damn it, cant find a topic i was posting on a few days ago, was about staking meythl dien and m1t!

anyway the point i was making on it was that staking the two wouldnt be that bad, given that the liver tox is directly related to the amount of meythlated substance in mg! so bosing methyl dien at 2-3mg per day for say 4-weeks, then adding 5-10mgs per day for 1-2 weeks for a kick at the end would be ok as you would only be taking in 7-13mg per day! compare this to m1,4ad which is doesed at 30mg per day and you see where im coming from!

also in relation to illegal substances, they are in the 40mg + per day without any severe side effects. (although im not condoning there use)

Im saying all this with the given that if someone is using a methylated substance they would not be taking any other liver toxic substance, like alcohol or other medications, and also be using some sort of pro-liver supplement!

look forward to your replies.

That arguement is stupid, you cannot compare them on a mg to mg basis as they are not the same.

The reason why you take more m1,4ad is because its not as strong or as toxic as either m1t or mdione.

From the sounds of it you have already made up your mind that stacking methylls is for you, why take the risk for what would be a marginal difference in the gains?

no, i have not decided to take any methylated subsyance, staked or not, it was just for discusions sake and in relation to a prior post that i could not find again, which was stated in the origonal post!

and would you like to elaborate as to why you cannot compare them on a miligram basis as this is the toxic part, the methylated active compound, in milligrams!

let me elaborate, if you are taking 30-40mg of a methylated substance, then your liver is having to process that 30-40mg of substance, where as if you are only taking 10-15mg of methylated substance, then your liver is only processing 50% less methylated substance! simple maths, and as stated the toxisity is related to how much, in mg terms, that you make your liver process. perhaps what you are thinking that the other, non liver related side effects related especially with M1t, would be the decicing factor in not staking the Methyls, such as cramping, water retention and high blood preasure, and i would agree, but as the point was actualy about liver toxicity, then its a moot point!

If you, or anyone else has an actual valid reason for disagreeing, other than 'thats stupid' then i would love to hear them, prove me wrong, it was as much of a question as it was a statement, thats why i asked for replies, so any well thought replies are still welcome, adn lets try and stay away from insults as an arguement, cause'my dads bigger than yours'!

The toxicity is not related on how many miligrams you are taking it is related to the strength of the compound.

Just because mdione, m1t & m1,4add and any other methyll compound you can think of share the "Methyll" tag does make them the same - as far as im aware (i apologise if im wrong) it is not the "methyll" that make the compound toxic. The "Methyll" makes the compound more bioavailible when administered orally and as such makes the effects stronger.

The toxicity of each of the M compounds is related to to the compound that has been methyllated not the other way around.

E.G.

m1,4add converts into dbol. It is not the M that is toxic it is the Dbol.
m1t doesnt convert , it is not the M that is toxic it is the suped up 1 test.
m1dione converts into some bad ass steriod, its not the M thats toxic its this uber steroid.

The basis of your arguement is that it is the M causes toxicity, this is flawed. The toxicity is from the compound not the process of making it more bioavailible

You are referring to this thread:

http://forums.bulknutrition.com/?showtopic=1612

I don't see how you are making an argument, when you don't even understand how methylated steroids are toxic to the liver. Each individual methylated compound is different and will place a different amount of stress on the liver. Taking any steroid orally will place stress on the liver. It just happens that the 17aa modification tends to make a steroid much harder on the liver. It doesn't automatically render each substance equally hepatotoxic on an mg per mg basis. If your argument were true, each steroid would be equally effective on an mg per mg basis. Different steroids have different activity and toxicity profiles, it is as simple as that. And, blood tests from people taking different methylated steroids at different doses correspond with this contention. Methyl-1,4-ADD at doses higher than those of M1T does not change liver values nearly as much.

Mate, the proces of methylating it is what makes it toxic to your liver! think about it, the PH's in there normal state are not toxic, and the only difference between, say, 1-test and m1-test is the methyl bond, thats it, the only difference, so the proces of adding the methyl bond, which is to make it more orally available, is also what makes it toxic, period.

i appreciate where you are coming from, but, sorry you are wrong, it is soley the methyl atachment that makes these products toxic to your liver, the methyl group attachment means that your liver can not break them down, or metabolize them,thats its purpose, but this means that basically that when it passes through your liver, its fucking it up (if you beleive that methyls are as bad as reported, which i dont, i would be quicker to swallow a tub of m1t than i would a tub of asprin, silly comparison, but u get the idea), so my earlier statements still stand!

cheers for the reply though!

Once and for all, Methylation renders a steroid INHERENTLY hepatotoxic, regardless of its structure. Now, as Sldghmmer & I (and others) have explained many times, the actual, acute, permanent harm that comes from this hepatotoxicity is a.) overstated, b.) generally temporary, and c.) can be alleviated/mitigated with proper anti-oxidant supplementation (assuming one is not needlessly over-dosing their steroid(s) & binge-drinking constantly), so take that for what it's worth, but the fact of the matter is that a 17-alkyl substituent into the molecule @ C-17 affects how your body can metabolize the steroid (in this case it can't break it down into a 17-ketosteroid) [1]. This can also be backed up by the fact that liver-tests on subjects using 17aa-AASs showed a distinct (not dangerous, but significant) rise in sulfobromophthalein retention [2], which is a triphenylmethane that your liver secretes at a certain rate (don't know what it is), when it's functioning "properly/optimally." If your urine starts showing less sulfobromophthalein, it means your liver is holding on to more of it, and hence isn't working as efficiently-- because the 17-alkyl substituent BY ITSELF is taxing the liver and forcing it to process at a higher level/rate. Yes, different compounds themselves will have different toxicity levels once metabolized, but to think that the 17aa- isn't having an effect in and of itself is pretty much kidding yourself...


Sources Cited:

1. Levedahl, BH & Samuels, LT, J. of Biological Chem., 1950; 186, 257.

2. Kruskemper, HL, Klin. Wochschr., 1966; 44, 1127.

Very nicely stated, Loki.

Why thank you.

Loki lives to give...

Word. Now tell Bactuffguy why he shouldn't be taking M1t and giving out advice!