Repigmentation in Vitiligo
One in every 200 Americans suffers vitiligo, a localized loss of pigment produced by the melanocytes in the skin. During embryogenesis, melanocytes come from the neural crest tissue which forms the endocrine glands and the peripheral nervous system, so they are part of the Communication System, and melanin is actually made of neurotransmitters!
Vitiligo of the hand in a person with dark skin. (Photo credit: Wikipedia)
Related conditions include:
- Thyroid Disease
- Adrenal Exhaustion and Addison’s Disease
- Hearing Loss
- Sweating Abnormalities
- Depigmentation and Inflammation in the Eyes
- Mental Depression
- Parkinson’s Disease
- Vitiligo is also clinically linked with:
- Pernicious Anemia
- Diabetes 1 & 2
- Hair Loss (Alopecia Areata)
- Nutritional Deficiencies
- Chronic Candidiasis
- PolyGlandular Syndromes 1 & 2
Psoralen: Psoralea corylifolia (breadroot) contains the phenolic compound psoralen that sensitizes to UV light. Soak seeds for 4 days, dry, and grind to a paste. Topical application in oil is followed by 10 – 15 minutes of sunlight. Oral psoralen supplementation is also effective. For dietary support, celery contains psoralen.
Nigella (Black Cumin) regenerates pigmentation.
Piperine from black pepper stimulates repigmentation (King’s College London)
Polypodium leucotomos (Anapsos) regenerates pigmentation. (Int J Dermatol. 1989; Mohammad A.)
Khella (Ammi visnaga) contains Khellin, which works similar to psoralen, as it stimulates repigmentation of the skin by increasing the sensitivity of the melanocytes to sunlight. Studies use 120–160 mg of khellin per day. (Abdel-Fattah, Aboul-Enein MN, Wassel GM, El-Menshawi BS. An approach to the treatment of vitiligo by khellin. Dermatologica 1982;165:136–40.)
Hypochlorhydria: Lack of stomach acid reduces digestion and absorption of a wide range of essential nutrients, and is associated with vitiligo. Supplementation after meals caused gradual repigmentation after one year or more. (Francis HW. Achlorhydria as an etiological factor in vitiligo, with a report of four cases. Nebraska State Med J 1931;16(1):25–6.) In order to prevent dependence on supplementation, hydrochloric acid, taken as betaine HCl, should only be used for over two weeks if taken together with bitter botanicals that stimulate endogenous production of digestive juices.
Picrorhiza improved response to methoxsalen and sun exposure. 400 to 1,500 mg per day of encapsulated picrorhiza powder is used in studies. (Bedi KL, Zutshi U, Chopra CL, Amla V. Picrorhiza kurroa, an Ayurvedic herb, may potentiate photochemotherapy in vitiligo. J Ethnopharmacol 1989;27:347–52.)
Ginkgo: Cessation of active progression of depigmentation was noted in patients treated with Ginkgo biloba 40 mg (24% ginkgo flavon glycosides) three times a day (P = 0.006) in a double-blind trial. Marked to complete repigmentation was seen in 10 out of 25 patients (40%) in the treatment group, versus only two patients out of 22 (9%) in the control group. (Effectiveness of oral Ginkgo biloba in treating limited, slowly spreading vitiligo. Clin Exp Dermatol. 2003)
Xiaobai Mixture (XBM) better than 8-MOP: The therapeutic effect of XBM was better than that of 8-MOP. XBM improved nail-fold microcirculation, elevated the plasma endothelin-1 level, and lowered the serum IgG in vitiligo. (Clinical observation on treatment of vitiligo with xiaobai mixture. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2003)
Mitochondrial dysfunction: Intracellular levels of reactive oxygen species and antioxidants, the activity of Krebs cycle enzymes, and the effects of inhibitors of the electron transport chain were measured in peripheral blood mononuclear cells from patients with active or stable disease vs. normal subjects. Plasma glyoxal levels were also measured as an index of systemic oxidative stress. In patients with active vitiligo, increased intracellular production of reactive oxygen species with a consequent imbalance of the prooxidant/antioxidant equilibrium was found, whereas plasma glyoxal levels were normal, ruling out systemic oxidative stress. In patients with stable disease, there was a balance between pro-oxidants and antioxidants. A marked increase in expression of mitochondrial malate dehydrogenase activity and a specific sensitivity to electron transport chain complex I inhibitor were seen. (Alterations of mitochondria in peripheral blood mononuclear cells of vitiligo patients. Pigment Cell Res. 2003) Remedies to consider: PQQ and Bacillus subtilis to stimulate mitochondrial regeneration; CoQH (coenzyme form: reduced CoQ10) and shilajit for mitochondrial protection.
