Alcohol – who doesn’t drink it. A name day toast, a glass of champagne on New Year’s Eve or a cold beer on a hot day 🙂 But do you know what it may be like? Our body treats the elimination of alcohol as a fight against an enemy, and alcohol also acts as an insidious opponent in this process. The most important goal for him is to neutralize the command center – our brain. After the first drink, the worries disappear and we feel nice and pleasant, but after the next drink we experience difficulties in walking, blurred vision, slurred speech, slower reaction time. All of these symptoms are caused by a disturbance in the activity of neurotransmitters such as GABA, glutamate, serotonin and dopamine.
Alcohol has been consumed by people practically since the dawn of time, fulfilling various functions. Initially, it served as a pain and fatigue reliever. Later it was used for relaxation purposes and finally became a contact aid. Perhaps surprisingly, alcohol kills more people than all other drugs (excluding nicotine) combined. Among the narcotic drugs, it’s our biggest killer.
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Alcohol Versus The Body
Ethanol (C2H5OH) is the basic ingredient of any drink. In the digestive tract, alcohol passes through the stomach walls and small intestine into the bloodstream. Carried with blood, it reaches numerous organs and tissues. A small part of it leaves the body in the form in which it got there (about 2% is excreted in the urine, 2% in the exhaled air). The liver is the main organ in the body to break down alcohol, although it does so very slowly (it takes about an hour to break down each unit of an alcoholic drink). A small amount of alcohol is metabolized in the stomach with the participation of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH).
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The biochemical processing of ethyl alcohol in hepatic cells is very complex. Metabolic changes occur through two pathways involving three enzymes located in different cell structures.
The First Trail Consists Of Two Stages:
The first, catalyzed by alcohol dehydrogenase (ADH), takes place in the cytoplasm:
ethanol + NAD + -> acetaldehyde + NADH + H +
The second, catalyzed by aldehyde dehydrogenase (ALDH), takes place in the mitochondrion:
acetaldehyde + NAD + + H2O -> acetate + NADH + H +
The second pathway is the Microsomal Ethanol-Oxidizing System (MEOS) located in the endoplasmic reticulum.
The main product of alcohol oxidation is acetaldehyde. It shows 10 times higher toxicity than ethanol. It is a very reactive compound, forming covalent bonds with many important functional groups of proteins, as a result of which their basic functions are damaged. Acetic acid is formed from oxidized acetaldehyde, which when released into the bloodstream, is broken down into CO2 and H2O.
Why Is Alcohol Considered A Depressant?
The answer is simple: it affects two key neurotransmitters – GABA (gamma-aminobutyric acid) and glutamate, reducing overall levels of brain activity.
GABA is the major inhibitory neurotransmitter in the brain. It can bind to two receptors, GABAA and GABAB. The binding of GABA to the GABAA receptor causes the opening of ion channels for chloride ions, causing hyperpolarisation of the cell membrane, extinction of action potentials and a reduction in the influx of calcium ions into the cell. It is this receptor that alcohol interacts with to increase the GABA effect. As a consequence, more chloride ions pass into the cell. However, this is not a general mechanism, as it only happens when you take a large dose of alcohol at a time.
On the other hand, in chronic alcohol users, both GABA and alcohol have a lower effect on GABAA receptors. As a result, less Cl- ions flows in and neurons are more activated, which can be the basis of anxiety and convulsions in people addicted to alcohol and hunger. GABAA receptors are widely present throughout the brain, but many have been found, for example, in the hippocampus, which is a part of the brain important for remembering and cognition.