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**dinoiii** · 12-10-2007, 07:23 PM

Alcohol + C17 alkylated PH/PS/AAS

C17-alkylated prohormones reach a peak plasma level within several hours, and the exogenous product is slowly cleared with a plasma half-life of 20-40 hours (dependent on the various PH’s mentioned in this thread above). In plasma, many become bound to an alpha 1-acid glycoprotein which contributes to the long half life.

Now, it is not the PH per se but the metabolites, usually of either the mono- or di-demethylated products (which are thought to be the active components) formed via cytochrome P450 (CYP) 3A4-catalyzed reactions, and to a lesser extent hydroxylated compounds. The drug undergoes continued hepatic metabolism, now 2nd pass (1st pass was the CYP transformation) and enterohepatic circulation to be excreted in the feces (predominantly).

With this by-product formation, free-radical products offer some local detriment to the liver in the meantime - voila … your hepatotoxic effect. In addition to this, due to the prolongation (ie. - recall our PH half-lives), it makes an interaction with other pharmaceuticals very likely. Fortunately, alcohol is metabolized primarily by the CYP2E1 enzyme and NOT 3A4. This doesn’t mean you are free and clear….the hepatotoxic effects of alcohol remain and in addition to the radical damaging effects of the above could prove significant enough to warrant true concern.

The effects of alcohol on the liver are DOSE-related and primarily of fatty infiltrative, inflammatory (hepatitis), and cirrhotic (fibrotic, necrotic) in nature. It only takes relatively small amounts of alcohol to induce a fatty-change from inhibition of both the tricarboxyllic acid cycle and oxidation of fat (coupled to PH actions), in part owing to the generation of excess NADH produced by the actions of ADH and ALDH. After this, inflammation/necrosis/cirrhosis will likely set in. Now, this is sometimes irreversible fat accumulation, but most often dead hepatocytes (liver cells) can regenerate - we just hope to NOT overwhelm them in loss. It may, therefore come down to yet again a USE VERSUS ABUSE argument.

Summary: I advise against concurrent use of these items. Now you have the science of why.

D_

jomi822 · 12-10-2007, 09:42 PM

awesome man, ill be linking this to the next suicidal teenage wanting to run a cycle of m-drol with "a couple beers" here and there.

Right Hook · 12-10-2007, 09:44 PM

No more on cycle Yaga bombz...

thesinner · 12-10-2007, 10:36 PM

Acetaldehyde: it's radical. :D

There appears to be a correlation between androgenic effect and "kills yer liver" effect. (Methyltren > Methyltest > methylbold) Is this a coincidence, or is there something behind that?

thesinner · 12-11-2007, 09:32 PM

I was reading Fogler's 4th Ed. Chemical Reaction Engineering today, and came across an interesting problem regarding to enzyme inhibition.

Methanol -(ADH)-> Formaldehyde -> Formic acid (Formate) which causes Blindness.

When a person ingests a toxic amount of methanol, they are given an IV of ethanol as a means to inhibit ADH from converting Methanol to Formaldehyde.

Thought that was interesting.

**growstrong** · 12-11-2007, 10:19 PM

This is great info... even though we dont like to admit, Sampson's thread illustrates how we all like to party

**Sampson** · 12-12-2007, 02:17 AM

as long as its done in a safe manner there shouldn't be a problem. however, Doc, what are your thoughts about drinking during PCT? Better? Worse?

Voodoo · 12-12-2007, 05:13 AM

Quote:

Originally Posted by dinoiii

Alcohol + C17 alkylated PH/PS/AAS

C17-alkylated prohormones reach a peak plasma level within several hours, and the exogenous product is slowly cleared with a plasma half-life of 20-40 hours (dependent on the various PH’s mentioned in this thread above). In plasma, many become bound to an alpha 1-acid glycoprotein which contributes to the long half life.

Now, it is not the PH per se but the metabolites, usually of either the mono- or di-demethylated products (which are thought to be the active components) formed via cytochrome P450 (CYP) 3A4-catalyzed reactions, and to a lesser extent hydroxylated compounds. The drug undergoes continued hepatic metabolism, now 2nd pass (1st pass was the CYP transformation) and enterohepatic circulation to be excreted in the feces (predominantly).

With this by-product formation, free-radical products offer some local detriment to the liver in the meantime - voila … your hepatotoxic effect. In addition to this, due to the prolongation (ie. - recall our PH half-lives), it makes an interaction with other pharmaceuticals very likely. Fortunately, alcohol is metabolized primarily by the CYP2E1 enzyme and NOT 3A4. This doesn’t mean you are free and clear….the hepatotoxic effects of alcohol remain and in addition to the radical damaging effects of the above could prove significant enough to warrant true concern.

The effects of alcohol on the liver are DOSE-related and primarily of fatty infiltrative, inflammatory (hepatitis), and cirrhotic (fibrotic, necrotic) in nature. It only takes relatively small amounts of alcohol to induce a fatty-change from inhibition of both the tricarboxyllic acid cycle and oxidation of fat (coupled to PH actions), in part owing to the generation of excess NADH produced by the actions of ADH and ALDH. After this, inflammation/necrosis/cirrhosis will likely set in. Now, this is sometimes irreversible fat accumulation, but most often dead hepatocytes (liver cells) can regenerate - we just hope to NOT overwhelm them in loss. It may, therefore come down to yet again a USE VERSUS ABUSE argument.

Summary: I advise against concurrent use of these items. Now you have the science of why.

D_

you know dana "dont do it cause its stupidly bad" would have been a fine post under that big bold heading.