Ross, important question for you!

[jnef]

Tat;

once you start a cycle at high enough total levels, your body will cease producing its own test or cut back severely. some compounds are more suppressive than others, but at the doses an intermediate level BB would take you'll likely end up shut down.

I cant take it down to a molecule level, but going by my own experience and that of others that I've talked to or read about, you just never feel quite right without some Test cruising tru your system.

even supplying dht via masteron or proviron doesnt get it quite right mentally or physically. I've tried.

It might be the absence of metabolites that only reduce from test? might even be the small amount of estrogen that aromatized test will provide. dont know. there's alot the scientific community doesnt know about how and why drugs do all of what they do, and steroids are no exception.

absent any studies one way or the other, my opinion is just err on the side of safety and always add at least a replacement dose of test to a suppressive cycle (200-300 mg weekly). It doesnt need to be the base compound, just needs to be in there.

lol here i thought i was setting myself up to get flamed with this post but damn turned out to be quite a post i learned a lot from - thanks everybody

 

[Ross]

Elaborate on the bits in bold please.

I am especially interested in the affinity of the different steroids for androgen (or other sex hormone receptors).

I did a wee bit of a search and couldn't find anything.

This is textbook Endocrinology 101; The hypothalamus contains ANDROGEN, ESTROGEN, and PROGESTERONE receptors. Each anabolic steroid has different binding properties.

For example, Testosterone activates the Androgen and Estrogen receptors in the Hypothalamus and thus causes HPTA Shutdown. Trenbolone activates the Androgen and Progesterone receptors and thus causes HPTA shutdown. Primobolan and Anavar however, barely activate the Androgen receptors and have NO effect on estrogen or progesterone receptors and thus, DO NOT cause HPTA shutdown.

 

[Mavafanculo]

This is textbook Endocrinology 101; The hypothalamus contains ANDROGEN, ESTROGEN, and PROGESTERONE receptors. Each anabolic steroid has different binding properties.

For example, Testosterone activates the Androgen and Estrogen receptors in the Hypothalamus and thus causes HPTA Shutdown. Trenbolone activates the Androgen and Progesterone receptors and thus causes HPTA shutdown. Primobolan and Anavar however, barely activate the Androgen receptors and have NO effect on estrogen or progesterone receptors and thus, DO NOT cause HPTA shutdown.

^^ true - and most only focus on the estrogen negative feedback loop portion of the equation.

but as to var and primo barely binding to any of the receptors at he hypothalmus, that would also mean the same in muscle tissue receptors.

at levels high enough to sufficiently stimulate protein synthesis at the muscle, you'll also sufficiently stimulate the androgen receptor at the hypothalmus to cause suppression.

just going from my experience for example, var at 100+ mg daily made the boys disappear, and resulted in a crash if I tried to go without PCT

 

[Tatyana]

This is textbook Endocrinology 101; The hypothalamus contains ANDROGEN, ESTROGEN, and PROGESTERONE receptors. Each anabolic steroid has different binding properties.

For example, Testosterone activates the Androgen and Estrogen receptors in the Hypothalamus and thus causes HPTA Shutdown. Trenbolone activates the Androgen and Progesterone receptors and thus causes HPTA shutdown. Primobolan and Anavar however, barely activate the Androgen receptors and have NO effect on estrogen or progesterone receptors and thus, DO NOT cause HPTA shutdown.

No offense hun, but 'this is endocrinology 101' that does come across as being a bit condescending.

Especially as you still haven't stated what your formal education is in.

Molecular biology, especially cell cycle control and cell signalling really rocks my world, and I have studied it extensively.


The text in bold is not in endocrinology textbooks.

I am looking for a table, some numbers, a paper.

This is the sort of stuff that is in basic endocrinology textbooks, synthesis pathways and signalling pathways (MAP-kinase and tyrosine kinase, C-AMP and G-AMP).