Whole blood glutathione levels, erythrocyte glutathione peroxidase, and glucose-6-phosphate dehydrogenase activity were decreased significantly in a controlled study of people with vitiligo. (Pigment Cell Res. 2004. Agrawal D, Shajil EM, Marfatia YS, Begum R. Department of Biochemistry, Faculty of Science, M.S. University of Baroda, Vadodara, Gujarat, India)
In a randomized, double-blind, placebo-controlled multicentre trial, the treatment group received, for 2 months before and for 6 months during the NB-UVB treatment, a balanced oral antioxidant supplement containing alpha-lipoic acid, vitamins C and E, and polyunsaturated fatty acids, which significantly improved clinical effectiveness. (Antioxidants and narrow band-UVB in the treatment of vitiligo: a double-blind placebo-controlled trial. Clin Exp Dermatol. 2007 Nov;32(6):631-6. Spedali Civili, Brescia, Italy.)
Botanical antioxidants: Green Tea, Oregano, Ginkgo, Turmeric, Berberis vulgaris have been suggested for antioxidant benefits.
Home Remedies: Basil in lime juice topical three times a day. Carrier oils often used include coconut and olive.
Fumaria officinalis (contains fumaric acid): Esterified fumarates are used topically and orally in low doses (60 – 100 mg/day) for psoriasis and other skin conditions. Fumaric acid, a Kreb’s Cycle intermediary is produced in the skin on exposure to UV light.
Apoptosis as the mechanism of melanocytosis:
Histological and laboratory data support apoptosis, rather than necrosis, as the mechanism for the loss of melanocytes. Apoptosis can be induced by immune cytokines, environmental chemicals (e.g. substituted hydroquinones such as monobenzone) and other molecular mechanisms. Current therapies, such as corticosteroids and ultraviolet light, affect apoptosis in a variety of ways. (Vitiligo: a manifestation of apoptosis? Am J Clin Dermatol. 2002. Huang CL, Nordlund JJ, Boissy R. Department of Dermatology, University of Cincinnati, Pavilion A, Ohio)
Vitilax capsule ingredients: Psoralea Fruit; Astragalus Root; Chinese Peony Root Without Bark, Cnidium Fruit; Chinese Salvia Root and Rhizome; Tribulus Fruit, Chinese Dodder Seed; Fo-Ti Root; Turmeric Root, Bai-zhu Atractylodes Rhizome; Dong Quai Root, Safflower Flower, Fragrant Angelica Root, Cassia Twig.
Munzij Balgham, another botanical formula, contains Glycyrrhiza glabra, Ficus carica, Foeniculum vulgare, Foeniculum vulgare (root), Adiantum capillus-veneris, Althaea officinalis (seeds), Malva sylvastris (seeds), Rosa damascena, Vitis vinfera, Apium graneolens (root), Zingerber officinale, Cassia angustifolia (leaves), Operculina turpethum
Corticosteroids: consider 7-Keto, DHEA (Update 2021: Sublingual 7-Keto formula)
Autoimmune Modulation: Phytosterols (as well as Ginkgo) (Update 2021: Immune Modulation formula)
Vitamin D3 for Calcium Modulation: Calcium transport is defective in melanocytes and keratinocytes harvested from patients with vitiligo. Vitamin D3, also a hormone and a sterol made from tissue cholesterol by absorption of UV light, activates melanin synthesis. (Birlea SA, Costin GE, Norris DA. New insights on therapy with vitamin D analogs targeting the intracellular pathways that control repigmentation in human vitiligo. Med Res Rev 2009;29:514-46)
A topical form of vitamin D (calcipotriol) together with sunlight stimulates repigmentation in children with vitiligo. After 11 months, repigmentation was marked to complete in 55%, moderate in 22%, and little or none was seen in 22% of the children. No new areas of vitiligo developed. The first repigmentation was within 6 to 12 weeks in most children. (Parsad D, Saini R, Nagpal R. Calcipotriol in vitiligo: A preliminary study. Pediatr Dermatol 1999;16:317–20.)
