Nandi dispells a few BBing myths

[prolangtum]

TweetNandi from CEM posted this a while back, CEM is where i get all my "scientific" info:

1) The use of thyroid hormone damages the thyroid

See mind and muscle #10

2) GH administration builds muscle mass

No studies have ever confirmed this. Several have refuted it. Hepatic IGF-1 is probably not important to muscle growth

3) Estrogen promotes fat accumulation

Estrogen has been shown to be both anorectic and lipolytic, the latter via reduction of lipoprotein lipase levels

4) Aromatase inhibitors and SERMS reduce the anabolic effects of steroids

Again, there is no research to support this. The effect is claimed to be due to reduction in IGF-1. As mentioned, hepatic IGF-1 is probably relatively unimportant for muscle growth

5) Proviron prevents gynecomastia

This is based on the fact that Proviron is 5 alpha reduced, like DHT. Numerous other AAS are 5 alpha reduced and they are not claimed to prevent gyno. Proviron has never been used in a study to treat or prevent gyno

6) Winstrol prevents "progestigenic gyno"

There is no evidence that synthetic progestigenic androgens cause gyno, or even contribute to it. Winstrol has been shown to be a progesterone receptor agonist in the one study that looked at this effect

7) Insulin use damages your pancreas

Insulin is routinely used in type 2 diabetes to lower blood sugar. It has not been shown to harm the pancreas in these patients or in any other subjects.

8) Antiestrogens prevent bloat from AAS use

Rather than a myth, this is probably better called a half truth. Androgens can directly promote water retention without aromatizing

9) Androgen receptors need to be "cleaned out" periodically

Androgen receptors are continually being turned over in the body. There is no need to clean out existing receptors because they only have a halflife of a few hours

[FLEMS]

Tweetgood info

[Lift Chief]

TweetInteresting stuff.

I will say though in my personal experience and that of my friends proviron does help somewhat with gyno and water retention... although it is a certainly a weak anti-e.

[rado]

Tweetnice info, thanks kid.

[prolangtum]

TweetBump for the evening crew...............

[got_pinz]

Tweeti did not know that!!!!good info

[jipped genes]

Tweetcool stuff man,thanks

[JohnnyB]

TweetNandi has some good articles

JohnnyB

[AnotherUser]

TweetAhh.. thank you for posting that I've seen some heated debates on several of those points. I don't have the credentials to back my arguements up, but he does

[ARMed]

Tweetnice post!

[trancedelt]

Tweetgood info
know where to find the winny progesterone study?

[prolangtum]

Tweet

Originally posted by blm9376
Actually, Insulin is used to treat Type 1 Diabetes (IDDM) Insulin Dependent Diabetes Mellitus. And in this case the persons Islets of Langerhans in the pancreas is already destroyed. So this info does not appear to be to reliable.

Type 2 (NIDDM) NON-Insulin Dependent Diabetes, requires medications such as sulfonylureas, biguanides,meglitinides, glucophage and a few others. Not insulin.

Actually, i know for a fact some type II diabetics use insulin, my grandmother for one.


Trancedelt here is a post by him a while back on that subject:

Won't this notion ever die? One of the mods at elite posted this tired old abstract. I chimed in below:

Hi fellas...Was reading through some of my abstracts and found this interesting one,showing a definite stanozolol/Progesterone receptor interaction,thought you guys might enjoy it as well...

Ellis AJ, Cawston TE, Mackie EJ.

Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, UK.

The anabolic steroid stanozolol stimulates the production of prostaglandin E2 (PGE2) and the matrix metalloproteinases collagenase and stromelysin in human skin fibroblasts but not in rheumatoid synovial fibroblasts. The basis for these differential responses was investigated at the levels of DNA synthesis and steroid receptor binding. Stanozolol inhibited fibroblast growth factor (FGF)-stimulated DNA synthesis in both the skin and synovial fibroblasts, showing that both cell types were capable of responding to the compound. Competitive binding assays indicated that stanozolol bound specifically to both the skin and synovial fibroblasts. Binding of stanozolol to both cell types could be partially displaced by progesterone, indicating that stanozolol binds to the progesterone receptor. Immunocytochemical studies confirmed the presence of progesterone receptors on skin and synovial fibroblasts. However, progesterone failed to elicit any response with respect to collagenase production in either cell type. Nortestosterone, dexamethasone and 17 beta-oestradiol had no effect on binding of stanozolol to either cell type. These results indicate that the inhibition of DNA synthesis by stanozolol is elicited through the progesterone receptor. The effects of stanozolol on collagenase and PGE2 production are mediated by a different receptor, present on skin but not synovial fibroblasts, and as yet unidentified.

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Virtually all androgens bind to the progesterone receptor to some degree; similarly progestins (and antiprogestins) bind to the androgen receptor. RU 486 binds to the androgen receptor as an antiandrogen, rendering it useless for bodybuilders.

As far as the winstrol article goes, has anyone bothered to actually read the whole study? Presumably we are supposed to believe winstrol has some kind of antiprogestin capability because it blocked FGF stimulated DNA synthesis.

The effect on DNA synthesis was measured by thymidine uptake. Less thymidine uptake means less DNA synthesis. Quoting from page 38 of the article,

" A significant inhibition of thymidine uptake was seen in response to stanozolol in both cell types. The steroids nortestosterone, oxymetholone, and progesterone itself were also tested for their effect on thymidine uptake to determine whether the effects of stanozolol on DNA synthesis were unique. These other compounds also inhibited DNA synthesis in both cell types"

In other words, winstrol has THE SAME effect as progesterone on progesterone receptor mediated DNA synthesis: they both block it. So rather than acting as an antiprogesterone in this study, winstrol, as well as nandrolone and oxymetholone, act in the same manner as progesterone