Everyone understands that excessive consumption of alcoholic beverages is not good for our health, despite this, most people across the world consume it. The science and mechanisms behind hangovers are actively being investigated, however, we can say with certainty that a hangover is, among other things, the result of suppression of the immune system by significant amounts of alcohol.
More than 75% of alcohol users have experienced a hangover at least once, 15% experience the problem at least once a month, and 25% of college students experience symptoms weekly (NIAAA, 2021).
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Absorption of alcohol in the body
The state of alcoholic intoxication is characterized by the fact that ethanol – the primary component of alcohol, disrupts the interaction of nerve cells with each other, although the details of the effect of alcohol at the biochemical level remain largely unclear.
Science shows that ethanol is not a stimulant for the nervous system, but a sedative. The external euphoria that accompanies the consumption of alcoholic beverages is exclusively a function of the disinhibition effect of ethanol. Due to its good solubility in both water and fats, ethanol can penetrate any cell membrane.
The first biologically active molecule for which an interaction with ethanol was discovered - the GABAA receptor protein - was discovered in 2006. When ethanol binds to this receptor, there is a significant decrease in neuronal activity. Interestingly, other sedatives, such as barbiturates and benzodiazepines, bind to the same protein receptor.
When alcohol enters our circulatory system, it causes the pituitary gland in the brain to block the production of vasopressin (also known as an antidiuretic hormone). Without this chemical, the kidneys channel water directly to the bladder rather than to the body that needs it.
Drinking about 250 ml of an alcoholic beverage results in 800 to 1,000 ml of water excreted by the body. That is, the loss of liquid in proportion to the absorbed is 4/1.
Influence under alcoholic intoxication
As with all substances with a sedative and narcotic effect, a gradual increase in the concentration of ethanol in the blood is expressed in several stages of intoxication. The first problems occur with a blood alcohol concentration of 0.3% (ppm) where coordination of movement is reduced, as well as a loss of focus and weakening of lateral vision. Concentration above 0.5% (ppm) leads to a state of relaxation of consciousness and to sensations that can be called relaxed. Ethanol concentrations above 5% are usually fatal.
Since the body immediately begins to destroy ethyl alcohol that enters the bloodstream, fatal cases of poisoning with ethyl alcohol, and not with more toxic substances found in an alcoholic surrogate, for example, methyl alcohol, occur only when a person, for some reason known only to him, drinks in one gulp a bottle of spirits.
In clinical practice, isolated cases of patients with alcohol intoxication and an ethanol content in the blood of even about 6% (ppm) were admitted to the emergency department, which they managed to pump out.
Moreover, it is curious that our enzymes are very selective. They always start with ethanol and then move on to methanol. And if you drink alcohol again 8-10 hours after drinking alcohol, the enzymes will immediately leave the "old" methanol from the previous drink alone and start for the "new" ethanol. This is the biological meaning of the habit of getting drunk.
You will really feel better for a while, as enzymes will stop poisoning you by breaking down methanol. Alas, this is one of the reasons for alcoholism.
Hangover biology: acetaldehyde
A product of alcoholic metabolism, which is more toxic than alcohol itself, acetaldehyde is formed when alcohol in the liver is broken down by an enzyme called alcohol dehydrogenase. Acetaldehyde is attacked by acetaldehyde dehydrogenase and glutathione, which consists of a large amount of cysteine.
Conversion of ethanol
In the liver, ethyl alcohol (CH3CH2OH) is oxidized to acetaldehyde (CH3CHO), which is then converted to acetic acid (CH3COOH), which is further processed in a process known as the "citric acid cycle" or the Krebs cycle, turns into carbon dioxide and water.
The maximum ethanol content in the blood is determined according to the Widmark formula proposed in 1932 in the article "Theoretical Foundations and Practical Use of the Forensic Definition of Alcohol":
С = A / (r × W) where
С alcohol concentration in ppm (‰);
A is the mass of pure ethanol, expressed in grams;
W is the mass of a person in kilograms and
r is a reduction factor (the ratio of the alcohol content in the whole body to its content in the blood), which is 0.7 for men and 0.6 for women.
After reaching the maximum, the blood alcohol content, due to reactions catalyzed by enzymes (catalytic proteins), begins to decrease linearly at a rate of 0.1 to 0.2 % per hour.
The rate of decrease in blood alcohol content depends on the activity of the catalyst protein produced by the liver cells - the enzyme-alcohol dehydrogenase and, since the performance of the liver is different for everyone, it is individual for a person. It is not possible to speed up the elimination of alcohol from the body with the help of drugs or exercise.
Continue Reading: How alcohol affects the body.
References:
- Min JA, Lee K, Ki DJ (June 2010). The application of minerals in managing alcohol hangover: a preliminary review. Current Drug Abuse Reviews.
- Stephens R, Ling J, Heffernan TM, Heather N, Jones K (January 2008). A review of the literature on the cognitive effects of alcohol hangover. Alcohol and Alcoholism
- Hori H, Fujii W, Hatanaka Y, Suwa Y (August 2003). Effects of fusel oil on animal hangover models. Alcoholism, Clinical and Experimental Research.
- Piasecki TM, Robertson BM, Epler AJ (June 2010). Hangover and risk for alcohol use disorders: existing evidence and potential mechanisms.
- National Institute on Alcohol Abuse and Alcoholism (March 2021). Available at https://www.niaaa.nih.gov/publications/brochures-and-fact-sheets/hangovers
Further Reading
Researchers explore the link between alcohol consumption and androgenetic alopecia