 

[gjohnson5]

I like those charts. They show the metabolism of hormones and the enzymes which cause the catalytic reaction to convert Hormone A to Hormone B. It's also good that it shows cholesterol being converted to pregnenolone and the multiple pathways in which hormones can be created from pregnenolone. I wish it listed the names of the metabolic pathways themselves.

*edit*
I may want to find one of those which start at the testes and shows testosterone being secreted from the testes after interaction with LH and FSH from the pituitary to diagram out HPTA
*edit*

 

[Tatyana]

I like those charts. They show the metabolism of hormones and the enzymes which cause the catalytic reaction to convert Hormone A to Hormone B. It's also good that it shows cholesterol being converted to pregnenolone and the multiple pathways in which hormones can be created from pregnenolone. I wish it listed the names of the metabolic pathways themselves.

*edit*
I may want to find one of those which start at the testes and shows testosterone being secreted from the testes after interaction with LH and FSH from the pituitary to diagram out HPTA
*edit*

I did see one of those in my recent searches, I will see if I can find it again.

I have more elaborate description/diagrams of sex hormone synthesis, but they are in textbooks.

 

[Mavafanculo]

Elaborate on the bits in bold please.

I am especially interested in the affinity of the different steroids for androgen (or other sex hormone receptors).

I did a wee bit of a search and couldn't find anything.

Thats a great question.

its one of those things that is included in every steroid profile on any site or book, and everyone takes for granted as an article of faith, but I havent seen (or noticed) the source for the assertions. (ie. "this steroid or that one has a strong binding affinity for this or that receptor")

soooo, who better to ask than one of our new COTB who has written many of the best steroid profiles avaiable to us. That would be Bill Llewellyn

 

[Ross]

Thats a great question.

its one of those things that is included in every steroid profile on any site or book, and everyone takes for granted as an article of faith, but I havent seen (or noticed) the source for the assertions. (ie. "this steroid or that one has a strong binding affinity for this or that receptor")

soooo, who better to ask than one of our new COTB who has written many of the best steroid profiles avaiable to us. That would be Bill Llewellyn

There is not much data available, but I have composed a list based on the known properties of each anabolic steroid compound.

The Following drugs either DIRECTLY or INDIRECTLY activate ESTROGEN receptors, to varying degrees:

Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone

The Following drugs either DIRECTLY or INDIRECTLY activate PROGESTERONE receptors, to varying degrees:

Nandrolone
Trenbolone
Oxymetholone

The Following drugs activate Androgen receptors, to varying degrees:

Testosterone
Methandrostenolone
Mathandriol
Oxymetholone
Nandrolone
Boldenone
Trenbolone
Halotestin
Oxandrolone
Stanzolol
Chlorodehydromethltestosterone
Methyltestosterone
Methenolone...
(ALL AAS*)

As we can see, the steroids that cause HPTA SHUTDOWN either OVERSATURATE ONE SPECIFIC receptor, or they activate too many TOTAL receptors(Androgen/Estrogen/Progesterone)

For instance, Trenbolone causes HPTA SHUTDOWN because it OVERSATURATES BOTH, the ANDROGEN and the PROGESTERONE receptors. Testosterone causes SHUTDOWN because it converts to ESTROGEN and DHT, therefore, it oversaturates the Androgen/Estrogen receptors.

As we can ALSO SEE, the steroids that DO NOT cause SHUTDOWN of the HPTA, do NOT oversaturate ANY of the different hormone receptors, and thus, do NOT cause SHUTDOWN. Methenolone(Primobolan) does not possess ANY Estrogenic or Progestational ACTIVITY WHATSOEVER. It does, by virtue of being an anabolic steroid, posses a SMALL Androgenic component. Because it lacks ANY ESTROGENIC/PROGESTATIONAL component, and it lacks a strong Androgenic component, it WILL NOT CAUSE SHUTDOWN! Oxandrolone(Anavar) posseses NO Estrogenic/Progestational component either. AND, it also lacks a strong androgenic component. Thus, Anavar will NOT cause shutdown.

