Written by Marcia J. Egles, MD. In a small animal study those fed niacin had significantly less liver damage when given alcohol.
Excessive drinking of alcohol can cause damage to the liver. An early and potentially reversible stage of alcoholic liver damage is known as “alcohol-induced fatty liver” in which microscopic droplets of fats (also known as lipids) accumulate in the liver cells. With continued alcohol consumption, the damage can progress to worsened forms of alcohol-related liver disease including alcoholic hepatitis, cirrhosis and liver cancer (2). A recent study in rats exposed to alcohol shows a lessening of fatty liver development when the rats were supplemented with dietary niacin along with the alcohol (1).
Alcoholism is frequently associated with multiple nutritional deficiencies including niacin deficiency (3). Niacin, also known as nicotinic acid, is one of the naturally occurring B3 vitamins. Niacin’s role is crucial in energy metabolism including the body’s processing of fats. The two objectives of the recent study were to determine if niacin deficiency exaggerates alcohol-induced lipid accumulation in the liver and if niacin dietary supplementation might alleviate alcohol-induced lipid accumulation (1). Though the study was performed in laboratory rats, the information obtained is pertinent to human health, as alcohol has toxic effects on the rat liver similar to its toxic effects on the human liver.
Three-month old healthy male laboratory rats were used in this eight-week study. The control group consisted of six rats, and three experimental groups contained eight rats each. The control group received no ethanol. The first experimental group received ethanol as part of a liquid diet otherwise similar to the liquid diet of the control group. The second group received ethanol in a niacin deficient diet. The third group received ethanol plus niacin supplementation. The control group and the first ethanol group received 7.5milligrams of niacin per liter in their diets, the niacin deficient diet had zero mg of niacin, and the niacin supplemented diet had 750 mg of niacin per liter of liquid food. To achieve equal caloric feeding across the four groups, the first ethanol group was allowed to feed freely. The other groups were then fed to match the calories consumed by the first ethanol group.
After eight weeks, the rats’ livers were compared in several microscopic and chemical analyses. The control group had normal livers. The ethanol feeding caused significant lipid accumulation in the livers of the first group. This lipid accumulation was not worsened in the niacin deficient diet rats as compared to the first group. The group that received ethanol plus niacin supplementation, however, showed significantly less (p less than 0.05) lipid accumulation.
Vitamin B deficiencies in particular are well documented among alcohol-dependent individuals. Thiamine ( vitamin B1) deficiency and thiamine replacement are widely described in the medical literature (4). As compared to thiamine, niacin supplementation in alcoholism has been less researched. Niacin’s unpleasant side effects (such as “flushing”) can be worsened by concomitant alcohol use.
Source: Li, Qiong, et al. “Dietary Nicotinic Acid Supplementation Ameliorates Chronic Alcohol‐Induced Fatty Liver in Rats.” Alcoholism: Clinical and Experimental Research 38.7 (2014): 1982-1992.
© 2014 by the Research Society on Alcoholism.
Posted April 21, 2016.
References:
- Qiong Li, et al., Dietary Nicotinic Acid Supplementation Ameliorates Chronic Alcohol-Induced Fatty Liver in Rats, Alcohol Clin Exp Res, Vol 38, No 7, 2014: pp 1982-1992.
- Gamfi,MA, Wan YJ et al. Pathogenesis of alcoholic liver disease: the role of nuclear receptors Exp Biol Med (Maywood) May 2010, vol. 235 ,no. 5, 547-560. doi: 10.1258/ebm.2009.009249
- VarellaMorandi Junqueira-Franco M, et al (2006) Intestinal permeability and oxidative stress in patients with alcoholic pellagra. Clin Nutr 25: 977-983.
- Mark A. Oldham et al. Pellagrous encephalopathy presenting as alcohol withdrawal delirium: A case series and literature review. Addict Sci Clin Pract. 2012; 7(1): 12.
