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Cardiovascular effects of dietary copper deficiency
1US Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, ND 58202-9034, USA. jsaari@gfhnrc.ars.usda.gov
Insights
Dietary copper deficiency negatively impacts cardiovascular health, leading to issues like high blood pressure and inflammation. This review details how copper impacts heart and blood vessel function, contributing to cardiovascular defects.
Area of Science:
- Cardiovascular Science
- Nutritional Biochemistry
Background:
- Dietary copper is essential for numerous physiological processes.
- Copper deficiency is linked to various cardiovascular risk factors.
Purpose of the Study:
- To review the cardiovascular alterations associated with dietary copper deficiency.
- To elucidate the mechanisms by which copper deficiency impairs cardiovascular health.
Main Methods:
- Literature review of studies on copper deficiency and cardiovascular health.
- Compilation of data on cardiac, vascular, and hematological changes.
Main Results:
- Copper deficiency contributes to hypertension, inflammation, anemia, and arteriosclerosis.
- Structural and functional changes in the heart, blood vessels, and blood cells are observed.
- Reduced activity of copper-dependent enzymes underlies these detrimental effects.
Conclusions:
- Copper deficiency poses a significant risk to cardiovascular health.
- Restoring copper levels may mitigate or prevent cardiovascular complications.
Abstract:
Dietary copper deficiency may impair cardiovascular health by contributing to high blood pressure, enhancement of inflammation, anemia, reduced blood clotting and arteriosclerosis. The purpose of this review is to compile information on the numerous changes of the heart, blood and blood vessels that may contribute to these cardiovascular defects. These alterations include weakened structural integrity of the heart and blood vessels, impairment of the use of energy by the heart, reduced ability of the heart to contract, altered ability of blood vessels to control their diameter and to grow, and altered structure and function of circulating blood cells. The fundamental causes of these changes rest largely on reduced effectiveness of enzymes that depend on copper for their activity.