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vascular disease with hyperglicemia as a late manifestation [1]. It’s known that T2DM causes coronary morbility and mortality from two to six times more than in individuals without diabetes [2]. Mortality from stroke rised almost 3-fold when diabetics are matched to the persons without diabetes [3]. Peripheral arterial and retinal diseases are some common complications of diabetes mellitus [4]. Patients having diabetes have an enhanced myocardial dysfunction, often evolving in chronic heart failure [5–7]. Premature atherosclerosis, hyperglycemia, increased insulin resistance and glycosilation of some proteins are undelay all these cardiovascular occurrences. In addition, these impairments often are clouped with elevated blood pressure and hyperhomocisteine, obesity, rised levels of triglycerides and low HDL-cholesterol. These conditions further favour the atherosclerotic processes

Inheired or acquired hyperhomocysteinemia (HHcy) is associated with several impairments, as certain tumors, deep venous thrombosis, tube neural defects, osteoporosis, early atherosclerosis and vascular acute events (IMA, stroke, PVD), mild cognitive impairments till Alzheimer’s disease (AD). But, vascular and neuronal derangements are the most frequent HHcy-manifestations. As far as early atherosclerosis, some clinical trials demonstrated that folates and B6–12 vitamins supplementation is unable to reduce atherosclerotic lesions and cardiovascular events, even if it lowers HHcy levels. Thus, for atherosclerosis and its acute events (IMA, stroke, PVD) HHcy acts as a powerful biomarker rather than a risk factor. For that, the supplementation with folates and B vitamins to lower atherosclerotic lesions-events in hyperhomocysteinemic patients is not recommended. On the contrary, several clinical investigations demonstrated that folates and vitamins administration is able to reduce Hcy serum levels and antagonize some mechanisms favouring neurodegenerative impairments, as mild cognitive impairment, AD and dementia. Thus, contrarily to the atherosclerotic manifestations in hyperhomocysteinemic patients, preventive treatment with folates and B6–12 vitamins reduces Hcy concentration and could prevent or delay cognitive decline and AD.