NIACIN DEFICIENCY AND CANCER IN WOMEN

A new interest in the relationship between niacin and cancer has evolv ed from the discovery that the principal form of this vitamin, NAD, is consumed as a substrate in ADP-ribose transfer reactions. Poly(ADP-ri bose) polymerase, an enzyme activated by DNA strand breaks, is the ADP -ribosyltransferase of greatest interest with regard to effects on the niacin status of cells since its K(m) for NAD is high, and its activi ty can deplete NAD. Studies of the consequences of DNA damage in cultu red mouse and human cells as a function of niacin status have supporte d the hypothesis that niacin may be a protective factor that limits ca rcinogenic events. To test this hypothesis in humans, we used a bioche mical method based on the observation that as niacin nutriture decreas es, NAD readily declines and NADP remains relatively constant. This ha s been demonstrated in both fibroblasts and in whole blood from humans . Thus, we use ''niacin number,'' (NAD/NAD + NADP) x 100% from whole b lood, as a measure of niacin status. Healthy control subjects showed a mean niacin number of 62.8 +/- 3.0 compared to 64.0 for individuals o n a niacin-controlled diet. Analyses of women in the Malmo Diet and Ca ncer Study showed a mean niacin number of 60.4 with a range of 44 to 7 5. The distribution of niacin status in this population was nongaussia n, with an unpredictably large number of individuals having low values .