How is it that alcohol affects the human body?

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SUMMARY

Alcohol, specifically ethanol, affects the human body by altering cell membrane permeability and elasticity, leading to impaired ion channel function in neural cells. Chronic alcohol consumption results in fatty liver conditions due to the metabolism of ethanol into acetyl-CoA, which is stored as fatty acids in the liver. The toxic metabolite acetaldehyde, along with increased oxidative stress and altered fat metabolism, contributes to various organ damage, including the liver and heart. Additionally, acetaminophen (Tylenol) exacerbates alcohol toxicity by depleting glutathione and increasing the production of the harmful metabolite NAPQI, which can lead to severe liver injury.

PREREQUISITES
  • Understanding of ethanol metabolism and its effects on the liver
  • Knowledge of cell membrane structure and function
  • Familiarity with the cytochrome P450 enzyme system, particularly CYP2E1
  • Awareness of the interactions between acetaminophen and alcohol
NEXT STEPS
  • Research the mechanisms of ethanol-induced oxidative stress and its effects on cellular health
  • Study the role of cytochrome P450 enzymes in drug metabolism
  • Examine the relationship between acetaminophen and liver toxicity in the context of alcohol consumption
  • Explore the physiological effects of acetaldehyde and its role in alcohol-related organ damage
USEFUL FOR

This discussion is beneficial for medical professionals, toxicologists, pharmacologists, and anyone interested in understanding the biochemical effects of alcohol on the human body.

wasteofo2
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What is it about 2 carbons, 5 hydrogens and a hydroxyl that causes people to become intoxicated when they drink alcohol? Also, why does alcohol have a degenerative effect on the liver, kidney, heart, brain etc.?

Thanks,
Jacob
 
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alcohol, being slightly less polar than water, will absorb into the lipid bilayer of the cell and alter it's elasticity and permeability. this results in trans-cell membrane activity being altered, particularly the ion channels of neural cells. diethylether (and other forms of surgical anaestesia - sp?) work the same way.

it causes "fatty liver" conditions because alcohol winds up getting metabolized as acetyl-CoA, and unused acetyl-CoA gets stored as fatty acids chains. this process mainly takes place in the liver, since that is where the detox (cytochrome P450 enzymes) are primarily located.

as far as how it affects the heart...i don't know, but it would be natural to assume that it damages the nerve cells in the heart for the same reason that it damages other neural cells: damage to the cell membrane.
 
The initial metabolite of alcohol is acetaldehyde, a relative of formaldehyde - not a very nice compound. This metabolite is usually cleared fairly rapidly, but chronic use/exposure would likely increase risk to exposure. Numerous other mechanisms of ethanol-induced toxicity have been proposed including increased oxidative stress, the alterations in fat metabolism that quetzalcoatl9 mentioned, etc. You can check out PubMed for a good selection of papers, just search for ethanol, rather than alcohol, it will cut down on articles with non-ethanol alcohols. Take a look at this one on ethanol, brain and HPA axis, or this one on cadiomyopathy.
 
Good points, DocToxyn.

It is also interesting that acetominaphen (aka tylenol) greatly enhances the toxicity of alcohol, since the a.m. gets converted into a _more_ toxic metabolite which happens to affect the alcohol breakdown (i forget exactly how). This is relevant because what does someone do when they have a hangover? Many people are admitted to the hospitals for this very common problem...getting extremely drunk one night, and then taking a dosage of somewhere around 1500 mg of a.m. can be fatal!
 
quetzalcoatl9 said:
It is also interesting that acetominaphen (aka tylenol) greatly enhances the toxicity of alcohol, since the a.m. gets converted into a _more_ toxic metabolite which happens to affect the alcohol breakdown (i forget exactly how).
It is alcohol that enhances the toxicity of acetaminophen ;)

About 95% of acetaminophen gets conjugated by glucuronide and sulfate routes in the liver, 5% is metabolized by the hepatic oxidase enzymes (CYP2E1). The oxidation yields the reactive electrophilic metabolite NAPQI, which is toxic to the liver. Normally the small amount of NAPQI is detoxified by conjugation with glutathione, at high doses the glutathione stores are depleted: leading to liver injury.

Alcohol competes with acetaminophen for interaction with the oxidase enzyme, inducing it, and it competes with the glutathione, depleting it, leading to an overproduction of the acetaminophen metabolite NAPQI.

This is relevant because what does someone do when they have a hangover? Many people are admitted to the hospitals for this very common problem...getting extremely drunk one night, and then taking a dosage of somewhere around 1500 mg of a.m. can be fatal!
True, the risk of liver damage is high.
 

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