In view of the importance of alcoholic beverages in daily life as well as its absolute priority in metabolism, alcohol has considerable potential to affect the nutritional status and metabolism of all essential nutrients including the different energy sources. In view of the great variability among alcohol drinkers in patterns of drinking, amounts ingested, ingestion of other nutrients, metabolic characteristics, genetic factors, and lifestyle characteristics (such as exercise or smoking behavior), the effects of alcohol on nutritional status and disease risk are very heterogeneous. Alcohol -associated malnutrition includes both primary and secondary malnutrition. Because of the comparatively high energy content of alcohol, it displaces other energy sources and thus many essential nutrients in the diet, thereby lowering the intake of most nutrients (primary malnutrition). Gastrointestinal and metabolic complications of heavy alcohol intake (especially liver dysfunction) lead to so -called secondary malnutrition. Anorexia and vomiting from alcoholic gastritis further promote inadequate intakes of food. Malabsorption of nearly all nutrients can develop as a result of mucosal dysfunction, liver insuffi ciency, and pancreatic insuffi ciency. Alcoholic liver dysfunction causes a reduced capacity to transport nutrients in the blood, a reduced storage capacity, and an insuffi cient activation of nutrients such as vitamins. In addition, alcohol increases the excretion of nutrients in the urine and bile. In alcoholic patients, several mechanisms for the development of malnutrition usually occur simultaneously.The effect of alcohol on morbidity and mortality is biphasic, and the relationship is J -shaped: low levels of ingestion are associated with reduced morbidity and mortality risks, whereas abstinence and higher levels of ingestion are associated with a higher mortality risk due to different cancers, alcoholic liver disease, and cardiovascular diseases such as arrhythmias, alcoholic cardiomyopathy, hypertension, and stroke. The reduced mortality risk at lower intakes is explained by the risk of coronary artery disease and a reduced risk of ischemic stroke. The amount of alcohol ingestion at the nadir of mortality risk is not known and varies from study to study and from one individual to another. The hallmark of excessive alcohol intake is metabolic and structural alterations at the level of the liver, and liver cirrhosis is the leading cause of death in heavy drinkers.Often, both positive and negative effects occur. In view of the heterogeneity of responses for any given alcohol dose, the formulation of public health recommendations for safe consumption levels is becoming increasingly diffi cult. In any case, alcohol should not be recommended for health reasons or for health maintenance, especially as long as there are no specifi c, sensitive predictors for harmful alcohol use and abuse. In the setting of an overall healthy lifestyle with respect to nutrition and physical activity, light to moderate alcohol consumptio...