Disruptions in
iron homeostasis are linked to a broad spectrum of
chronic conditions including cardiovascular, malignant, metabolic, and
neurodegenerative disease. Evidence supporting this contention derives from a variety of analytical approaches, ranging from molecular to population-based studies. This review focuses on key epidemiological studies that assess the relationship between body
iron status and
chronic diseases, with particular emphasis on
atherosclerosis ,
metabolic syndrome and diabetes. Multiple surrogates have been used to measure body
iron status, including serum
ferritin,
transferrin saturation, serum
iron, and
dietary iron intake. The lack of a uniform and standardized means of assessing body
iron status has limited the precision of epidemiological associations. Intervention studies using depletion of
iron to alter risk have been conducted. Genetic and molecular techniques have helped to explicate the biochemistry of
iron metabolism at the molecular level. Plausible explanations for how
iron contributes to the pathogenesis of these
chronic diseases are beginning to be elucidated. Most evidence supports the hypothesis that excess
iron contributes to
chronic disease by fostering excess production of
free radicals. Overall, epidemiological studies, reinforced by basic science experiments, provide a strong line of evidence supporting the association between
iron and elevated risk of
cardiovascular disease and diabetes. In this narrative review we attempt to condense the information from existing literature on this topic.