Lyle McDonald's response to my theory on usenet

Posted by: jboldman

Got my I3C in and DIM and looking forward to giving that a try. was that all your idea wale or was it Dr. Nicks? I can not believe that i have missedout on that research all these years.

jb

DHT also plays a key role in this process, as it shifts the estrogenic balance away from estrone and toward estradiol, which is to our benefit.

Part of DIM/I3C effects on estrone comes from the fact that they deactivate androstenedione, making less direct substrate for estrone formation. But I for one am curious as to what we may or may not achieve with an actual 17aHSD blocker. That would not only reduce andro/estrone but it would also increase test/DHT/estradiol since it was never converted in the first place, and keeping the enzyme blocked may lead to upregulation, which would be to our advantage during recovery.

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Got my I3C in and DIM and looking forward to giving that a try. was that all your idea wale or was it Dr. Nicks? I can not believe that i have missedout on that research all these years.

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Dr. Nick is the first to introduce me to this idea. We discussed it over dinner following an A4M sponsored medical conference I spoke at a few weeks ago. We got quite excited about the idea, and continued on with it over the evening, across night club after night club (man, WE sure do know how to party, eh?). That is why we decided to try it out on a selected handful of my TRT patients.

Here's something you might get excited to hear: the FIRST guy to try it out, a doctor with a steroid history and longstanding hard gyno nodules, reported to me that same had ENTIRELY disappeared within two weeks of getting on the EstroBlock product. Granted, this single case has absolutely no validity from a scientific proof standpoint, but it sure did raise our eyebrows!

Hey, that was the first time 'Ol Doc tried to do a "quote" in a reply. Thanks, Miggy.

Now, how do I get the "originally posted by..." in there?

great news. keep us posted. thanx

Posted by: jboldman

The clear answer to all these questions is that we will probably never know beyond conjecture since tren is a steroid used exclusively in animals except for the few studies done to see the effets of animal by products getting into the food chain. Therre are 304 abstracts reported on medline and i have read every one of them and still have many unanswered questions.

jb

And there lies the inherent problem.

I have blood test dating back a good 2 1/2 years regarding Tren use.

I had everything done AST, ALT, GGT, Thyroid Panel etc...

I have also read all the abstracts concerning Trenbolone(And others), have talked a veritable panoply of athletes who use Tren, and thats where i get my conclusions from.

The only thing I never measured while on Tren is cortisol levels.(I never really saw the relevance for this).

Trenbolone can either:

a) Antagonize cortisol at the receptor sites(Same analogy to http://search.store.yahoo.com/cgi-bin/nsearch?catalog=yhst-20189112917352&query=tamoxifen&.autodone=http%3A%2F%2Fwww.cemproducts.com%2Fnsearch.htm l" target="_blank" rel="noopener">tamoxifen antagonizing estrogen at its receptor sites)

b) Reduce Cortisol levels by some means(I have no idea but lets hypothesize)

If its a)

- Cortisol levels will most likely be elevated above normal in a weight-lifitng athlete.

If its b)

- Cortisol levels will be reduced below threshold levels.

The we hit upon other problems.

If its b).....then how are Trenbolone's fat burning properties explained? You need cortisol to initiate FFA breakdown. In fact ECA stacks raise cortisol levels.

Fonz

Not to point out the painfully obvious, yet again, but the same would hold true for a).

And fact is it doesnt hold true for either. Cortisol is neither the end all or be all of fatburning, nor is it an absolute necessity. Secondly you need to remember that a reduction in corticosteroid activity is not a total inhibition of corticosteroid activity.

If receptors were totally blocked, or if cortisol release was completely inhibited, a host of problems would arise, and if that was the case I'm sure more tren users would have complained.

There is a variety of ways to explain tren's fat-reducing ability, independent of cortisol. I might also want to stress that tren's active fat-reducing ability is not that great at all, most studies referred to it as insignificant. Perhaps no more than other steroids, in which case the only difference between test and tren is that test has slight anti-lipolytic ability.

Posted by: Big Cat

Perhaps no more than other steroids, in which case the only difference between test and tren is that test has slight anti-lipolytic ability.

and this is the reason most people are finding tren to be better at lipid metabolism ?

Posted by: SWALE

And I am very excited about the potential benefits of manipulating the 2-OH/16-A ratio of estrogen metabolites as well, as we may then be able to let estrogen go even higher without its deleterious effects.

one thing bro, big cat pointed out to me once in a mail that would using diindolylmethane cause such a shift in the ratio , also estradiol is a much more potent regulator of GH release than estrones are. so letting estrogen go to higher levels becos of use of these supplements might not pay off as expected ?

another thing , i saw this study :

Plant derived 3,3'-diindolylmethane is a strong androgen antagonist in human prostate cancer cells.

