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How suppressive is primobolan compared to testosterone?
MESO-Rx
Anabolic Steroids
How suppressive is primobolan compared to testosterone?
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kosp
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It's like
I want a woman who is pretty, nice, got a gym body, smart, well-educated, gives me great sex whenever I want, has no exs, got money and gives me a lot of freedom.
JulianB
New Member
It will be almost similar.
If you want to use steroids, you will have to deal with the shutdown.
There is no exception.
Type-IIx
Well-known Member
Substantially less. You could use, e.g., oral primo ace tablets for a mild cosmetic benefit for months continuously and endogenous T secretion would proceed. The same applies to metenolone enanthate i.m.
Since this is a bodybuilding board, this would seem a waste of drugs to most, however. We generally like aromatizable drugs in our stack to augment IGF-I activity and total-body growth & our risk tolerance permits the risk of persistent hypogonadism. Testosterone is a great drug that synergizes well with many others. It also enhances subjective measures like libido, assertiveness, etc.
Nevertheless, strictly to your question, it is a bro-science myth that you must accept total shutdown. This belief arises from the arguably myopic experiences of those that use testosterone-based cycles exclusively (a potently suppressive androgen) where the use of AAS is directed at maximal anabolism. However, it excludes the legitimate use cases that include the use of orals in a pulsed fashion or for peaking strength/performance, prepping for a photo shoot that isn't in FLEX Magazine, etc.
Since this is a bodybuilding board, this would seem a waste of drugs to most, however. We generally like aromatizable drugs in our stack to augment IGF-I activity and total-body growth & our risk tolerance permits the risk of persistent hypogonadism. Testosterone is a great drug that synergizes well with many others. It also enhances subjective measures like libido, assertiveness, etc.
Nevertheless, strictly to your question, it is a bro-science myth that you must accept total shutdown. This belief arises from the arguably myopic experiences of those that use testosterone-based cycles exclusively (a potently suppressive androgen) where the use of AAS is directed at maximal anabolism. However, it excludes the legitimate use cases that include the use of orals in a pulsed fashion or for peaking strength/performance, prepping for a photo shoot that isn't in FLEX Magazine, etc.
It's been said that it doesn't mess with your testosterone levels too much, but that might not be totally true using more than 20 mg oral per day. In fact, one study found that over half of the people taking just a little bit (oral 30-45 mg per day) still noticed a drop in their gonadotropin levels (which is not ideal). But, compared to other stuff out there, Primobolan might not mess with your hormones as much. And if you don't go too crazy with it and only use it for a little while, you shouldn't have too much trouble bouncing back.
aren’t these contradicting to what you’ve stated before ? Or have you changed your mind on that ?
You seemed to mock me heavily for implying estradiol would benefit igf1 activity in any way.
Type-IIx
Well-known Member
Where is there a contradiction? Metenolone (Primo) is nonaromatizable, so does not augment IGF-I, unlike T, that does, by in situ aromatization (process) rather than by the action of its aromatic product, E2. Unfortunately E2 increases IGFBP-1 in man, which reduces IGF-I bioavailability (unlike in ruminants).
Here you are saying he would benefit from having estrogen to augment Igf 1. When I said that, you brought up how it was useless because estrogen increases Igfbp
Type-IIx
Well-known Member
I assure you that's not what I am saying. Aromatizable androgen ≠ E2. Refer back to Why you should NOT take estrogens (Exogenous E2 ≠ Test's aromatic product) that I know you have read, yet continue to refuse to accept.
GuerillaPete
Well-known Member
Could primo act the same way Aromasin would and actually stimulate testosterone by lovering estradiol? In the absence of exogenous testosterone of course.
Type-IIx
Well-known Member
No, because Primo will slow hypothalamic GnRH pulse frequency (as an androgen). Hypothetically, I'd also expect exemestane (Aromasin) to be less efficacious at this than, e.g., anastrozole (Arimidex) because of its steroidal backbone and exerting some androgenic effects, though this is primarily through its primary metabolite. But I could be wrong, it just occurred to me.
GuerillaPete
Well-known Member
I will look into it further as my time permits but it was prescribed at 200mg/week or two weeks so they must have done some trials and tested its suppressiveness I would imagine .
