Copper nutriture and ischemic heart disease: a brief review

Abstract

The idea that dietary fat is poisonous arose nearly ¾ of a century ago. Criteria for associating disease incidence with environmental change were published a couple decades later. Intakes of dietary fat did not increase while ischemic heart disease risk was increasing; in contrast, dietary copper decreased. Intakes of copper calculated from food tables are falsely high by an average of 77%. Approximately half of adults consume less than 0.9 mg of copper per day when chemical analyses are done. This amount is less than nutritional guidelines. When hypercholesterolemia was discovered in copper deficient rats, a search was begun for anatomical, chemical and physiological similarities between animals deficient in copper and people with ischemic heart disease; more than 80 of these similarities have been identified. The copper deficiency theory on the etiology and pathophysiology of ischemic heart disease is the simplest and most general theory that has been proposed because it incorporates other theories on fetal programming, homocysteine and iron overload. It satisfies classical criteria of nutritional deficiency and association of an environmental characteristic with disease prevalence.