Newer aspects of micronutrients in chronic disease: copper

Cu ions are pro-oxidants when added to biological material in vitro and excessive levels of Cu in the body, such as in Wilson's Disease (Yarze et al. 1992) promote oxidant-related pathologies. In contrast there is now substantial evidence that an optimum level of Cu is required to maintain antioxidant defence and that Cu deficiency in animals increases oxidant stress. There are abundant mechanistic relationships linking Cu deficiency and processes associated with IHD, some of which do not directly involve oxidant damage. These mechanistic relationships, however, have mostly been demonstrated in animal models and more information is urgently required concerning possible chronic mild Cu deficiencies in human populations. A major hurdle to advances in this area is the lack of indices of Cu status which are sensitive enough to detect marginal Cu deficiency in humans. The question, therefore, of whether or not there is a role for mild Cu deficiency in the onset of chronic disease processes, including IHD, remains unanswered.