Adverse Effects of Chronic Alcohol Consumption

Abstract

Chronic alcohol consumption has emerged as a leading cause of metabolic derangement in susceptible cohorts worldwide; ethanol has a high calorific value and excessive intake interferes with energy metabolism. It has a very high glycemic index, so the glucose homeostasis does not follow the normal physiological regulations in chronic consumption of ethanol. Chronic alcohol consumption is a global concern for its health issues. The detailed mechanism of alcohol-associated organ damage and health anomalies has been reviewed here. Almost all of its metabolic fates has minor to major impacts on any physiological process. The main rate-limiting markers of glucose homeostasis, i.e. NADH/NAD+ and ATP/ADP, are physiologically misjudged in ethanol consumption; as a result, excess acetoacetyl CoA becomes engaged in ketone body formation resulting in ketoacidosis. Ethanol induced ROS production and antioxidant depletion resulting in necrotic tissue damage especially in the stomach, intestine epithelial cells, and liver. Increased oxidative stress causes vascular dysfunction, NO deregulation, peripheral vascular resistance, increased blood pressure, and aldosterone-induced hypertension. Ethanol manipulates intracellular phosphorylation regulations by influencing MAPK and inflammatory molecule, like TNFa and IL-6, and transcriptional stress factor like NF-κβ, Nrf-2, and Hif-α via redox signalling. Activation of lipogenic factors and PPAR signalling drastically increase body fat accumulation. Direct damage to the pancreatic cells generates insulin resistance. Synergistic effects of several metabolic malfunctioning develop insulin resistance, chronic hyperglycaemia, and abnormal fat accumulation.