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Ross, important question for you!
- Thread starter jnef
- Start date
Tatyana
Elite Mentor
Someone explain this to me.
According to Bill Llewellyn, all steroids are based off one of three compounds, test, DHT and think it is pregnalone.
They are all derived from cholesterol and share the same five ring structure with just variable double bonds and side chains.
When you look at pics of the various steroids, they all follow the same pattern.
This is so they will fit into the androgen/testosterone receptor.
No binding with the receptor (and this sort of works like a lock and key principle), no 'switching' on of the DNA protein making machine.
Cause that is what hormones do, they are 'chemical messengers' to tell the cells to do things. THEY don't actually produce the result directly.
So if a steroid has to bind to a receptor to work, it has to be similar to test, so how can adding test make any difference?
They are still stimulating the same receptor (well there are two isoforms).
The structure only changes the pharmocodynamics, which is REALLY complicated and I would have to read more to refresh my really basic knowlege on it.
According to Bill Llewellyn, all steroids are based off one of three compounds, test, DHT and think it is pregnalone.
They are all derived from cholesterol and share the same five ring structure with just variable double bonds and side chains.
When you look at pics of the various steroids, they all follow the same pattern.
This is so they will fit into the androgen/testosterone receptor.
No binding with the receptor (and this sort of works like a lock and key principle), no 'switching' on of the DNA protein making machine.
Cause that is what hormones do, they are 'chemical messengers' to tell the cells to do things. THEY don't actually produce the result directly.
So if a steroid has to bind to a receptor to work, it has to be similar to test, so how can adding test make any difference?
They are still stimulating the same receptor (well there are two isoforms).
The structure only changes the pharmocodynamics, which is REALLY complicated and I would have to read more to refresh my really basic knowlege on it.
Tatyana said:
True , all steroids are based on the T molecule, but some impart more than others and since any exogenous T is suppressive, some wind up lowering T instead of elevating it. (Technically, this is a different pathway with nandrolones, but that's another story). All steroids also increase nitrogen, which is essentially what grows muscle and what makes Primo so coveted. It does so with less androgenic influx. The problem is, as you inferred, it's still going to suppressive, albeit slightly. So some people will add test to "kick it up."
Meanwhile, the increased androgen from something as basic as test increases strength and water retention which leads to increased muscle size -- IF -- the person makes the most of it. I'd say 90% of the people who like test do so because it works fast, increases strength, mood and libido, swells you up with water and gives the impression of "gains." And it's cheap. But a drug like Primobolan will be more subtle yet increase actual muscle tissue to a greater degree. (Remember, a pound of muscle tissue is quite a bit but will not change appearance as much as 10 pounds of water and increased blood volume).
Having said all that, I think the differences in steroids is sometimes overanalyzed. They all do the same thing. Some do it a little more effectively and a little less harshly than others, depending on your preference.
Last edited:
njmuscleguy
New member
Tatyana said:
Tatyana, let me see if I'm understanding your question (it's early)... are you asking that if an accompanying AAS compound that in theory is similar to test is already binding the receptors, then of what benefit is it to add test on top of that?
I know I can't readily answer that with any medical / scientific evidence... and I can't really answer that by experience or "FEEL" since I always run test in any of my cycles. So I can't compare it to a cycle *without test*.
However, if there was no benefit of running test along with say tren, or deca, or primo, etc. etc. etc., then why would countless people over the years be doing it? Why do people say "primo is enhanced when running test" or "proviron and test are syngergistic". Now that I think of it, primo and proviron are dht-derivitives and test is, well test... so I guess they each bind to different receptors? Forgive my ignorance, just thinking out loud
Tatyana
Elite Mentor
I am at work, and working on my research project, I will read the responses more carefully when I get home.
BUT, I did make a few boo-boos.
Testosterone is a 4 ring molecule.
I think the three basic forms of test are test, dihydrotest and dihydroepiandrosterone.
Most of my stuff is with the pathology of endocrinology, so what goes wrong, and only the basics of the normal physiology.
It is rather involved.
BUT, I did make a few boo-boos.
Testosterone is a 4 ring molecule.
I think the three basic forms of test are test, dihydrotest and dihydroepiandrosterone.
Most of my stuff is with the pathology of endocrinology, so what goes wrong, and only the basics of the normal physiology.
It is rather involved.
gjohnson5
New member
I think this is a good start to the question.
I will try to explain this as best as I can, because this won't be a very good explanation...
What we need to look at is where the androgen receptor is located and androgen-dependant gene expression. When an androgen attaches to an androgen receptor, that androgen act son certain functions in the body and this can be dependant on what type of androgen attached to the androgen receptor. Also the type of physiological change from that androgen attahching to the androgen receptor will also depend on what type of cell that androgen receptor was located on. Steroid hormones (or lack of steroid hormones) can cause different physiological changes in muscle , bone , nerve, gland and organ tissue.