Le HT, Schaldach CM, Firestone GL, Bjeldanes LF.

Nutritional Sciences and Toxicology, University of California at Berkeley, Berkekey, CA 94720.

3,3-Diindolylmethane (DIM), is a major digestive product of indole-3-carbinol (I3C), a potential anticancer component of cruciferous vegetables. Our results indicate that DIM exhibits potent antiproliferative and antiandrogenic properties in androgen dependent human prostate cancer cells. DIM suppresses cell proliferation of LNCaP cells and inhibits dihydroTestosterone(DHT) stimulation of DNA synthesis. These activities were not produced in androgen independent PC-3 cells. Moreover, DIM inhibited endogenous PSA transcription and reduced intracellular and secreted PSA protein levels induced by DHT in LNCaP cells. Also, DIM inhibited, in a concentration dependent manner, the DHT-induced expression of a PSA promoter regulated reporter gene construct in transiently transfected LNCaP cells. Similar effects of DIM were observed in PC-3 cells only when these cells were co-transfected with a wild type androgen receptor expression plasmid. Using fluorescence imaging with GFP-AR and Western blot analysis, we demonstrated that DIM inhibited androgen-induced AR translocation into the nucleus. Results of receptor binding assays indicated further that DIM is a strong competitive inhibitor of DHT binding to the AR. Results of structural modeling studies showed that DIM is remarkably similar in conformational geometry and surface charge distribution to an established synthetic AR antagonist although the atomic compositions of the two substances are quite different. Taken together with our published reports of the estrogen agonist activities of DIM, the present results establish DIM as a unique bifunctional hormone disrupter. To our knowledge, DIM is the first example of a pure androgen receptor antagonist from plants.

if DIM is a competitive antagonist at the AR receptor affecting the
androgen dependant tissues in the body (muscle) , then its not a very good thing is it ?

Excellent point, RayBravo. This is something we are also looking into.

When considering the respective effects of DIM on estrone and estradiol, it is important to remember that estradiol concentrations are many times that of estrone.

Specifically, if cortisol levels drop "below threshold" your body would quickly assume room temperature. Cortisol is the only hormone our bodies cannot maintain life without.

And just because dim is an androgen antagonist in the prostate does not mean that it has that same effect inother tissues. A prostate andro antagonist would be a good thing.

jb

Posted by: raybravo

and this is the reason most people are finding tren to be better at lipid metabolism ?

Its merely one way of looking at it, there is absolutely no data on this whatsoever. Its all conjecture, it just seems less likely that cortisol is the cause of the difference in this regard.

Posted by: jboldman

And just because dim is an androgen antagonist in the prostate does not mean that it has that same effect inother tissues.

They state its a pure androgen receptor antagonist and to my knowledge there is only one androgen receptor ...

Re: Lyle McDonald's response to my theory on usenet

Posted by: JGUNS

I was going through an old post of mine on usenet from several months ago and I realized that Lyle McDonald "steroid guru" had responded to my post. I felt that I would crosspost his responses here for debate. I realize that my own theory in this regard is by no means "solid" but Lyle attacks it without backing any of his statements up,nor making much sense to me. I also emailed him with a response, which I have also posted. We will see if he comes here for a friendly debate.

I'm next to you.
I think lyle is the most stupid person on the net. presto.
he flames people just if they don't say he is the best.
I remeber when I said nandi is the most brillant mind in bbing community, and he wrote "nandi can be as good as I'm, if he just stops using shitty word, and makes things easy like I do".
he says he got the testimonial from dan duchaine. I don't know when dan gave it to him!
on avantlabs some people hate me, because I write his book is a fake. but it is.
you should read the introduction of the ultimate diet 2.0. the only thing u can do is laught!

Well, I used to be able to break harder stuff down into simpler language as well, but I find the more you know and the deeper you dig, the harder it becomes to say things in simple terms, simply because it would take you a fucking age to explain everything.

That is in essence why we have scientific language, so everybody knows what we are talking about, its universal, its specific and it says so much with so little words. If Lyle is content explaining that stuff to those who are too stupid to do the slightest bit of research, it is after all his perogative. But i know that stands in the way of my development, and so does he.

So trust me, its all show. He knows he can't touch most of the brainpower on this board.

And maybe the critiscism you get is correct, you don't need to keep saying his book is crap. You've told them once, if they are dumb enough not to listen, its their money after all.