autonmousone1980
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So like, angiogenesis(new blood vessel growth) is supposedly required for hair to enter the anagen phase. Vegf is vascular endothelial growth factor, and is supposedly being developed to treat hairloss, but the thing is, copper is involved in its synthesis. Is it possible some hairloss could be attributed to decreased copper stores?? as you body stores this mineral i would think it would prioritize what process got more copper to ensure the most critical would be met.
Also a new cancer fighting strategy is to develop a copper chelation technology which depletes copper to inhibit tumors ability to use angiogenesis to form new blood vessels.
Pretty interesting hey?
Also, if anyone takes zinc hoping it will inhibit dht, you are probably going to cause hairloss this way because too much zinc blocks the absorption of copper. the zinc myth for any benefits for hairloss must be stopped now!! And start taking copper instead.
here is some evidence to back up my words.
1: J Exp Med. 2007 Mar 19;204(3):657-66. Epub 2007 Mar 5.Links
Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice.
Jiang Y, Reynolds C, Xiao C, Feng W, Zhou Z, Rodriguez W, Tyagi SC, Eaton JW, Saari JT, Kang YJ.
Department of Medicine, University of Louisville School of Medicine, Louisville, KY 40202, USA.
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)-1alpha and HIF-1alpha gene silencing blocks IGF-1- or Cu-stimulated VEGF expression. HIF-1alpha 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-1alpha activation and VEGF expression. Therefore, dietary Cu supplementation improves the condition of hypertrophic cardiomyopathy at least in part through CCS-mediated HIF-1alpha activation of VEGF expression and angiogenesis.
Also a new cancer fighting strategy is to develop a copper chelation technology which depletes copper to inhibit tumors ability to use angiogenesis to form new blood vessels.
Pretty interesting hey?
Also, if anyone takes zinc hoping it will inhibit dht, you are probably going to cause hairloss this way because too much zinc blocks the absorption of copper. the zinc myth for any benefits for hairloss must be stopped now!! And start taking copper instead.
here is some evidence to back up my words.
1: J Exp Med. 2007 Mar 19;204(3):657-66. Epub 2007 Mar 5.Links
Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice.
Jiang Y, Reynolds C, Xiao C, Feng W, Zhou Z, Rodriguez W, Tyagi SC, Eaton JW, Saari JT, Kang YJ.
Department of Medicine, University of Louisville School of Medicine, Louisville, KY 40202, USA.
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)-1alpha and HIF-1alpha gene silencing blocks IGF-1- or Cu-stimulated VEGF expression. HIF-1alpha 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-1alpha activation and VEGF expression. Therefore, dietary Cu supplementation improves the condition of hypertrophic cardiomyopathy at least in part through CCS-mediated HIF-1alpha activation of VEGF expression and angiogenesis.