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Monday, October 9, 2017 9:47 PM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases,
Douglas B Kell, Medical Genomics2009

"...Cardiovascular diseases
It is well known that elevated iron stores can predispose to coronary artery disease and thence myocardial infarction. The 'iron hypothesis' of the benefits of some iron depletion due to menstruation was devised to account for the lowering of heart-disease risk in young women (that disappears in those post-menopause) and was proposed by Jerome Sullivan in 1981 [695, 696, 697, 698] (and see also [699, 700]). (In this sense, the lack of menstruation during pregnancy would predispose to a comparative abundance of iron, as is indeed found – see above.) It is of particular interest that the well-known adverse vascular effects of homocysteine (in inhibiting flow-mediated dilatation) are in fact iron-dependent [701, 702, 703], and that reducing homocysteine (e.g. by folate supplementation) in the absence of lowering iron has shown no clinical benefit to date [704], thereby suggestion iron mediation. By contrast, iron stores represent an established risk factor for cardiovascular disease [705].

Of course many factors such as lipid levels, stress, smoking and so are well-known risk factors for cardiovascular, coronary artery disease and related diseases. Indeed kidney disease is well established as a risk factor for cardiovascular disease [706, 707, 708] (and indeed stroke [709]), all consistent with their having in part a common cause – we believe inflammation). Our purpose here, within the spirit of this review, is to indicate the evidence for the involvement of inappropriately chelated iron in cardiovascular diseases too. There is no doubt that the iron-mediated causal chain of ischaemia ? (su)peroxide ? OH• radical formation occurs during the development of heart disease, especially during reperfusion injury [710, 711, 712, 713], and suitable iron chelators inhibit this [714, 715] (see also [716, 717], and for thalassaemia [718]). Iron is also involved in the protection that can be produced by ischaemic preconditioning [719, 720]. Erythropoietin, a hormone with multiple effects that may involve iron metabolism, is also protective [721, 722]..."

full paper: https://bmcmedgenomics.biomedcentral.com/articles/10.1186/1755-8794-2-2
Venöse Multiple Sklerose, CVI & SVI, CCSVI