Stress Vitamins: Electron & Methyl Donors
A clinical report describes vitamin therapies in vitiligo. Folic acid and/or vitamin B12 and vitamin C levels were abnormally low in most of the 15 people studied. Supplementation with high dose folic acid (1–10 mg a day), vitamin C (1 gram a day), and intramuscular vitamin B12 injections (1,000 mcg every two weeks), produced marked repigmentation in eight people apparent at three months, and with full repigmentation after one to two years of supplementation. (Montes LF, Diaz ML, Lajous J, Garcia NJ. Folic acid and vitamin B12 in vitiligo: a nutritional approach. Cutis 1992;50:39–42.)
B12 & Folate: Repigmentation occurred in 3 to 6 months in 52 out of 100 patients taking oral B12 (2,000 mcg per day) & folic acid (10 mg a day), including 37 who exposed their skin to summer sun and 6 who used UVB lamps in winter. Repigmentation was most evident in sun-exposed areas. Total repigmentation was seen in 6 patients, and the spread of vitiligo stopped in 64%. Repigmentation was better than with vitamins or sun exposure alone. Treatment should continue as long as the white areas continue to repigment. (Juhlin L, Olsson MJ. Improvement of vitiligo after oral treatment with vitamin B12 and folic acid and the importance of sun exposure. Acta Derm Venereol 1997;77:460–2.)
PABA (para-aminobenzoic acid): 100 mg three to four times per day, along with injectable PABA and hormones tailored to individual needs, resulted, in many cases, in repigmentation of vitiligo. (Sieve BF. Further investigations in the treatment of vitiligo. Virginia Med Monthly 1945; Jan:6–17.)
Minerals: Copper is antifungal, and antioxidant in small quantities, while Sulfur is a major remedy for the skin.
NAC: Dopamine, a monoamine neurotransmitter, is a neurotoxin via the generation of reactive oxygen species and quinones. Dopamine levels increase with the onset and progression of vitiligo as well as Parkinson’s, both involving tissues that produce pigments from neurotransmitters. To investigate the cytoprotective activity of antioxidants, vitamin C, vitamin E, Trolox, quercetin, N-acetylcysteine (NAC), and l-glutathione (GSH) were tested. Among the various antioxidants in the study, only thiol-containing antioxidants such as NAC or GSH inhibited both JNK and p38 MAPK activation and apoptosis. (Glutathione prevented dopamine-induced apoptosis of melanocytes and its signaling. J Dermatol Sci. 2007. Department of Dermatology, Seoul National University College of Medicine, Chongno-Gu, Seoul, Republic of Korea)
L-Phenylalanine: several studies have found that L-phenylalanine produces repigmentation, and was even more effective when taken in conjunction with UVA or UVB therapy. (Siddiqui AH, Stolk LM, Bhaggoe R, et al. L-phenylalanine and UVA irradiation in the treatment of vitiligo. Dermatology 1994;188:215–8.; Schulpis CH, Antoniou C, Michas T, Strarigos J. Phenylalanine plus ultraviolet light: preliminary report of a promising treatment for childhood vitiligo. Pediatr Dermatol 1989;6:332–5.)
The therapeutic dosage is 50 to 100 mg/kg of body weight, and a topical LPA gel can also be used to achieve improvement in 83% of participants. 57% reported improvement of at least 75%. (Camacho F, Mazuecos J. Treatment of vitiligo with oral and topical phenylalanine: 6 years of experience. Arch Dermatol 1999;135:216–7.)
