why is ethanol the only drinkable alcohol?

ShawnD

People can drink ethanol and not have a problem, but other alcohols like methanol and propanol are very poisonous; why is that?

Monique

Ethanol is a poison too, why do you think you get drunk?

Monique

OK, more about the metabolism:

The problem with methanol is that the body tries to break it down in the same way as ethanol is broken down. Unfortunately, in the case of methanol, the metabolic byproducts are highly toxic.

Methanol is metabolised first to formaldehyde, then to formic acid.
(Assuming the methanol isn't first secreted in urine or exhaled in the breath.) After large doses of methanol, the formic acid can build up to toxic levels.

http://www.mnpoison.org/index.asp?pageID=145

Monique

Interesting, when you come to an emergency room with ethyl glycol or methanol poisoning, they will probably give you a dose of ethanol: it competes with the receptor sites and thus prevents more damage from the (intermediate) metabolites..

suyver

I think the longer-chain alcohols (> decanol) are non-toxic to humans too, aren't they? Of course, they are also solid at room temperature so you won't mix a drink out of them...

Monique

Everything is toxic, at the most they might be less toxic.

How about that Russian, not too long ago, who won a contest of drinking wodka and received the trophee: a bottle of wodka. Unfortunately he was unable to enjoy it since he dropped down dead.

suyver

Well... du'h! [:D] (i.e.: so is water)

But, that's cheating your way out of answering my question, and I am not letting you off that quick! If I remember correctly from my studies (shady Dutch university [;)] ) then the long-chain alcohols are not toxic, at least to the same degree that ethanol is non-toxic. And the longer the chain, the lower the toxicity. I think that some of these long-chain alcohols (for example hexadecanol) are also used in cosmetics.

Correct, or not?

adrenaline

Monique is right in alluding to the fact that ethanol is just as much a toxin, just a slower killer than drinking outright propanol or methanol.

Ethanol is the preferred fuel for the liver,so let's look at what it does to this organ specificaly. Thus, ethanol displaces other substrates when present. Metabolism leads to the elimination of ethanol at the risk of toxicity. A variable proportion of ethanol undergoes first-pass metabolism mainly by the gastric isoenzymes of alcohol dehydrogenase (ADH).
Ethanol metabolism involves oxidative and non-oxidative pathways. In the first step of oxidation, ethanol is converted to acetaldehydeAlcohol dehydrogenase is the major enzyme. The microsomal ethanol-oxidizing system (MEOS) involves several cytochrome P450 isoenzymes, of which cytochrome P450 2E1 (CYP2E1) is the major constituent. Expression of CYP2E1 is increased by chronic ethanol consumption and this is thought to account for increased hepatic ethanol oxidation observed in this setting. This pathway generates reactive oxygen species (ROS) that contribute to tissue injury. A peroxisomal system involving catalase is capable of substantial ethanol oxidation, but its activity in vivo is limited by the availability of the cofactor H2O2. The products of these enzyme systems are all thought to contribute significantly to liver injury. Non-oxidative ethanol metabolism involves formation of fatty acid ethyl esters (FAEE) from free fatty acids and ethanol. The potential for FAEE to contribute to liver injury has received little attention.

Of course there seems to be a genetic predisposition for the liver injury and thus, this is not just an affliction of alcoholics or those who imbibe excessively.


Genetically determined polymorphisms of acetaldehyde dehydrogenase (ALDH) with low enzyme activity may lead to accumulation of higher levels of acetaldehyde that promote liver injury. Japanese persons withALDH2 deficiency are susceptible to liver diseas. In Caucasians populations, the ALDH polymorphisms found to date are uncommon and do not explain individual variations in ALDH activity or susceptibility to ALD. Levels of acetaldehyde in blood and liver tissue are increased in patients with ALD This has been attributed to mitochondrial damage, which is an early feature of ALD. Mitochondrial reoxidation of the cofactor nicotine adenine dinucleotide (NADH) to NAD+ is reduced, leading to impaired acetaldehyde elimination.

Any hoo, just my two cents worth.

Monique

I knew a Japanese person with ALDH (or just ADH?) deficiency. He would flush when drinking half a bottle of beer and feel the effects for hours :P

nautica

That would make for a cheap date

nautica