Alcoholics often eat poorly, limiting their supply of essential nutrients and affecting both energy supply and structure maintenance. Furthermore, alcohol interferes with the nutritional process by affecting digestion, storage, utilisation and excretion of nutrients.
Once ingested, food must be digested (broken down into small components) so it is available for energy and maintenance of body structure and function. Digestion begins in the mouth and continues in the stomach and intestines, with help from the pancreas. The nutrients from digested food are absorbed from the intestines into the blood and carried to the liver. The liver prepares nutrients either for immediate use or for storage and future use.
Alcohol inhibits the breakdown of nutrients into usable molecules by decreasing secretion of digestive enzymes from the pancreas. Alcohol impairs nutrient absorption by damaging the cells lining the stomach and intestines and disabling transport of some nutrients into the blood. In addition, nutritional deficiencies themselves may lead to further absorption problems. For example, folate deficiency alters the cells lining the small intestine, which in turn impairs absorption of water and nutrients including glucose, sodium, and additional folate.
Even if nutrients are digested and absorbed, alcohol can prevent them from being fully utilised by altering their transport, storage and excretion. Decreased liver stores of vitamins such as vitamin A, and increased excretion of nutrients such as fat, indicate impaired utilisation of nutrients by alcoholics.
The three basic nutritional components found in food – carbohydrates, proteins and fats – are used as energy after being converted to simpler products. Some alcoholics ingest as much as 50 per cent of their total daily calories from alcohol, often neglecting important foods. Even when food intake is adequate, alcohol can impair the mechanisms by which the body controls blood glucose levels, resulting in either increased or decreased blood glucose.
In non-diabetic alcoholics, increased blood sugar, or hyperglycemia – caused by impaired insulin secretion – is usually temporary and without consequence. Decreased blood sugar, or hypoglycemia, can cause serious injury even if this condition is short-lived. Hypoglycemia can occur when a fasting or malnourished person consumes alcohol. When there is no food to supply energy, stored sugar is depleted, and the products of alcohol metabolism inhibit the formation of glucose from other compounds such as amino acids. As a result, alcohol causes the brain and other body tissue to be deprived of glucose needed for energy and function.
Although alcohol is an energy source, how the body processes and uses the energy from alcohol is more complex than can be explained by a simple calorie-conversion value. For example, alcohol provides an average of 20 per cent of the calories in the diet of the upper third of drinking Americans, and we might expect many drinkers who consume such amounts to be obese. Instead, national data indicate that, despite higher caloric intake, drinkers are no more obese than non-drinkers. Also, when alcohol is substituted for carbohydrates, calorie for calorie, subjects tend to lose weight, indicating that they derive less energy from alcohol than from food.
The mechanisms accounting for the apparent inefficiency in converting alcohol to energy are complex and incompletely understood, but several mechanisms have been proposed. For example, chronic drinking triggers an inefficient system of alcohol metabolism, the microsomal ethanol-oxidising system (MEOS). Much of the energy from MEOS-driven alcohol metabolism is lost as heat rather than used to supply the body with energy.
Cell structure and function
Because cells are made mostly of protein, a diet with enough protein in it is important for maintaining cell structure, especially if cells are being damaged. Research indicates that alcohol affects protein nutrition by causing impaired digestion of proteins to amino acids, impaired processing of amino acids by the small intestine and liver, impaired synthesis of proteins from amino acids, and impaired protein secretion by the liver.
Nutrients are essential for proper body function; proteins, vitamins, and minerals provide the tools that the body needs to perform properly. Alcohol can disrupt body function by causing nutrient deficiencies and by usurping the machinery needed to metabolise nutrients.
Vitamins and minerals
Vitamins are essential to maintaining growth and normal metabolism because they regulate many physiological processes. Chronic heavy drinking is associated with deficiencies in many vitamins because of decreased food ingestion and, in some cases, impaired absorption, metabolism and utilisation. For example, alcohol inhibits fat absorption and thereby impairs absorption of the vitamins A, E, and D, which are normally absorbed along with dietary fats. Vitamin A deficiency can be associated with night blindness, and vitamin D deficiency is associated with softening of the bones.
Vitamins A, C, D, E, K, and the B vitamins, also deficient in some alcoholics, are all involved in wound healing and cell maintenance. In particular, because vitamin K is necessary for blood clotting, deficiencies of that vitamin can cause delayed clotting and result in excess bleeding. Deficiencies of other vitamins involved in brain function can cause severe neurological damage.
Deficiencies of minerals such as calcium, magnesium, iron and zinc are common in alcoholics, although alcohol itself does not seem to affect the absorption of these minerals. Rather, deficiencies seem to occur secondary to other alcohol-related problems: decreased calcium absorption due to fat malabsorption; magnesium deficiency due to decreased intake, increased urinary excretion, vomiting, and diarrhoea; iron deficiency related to gastrointestinal bleeding; and zinc malabsorption or losses related to other nutrient deficiencies. Mineral deficiencies can cause a variety of medical consequences from calcium-related bone disease to zinc-related night blindness and skin lesions.