Androsterone

JKVol

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Its alright, nothing mind blowing. Yes it is an andro.
I agree with this take. It has good nitrogen uptake so I like it on a cut so I don’t feel flat. If someone is not going for a major cycle and wanted to cut or recomp, using this with something like 11KT would be alright.
 

Dmzjne

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Yeah 3AD isn’t anything crazy but it was a nice compound if you wanted something more chill to run or stack.
I will have to look into it. Alot of new andro products; since they are legal and fairly safe. However again, half life and bioavailability become an issue.

I miss the old furaza/ orastan compounds. Always had great results and literally zero side effect profile
 
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wfreiling

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Yeah 3AD isn’t anything crazy but it was a nice compound if you wanted something more chill to run or stack.
In my experience, as a stacker I feel it’s more of an “enhancer” of whatever the primary compound is. Also, doesn’t have the same bp issues high dosed epiandro gives me.
 
ZOO

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I will have to look into it. Alot of new andro products; since they are legal and fairly safe. However again, half life and bioavailability become an issue.

I miss the old furaza/ orastan compounds. Always had great results and literally zero side effect profile
Sucks I don’t think I ever got to use Furuza although I used to have some at one point.

In my experience, as a stacker I feel it’s more of an “enhancer” of whatever the primary compound is. Also, doesn’t have the same bp issues high dosed epiandro gives me.
Good feedback man. It’s a game of give and take.
 
wfreiling

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I will have to look into it. Alot of new andro products; since they are legal and fairly safe. However again, half life and bioavailability become an issue.

I miss the old furaza/ orastan compounds. Always had great results and literally zero side effect profile
I have 2 bottles of cel p-stanz. That was similar, correct? I used every cel ph other than these back in the day
 
50Magnum

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In my experience, as a stacker I feel it’s more of an “enhancer” of whatever the primary compound is. Also, doesn’t have the same bp issues high dosed epiandro gives me.
I've been running it at 75mg now, I see people running it at a 100-150, is there a difference or should I just stay at the same dose??
 
wfreiling

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I've been running it at 75mg now, I see people running it at a 100-150, is there a difference or should I just stay at the same dose??
I like 100 a lot, 125 was too much. I guess try for a few days and see how it treats you
 
BigGame84

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Yes prostanozol; the non methylated ph to stanozolol (winstrol)

Furuza was only marketed as a pro hormone, however IMO already an active compound
Never got around to trying Furuza. From what I recall, you needed a lot. For whatever reason, it got banned back in 2014.
 
wfreiling

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Yes prostanozol; the non methylated ph to stanozolol (winstrol)

Furuza was only marketed as a pro hormone, however IMO already an active compound
Yup that’s the one. I remember it being dosed high. I’m not even sure i have enough to make it worth while
 
BigGame84

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A few years ago a local shop had OL Furuza for sale but only had 1 bottle. I was shocked to see it but there was just no point buying it for only 1 bottle. Probably needed 3 bottles to make it worth it.
 
GQdaLEGEND

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A few years ago a local shop had OL Furuza for sale but only had 1 bottle. I was shocked to see it but there was just no point buying it for only 1 bottle. Probably needed 3 bottles to make it worth it.
i woulda still picked it up if it was decent price
 

Dmzjne

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Never got around to trying Furuza. From what I recall, you needed a lot. For whatever reason, it got banned back in 2014.
Yeah that's how I feel about pheraplex, was slightly before my time.

Furaza was an excellent compound IMO. And the ONLY compound, to my knowledge, to have a furazan ring
 
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delsolrob

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sorry, I'm jumping back a little in the conversation - one of the cool things about androsteone is that it's also a GABA agonist and neurosteroid. It is a PH to DHT that also side steps the 5AR mechanism, additionally, DHT also converts back to Androsterone down stream
 

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sorry, I'm jumping back a little in the conversation - one of the cool things about androsteone is that it's also a GABA agonist and neurosteroid. It is a PH to DHT that also side steps the 5AR mechanism, additionally, DHT also converts back to Androsterone down stream
Oh its all good, bro. I hijacked this thread days ago!

Androsterone has a backway door mechanism to DHT. Therefore, although it bypasses 5 alpha reductase; there is no direct conversion to DHT
 
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delsolrob

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Oh its all good, bro. I hijacked this thread days ago!

