Copper nutrition and biochemistry and human (patho)physiology.

Abstract

The essential trace mineral copper plays important roles in human physiology and pathophysiology. Disruption of copper homeostasis may underlie the development of ischemic heart disease, and connective tissue and neurodegenerative disorders. Copper also likely participates in the host response to bacterial infection and is further implicated more broadly in regulating immunity. Recent studies further associate copper with disruption of lipid homeostasis, as is frequently seen in, for example, non-alcoholic fatty liver disease (NAFLD). Moreover, continuing investigation of copper chaperones has revealed new roles for these intracellular copper-binding proteins. Despite these (and many other) significant advances, many questions related to copper biology remain unanswered. For example, what are the most sensitive and specific biomarkers of copper status, and which ones are useful in marginal (or "sub-clinical" copper deficiency)? Further research on this topic is required to inform future investigations of copper metabolism in humans (so the copper status of study participants can be fully appreciated). Also, are current recommendations for copper intake adequate? Recent studies suggest that overt copper deficiency is more common than once thought, and further, some have suggested that the copper RDAs for adults may be too low. Additional human balance and interventional studies are necessary and could provide the impetus for reconsidering the copper RDAs in the future. These and myriad other unresolved aspects of copper nutrition will undoubtedly be the focus of future investigation.