posted on Apr, 4 2006 @ 11:36 PM
My pharmacology friends and I call alcohol the pharmacological hand grenade.
To get much of this data, I restate much of Robert Julien's "A Primer for Drug Action" tenth edition.
Before I get labeled as a modern day prohibitionist, I will state that I am 23 and I do drink, but not often and never excessively. The last time I
drank was in November and I only had two beers at the time.
First off, recreational alcohol is actually ethyl alcohol (ethanol). To understand its effects, we have to look at this compound and its actions as
we would a drug.
One of the issues with alcohol is that it acts sloppily by being absorbed by many different parts of the body (which also adds to the fun of it). It
is rapidly absorbed throughout the entire GI tract. The first part of absorbtion can occur within 20 minutes of consumption and absorbtion can
continue from the intestines up to 80 minutes later.
Roughly 95% of consumed alcohol is absorbed by the body. Women absorb more than men. The extra 5% and the difference in sex is due to differences in
the presense of alcohol dehydrogrenase, the enzyme that breaks down alcohol. When we discuss tolerance for alcohol, we refer to the presense of this
enzyme. Many people brag that they can drink others under the table due to increased tolderance. This is mostly false. One can produce increased
levels of the enzyme, but it does not have that much of an effect in the large scheme of things. What is primarily changed is the psychological way
these people have gotten used to being drunk. Physiologically very little difference in the presense of enzyme exists between someone who rarely
drinks and those who consume a 6-pack daily. Habitual drinkers may slightly lower their absorbtion to 93% due to increased enzyme.
The 90%+ that remains in the body that is absorbed goes many places.
In my personal experience in working with neurons, I have had to do controls for many drug studies (which are sometimes suspended in alcohol)
To control for the suspension a neuron + alcohol cell line is always used. Apply a small concentration of alcohol in the neuron media and the neurons
die - regardless of the concentration in the media (when compared to the pure control)
But what is it doing?
Alcohol is a major inhibitor of NMDA Glutamate (excitatory neurotransmitter) receptors. It also causes an increase in chloride ions at GABA receptors
causing neuronal inhibition. At the same time it activates the reward pathway due to activation of opioid receptors. Finally, it also disrupts the
Serotonin pathways (serotonin is a derivative of tryptophan - like the turkey at thanksgiving that makes you sleepy, alcohol dirupts the sleep cycle
in a similar way)
All in all the first neurons to die are those associated with higher processing
(see wiki on Korsakoff's syndrome). This data goes hand in hand with the teratogenic effects. When a pregnant mother consumes alcohol, the fetus
develops FAS and higher skills are impared.
As neurons die, their neighbors, the ones they form synapse with continue to look for the synapses (connections they once had). This process is known
as plasticity and is linked to hallucinations, motor aggistations, confusion, disorientation and the delirium tremens (DTs). 30-50% of alcoholics
meet criteria for major depression due to such physiological changes.
In addition to the above stated, alcohol is also linked to a promoter of cancer , pancreatitis, liver damage and chronic gastritis. Alcohol is also
metabolized into acetaldehyde and free radicals which do their own damage to cells.
Alcohol is an anticonvulsant (but not clinically used)
In light to moderate doses, it has shown to lessen risk of stroke. (perhaps since there are fewer neurons to dose)
There's a lot more, but I'll save that for later posts since it is getting rather late here.