Primo: risk-reward profile... is it 'conspicuous consumption' or does it really only 'shine' with long-term use?

[Jbagel132]

DHT displacement from what, SHBG? Wouldn't that yield more active DHT in circulation? There is something called the Megalin hypothesis that might impact uptake of an SHBG-DHT complex, but this is speculative. What is the connexion between SHBG-bound DHT and sexual function or libido, anyhow?

Finasteride on the other hand is a 5α-reductase inhibitor that actually reduces DHT synthesis by this mechanism. It also, separately, has been associated with a post-finasteride syndrome that may (very speculatively) implicate neurosteroids (synthesized in the CNS).

Are you saying that primobolan could inhibit libido in the same way that Finasteride can? That’s confusing, because it’s also always said that Finasteride cannot protect from hair loss due to the DHT-derivatives, and I’m pretty sure the studies that are out there indicate ED from Finasteride is rare, all things considered.

 

[Type-IIx]

Are you saying that primobolan could inhibit libido in the same way that Finasteride can? That’s confusing, because it’s also always said that Finasteride cannot protect from hair loss due to the DHT-derivatives, and I’m pretty sure the studies that are out there indicate ED from Finasteride is rare, all things considered.

Nope, I'm saying the opposite! That's what VenomYo was suggesting.

I agree with both of your statements, that finasteride doesn't mitigate hair loss due to the androgens described as "DHT-derivatives" being already 5a-reduced and that ED from finasteride is very rare.

 

[T&H]

DHT displacement from what, SHBG? Wouldn't that yield more active DHT in circulation? There is something called the Megalin hypothesis that might impact uptake of an SHBG-DHT complex, but this is speculative. What is the connexion between SHBG-bound DHT and sexual function or libido, anyhow?

Finasteride on the other hand is a 5α-reductase inhibitor that actually reduces DHT synthesis by this mechanism. It also, separately, has been associated with a post-finasteride syndrome that may (very speculatively) implicate neurosteroids (synthesized in the CNS).

Wanted to ask you a question. Would a drastic slowing of facial hair growth be caused by low estrogen?

 

[Type-IIx]

Wanted to ask you a question. Would a drastic slowing of facial hair growth be caused by low estrogen?

Don't think so.

 

[Jbagel132]

Nope, I'm saying the opposite! That's what VenomYo was suggesting.

I agree with both of your statements, that finasteride doesn't mitigate hair loss due to the androgens described as "DHT-derivatives" being already 5a-reduced and that ED from finasteride is very rare.

My rationale always went along with this: If Finasteride has a small chance of causing ED, then using a compound known as a “DHT-derivative” must cause the opposite effect, that’s to say, MORE libido.

 

[GreenAmine]

DHT displacement from what, SHBG? Wouldn't that yield more active DHT in circulation? There is something called the Megalin hypothesis that might impact uptake of an SHBG-DHT complex, but this is speculative. What is the connexion between SHBG-bound DHT and sexual function or libido, anyhow?

Finasteride on the other hand is a 5α-reductase inhibitor that actually reduces DHT synthesis by this mechanism. It also, separately, has been associated with a post-finasteride syndrome that may (very speculatively) implicate neurosteroids (synthesized in the CNS).

This was a hypothesis I have been mulling over for a while, and one that I mentioned in @VenomYo 's thread about primo and loss of libido.

I did not actually mean that it displaces DHT from SHBG (although that could be an issue; I'm not completely sold on the current thinking in regards to free/unbound androgens, but I digress), but from the NR3C4 receptor by competitive binding.

Further (and I hope you can provide input on this, since it's not something I've thoroughly researched), an excess of DHT derivatives could be providing feedback that DHT is plentiful, downregulating 5a-reductase activity. The decreased amount of actual DHT could cause libido issues.

 

[Type-IIx]

This was a hypothesis I have been mulling over for a while, and one that I mentioned in @VenomYo 's thread about primo and loss of libido.

I did not actually mean that it displaces DHT from SHBG (although that could be an issue; I'm not completely sold on the current thinking in regards to free/unbound androgens, but I digress), but from the NR3C4 receptor by competitive binding.