The easiest way for me to demonstrate this is by using ATD as an example. The location with the highest number of androgen receptors is the hypothalamus gland. One of it's purposes it to regulate androgen production from other hormones. When ATD (which has a higher affinity for those same receptors as testosterone) attaches to those androgen receptors the function that ATD carries out on those receptors does not initiate the sequence of events which lead to reduces if not completely stopped production GrNH. The ATD androgen itself is too weak an androgen to trigger the sequence of events in the hypothalamus which leads to shutdown. The expression that which androgen initiates is different then other androgens which attach to the AR's of the hypothalamus. Hence ATD is used to "trick" the hypothalamus into thinking there are less circulating androgens in your blood then there really are. But there is a cost associated with ATD attaching to androgen receptors in other parts of the body then a "real" androgen
The expression initiated by testosterone attaching to muscle is different then say a 19-nor-testosterone molecule. Also this expression is different if the androgen attaches to bone or nerve or the testes. So what we would need to look at is the sequence of events which take place after testosterone attaches to AR's in muscle as compared to a DHT like drug such as masteron. This is why we'd listen to bodybuilders because they would have more anectdotal answers to these questions, where as a scientists would need to study this in a lab setting as well as injecting someone with the chemicals if they are doing a human study.
Hopefully I didn't fuck up too bad
I will try to explain this as best as I can, because this won't be a very good explanation...
What we need to look at is where the androgen receptor is located and androgen-dependant gene expression. When an androgen attaches to an androgen receptor, that androgen act son certain functions in the body and this can be dependant on what type of androgen attached to the androgen receptor. Also the type of physiological change from that androgen attahching to the androgen receptor will also depend on what type of cell that androgen receptor was located on. Steroid hormones (or lack of steroid hormones) can cause different physiological changes in muscle , bone , nerve, gland and organ tissue.
The easiest way for me to demonstrate this is by using ATD as an example. The location with the highest number of androgen receptors is the hypothalamus gland. One of it's purposes it to regulate androgen production from other hormones. When ATD (which has a higher affinity for those same receptors as testosterone) attaches to those androgen receptors the function that ATD carries out on those receptors does not initiate the sequence of events which lead to reduces if not completely stopped production GrNH. The ATD androgen itself is too weak an androgen to trigger the sequence of events in the hypothalamus which leads to shutdown. The expression that which androgen initiates is different then other androgens which attach to the AR's of the hypothalamus. Hence ATD is used to "trick" the hypothalamus into thinking there are less circulating androgens in your blood then there really are. But there is a cost associated with ATD attaching to androgen receptors in other parts of the body then a "real" androgen
The expression initiated by testosterone attaching to muscle is different then say a 19-nor-testosterone molecule. Also this expression is different if the androgen attaches to bone or nerve or the testes. So what we would need to look at is the sequence of events which take place after testosterone attaches to AR's in muscle as compared to a DHT like drug such as masteron. This is why we'd listen to bodybuilders because they would have more anectdotal answers to these questions, where as a scientists would need to study this in a lab setting as well as injecting someone with the chemicals if they are doing a human study.
Hopefully I didn't fuck up too bad
Nelson Montana said:
AR-binding is only one pathway for anabolism, some steroids(such as Dianabol) barely bind to the A-R at all and yet are still extremely anabolic.Tatyana said:
In terms of HPTA inhibition, each steroid has different binding affinity for the Androgen/Estrogen/Progesterone receptors. Steroids which ACTIVATE these receptors(bind) cause greater HPTA inhibition than those that do not.
gjohnson5
New member
Another example is hair growth /loss
Hair loss is said to be triggered by an androgen DHT attaching to AR in hair follicle.
The exact opposite would be testosterone attaching to AR in hair follicle causing hair growth
So yes , the type of androgen and where the AR is located will determine which expression is initiated
Hair loss is said to be triggered by an androgen DHT attaching to AR in hair follicle.
The exact opposite would be testosterone attaching to AR in hair follicle causing hair growth
So yes , the type of androgen and where the AR is located will determine which expression is initiated
digitizedsoul
New member
This is one of the most mind excercising and educational threads I have ever seen in my time here.
Tat especially but the rest of you as well are displaying knowledge of chemistry / biochemistry that just amazes me. I commend you all for pursuing such complicated wisdom.
I only wish I could contribute, however my knowledge is rather limited on the subject, although so far I have been able to follow along.
Tat especially but the rest of you as well are displaying knowledge of chemistry / biochemistry that just amazes me. I commend you all for pursuing such complicated wisdom.
I only wish I could contribute, however my knowledge is rather limited on the subject, although so far I have been able to follow along.
