Vitamin Supplements as a Nutritional Strategy against Chronic Alcohol Consumption? An Updated Review

Abstract

Several studies have shown that blood vitamin levels are low in alcoholic patients. In effect, alcohol use abuse is considered a chronic disease that promotes the pathogenesis of many fatal diseases, such as cancer and liver cirrhosis. The alcohol effects in the liver can be prevented by antioxidant mechanisms, which induces enzymatic as well as other nonenzymatic pathways. The effectiveness of several antioxidants has been evaluated. However, these studies have been accompanied by uncertainty as mixed results were reported. Thus, the aim of the present review article was to examine the current knowledge on vitamin deficiency and its role in chronic liver disease. Our review found that deficiencies in nutritional vitamins could develop rapidly during chronic liver disease due to diminished hepatic storage and that inadequate vitamins intake and alcohol consumption may interact to deplete vitamin levels. Numerous studies have described that vitamin supplementation could reduce hepatotoxicity. However, further studies with reference to the changes in vitamin status and the nutritional management of chronic liver disease are in demand.

Keywords: alcoholic liver disease; vitamin B1; vitamin C; vitamin D; vitamin E.

Figure 1

Flow diagram for the review process.

Figure 2

Oxidative pathway involved during ethanol metabolism.

Figure 3

Vitamins and their possible mechanisms of action against the liver injury caused by al-cohol consumption. Tetrahydrofolate (THF), 5,10-methylenetetrahydrofolate (5,10-Methylene THF), methylenetetrahydrofolate reductase (MTHFR), and 5-methyltetrahydrofolate (5-Methyl THF), the initial methyl donor for transmethylation processes, are all involved in vitamin metabolism. 5-Methyl THF and homocysteine (Hcy) are substrates for methionine synthase (MS) in the synthesis of methionine, which is converted to S-adenosylmethionine (SAM) by methionine adenosyltransferase (MAT) in transmethylation processes. S-adenosylhomocysteine (SAH) is a product and inhibitor of methyltransferase reaction (MTs) as well as a substrate for the bidirectional enzyme SAH hydrolase (SAHH), which creates homocysteine or SAH when SAH is in excess. Hcy is metabolized by cystathionine beta-synthase (CBS) and cystathionase to produce cysteine and glutathione (GSH) in transsulfuration processes. It is also important to note that SAM inhibits MTHFR while promoting CBS expression. As a result, a SAM shortage boosts 5-Methyl THF production while lowering 5,10-Methyl THF and GSH production.