Androsterone has a backway door mechanism to DHT. Therefore, although it bypasses 5 alpha reductase; there is no direct conversion to DHT
Sorry bud, you're speaking in circles - yes, Androsterone is a PH to DHT - it's a 2 step conversion via androstanediol
 
tubzy

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Its a downstream hormone. Conversion to DHT is inevitable. Doubtful anyone is taking pure DHT anymore, as this will destroy you with sides (hair loss/ prostate enlargment, voice changes)

IMO stanolone is an outdated drug
We don't really know how much androsterone actually converts to DHT versus androsterone direct effect. DHT and androsterone are very similar its just DHT is much more androgenic hence the result of being exposed to more potential sides. DHT is also a neurosteroid. Actually, androsterone increases DHT concentration in the brain as well.

I'm just curious how they compare in terms of the androgenic benefits i.e. CNS stimulation, strength gains, vascularity etc. pure DHT is much more potent on paper.

The only "negative" I have seen is due to stanolone's oral bioavailability people don't use it too much anymore but androsterone is the same situation - they are both non methylated but seem to still absorb
 

Dmzjne

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Sorry bud, you're speaking in circles - yes, Androsterone is a PH to DHT - it's a 2 step conversion via androstanediol
Incorrect. It may act as a precursor; indirectly converting to DHT. Androsterone is a metabolite of DHT and T. Although slight conversion may be taking place, this is not direct conversion. Therefore androsterone is a metabolic intermediate; not a prohormone

The 3b isomer of androsterone is epiandrosterone; however, although epiandro is ALSO considered a metabolic intermediate, it converts more directly to DHT via 5 alpha reductase. I still wouldn't consider this a prohormone, as natural metabolic intermediates would be considered precursors. Tell me again how androsterone directly converts to DHT, or show me some literature bud
 
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ZOO

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I interrupt this intellectual battle to inform everyone that I am willing to do a 100 unit run of Androsterone (250mg x 60 capsules). Cost would be $90-100 per bottle before discounts. So basically $80 average

Let me get a sound off and if you are down for a presale.
 

Dmzjne

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We don't really know how much androsterone actually converts to DHT versus androsterone direct effect. DHT and androsterone are very similar its just DHT is much more androgenic hence the result of being exposed to more potential sides. DHT is also a neurosteroid. Actually, androsterone increases DHT concentration in the brain as well.
Again. I would need to see some literature. I'm not saying there is NO conversion to DHT, but I wouldn't even compare it to something like proviron/ masteron/ stanolone.

How do we know androsterone will even cross the blood brain barrier? These are intermediate hormones in our body. We know the nueroprotective properties of T. But T is the master hormone, so our body will allow it to cross into the brain. Androsterone IS a neurosteriod, but most likely ONLY in vivo
 
tubzy

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Again. I would need to see some literature bro. I'm not saying there NO conversion to DHT, but I wouldn't even compare it to something like proviron/ masteron/ stanolone.

How do we know androsterone will even cross the blood brain barrier. These are intermediate hormones in our body. We know the nueroprotective properties of T. But T is the master hormone, so our body will allow it to cross into the brain. Androsterone IS a neurosteriod, but most likely ONLY in vivo
This was in vivo


DHEAS administration augmented concentrations of DHEA, pregnenolone, androstendiol and androstentriol in both brain structures, while androsterone injections increased brain levels of androsterone, epiandrosterone, 5α-dihydrotestosterone, and androstandiol. Present data document that although psychobehavioral and neurochemical effects of DHEAS and androsterone differ in several aspects; both neurosteroids have rewarding properties at certain dose ranges, suggesting their likely involvement in addictions, which entail different mechanisms.

And for anecdotal evidence, it definitely crosses the blood brain barrier. I have experimented with 1000mg+ of oral androsterone per day. I felt so tired and could literally fall asleep on my couch. The GABA agonism is definitely real. The fatigue would immediately lift after ingesting caffeine pills (caffeine upregulates GABA).

However - my point is I don't know if it is solely androsterone for this effect or its metabolites like shown in the study above.

Proviron and Masteron are not the same as stanolone or androsterone. Just because they are DHT derivatives doesn't mean they act exactly the same as DHT in the body. Androsterone and Stanolone (DHT) are actual bioidentical hormones that can convert into other endogenous hormones in the body while proviron and masteron cannot.
 
delsolrob

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Incorrect. It may act as a precursor; indirectly converting to DHT. Androsterone is a metabolite of DHT and T. Although slight conversion may be taking place, this is not direct conversion. Therefore androsterone is a metabolic intermediate; not a prohormone

The 3b isomer of androsterone is epiandrosterone; however, although epiandro is ALSO considered a metabolic intermediate, it converts more directly to DHT via 5 alpha reductase. I still wouldn't consider this a prohormone, as natural metabolic intermediates would be considered precursors. Tell me again how androsterone directly converts to DHT, or show me some literature bud
I believe you're getting caught up with semantics. I believe my statement to be correct, Androsterone offers a 2 step conversion to DHT via androstanediol.

