Thread: Some of the Science Behind LG Sciences MMV2!!

A few folks on this forum asked, and for those who care to know...we at LG Sciences, wanted to deliver, this comes to me passed down from the 'higher up's in the LG Science hiearchy, so here you go:

Why it works:

What used to disable the old prohormones is the same system we use to ACTIVATE our ANDROSTANES.

It’s not the liver that causes the issues it’s the “gut” or intestinal systems! To quote a study “Our findings suggest that the gut, rather than the liver, is responsible for the failure of oral testosterone to provide effective androgen replacement therapy.”

Oral Stanolone (illegal active steroid) + Gut Enzymes (17bHSD) = Androstanedione (inactive prohormone) + Liver/Muscle Enzymes (3bHSD) = Androsterone (inactive prohormone)

Oral Androstanedione (illegal inactive prohormone) + Gut Enzymes (17bHSD) = Stanolone (active steroid) + Liver/Muscle Enzymes (3bHSD) = Androstanediol (inactive prohormone)

Oral Androstanediol (illegal inactive prohormone) + Gut Enzymes (17bHSD) = Androsterone (inactive prohormone) + Liver/Muscle Enzymes (3a/3bHSD) = Androstanedione (inactive prohormone)

So, you can see that with the prohormones of old, you get INACTIVE hormones in the muscle no matter what path you take, EXCEPT for Methyl Masterdrol V2’s Androstane ester:

Methyl Masterdrol V2 Androstane Ester (DSHEA compliant prohormone) + Gut Enzymes (17bHSD) = Androstanediol (prohormone) + Liver/Muscle Enzymes (3a/3bHSD) = Stanolone (ACTIVE STEROID)

Better conversion is due to taking advantage of the body's enzymes instead of working against them. As I stated in my Masterdrol write up, the gut is the primary deactivation site for 17b-OH steroids. Using a dione would be preferable, if it stopped there but there is also a fair amount of 3bHSD in the liver/muscle/blood so you end up with Androstane-3a/b-ol, 17-one the opposite of what you want. This is a theory but we are getting good results with Androsterone, equally as good as any Androstane prohormone that I can tell (3-alpha, 5aa etc...)

I stick heavily by my postion and I have tons of information supporting my arguement and theory. Including the papers showing 17bHSD in the gut and the studies showing titrated diols and dione conversions that show pretty conclusively that 3-HSD's are expressed somewhere outside the gut, but certainly occuring in the blood somehow... You may win debates, but Seth was a very competent pharmacologist, I miss his knowledge quite a bit. He thought my theory had merit, but he tended to agree with you that the diols had the best efficacy yet admitted that the theory I have is possible and has merit. I agree that 3a-HSD seems to be uni-directional but there are not many studies that show the effect of high doses of 3a hydroxyls that could potentially reverse the enzyme. You have to admit that all the HSD enzymes I know of are bi-directional. For example Methyl 5aA seemed to have much better activity than Methyl DHT...so it seems entirely possible that 3a-HSD is bi-directional as well.

Testosterone metabolism by the rat gastrointestinal tract, in vitro and in vivo.

We have shown previously that the capacity of the jejunal mucosa to oxidise testosterone to the weaker androgen, androstenedione, by the enzyme 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD), is considerable. The present study extends these earlier observations by measuring 17 beta-HSD activity in different regions of the gastrointestinal tract, by investigating the potential for testosterone metabolism by slices and everted sacs of rat jejunum, and estimating the contribution of intestinal testosterone metabolites to circulating levels of plasma androgens, by portal vein sampling in the rat, in vivo. 17 beta-HSD activity in homogenates of gastric and duodenal mucosa was significantly higher than that in jejunum, and was also present in ileum and colon. In addition to androstenedione, slices and everted sacs of rat jejunum produced various metabolites, one of which was probably dihydrotestosterone. It was not, however, a major metabolite in vivo. It is suggested that 5 alpha-reduction may be favoured in vitro by a lower oxidation-reduction potential resulting from tissue anoxia. The major portal vein metabolite was androstenedione, the same major metabolite produced by mucosal homogenates. We conclude that oxidation of testosterone is the major metabolic pathway in intestinal mucosa and the capacity of the gastrointestinal tract to reduce the potency of testosterone is considerable. Our findings suggest that the gut, rather than the liver, is responsible for the failure of oral testosterone to provide effective androgen replacement therapy. The qualitative difference in testosterone metabolism between in vitro and in vivo preparations emphasises the need for caution in the interpretation of similar in vitro experiments.


*****Nothing claimed above, is medical advise

Great stuff looking forward to it.