Further (and I hope you can provide input on this, since it's not something I've thoroughly researched), an excess of DHT derivatives could be providing feedback that DHT is plentiful, downregulating 5a-reductase activity. The decreased amount of actual DHT could cause libido issues.

Oh man, I don't know about this, can you put together a case for why this might be with some references? It's never been something I looked into, sexual function and AR potency, competitive inhibition by androgens vs. DHT. It's not something I'm inclined to investigate with vigor honestly. It would surprise me to see methenolone inhibiting DHT by competitive binding at the AR to begin with. Everything coming to mind regarding methenolone's AR binding across species hints at methenolone being a fairly weak AR ligand (Saartok, 0.09RBA vs. DHT in rabbit skeletal muscle, 0.14RBA vs. DHT in rat prostate). It's not markedly potent in Houtman (the AR CALUX mammalian reporter gene bioassay) or anything.

DHT derivatives is a misnomer, bad broscience. Basically these are androgens without a C-4,5 double bond (so relatively reduced AR binding), but claw back some AR affinity by providing a still hydrophobic backbone (versus their 5B-reduced counterparts). I don't think an asymmetric junction between rings A & B at C-5 confuses the body into downregulating 5a-reductase activity or anything. IDK, it seems pretty hypothetical without any supporting data brother.

 

[hometeam]

DHT derivatives is a misnomer, bad broscience. Basically these are androgens without a C-4,5 double bond (so relatively reduced AR binding), but claw back some AR affinity by providing a still hydrophobic backbone (versus their 5B-reduced counterparts).

Interesting... they do all kind of act similarly to DHT though: being a weaker anabolic than testosterone, the oily skin, positive effects on mood, lack of aromatization and hair loss.

 

[Type-IIx]

Interesting... they do all kind of act similarly to DHT though: being a weaker anabolic than testosterone, the oily skin, positive effects on mood, lack of aromatization and hair loss.

I mean, not really. Superdrol is not a weaker anabolic than testosterone, nor does it have many positive effects on mood. Oily skin, hair loss are class effects of androgens. Aromatization is more an exception when looking at AAS than the rule.

 

[hometeam]

I mean, not really. Superdrol is not a weaker anabolic than testosterone, nor does it have many positive effects on mood. Oily skin, hair loss are class effects of androgens. Aromatization is more an exception when looking at AAS than the rule.

It is interesting how they can take boldenone and add 17aa methylation and get dianabol, with completely different properties. And same can be said for masteron and superdrol.

 

[Type-IIx]

It is interesting how they can take boldenone and add 17aa methylation and get dianabol, with completely different properties. And same can be said for masteron and superdrol.

It is really interesting. I try to visualize how the molecule binds to the AR, given the structure of both. There are some key characteristics that increase AR binding affinity, a tertiary 17α-methyl group addition to the structure is a good way to flatten the steroid so it fits into the AR more like a knife, it also prolongs hepatic clearance and prevents aromatization of the A-ring.

 

[GreenAmine]

Oh man, I don't know about this, can you put together a case for why this might be with some references? It's never been something I looked into, sexual function and AR potency, competitive inhibition by androgens vs. DHT. It's not something I'm inclined to investigate with vigor honestly. It would surprise me to see methenolone inhibiting DHT by competitive binding at the AR to begin with. Everything coming to mind regarding methenolone's AR binding across species hints at methenolone being a fairly weak AR ligand (Saartok, 0.09RBA vs. DHT in rabbit skeletal muscle, 0.14RBA vs. DHT in rat prostate). It's not markedly potent in Houtman (the AR CALUX mammalian reporter gene bioassay) or anything.

DHT derivatives is a misnomer, bad broscience. Basically these are androgens without a C-4,5 double bond (so relatively reduced AR binding), but claw back some AR affinity by providing a still hydrophobic backbone (versus their 5B-reduced counterparts). I don't think an asymmetric junction between rings A & B at C-5 confuses the body into downregulating 5a-reductase activity or anything. IDK, it seems pretty hypothetical without any supporting data brother.

