
Ethanol, commonly known as alcohol, is a molecule responsible for causing drunkenness. Despite its simple structure, ethanol has the ability to traverse membranes and interact with various targets in the body, leading to a wide range of effects compared to more complex molecules. To understand the mechanism behind alcohol-induced drunkenness and the variations in its effects among individuals, let us follow the journey of alcohol through the body.
After consumption, alcohol enters the stomach and is subsequently absorbed into the bloodstream through the digestive tract, particularly the small intestine. The contents of the stomach, including food, can impact the rate at which alcohol is absorbed. For instance, after a meal, the pyloric sphincter—separating the stomach from the small intestine—closes, slowing down the absorption process. As a result, the level of alcohol reaching the blood after a substantial meal may be only a quarter of what is absorbed on an empty stomach.
Once in the bloodstream, alcohol is distributed to various organs, with the liver and brain receiving the highest blood flow. Alcohol first reaches the liver, where enzymes break it down in two steps. The enzyme alcohol dehydrogenase (ADH) converts alcohol into acetaldehyde, a toxic substance. Subsequently, aldehyde dehydrogenase (ALDH) converts acetaldehyde into non-toxic acetate. The liver continuously eliminates alcohol as the blood circulates, and the initial breakdown in the liver determines the amount of alcohol reaching the brain and other organs.
The effects of alcohol on the brain are responsible for the emotional, cognitive, and behavioral changes associated with drunkenness. Alcohol enhances the activity of the neurotransmitter gamma-aminobutyric acid (GABA), which acts as the brain's primary inhibitory signal, while reducing the activity of glutamate, the brain's primary excitatory neurotransmitter. This dampens neuronal communication, resulting in feelings of relaxation at moderate doses, drowsiness at higher doses, and potential impairment of vital brain functions at toxic doses.

Alcohol also stimulates a specific group of neurons that extend from the midbrain to the nucleus accumbens, a region involved in motivation. Similar to other addictive substances, alcohol triggers the release of dopamine in the nucleus accumbens, leading to a pleasurable sensation. Furthermore, alcohol can cause certain neurons to synthesize and release endorphins, which contribute to the euphoric and calming effects associated with alcohol consumption.
As the liver continues to break down alcohol at a faster rate than the brain absorbs it, the effects of drunkenness gradually fade away. However, individual differences at any stage of alcohol's journey through the body can cause people to exhibit varying degrees of intoxication. Factors such as body composition, genetics, and previous alcohol consumption play crucial roles.
For instance, even if a man and a woman of the same weight consume the same amount of alcohol during an identical meal, their blood alcohol concentrations (BACs) can differ. Women generally have a higher percentage of body fat compared to men, which requires less blood for distribution. As a result, a smaller blood volume carrying the same amount of alcohol leads to a higher concentration in women. Genetic variations in the liver's alcohol-processing enzymes can also influence BAC. Regular alcohol consumption can increase the production of these enzymes, contributing to the development of tolerance.
Moreover, genetic differences in the transmission of dopamine, GABA, and endorphins can influence an individual's risk of developing an alcohol use disorder. Those with naturally low levels of endorphins or dopamine may be more prone to self-medicate with alcohol. Some individuals have a heightened endorphin response, increasing the pleasurable effects of alcohol and raising the risk of excessive drinking. Others may have variations in GABA transmission that make them particularly sensitive to the sedative effects of alcohol, reducing their risk



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