune system & mutations in NLRP1 have been associated with the presence of autoimmune disorders. The rs6502867 variant of the NLRP1 gene (risky allele: T) was associated with vitiligo in an Indian study (Dwivedi M et al., 2013).
Phytonutrient (EGCG) in green tea has been shown to inhibit the action of the NLRP1 gene (Ellis L et al., 2010).
Methylation is a process responsible for many functions in the body including cell replication and DNA repair. A study published among 80 individuals (40 with vitiligo & 40 controls) (Yasar, A et al., 2012) showed no correlation between mutations in MTHFR or the levels of serum folate & vitamin B12 among the patients. Had the study measured red blood cell folate and vitamin B12 their findings would have been more significant.
Both folate & vitamin B12 (which directly support the methylation pathway) have been used by vitiligo patients with positive outcomes.
The photos in the image above are from a female client in her 50’s. She was following the Wahls dietary protocol for 6 months as an anti-inflammatory / auto-immune friendly approach. The main adjustments in her diet where the increase of fats through nuts & seeds as well as progressing from 2 meals and 1 snack a day to a 16-8 hours fast and then to 1 meal a day (twice per week). Breathing exercises as well as progressive exposure to cold (through showers) were also part of her protocol.
Boone, B., Ongenae, K., Van Geel, N., Vernijns, S., De Keyser, S. and Naeyaert, J.M., 2007. Topical pimecrolimus in the treatment of vitiligo. European Journal of Dermatology, 17(1), pp.55-61.
Dwivedi, M., Laddha, N.C., Mansuri, M.S., Marfatia, Y.S. and Begum, R., 2013. Association of NLRP1 genetic variants and mRNA overexpression with generalized vitiligo and disease activity in a Gujarat population. British Journal of Dermatology, 169(5), pp.1114-1125.
Ellis, L.Z., Liu, W., Luo, Y., Okamoto, M., Qu, D., Dunn, J.H. and Fujita, M., 2011. Green tea polyphenol epigallocatechin-3-gallate suppresses melanoma growth by inhibiting inflammasome and IL-1β secretion. Biochemical and biophysical research communications, 414(3), pp.551-556.
Grimes, P. E. (2005). New insights and new therapies in vitiligo. Jama, 293(6), 730-735.
Njoo, M. D., Bos, J. D., & Westerhof, W. (2000). Treatment of generalized vitiligo in children with narrow-band (TL-01) UVB radiation therapy. Journal of the American Academy of Dermatology, 42(2), 245-253.
Njoo, M. D., Spuls, P., Bos, J. T. A., Westerhof, W., & Bossuyt, P. M. M. (1998). Nonsurgical repigmentation therapies in vitiligo: meta-analysis of the literature. Archives of dermatology, 134(12), 1532-1540.
Yasar, A., Gunduz, K., Onur, E. and Calkan, M., 2012. Serum homocysteine, vitamin B12, folic acid levels and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism in vitiligo. Disease markers, 33(2), pp.85-89.