Eh, it was more of a hunch than anything concrete. You've studied this particular area a lot more than I have, so if you don't think it's worth pursuing, I trust your judgement. It's the only plausible explanation I could think of at the moment to explain an immediate loss of libido upon injection of primo. Libido is a very complicated concept, so even if it is a part of the explanation, I'm sure it's not as simple as DHT binding inhibition.

 

[Type-IIx]

Eh, it was more of a hunch than anything concrete. You've studied this particular area a lot more than I have, so if you don't think it's worth pursuing, I trust your judgement. It's the only plausible explanation I could think of at the moment to explain an immediate loss of libido upon injection of primo. Libido is a very complicated concept, so even if it is a part of the explanation, I'm sure it's not as simple as DHT binding inhibition.

That's my thinking as well, libido is usually 80% psychological. I'm sure T increases libido, but these compounds cross the BBB as well, it could be for myriad reasons. And yes, I think that competitive inhibition vs DHT at the AR would be rather far down the list. Actually, given that it's a rapid action as you describe, this means (aside from a possible psychological cause) it's likely due to nongenomic action - it could be mediated by a membrane receptor/GPCR or some effect by crossing the BBB - this would be more likely than any AR-mediated effect.

 

[hometeam]

That's my thinking as well, libido is usually 80% psychological. I'm sure T increases libido, but these compounds cross the BBB as well, it could be for myriad reasons. And yes, I think that competitive inhibition vs DHT at the AR would be rather far down the list. Actually, given that it's a rapid action as you describe, this means (aside from a possible psychological cause) it's likely due to nongenomic action - it could be mediated by a membrane receptor/GPCR or some effect by crossing the BBB - this would be more likely than any AR-mediated effect.

Well I know one thing for sure: a man's libido is naturally much higher than a woman. And with those women who have had a hysterectomy and are on HRT, they tend to be the horniest.

 

[Rido]

Well I know one thing for sure: a man's libido is naturally much higher than a woman. And with those women who have had a hysterectomy and are on HRT, they tend to be the horniest.

I am a swinger, some of the best women to do stuff with are cougars.. fucking horny as hell and know what they want. They are straight up on the prowl ready to throw down. no holes off limits.

 

[Rido]

@Type-IIx . IDK wtf happened to my test levels here but
first pic is 600 test C, 300 primo

2nd is 600 test C, 300 primo, 500 hcg twice a week


3rd is 600 test C, 600 mast. 500 hcg twice a week

 

[Type-IIx]

@Type-IIx . IDK wtf happened to my test levels here but
first pic is 600 test C, 300 primo
View attachment 160764
2nd is 600 test C, 300 primo, 500 hcg twice a week
View attachment 160768

3rd is 600 test C, 600 mast. 500 hcg twice a week

View attachment 160765

Nice, more evidence of Primo modulating serum E2. Depending on the assay used, there is some degree of cross-reactivity with Primo and Testosterone.

 

[T&H]

Nice, more evidence of Primo modulating serum E2. Depending on the assay used, there is some degree of cross-reactivity with Primo and Testosterone.

Just got bloodwork back myself. 300 test from private source, 500mg @Stanfordpharma1 Primo with no ai. No sex drive at all, even noticed slow facial hair growth as I don't need to shave once a week like I used to for years. I've had an estrogen lvl of 9 years ago running test mast Primo but still had a sex drive.

 

[Rido]

Just got bloodwork back myself. 300 test from private source, 500mg @Stanfordpharma1 Primo with no ai. No sex drive at all, even noticed slow facial hair growth as I don't need to shave once a week like I used to for years. I've had an estrogen lvl of 9 years ago running test mast Primo but still had a sex drive.

Do you think it's possible that you didn't have primo 9 years ago?

My friend ran 450 test and 450 primo. Same bottle from me. We couldnt get follow up blood work because he is in jail now...

 

[T&H]

Do you think it's possible that you didn't have primo 9 years ago?

My friend ran 450 test and 450 primo. Same bottle from me. We couldnt get follow up blood work because he is in jail now...

Estrogen level of 9. My last bloodwork about 1.5 years ago.