From: Kofi on
It would appear as if nicotinamide supplementation might render yeast
infections vulnerable to antifungal agents. This might tie into the
recently advanced hypothesis that nicotinamide overload plays a role in
the development of type II diabetes [PMID 19960564]. Enhanced niacin
could impair fungal overgrowth and fungal overgrowth impairs intestinal
repair in colitis [PMID 19439813] - making niacin a potentially
important anti-Crohn's strategy (perhaps not so surprising given how
PGD2 helps in Crohn's
<>; PGD2 is
downstream of the niacin flush that is defective in schizophrenics).
Recent evidence points to an interesting genetic relationship between
diabetes and Crohn's. Genes that raise the risk of diabetes appear to
help with Crohn's and vice versa. That is to say, genes protective in
one are harmful in the other

Notice the connection to IDO in my previous post...

nicotinamide impairs fungus survival;; Vitamin B3 is a Novel Approach to
Treat Fungal Infections; a Candida albicans enzyme, Hst3, is essential
to the growth and survival of the yeast; genetic or pharmacological
inhibition of Hst3 with nicotinamide, a form of vitamin B3, strongly
reduced C. albicans virulence in a mouse model; Both normal and
drug-resistant strains of C. albicans were susceptible to nicotinamide;
nicotinamide also prevented the growth of other pathogenic Candida
species and Aspergillus fumigatus (another human pathogen), thus
demonstrating the broad antifungal properties of nicotinamide; Hugo
Wurtele, Sarah Tsao, Guylaine L�pine, Alaka Mullick, Jessy Tremblay,
Paul Drogaris, Eun-Hye Lee, Pierre Thibault, Alain Verreault, Martine
Raymond. Modulation of histone H3 lysine 56 acetylation as an antifungal
therapeutic strategy. Nature Medicine, 2010; 16 (7): 774 DOI:

In yeast, histone H3 Lys56 acetylation (H3K56ac) is an abundant
modification regulated by enzymes that have fungal-specific properties,
making them appealing targets for antifungal therapy; H3K56ac in C.
albicans is regulated by the RTT109 and HST3 genes, which respectively
encode the H3K56 acetyltransferase (Rtt109p) and deacetylase (Hst3p);
reduced levels of H3K56ac sensitize C. albicans to genotoxic and
antifungal agents. Inhibition of Hst3p activity by conditional gene
repression or nicotinamide treatment results in a loss of cell viability
associated with abnormal filamentous growth, histone degradation and
gross aberrations in DNA staining; genetic or pharmacological
alterations in H3K56ac levels reduce virulence in a mouse model of C.
albicans infection; modulation of H3K56ac is a unique strategy for
treatment of C. albicans and, possibly, other fungal infections [PMID