Ethanol metabolism

The majority of ethanol (alcohol and its impact on the body) is metabolized in the liver, with 90% of it being converted by the enzyme ADH. This process (Ethanol metabolism) occurs at a rate of about 0.25 ounces per hour. The remaining 10% is excreted through various bodily fluids. The liver’s ability to metabolize ethanol does not increase with higher levels of ethanol in the bloodstream, which results in a rise in blood alcohol content (BAC) and increased intoxication. Ethanol metabolism by ADH forms acetaldehyde, which is toxic and immediately metabolized by the enzyme ALDH2 into acetate.

Acetate produced by the metabolism of ethanol is converted into acetyl-CoA, which then participates in the Krebs cycle, leading to its breakdown into CO2 and H2O, through the electron transport chain. The majority of this non-toxic acetate is taken up by cells in the brain, skeletal and cardiac muscles.

Metabolism of Ethanol
How Is Alcohol Metabolized by the Body.
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Nutrition Coach.

Efforts to lose body fat and alcohol

Consuming alcohol frequently can impede efforts to lose body fat. Alcohol metabolism provides an abundant source of acetyl-CoA, reducing the need for the body to use its own stored fat. Additionally, excess calories from carbohydrates and fats consumed with alcohol are stored as fat, creating a double obstacle to managing optimal body composition.
  • Acetaldehyde
    The toxic product of ethanol metabolism is acetaldehyde, which must be quickly metabolized to prevent its toxic effects.
  • Acetaldehyde Dehydrogenase
    Acetaldehyde is primarily metabolized by the enzyme Aldehyde Dehydrogenase (ALDH).

There is another way for ethanol to be metabolized, in addition to the ADH pathway in the liver. This is the microsomal ethanol-oxidizing system (MEOS), which takes place in liver microsomes. It is activated when the ADH pathway becomes saturated, such as when large amounts of alcohol are consumed or when an individual is a heavy drinker. The MEOS also leads to the formation of acetaldehyde, which is then converted to acetate. However, unlike the ADH reaction, the MEOS oxidizes NADPH and changes the energy coupling of ethanol oxidation, leading to heat production.



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This production of ATP from ethanol oxidation is relatively low compared to other macronutrients, such as glucose, and is, therefore, not a significant source of energy for the body. Rather, ethanol oxidation is seen as a way to dispose of the toxic acetaldehyde produced in ethanol metabolism. The end result of both the ADH and MEOS pathways is the production of acetate, which can be used as an energy source, but the net effect on energy balance is negative due to the decreased utilization of other macronutrients.

This results in a build-up of NADH and a decrease in the NAD+/NADH ratio within the cytosol, disrupting cellular respiration and leading to the generation of reactive oxygen species (ROS). This is one of the mechanisms by which ethanol leads to cellular damage and liver injury. Additionally, as the liver tries to maintain the NAD+/NADH ratio, it may divert resources from other metabolic processes, leading to impaired detoxification of other toxic substances and decreased overall liver function.

The liver's primary method of metabolizing ethanol is through the alcohol dehydrogenase (ADH) pathway, which is responsible for up to 90% of ethanol metabolism. The microsomal ethanol-oxidizing system (MEOS) and the catalase pathway contribute to a lesser extent.

The elevated NADH levels also interfere with the oxidation of fatty acids, leading to the accumulation of fat in the liver, a condition known as fatty liver, which can progress to more serious liver conditions such as steatohepatitis (alcoholic hepatitis) and cirrhosis.

Additionally, the increased NADH also leads to decreased ATP production and oxidative phosphorylation, which can result in cellular dysfunction and injury, leading to liver damage and disease. Ethanol consumption should be limited and monitored to prevent these harmful effects on the liver and overall health.

Individuals with a deficiency in the acetaldehyde dehydrogenase enzyme experience an accumulation of acetaldehyde and may experience side effects such as skin flushing, nausea, and an increased risk of esophageal cancer.