Why is a chronic alcoholic likely to be prone to lactic acidosis

Alcohol acidosis is a result of prolonged starvation with glycogen depletion, counter-regulatory hormone production, dehydration, and the metabolism of ethanol itself.

When the dietary intake of carbohydrates is insufficient to supply glucose for the body's needs and hepatic glycogen stores are depleted by fasting, ketones are produced in the liver as an alternative source of energy. Two steps are required for ketogenesis: (1) enhanced lipolysis with an increased delivery of free fatty acids to the liver and (2) an alteration in hepatic metabolism by which these free fatty acids are converted preferentially into ketones instead of into triglycerides. Decreased insulin activity, increased counter-regulatory hormone levels (primarily glucagon, but also cortisol, catecholamines, and growth hormone), and volume depletion all play a role in ketogenesis.

The body's response to starvation is a decrease in insulin activity and an increase in the production of counter-regulatory hormones. These counter-regulatory hormones cause the release of free fatty acids from peripheral adipose tissue. However, excess fatty acids alone are insufficient to cause ketoacidosis since, normally, the liver metabolizes free fatty acids into triglycerides. The key difference in the starvation state is in mitochondrial enzyme activity鈥攕pecifically, the rate at which carnitine acyltransferase (CAT) transports free fatty acids into the mitochondria for oxidation. CAT activity is low in the fed state and accelerated in the starvation state. Glucagon excess is believed to have the major role in this hepatic response.