An elevated level of total homocysteine (tHcy) in blood, denoted hyperhomocysteinemia, is emerging as a prevalent and strong risk factor for atherosclerotic vascular disease in the coronary, cerebral, and peripheral vessels, and for arterial and venous thromboembolism. The basis for these conclusions is data from about 80 clinical and epidemiological studies including more than 10,000 patients. Elevated tHcy confers a graded risk with no threshold, is independent of but may enhance the effect of the conventional risk factors, and seems to be a particularly strong predictor of cardiovascular mortality. Hyperhomocysteinemia is attributed to commonly occurring genetic and acquired factors including deficiencies of folate and vitamin B12. Supplementation with B-vitamins, in particular with folic acid, is an efficient, safe, and inexpensive means to reduce an elevated tHcy level. Studies are now in progress to establish whether such therapy will reduce cardiovascular risk.

/pdf/homocysteine-and-cardiovascular-disease-1zad76k6jt.pdf

Homocysteine and Cardiovascular Disease

https://www.gastrojournal.org/article/S0016-5085(03)00276-2/pdf

Betaine decreases hyperhomocysteinemia, endoplasmic reticulum stress, and liver injury in alcohol-fed mice

After a thorough review of the available literature, it appears that hyperhomocysteinemia is an independent risk factor for CHD. Furthermore, folic acid has been shown to reduce homocysteine concentration. Nevertheless, CHD is a multifactorial process, and many risk factors play a role in its pathogenesis. Several unanswered questions remain regarding the role of folic acid supplementation in hyperhomocysteinemia (Table 3). The absolute homocysteine concentration at which cardiovascular risk increases is not certain, and the magnitude of homocysteine-lowering needed to prevent events is unknown. Consequently, the number needed to treat cannot be calculated for folic acid supplements. Based on these data, the populations in whom to evaluate a homocysteine concentration have yet to be described. Because the POEMs are not yet available, it is unknown whether supplemental folic acid to lower homocysteine concentration will reduce CHD morbidity and mortality. It will take several years before any randomized, controlled trials are done, and primary prevention trials will need to be of very long duration to show any change in outcomes. Widespread use of folic acid supplementation has been recommended, however, and the need for clinical outcomes might be precluded. Even in the absence of outcome data, the potential benefits of using folic acid appear to outweigh any risks. A diet high in folic acid should be encouraged in everyone (Table 4). The FDA-mandated folic acid fortification of enriched grain products is most likely insufficient to lower homocysteine concentrations meaningfully, and a daily multivitamin that contains 400 microg of folic acid should be considered for patients who have documented CHD (especially when other risk factors are absent or in patients with premature atherosclerosis) and men and women who have cardiovascular risk factors, in addition to women of childbearing potential. Folic acid supplementation in the form of a multivitamin once daily is safe and inexpensive and might prevent the development and progression of CHD.

On the basis of recent retrospective and prospective studies, it is now widely accepted that increased total plasma homocysteine is a risk factor for cardiovascular disease. Impaired enzyme function as a result of genetic mutation or deficiency of the essential B vitamins folic acid, B12, and B6 can lead to hyperhomocysteinemia. Oxidized forms of homocysteine account for 98-99% of total plasma homocysteine. Although there is uncertainty as to whether increased homocysteine is causal or merely a proxy for cardiovascular disease, several lines of evidence suggest that it may play a role in atherothrombotic disease. Homocysteine appears to alter the anticoagulant properties of endothelial cells to a procoagulant phenotype. Mildly increased homocysteine causes dysfunction of the vascular endothelium. Folic acid effectively lowers homocysteine concentration in the plasma. Intervention studies are urgently needed to determine if lowering homocysteine is effective in decreasing the morbidity and mortality of cardiovascular disease.

/pdf/homocysteine-and-vitamins-in-cardiovascular-disease-2bci7lvdj8.pdf

Homocysteine and vitamins in cardiovascular disease

Alcoholic liver disease (ALD) develops as a consequence of priming and sensitizing mechanisms rendered by cross-interactions of primary mechanistic factors and secondary risk factors. This concept, albeit not novel, is becoming widely accepted by the field, and more research is directed toward identifying and characterizing the interfaces of the cross-interactions to help understand individual predisposition to the disease. Another pivotal development is the beginning of cell type-specific research to elucidate specific contributions not only of hepatocytes, but also of hepatic macrophages, liver-associated lymphocytes, sinusoidal endothelial cells, and hepatic stellate cells to sensitizing and priming mechanisms. In particular, the critical role of hepatic macrophages has been highlighted and the priming mechanisms concerning this paracrine effect have been proposed. Glutathione depletion in hepatocyte mitochondria is considered the most important sensitizing mechanism. One of the contributing factors is decreased methionine metabolism. Remaining key questions include how altered methionine metabolism contribute to the pathogenesis of ALD; how cross-talk among nonparenchymal liver cells or between nonparenchymal cells and hepatocytes leads to ALD; how dysfunctional mitochondria determine the type of cell death in ALD; and what secondary factors are critical for the development of advanced ALD such as alcoholic hepatitis and cirrhosis.

Current concepts in the pathogenesis of alcoholic liver injury

Hyperhomocysteinemia in chronic alcoholism: correlation with folate, vitamin B-12, and vitamin B-6 status.

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Hyperhomocysteinemia in chronic alcoholism: correlation with folate, vitamin B-12, and vitamin B-6 status.