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Vitamin B3 May Help Treat Fungal Infections

By Greg Arnold, DC, CSCS, August 17, 2010, abstracted from “Modulation of histone H3 lysine 56 acetylation as an antifungal therapeutic strategy” in the 2010 issue

The bacteria C. albicans (Candida albicans) is responsible for most fungal infections in humans, with severity ranging from minor skin and mucosal infections to life-threatening infections in the body (1). Ironically, it does not pose a threat and is one of a number of bacteria in the mouth and digestive system of healthy individuals. In those with weakened immune systems (patients undergoing cancer chemotherapy, organ or bone marrow transplantation and AIDS sufferers), C. albicans can become very dangerous (2).

C. albicans infections are difficult to treat and “create very serious challenges” in medicine. Death rates among patients with candidiasis have been increasing and can be as high as 40% to 60%, especially when C. albicans infections enter the bloodstream (3). It’s estimated that C. albicans is estimated to cause $2.6 billion in the U.S. alone (4).

Now a new study in mice (5) has now found that vitamin B3, shown to be effective at treating skin lesions (6), may have the potential to help treat fungal infections caused by C. albicans. In the study, researchers injected 12 mice with vitamin B3 (500 mg per kg of bodyweight, which is about 35 grams or 1 ¼ oz. for a 70 kg human) 30 minutes before and 8 hours after infecting them with C. albicans. Kidney tissue samples obtained from the mice found that vitamin B3 prevented the growth of C. albicans by acting on a gene in the bacteria called Hst3p which is crucial for reproduction (7). Acting on Hst3P increased levels of another protein called H3K56ac which is toxic to C. albicans.

For the researchers, “Our results demonstrate that [altering]…H3K56ac is a unique strategy for treatment of C. albicans and, possibly, other fungal infections.” The importance of these results lies in the fact that it presents vitamin B3 may now be a viable treatment option for C. albicans infections as the bacteria frequently develops resistance to azoles and echinocandins, the prescription medications most commonly used to treat fungal infections (8, 9).

Greg Arnold is a Chiropractic Physician practicing in Danville, CA. You can contact Dr. Arnold directly by emailing him at PitchingDoc@msn.com or visiting his web site at www.PitchingDoc.com

Reference:

1. Ihmels J. Comparative gene expression analysis by differential clustering approach: application to the Candida albicans transcription program. PLoS Genet 2005;1:e39
2. d'Enfert C, Hube B: Candida: comparative and functional genomics. Wymondham: Caister Academic; 2007
3. Seneviratne CJ. Biofilm lifestyle of Candida: a mini review. Oral Dis 2008;14:582-590
4. Wilson LS, Reyes CM, Stolpman M, Speckman J, Allen K, et al. (2002) The direct cost and incidence of systemic fungal infections. Value Health 5: 26–34.
5. Wurtele H. Modulation of histone H3 lysine 56 acetylation as an antifungal therapeutic strategy. Nature Medicine, 2010; 16 (7): 774 DOI: 10.1038/nm.2175
6. Niren, N.M. Pharmacologic doses of nicotinamide in the treatment of inflammatory skin conditions: a review. Cutis 77, 11–16 (2006)
7. Celic I. The sirtuins hst3 and Hst4p preserve genome integrity by controlling histone h3 lysine 56 deacetylation. Curr Biol 2006 Jul 11;16(13):1280-9.
8. Akins, R.A. An update on antifungal targets and mechanisms of resistance in Candida albicans . Med. Mycol 2005; 43:285–318
9. Perlin, D.S. Resistance to echinocandin-class antifungal drugs. Drug Resist. Updat 2007; 10:121–130