Lyle McDonald's response to my theory on usenet

Posted by: Big Cat

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.

this is the point.
the thing I do not tollatate is he says he about himself he is the best in writing diets...when he has just written a fake.

I wil be the first to admit that i am getting a little out of my depth here. As i undererstand it a "pure" anti-androgen simply means that it exhibits "only" antiandrogen effects opposed to other steroidal antiandrogens that are agonists in some tissues. It would be nice to see some more studies, this sounds like an in vitro study based on the abstract, frequently we see different results when in vivo studes are done. Another issue is that most "pure" antiandrogens are weak in vivo. This might make sense re DIM since it has very poor absorbtion rates and might be difficult to dose enough orally to have this effect in vivo. Certainly, intuitively we would think that DIM would have made the short list for prostate cancer research if it were as potent in vivo as suggested.

In a study done with rats fed a diet of up to 10X human recommended dose of an absorbtion enhanced DIM or 7X times the recommended dose of I3C, they found "There were no observable differences grossly or histologically between groups". One might expect some weight changes and other changes if there were significant ar blockade going on, ei wasting.

This is a serious issue and if you or anyone has more info to impart it would be appreciated.

jb
==============
Toxicol Sci. 2003 Jul;74(1):10-21. Epub 2003 May 02.

Evaluation of chronic dietary exposure to indole-3-carbinol and absorption-enhanced 3,3'-diindolylmethane in sprague-dawley rats.

Leibelt DA, Hedstrom OR, Fischer KA, Pereira CB, Williams DE.

Posted by: Big Cat

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

Raybravo, since estradiol plays an important role in gh, why woul dnot having more of it be a good thing?

jb

==================

Endocrine. 2003 Oct;22(1):25-40.
Sex-steroid modulation of growth hormone (GH) secretory control: three-peptide ensemble regulation under dual feedback restraint by GH and IGF-I.

Raybravo, since estradiol plays an important role in gh, why woul dnot having more of it be a good thing?

jb

==================

Endocrine. 2003 Oct;22(1):25-40.
Sex-steroid modulation of growth hormone (GH) secretory control: three-peptide ensemble regulation under dual feedback restraint by GH and IGF-I.

I thought Lyle was only into dieting, learn something new.

Posted by: jboldman

I wil be the first to admit that i am getting a little out of my depth here. As i undererstand it a "pure" anti-androgen simply means that it exhibits "only" antiandrogen effects opposed to other steroidal antiandrogens that are agonists in some tissues. It would be nice to see some more studies, this sounds like an in vitro study based on the abstract, frequently we see different results when in vivo studes are done. Another issue is that most "pure" antiandrogens are weak in vivo. This might make sense re DIM since it has very poor absorbtion rates and might be difficult to dose enough orally to have this effect in vivo. Certainly, intuitively we would think that DIM would have made the short list for prostate cancer research if it were as potent in vivo as suggested.

In a study done with rats fed a diet of up to 10X human recommended dose of an absorbtion enhanced DIM or 7X times the recommended dose of I3C, they found "There were no observable differences grossly or histologically between groups". One might expect some weight changes and other changes if there were significant ar blockade going on, ei wasting.

This is a serious issue and if you or anyone has more info to impart it would be appreciated.

I agree, the real question is does its effect on estrogen outweigh its effect on androgens ?

well, at least anecdotally, i will be able to give some reports in a few weeks since i have just started taking both I3C and DIM.

jb

I'm curious as to why yu are taking both of them.

What are the dose(s)?

That's a good question. I was a little concerned about the poor absorbtion of DIM so I am taking both. I will probably opt out of the I3C for the DIM since the I3C was more expensive.

jg

Posted by: Big Cat

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.

BC, ever find anything that bocks the 17aHSD?

whats the full term, word for 17aHSD?

Can't say I have.

17alpha hydroxysteroid dehydrogenase.

Posted by: Big Cat

Well, in my opinion .......................

Coming from a man who rehashes ketogenic dieting while every bodybuilder had it down cold 10 years ago ... proper, polite too. But then I guess that's the usenet attitude. And you guys thought I was bad.

Well, tren binds more avidly and more importantly shows little affinity for binding proteins. This has nothing to do with receptors, nor were different receptpors implied in JGUNS original post. The difference in affinity could most certainly account for a difference in action.

Since when do androgens cause 'severe' water and mineral retention ? Water retention for the most part is caused by estrogenic upregulation of aldosterone . And this would account for jack shit, since the use of aldosterone blockers which is pretty common practice among top athletes who do a lot of guest posing still doesn't make up for the difference in effect.

a lot! androgens can cause severe water retention and estradiol levels can be lower than normal or low normal , that way,water retention can be non estrogenic mediated.

problems of over-generalizing.

That's your problem, you don't understand what 'for the most part' means. Secondly, even non-estrogen related water retention is still adressed by the standard diuretics, and regardless of association, androgens do not cause 'severe' water and mineral retention.

And why are you bumping threads that have been dead for a year ? You never contribute anything.

Posted by: Big Cat

That's your problem, you don't understand what 'for the most part' means. Secondly, even non-estrogen related water retention is still adressed by the standard diuretics, and regardless of association, androgens do not cause 'severe' water and mineral retention .

