Dr. Ron’s Research Review – September 14, 2016

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This week’s research review focuses on copper and heart disease.

Over the last couple of decades, dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance. Interestingly, these changes are common in the United States where people consume processed foods marginally deficient in copper and replete with sugar. Improving levels of copper in the diet, by appropriate food selection or by addition of a daily multi-vitamin, is recommended. (Aliabadi, 2008)

Although the nutritional essentiality of copper was established in 1928, a preoccupation with hematology delayed the discovery of cardiovascular disease from copper deficiency for more than a decade. Anatomical studies of several species of deficient animals revealed, interalia, aortic fissures and rupture, arterial foam cells and smooth muscle migration, cardiac enlargement and rupture, coronary artery thrombosis and myocardial infarction. Abnormal biochemistry in deficiency probably contributes to these lesions, e.g., decreased activities of lysyl oxidase and superoxide dismutase, which result in failure of collagen and elastin crosslinking and impaired defense against free radicals. Copper deficiency also decreases copper in hearts and other organs and cells and increases cholesterol in plasma. Abnormal physiology from deficiency includes abnormal electrocardiograms, glucose intolerance and hypertension. Copper depletion experiments with men and women have revealed abnormalities of lipid metabolism, blood pressure control, and electrocardiograms plus impaired glucose tolerance. The Western diet often is as low in copper as that proved insufficient for these people. (Klevay, 2000)

Dr. Ron

 


Articles

 

A deleterious interaction between copper deficiency and sugar ingestion may be the missing link in heart disease.
            (Aliabadi, 2008) Download
Copper deficiency plays a vital role in atherogenesis. To the long list of risk factors for atherosclerotic cardiovascular disease should be added the deleterious interaction between copper deficiency and carbohydrate consumption. Here we critically evaluate the role of copper in the diet and its role as a possible etiological factor in the development of cardiovascular disease. A possible mechanism for the development of heart disease due to copper deficiency is proposed. There are many known risk factors for the development of heart disease, including hyperlipidemia and hypertension; however, little emphasis has been placed on the role of copper on heart disease. Over the last couple of decades, dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance. Interestingly, these changes are common in the United States population and they are known risk factors for heart disease. Further research in this field is warranted considering the profound implications to people in the United States and around the world who consume processed foods marginally deficient in copper and replete with sugar. The only nutritional condition with signs and symptoms of atherosclerotic cardiovascular disease may be copper deficiency. Improving levels of copper in the diet, by appropriate food selection or by addition of a daily multi-vitamin, is recommended.

Cardiovascular disease from copper deficiency--a history.
            (Klevay, 2000) Download
Although the nutritional essentiality of copper was established in 1928, a preoccupation with hematology delayed the discovery of cardiovascular disease from copper deficiency for more than a decade. Anatomical studies of several species of deficient animals revealed, interalia, aortic fissures and rupture, arterial foam cells and smooth muscle migration, cardiac enlargement and rupture, coronary artery thrombosis and myocardial infarction. Abnormal biochemistry in deficiency probably contributes to these lesions, e.g., decreased activities of lysyl oxidase and superoxide dismutase which result in failure of collagen and elastin crosslinking and impaired defense against free radicals. Copper deficiency also decreases copper in hearts and other organs and cells and increases cholesterol in plasma. Abnormal physiology from deficiency includes abnormal electrocardiograms, glucose intolerance and hypertension. People with ischemic heart disease have decreased cardiac and leucocyte copper and decreased activities of some copper-dependent enzymes. Copper depletion experiments with men and women have revealed abnormalities of lipid metabolism, blood pressure control, and electrocardiograms plus impaired glucose tolerance. The Western diet often is as low in copper as that proved insufficient for these people. Knowledge of nutritional history can be useful in addressing contemporary nutritional problems.

 

References

Aliabadi, H (2008), ‘A deleterious interaction between copper deficiency and sugar ingestion may be the missing link in heart disease.’, Med Hypotheses, 70 (6), 1163-66. PubMed: 18178013
Klevay, LM (2000), ‘Cardiovascular disease from copper deficiency--a history.’, J Nutr, 130 (2S Suppl), 489S-92S. PubMed: 10721936