 

[Mavafanculo]

........As we can ALSO SEE, the steroids that DO NOT cause SHUTDOWN of the HPTA, do NOT oversaturate ANY of the different hormone receptors, and thus, do NOT cause SHUTDOWN. Methenolone(Primobolan) does not possess ANY Estrogenic or Progestational ACTIVITY WHATSOEVER. It does, by virtue of being an anabolic steroid, posses a SMALL Androgenic component. Because it lacks ANY ESTROGENIC/PROGESTATIONAL component, and it lacks a strong Androgenic component, it WILL NOT CAUSE SHUTDOWN!

Oxandrolone(Anavar) posseses NO Estrogenic/Progestational component either. AND, it also lacks a strong androgenic component. Thus, Anavar will NOT cause shutdown.

you calling my nads liars? lol

----------
Clin Endocrinol (Oxf). 1997 Feb;46(2):209-16.

Effect of low dose oxandrolone and testosterone treatment on the pituitary-testicular and GH axes in boys with constitutional delay of growth and puberty.

Crowne EC, Wallace WH, Moore C, Mitchell R, Robertson WH, Holly JM, Shalet SM.
Department of Endocrinology, Christie Hospital Trust, Manchester, UK.

OBJECTIVE: To investigate the effect of low dose oxandrolone and testosterone on the pituitary-testicular and GH-IGF-I axes. DESIGN: Prospective double-blind placebo-controlled trial. PATIENTS: Sixteen boys with constitutional delay of growth and puberty (CDGP) with testicular volumes 4-6 ml were randomized to 3 months treatment: Group 1 (n = 5), daily placebo: Group 2 (n = 5), 2.5 mg oxandrolone daily or Group 3 (n = 6), 50 mg testosterone monthly intramuscular injections with assessment (growth, pubertal development and overnight hormone profiles) at 0, 3, 6 and 12 months. MAIN OUTCOME MEASURES: LH and GH profiles (15-minute samples) were analysed by peak detection (Pulsar), Fourier transformation and autocorrelation. Testosterone levels were measured hourly and insulin, SHBG, IGF-I, and IGFBP-3 levels at 0800 h. Statistical analysis was by multivariate analysis of variance for repeated measures. RESULTS: LH and testosterone parameters increased significantly with time in all 16 (LH AUC, P < 0.001; peak amplitude, P = 0.02; number of peaks, P = 0.02; testosterone AUC, P = 0.02; morning testosterone, P = 0.002). In Group 2, however, LH and testosterone parameters decreased at 3 months followed by a rebound increase at 6 and 12 months. SHBG levels were markedly reduced at 3 months (P = 0.006) and a wider range of dominant GH frequencies was present although GH AUC was not increased until 6 months, with an increase in GH pulse frequency but not amplitude. IGF-I levels were increased at both 3 and 12 months. In Group 3, pituitary-testicular suppression was not apparent, but GH levels increased with an increase in GH amplitude at 3 and 12 months. CONCLUSION: Oxandrolone transiently suppressed the pituitary-testicular axis and altered GH pulsatility. Testosterone increased GH via amplitude modulation.
-----------

also, this suppression was at baby sized doses. BB's take up to FIFTY times the study dose.

 

[gjohnson5]

I agree that the steroid profiles have marginal accuracy since there are very few human studies on this stuff. The other portion of the data is based on mice and rat studies since noone gives a fuck about the long terms effects of studies on lab rodents.... We should most definitly be studying the long term effects of steroid medication/use/abuse on humans IMHO. But some people are still basing what they say on some of the Dan Duchaine work because he would inject heavy dosages of steroid and in a marginally accurate way publish data about the changes he noticed in his genetics. But there is no profit potential in investigating this stuff until we vote in politicians who are pro-steroid use and get the Scheduled drug stuff overturned.

Thats a great question.

its one of those things that is included in every steroid profile on any site or book, and everyone takes for granted as an article of faith, but I havent seen (or noticed) the source for the assertions. (ie. "this steroid or that one has a strong binding affinity for this or that receptor")

soooo, who better to ask than one of our new COTB who has written many of the best steroid profiles avaiable to us. That would be Bill Llewellyn