And why are you bumping threads that have been dead for a year ? You never contribute anything.

oughhhh

J Clin Endocrinol Metab. 2005 Jul;90(7):3989-94. Epub 2005 Apr 12.
Independent and combined effects of testosterone and growth hormone on extracellular water in hypopituitary men.

Johannsson G, Gibney J, Wolthers T, Leung KC, Ho KK.

Pituitary Research Unit, Garvan Institute of Medical Research, St. Vincent's Hospital, 384 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.

CONTEXT: Symptoms of fluid retention in GH-deficient patients during GH replacement are greater in men than in women, suggesting that testosterone may augment or estradiol may attenuate the antinatriuretic actions of GH. The mechanisms underlying the sodium-retaining effects of GH are poorly understood. AIM: The aim of this study was to investigate the effects of GH and testosterone, alone and in combination, on extracellular water (ECW) and the hormonal mechanisms involved. DESIGN: Two separate, open-label, randomized, two-period, crossover studies were performed; the first compared the effects of GH alone with those of GH and testosterone, and the second compared the effects of testosterone alone with those of GH and testosterone. PARTICIPANTS: Twelve hypopituitary men with GH deficiency and hypogonadism were studied. INTERVENTION: During the weeks of intervention, GH (0.5 mg/d) and Testosterone Enanthate (250 mg) were administered by im injection. OUTCOME MEASURES: The outcome measures were ECW, IGF-I, plasma renin activity (PRA), aldosterone (Aldo), and atrial natriuretic peptide (ANP). RESULTS: GH treatment significantly increased (P < 0.05) both IGF-I and ECW, and these changes were enhanced by cotreatment with testosterone (P = 0.07 for both). PRA, Aldo, and ANP levels did not change. Testosterone treatment alone did not change the IGF-I concentration, whereas cotreatment with GH induced a marked increase. Testosterone alone increased (P < 0.05) ECW, and the effect was augmented (P < 0.01) by cotreatment with GH. Although PRA and ANP did not change, plasma Aldo decreased after single and combined treatments. CONCLUSION: GH and testosterone exerted independent and additive effects on ECW. The mechanisms of fluid retention for both hormones are likely to be exerted on the renal tubules. This is the first direct evidence that testosterone increases ECW.

wish more............................

a year dead? ah, 'for the most part�

07-10-2006 02:02 PM

Posted by: triguy

BC, ever find anything that bocks the 17aHSD?

whats the full term, word for 17aHSD?

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 ..................................................................................As for how the GR comes into play: The binding of cortisol to the GR
can cause an increase in LPL
Effects of physiological hypercortisolemia on the regulation of
lipolysis in subcutaneous adipose tissue.
J Clin Endocrinol Metab. 1998 Feb;83(2):626-31............................................................................................

J Clin Endocrinol Metab. 1998 Feb;83(2):626-31. Related Articles, Links

Effects of physiological hypercortisolemia on the regulation of lipolysis in subcutaneous adipose tissue.

Samra JS, Clark ML, Humphreys SM, MacDonald IA, Bannister PA, Frayn KN.

Oxford Lipid Metabolism Group, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, United Kingdom.

Cortisol is known to increase whole body lipolysis, yet chronic hypercortisolemia results in increased fat mass. The main aim of the study was to explain these two apparently opposed observations by examining the acute effects of hypercortisolemia on lipolysis in subcutaneous adipose tissue and in the whole body. Six healthy subjects were studied on two occasions. On one occasion hydrocortisone sodium succinate was infused i.v. to induce hypercortisolemia (mean plasma cortisol concentrations, 1500 +/- 100 vs. 335 +/- 25 nmol/L; P < 0.001); on the other occasion (control study) no intervention was made. Lipolysis in the s.c. adipose tissue of the anterior abdominal wall was studied by measurement of arterio-venous differences, and lipolysis in the whole body was studied by constant infusion of [1,2,3-2H5]glycerol for measurement of the systemic glycerol appearance rate. Hypercortisolemia led to significantly increased arterialized plasma nonesterified fatty acid (NEFA; P < 0.01) and blood glycerol concentrations (P < 0.05), with an increase in systemic glycerol appearance (P < 0.05). However, in s.c. abdominal adipose tissue, hypercortisolemia decreased veno-arterialized differences for NEFA (P < 0.05) and reduced NEFA efflux (P < 0.05). This reduction was attributable to decreased intracellular lipolysis (P < 0.05), reflecting decreased hormone-sensitive lipase action in this adipose depot. Hypercortisolemia caused a reduction in arterialized plasma TAG concentrations (P < 0.05), but without a significant change in the local extraction of TAG (presumed to reflect the action of adipose tissue lipoprotein lipase). There was no significant difference in plasma insulin concentrations between the control and hypercortisolemia study. Site-specific regulation of the enzymes of intracellular lipolysis (hormone-sensitive lipase) and intravascular lipolysis (lipoprotein lipase) may explain the ability of acute cortisol treatment to increase systemic glycerol and NEFA appearance rates while chronically promoting net central fat deposition