Epidemiological studies assessing cadmium (Cd) body burden by determining its creatinine-corrected level in urine strongly suggest that non-occupational Cd exposure can boost systemic oxidative stress and inflammation, and is a major mediating factor in the pathogenesis of various common cancers, vascular disease, and other health disorders. Cadmium’s effects in this regard often appear to reflect competition with zinc for binding to regulatory proteins. Indeed, increased intakes of zinc counteract Cd toxicity in rodent models. Zinc’s protective impact in this regard is mediated in part by induction of metallothionein; this sequesters Cd is such a way as to reduce its intestinal absorption and alleviate its pathogenic effects. Zinc’s Cd antagonistic effects may rationalize epidemiology associating increased zinc intakes with lower cancer risks. The significant 27% decrease in total mortality noted in zinc-supplemented subjects (80 mg daily) in the AREDS1 study might also be partially attributable to Cd antagonism. In light of growing evidence that Cd is a major mediator of a number of life-threatening disorders throughout the world, and that zinc can notably lessen its pathogenicity, a large and long-term controlled trial of high-dose zinc supplementation in an older population, with mortality as its primary endpoint, can be strongly recommended. Targeting a population with relatively high Cd exposure, such as that of Japan, would be most appropriate in this regard.
Mark McCarty F, James DiNicolantonio J
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