Posted 26 February 2006 - 03:43 AM
I've seen references to excess niacin using up methyl equivalents (certain molecules donate methyl groups in Niacin metabolism) which are otherwise unavailable for other purposes. Lack of sufficient methylation of DNA could be associated with genetic "unsilencing" of genes that should be kept from being expressed. This may be what's being addressed in references to DNA damage. I'm not familiar with telomere damage, specifically.
It's suggested that folate, B12, TMG, and Choline can take part in methyl donation reactions, so you might want to supplement with these to compensate for excess niacin intake.
On the other hand, all of the references I see on a quick-n-dirty search suggest lack of niacin results in increased risk of DNA damage. For example, niacin is required in RDA levels to ensure DNA repair process integrity (see below).
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Nutr Cancer. 2003;46(2):110-8. Related Articles, Links
Niacin and carcinogenesis.
Kirkland JB.
Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
The dietary status of niacin (vitamin B3) has the potential to influence DNA repair, genomic stability, and the immune system, eventually having an impact on cancer risk, as well as the side effects of chemotherapy in the cancer patient. In addition to its well-known redox functions in energy metabolism, niacin, in the form of NAD, participates in a wide variety of ADP-ribosylation reactions. Poly(ADP-ribose) is a negatively charged polymer synthesized, predominantly on nuclear proteins, by at least seven different enzymes. Poly(ADP-ribose) polymerase-1 (PARP-1) is responsible for the majority of polymer synthesis and plays important roles in DNA damage responses, including repair, maintenance of genomic stability, and signaling events for stress responses such as apoptosis. NAD is also used in the synthesis of mono(ADP-ribose), often on G proteins, with poorly understood roles in signal transduction. Last, NAD and NADP are required for the synthesis of cyclic ADP-ribose and nicotinic acid adenine dinucleotide (NAADP), two mediators of intracellular calcium signaling pathways. Disruption of any of these processes has the potential to impair genomic stability and deregulate cell division, leading to enhanced cancer risk. There are various sources of evidence that niacin status does have an impact on cancer risk, including animal models of leukemogenesis and skin cancer, as well as epidemiological data from human populations.
Publication Types:
Review
PMID: 14690785 [PubMed - indexed for MEDLINE]