The aftermath of alcohol misuse: Linking cellular damage, suboptimal micronutrient nutrition, and organ dysfunction

Alcohol consumption has broad consequences at the cellular level, affecting a wide variety of biochemical pathways and cellular functions. Examples include compromising cell membrane integrity, disrupting normal signal transduction, altering gene expression, impairing mitochondrial function, exacerbating oxidative stress, diminishing energy production, and triggering cell death through apoptosis. Prolonged chronic alcohol exposure induces significant oxidative stress, resulting in lipid peroxidation, damage to essential cellular components, and depletion of antioxidant capacity. Many of these processes require vitamins and minerals, which are essential for regulating the aforementioned biochemical pathways and cellular functions. Most people's diets contain at least one or more vitamins and/or minerals in amounts that are inadequate (suboptimal) for the robust functioning of these pathways, further exacerbating alcohol's effect. Additionally, alcohol, when consumed chronically in extreme amounts, can damage the mucosal lining of the small intestine, reducing its capacity to absorb vitamins and minerals, further contributing to a suboptimal nutritional state. Both impaired nutrient absorption and suboptimal nutrient intake exacerbate the declining cellular homeostasis caused by alcohol, contributing to the development of alcohol-associated chronic conditions including, but not limited to liver disease, neurodegeneration, cardiovascular disorders, and metabolic syndromes. Therefore, this review aims to summarize our current understanding of the direct cellular effects of alcohol consumption in conjunction with suboptimal micronutrient nutrition, with a special emphasis on its cellular metabolic consequences. These insights will lead to a better appreciation of alcohol's aftermath on cellular physiology and metabolism.