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Reversing Vitiligo

(Updated: 18th Dec 2017)

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 autoimmune) 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 elimination diet for foods.

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)

This is the 1st step of the ROSE system I base most cases on (i.e. Removal of ongoing pathogens).

 

Which nutrients can help & why?

In search for re-pigmentation solutions for vitiligo, a group of scientists in Amsterdam – NL (Cormane R et al., 1985), noted that patients with phenylketonuria (who among other symptoms have lighter than normal skin) when administrated tyrosine and were incubated with UV-light had normal melanin production. Cormane’s team initially tried the tyrosine & UV-A protocol in a pilot study of 5 without any success. Sequentially they tried phenylalanine (a precursor of tyrosine) seeing improvement in 95% of the subjects after 6 to 8 months. The theory put forward on why phenylalanine benefits vitiligo patches was that it stops antibodies and allows sun radiation to stimulate melanocytes from other areas to migrate to the damaged ones (Camacho, F. and Mazuecos, J., 1999).

 

50 mg/kg of body weight per day of phenylalanine was administered 1 hour prior to UV A irradiation (twice per week). Of the 19 participants:

i. 5 noted dense re-pigmentation in 6 to 8 months

ii. 13 saw sparse re-pigmentation in the same period

iii. and 1 had no re-pigmentation even after 8 months.

Since the 1980’s there has been no more research examining the benefits of phenylalanine for vitiligo. All 3 studies combining the administration of the amino acid & UVA exposure as well as the 1 that used just the amino acid reported positive outcomes (Szczurko, O. and Boon, H.S., 2008).

 

Vitamin E (Szczurko, O. and Boon, H.S., 2008) and vitamin C have also been shown to support re-pigmentation potentially due to their antioxidant properties.

 

 

Which Genes are responsible for Vitiligo?

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.

 

Case Studies.

Case 1

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.

 

References.

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.

 

Camacho, F. and Mazuecos, J., 1999. Treatment of vitiligo with oral and topical phenylalanine: 6 years of experience. Archives of dermatology, 135(2), pp.216-217.

 

Cormane, R.H., Siddiqui, A.H., Westerhof, W. and Schutgens, R.B.H., 1985. Phenylalanine and UVA light for the treatment of vitiligo. Archives of Dermatological Research, 277(2), pp.126-130.

 

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.

 

Szczurko, O. and Boon, H.S., 2008. A systematic review of natural health product treatment for vitiligo. BMC dermatology, 8(1), p.2.

 

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.

 

 

Underactive thyroid and gut health

The relationship between underactive thyroid and gut health is reciprocal. While a compromised thyroid health will affect the gut function, the reverse also holds true.

How does an underactive thyroid affect the gut

i. For proper digestion of protein the stomach needs to secrete hydrochloric acid (HCl) – a very expensive energy-wise process. When the thyroid is underactive the production of HCl is low (hypochloridia)  (1). The implications of hypochloridia are massive as undigested proteins can cause increased intestinal permeability in the gut.

ii. Underactive thyroid will slow down other high energy demanding processes in the body such as liver and gallbladder function (2,3). The consequence is poor fat digestion and detoxification.

 

“Whatever the reason of the cause, slow thyroid function will compromise macronutrient digestion”

 

How can poor gut health cause hypothyroidism

i. While most of the T4 (inactive form of thyroid hormone) is activated in the liver, 20% of the conversion takes place in the intestines, in the presence of healthy gut flora.

ii. Inflammation in the gi track can exhaust the adrenals (4) which will then drug down the function of thyroid.

iii. Constipation can compromise the elimination of estrogen from the body. High estrogen levels by binding to thyroid hormone receptors can slow down thyroid function.

iv. Faulty digestion is one of the primary causes of autoimmune disease (5,6). With 60% of the immune system located in the gi track this should come as no surprise. Hashimoto’s is an automimmune disorder where the body attacks the TPO enzyme in the thyroid gland.

v. Elevated levels of Yersinia enterocolitica bacteria have been associated with patients suffering from Hashimoto’s disease (7).

 

 How to address hypothyroid-gut issues

Nobel prize winner and microbiologist Elie Metchnikoff said: “Death begins in the colon.” But so does health. Healing the gut should be your primary concern if you are presenting with gi and thyroid problems. A comprehensive stool analysis is a great starting point.

 

Knowing how underactive thyroid can put a burden on gut health what can you do?

If you suffer from gastrointestinal problems make sure your thyroid function is good shape. While supplementation and natural remedies can support digestion initially, on the long run you want the body to produce adequate levels of HCl and digestive enzymes. If underactive thyroid symptoms are present work with a healthcare practitioner to improve your thyroid health.

 

 

 

References

1. Atrophic body gastritis in patients with autoimmune thyroid disease: an underdiagnosed association. Arch Intern Med 1999 159:1726-1730.

2. Possible chronic thyroiditis revealed by [18F]-FDG-PET/CT scan in a euthyroid patient with recurrent gallblader carcinoma. Thyroid 2007 17:1157-1158.

3. Is bile flow reduced in patients with hypothyroidism? Surgery 2003, 133: 288-293.

4. Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions. Curr Rheumatol Rep 2007 9:482-487.

5. The gut immune system and type 1 diabetes. Ann NY Acad Sci 2002; 958:39-46.

6. The “perfect storm” for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability and mucosal immunity. Diabetes 2008;57:2555-2562.

7. Clin Microbiol Infect 2001 Mar 7:138-143.