How is it that alcohol affects the human body?

  • Thread starter wasteofo2
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  • #1
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Main Question or Discussion Point

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
 

Answers and Replies

  • #2
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.
 
  • #3
DocToxyn
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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.
 
  • #4
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!
 
  • #5
Monique
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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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