Koper goed voor het hart.*

Voldoende koper in de voeding is goed voor hart en bloedvaten volgens Amerikaanse wetenschappers. Koper vermindert de stress op het hart en gaat hartvergroting tegen. Koper in de voeding staat bekend als cholesterol verlagend tegen bloedstolsels en hartziektes. Uit deze nieuwe studie weliswaar met muizen blijkt dat voldoende koper in de voeding ook bij een zwaar belast hart de normale functies weer herstellen. Koper doet de productie van een proteïne toenemen welke zorgt voor de aanmaak van nieuwe bloedvaatjes. Uit deze studie blijkt dat voldoende koper betekent voor een mens ongeveer 3 mg/dag en dat is toch wel wat meer als doorgaans geadviseerd wordt (in NL 1,5 mg/dag).

Heavy metal for a troubled heart

Including more copper in your everyday diet could be good for your heart, according to a study on page 657. Jiang et al. now find that dietary supplementation of copper offsets the effects of stress on an overworked heart by preventing its enlargement.

Copper-carrying proteins disarm oxygen radicals and power electron transport. Humans with copper deficiency have increased cholesterol levels, clot formation, oxidative tissue damage, and heart disease. Cardiac tissue biopsies of heart attack victims show a great reduction in copper levels.

In mice with stress-induced heart disease, the team now shows, increased heart size and decreased heart function can both be restored to normal levels by a small increase in the daily intake of copper, even when the stress stimulus is maintained. But without the copper supplement, stressed mice suffer heart failure after two months.

The authors show that mice receiving dietary copper supplements have increased activity of a transcription factor called HIF-1-alfa, leading to increased production of the vascular endothelial growth factor (VEGF) protein, which promotes angiogenesis. Blocking VEGF activity inhibits the ability of copper to reverse heart enlargement and dysfunction. It is not clear, however, how angiogenesis helps decrease muscle mass or how copper gets pushed out of the heart during stress.

The human equivalent of the beneficial dose of copper used in 3.0 mg/day. The current recommended daily intake for humans, however, is only 0.9 mg/day. Increasing copper intake may be a cheap way to reduce mortality associated with heart disease.

Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice
Youchun Jiang¹, Corey Reynolds², Chang Xiao¹, Wenke Feng¹, Zhanxiang Zhou¹, Walter Rodriguez², Suresh C. Tyagi², John W. Eaton^1,4, Jack T. Saari³, and Y. James Kang^1,2,4

¹ Department of Medicine, ² Department of Physiology and Biophysics, and ⁴ Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville KY 40202
³ U.S. Department of Agriculture Human Nutrition Research Center Grand Forks, ND 58202

CORRESPONDENCE Y. James Kang: yjkang01@louisville.edu

Sustained pressure overload causes cardiac hypertrophy and the transition to heart failure. We show here that dietary supplementation with physiologically relevant levels of copper (Cu) reverses preestablished hypertrophic cardiomyopathy caused by pressure overload induced by ascending aortic constriction in a mouse model. The reversal occurs in the continued presence of pressure overload. Sustained pressure overload leads to decreases in cardiac Cu and vascular endothelial growth factor (VEGF) levels along with suppression of myocardial angiogenesis. Cu supplementation replenishes cardiac Cu, increases VEGF, and promotes angiogenesis. Systemic administration of anti-VEGF antibody blunts Cu regression of hypertrophic cardiomyopathy. In cultured human cardiomyocytes, Cu chelation blocks insulin-like growth factor (IGF)-1– or Cu-stimulated VEGF expression, which is relieved by addition of excess Cu. Both IGF-1 and Cu activate hypoxia-inducible factor (HIF)-1-alfa, and HIF-1-alfa gene silencing blocks IGF-1– or Cu-stimulated VEGF expression. HIF-1-alfa, coimmunoprecipitates with a Cu chaperone for superoxide dismutase-1 (CCS), and gene silencing of CCS, but not superoxide dismutase-1, prevents IGF-1– or Cu-induced HIF-1-alfa activation and VEGF expression. Therefore, dietary Cu supplementation improves the condition of hypertrophic cardiomyopathy at least in part through CCS-mediated HIF-1-alfa activation of VEGF expression and angiogenesis. (Maart 2007) (Opm. Meer over koper in de voeding. Let op meer koper in de voeding is geen goede oplossing bij kanker. Meer koper in de voeding is verder voor iedereen goed doch zij die behalve veel koper ook nog langdurig veel verzadigde vetzuren en transvetten consumeren doen hun cognitieve functies sterk verminderen.)