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The condition described is characterized by decreased glycogen stores and impaired gluconeogenesis as a result of excess alcohol consumption. In alcohol use disorder, ethanol metabolism alters the liver's normal metabolic functions.

Ethanol is predominantly metabolized in the liver, which leads to the accumulation of reduced cofactors such as NADH. This shift in the redox state disrupts various metabolic pathways, particularly gluconeogenesis—the process by which glucose is produced from non-carbohydrate sources. The accumulation of NADH promotes the conversion of pyruvate into lactate, creating lactic acidosis, and results in decreased availability of substrates necessary for gluconeogenesis.

Additionally, excessive alcohol intake leads to glycogen depletion because the liver prioritizes ethanol metabolism over glycogenolysis and gluconeogenesis. As glycogen stores are depleted and gluconeogenesis is impaired, individuals can experience hypoglycemia, especially during fasting states or when they do not consume enough carbohydrates to meet their energy needs.

This metabolic state can be particularly concerning in a fasting individual who consumes alcohol, as their body’s ability to maintain blood glucose levels through glucose production is compromised. Consequently, fasting hypoglycemia can occur in the context of excessive ethanol consumption due to both depleted glycogen stores and inhibited