Homeopathy: remedies to consider include Alum, Natrum carbonicum, Phosphorus, Sepia, Silicea, and Sulfur
Eat millet, pulse, ghee, broad bean, French bean, spinach, bitter gourd, ridge gourd, onions, beetroot, carrot, chilies, red pepper, pistachio, walnut, date, mango, apricot, grape, potato, papaya, amaranth, fenugreek, turnip, almond.
Avoid Milk, curd, buttermilk, lemon, lime, tamarind, orange, all citrus, sorrel, parsley, custard apple, guava, prune, cashew, melon, watermelon, Chinese date, tomato, amla.
Possible Etiology: Tinea versicolor is a fungal infection that causes depigmentation. Natural topical remedies include Selenium, Sulfur, Tea Tree Oil, aloe gel, eucalyptus oil, senna alata (candle bush), and dilute apple cider vinegar.
Among the herbs that slow down or halt the growth of fungus are goldenseal (Hydrastis canadensis), myrrh (Commiphora molmol), garlic (Allium sativa), pau d’arco (Tabeebuia impestiginosa), turmeric (Curcuma longa), oregano (Origanum vulgare), cinnamon (Cinnamonum zeylanicum), jewelweed, sage (Salvia officinalis), Impatiens aurea, yellow dock (Rumex crispus), the lichen known as old man’s beard (Usnea barbata), black walnut husks and bark (Juglans nigra), licorice (Glycyrrhiza glabra), and Calendula officinalis. These herbs can be applied to external fungus as infusions, salves, powders, or vinegar. Many of them can also be taken internally as capsules or tinctures. Antifungal herbs can be very strong, and care should be taken that a given remedy is suitable for internal use. Dosage should be gradually increased according to tolerance, taking plenty of water to flush out endotoxins released as fungi die off to avoid strong Herxheimer reactions.
When an infusion is used, the affected area should be washed or soaked in the herbal water for at least 15 minutes twice daily. Store-bought or homemade tea bags can be soaked in water or vinegar for 10 minutes and then used as a poultice. Herbal vinegar makes excellent remedies for fungus, as acetic acid is antifungal. Gourmet vinegar with antifungal ingredients like oregano and garlic are often available at grocery stores. Vinegar can be applied a few times a day with cotton or compresses. Also, bentonite clay powder can be used to dry moist skin that breeds fungus. It works best mixed with powdered antifungal herbs like myrrh or Oregon grape root. The powder is especially helpful for athlete’s foot.
Many herbs high in essential oils also have antifungal activity, especially tea tree (Melaleuca alternifolia), oregano, lavender (Lavandula officinalis), Eucalyptus spp., rose geranium (Pelargonium graveolens), peppermint (Mentha piperita), chamomile (Matricaria recutita), and myrrh. Peppermint oil is helpful for relieving the itching of fungal infections. Add several drops of essential oil to the bathwater. The essential oil can also be added to mixtures for soaking or compresses. Tea tree is the most frequent recommendation for fungal skin infection. With all essential oils, the full-strength oil should be diluted in a carrier, such as coconut oil, olive oil, or grapeseed oil. Coconut oil contains caprylic acid which is antifungal.
A healthy diet should be maintained. Foods that are high in yeast, such as beer and wine, bread, and baked goods should be avoided. Fermented foods and sugary foods, including honey and fruit juices, should also be avoided until symptoms clear. Antifungal culinary herbs such as garlic, turmeric, oregano, sage, and cinnamon should be used liberally. Yogurt containing live cultures can be incorporated into the diet to supply needed gut bacteria and help reduce digestive infections such as candidiasis and thrush. Lactobacillus acidophilus and Lactobacillus bulgaricus can also be taken directly as supplements. Bacillus subtilis produces PQQ which stimulates regeneration of the mitochondria. Supplements that can be taken for fungal infections include vitamins A, B complex, C, and E. Caprylic acid from coconut is also recommended as an antifungal, as well as grapefruit seed extract. Essential fatty acids in evening primrose oil, fish oil, and flaxseed oil, can help reduce inflammation in fungal infections. A daily dose is recommended.