There was a study on Aromasin and it did a good job at increasing testosterone levels and did not crash estrogen strangely even at 25/50mg per day .
I don't remember how long this trials lasted .
Before adopting the blast and cruise lifestyle i have tried this with 25mg x3 week and it felt quite good to be honest i am tempted to go back to it after some further research.
i still have this image saved from the study but i don't remember all the details without searching for it.
I suppose It’s not as though I refuse to accept. I just fail to understand the difference between serum e2 being the same level, and whether or not that same e2 level comes from aromatized testosterone or from exogenous estradiol.
Lipophilic steroids ultimately go to the same places in the body, so i fail to understand why the same Ligand would produce different results depending on its source( either aromatized testosterone or exogenous estradiol).
Now, I do understand there is a difference with varying administration methods of estradiol resulting in different metabolites- such as Greatly disproportionate levels of Estrone with oral administration of estradiol and also more significant increases in Shbg and other binding proteins. When you take into account IM estradiol, or even sublingual, you have an equal profile when compared to testosterone being aromatized.
Type-IIx
Well-known Member
If you say so. Do you want me to give you studies showing a) women having lower IGF-I than men, despite b) higher GH levels; c) women on exogenous estrogens requiring rhGH dose increases. I've already given you evidence that this occurs because E2 increases IGFBP-1 in man, while aromatizing androgen, e.g., testosterone, doesn't.
Or will you just continue this thick, "I just fail to understand" shit? Does it really affect the validity of anything I've been saying that YOU don't understand it, Para?
I cannot say I can trace out the cellular effects to explain the phenomenon either (I don't know that anyone can?), but I can still see that a - c are all true above, without being able to explain the nuance.
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I don’t disagree with you or fail to understand that (on exogenous estrogens increasing igfbp-1) I Believe that. Do you know the administration methods used here?
I also think it’s highly possible and likely that exogenous test that results in increased estradiol does the same thing. There just isn’t many studies in women or men where they’re doing this. I’ve looked but may have come up short.
Long story short, I’d expect the same result regardless of the estrogen source. Either aromatized test or exogenous. I’ve never seen anything to the contrary- Which gives me the strong hypothesis that the trend would continue. I see no reason why it wouldn’t. Again maybe I’m just missing information showing otherwise.
Type-IIx
Well-known Member
OK, @Para_33 I'm going to make one last ditch attempt to explain the phenomenon simply.
If a person takes nandrolone (Deca) only, an aromatizing androgen, and achieves sub-normal or low-normal E2, they will have significantly elevated IGF-I.
If you stop looking at the product (E2) as a factor - OK? If you can do that, it will begin to make sense.
I've seen it many times, I think falseprophet09 or has posted bloodwork that supports this here somewhat recently.
In fact, I am sure that E2 is a factor for IGF-I bioavailability - a negative one. That is, once aromatization is very high, E2 feeds back negatively on IGF-I levels because of IGFBP-1.
E2, then, is not a positive factor for enhancing IGF-I. Rather, aromatization as a process is.
If that thought exercise fails, I'm giving up on you.
If a person takes nandrolone (Deca) only, an aromatizing androgen, and achieves sub-normal or low-normal E2, they will have significantly elevated IGF-I.
If you stop looking at the product (E2) as a factor - OK? If you can do that, it will begin to make sense.
I've seen it many times, I think falseprophet09 or has posted bloodwork that supports this here somewhat recently.
In fact, I am sure that E2 is a factor for IGF-I bioavailability - a negative one. That is, once aromatization is very high, E2 feeds back negatively on IGF-I levels because of IGFBP-1.
E2, then, is not a positive factor for enhancing IGF-I. Rather, aromatization as a process is.
If that thought exercise fails, I'm giving up on you.
Type-IIx
Well-known Member
I just thought aloud that perhaps anastrozole > exemestane for increasing T synthesis as I was typing. Of course exemestane has this effect as an AI.
revono
New Member
I will also think out loud) theoretically, it is possible to increase T not only with anti-estrogens, but also with anti-androgens. If you use only non-flavored aas. For example, bicalutamide blocks ar, the brain receives a signal that there are no androgens in the system, as a result, the release of gonadotropins increases. I haven't tested it with tests, according to indirect sensations (erection, mood, muscle preservation) it works well. After bic, I take dutasteride, T increases even more.
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