I don't have all afternoon to dig up articles, but I'm pretty certain I've seen literature about androsterone crossing the blood brain barrier.
 
ANABOLICWRWLF

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Man, dat dere prostanozol sounds interesting...

So nobody is manufacturing that currently?
 
JKVol

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In my experience, as a stacker I feel it’s more of an “enhancer” of whatever the primary compound is. Also, doesn’t have the same bp issues high dosed epiandro gives me.
I’ve seen some say it’s proviron light which would be similar to what you are saying about it being an enhancer.
 

Dmzjne

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I believe you're getting caught up with semantics. I believe my statement to be correct, Androsterone offers a 2 step conversion to DHT via androstanediol.
Yes. However, I wouldn't classify any of the andros; as pro hormones

Most likely this conversion only takes place in the body, and when exogenous androsterone is detected; this conversion may or may not take place
 
thebigt

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Yes. However, I wouldn't classify any of the andros; as pro hormones

Most likely this conversion only takes place in the body, and when exogenous androsterone is detected; this conversion may or may not take place
seems to be a lot of interest though-eh?
 
StrongGuy

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I interrupt this intellectual battle to inform everyone that I am willing to do a 100 unit run of Androsterone (250mg x 60 capsules). Cost would be $90-100 per bottle before discounts. So basically $80 average

Let me get a sound off and if you are down for a presale.
I'm down. I'd be happy with just 100 mg per cap or anything in between to help with cost. Either way, I'd buy some.
 

Dmzjne

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This was in vivo


DHEAS administration augmented concentrations of DHEA, pregnenolone, androstendiol and androstentriol in both brain structures, while androsterone injections increased brain levels of androsterone, epiandrosterone, 5α-dihydrotestosterone, and androstandiol. Present data document that although psychobehavioral and neurochemical effects of DHEAS and androsterone differ in several aspects; both neurosteroids have rewarding properties at certain dose ranges, suggesting their likely involvement in addictions, which entail different mechanisms.

And for anecdotal evidence, it definitely crosses the blood brain barrier. I have experimented with 1000mg+ of oral androsterone per day
I'm sure @ 1000 mg/ day, eventually it is possible. Note that the compounds listed were given via injection!

Proviron and Masteron are not the same as stanolone or androsterone. Just because they are DHT derivatives doesn't mean they act exactly the same as DHT in the body. Androsterone and Stanolone (DHT) are actual bioidentical hormones that can convert into other endogenous hormones in the body while proviron and masteron cannot.
Agreed. But masteron and proviron are classic AAS, and they can't be counted out. IMO they have a higher affinity for dht receptors in the body/
work more efficiently at raising dht levels, compared to androsterone
 
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tubzy

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I'm sure @ 1000 mg/ day, eventually it is possible. Note that the compounds listed were given via injection!



Agreed. But masteron and proviron are classic AAS, and they can't be counted out. IMO they have a higher affinity for dht receptors in the body/
work more efficiently at raising dht levels, compared to androsterone
Why wouldn't sub 1000mg be possible for mental effects? People have reported mood changes in their logs at way lower doses than that.

Correct, it was injection but it was injection into serum not directly into the brain/CSF meaning it would still have to pass through the blood brain barrier just as if you took it oral or topically... it would just be less bioavailable orally compared to injections. :)

I understand your point but I'm saying a synthetic version of a parent hormone can be drastically different in the body. Easiest example is halotestin being a derivative of testosterone but being more androgenic than any of the DHT derivatives. And vice versa with anavar being DHT derivative but being insanely less androgenic than test and DHT.

Best way to measure this is to look at examples of bioidentical hormones rather than synthetics - this cuts out many of the variables.

Do you have any research on masteron and your claim? From my research, I thought masteron was developed mainly for women's breast cancer purposes and they took the DHT molecule and tailored it to be more selective for its anti estrogenic properties but made it less androgenic than actual DHT since women would be using it (i.e. since women don't want androgenic sides). I believe you mean androgen receptors instead of DHT receptors, right?
 

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Do you have any research on masteron and your claim? From my research, I thought masteron was developed mainly for women's breast cancer purposes and they took the DHT molecule and tailored it to be more selective for its anti estrogenic properties but made it less androgenic than actual DHT since women would be using it (i.e. since women don't want androgenic sides). I believe you mean androgen receptors instead of DHT receptors, right?
AAS binds to AR, DHT, IGF1, ER, PGR, etc. They all have different binding affinity for the receptor sites. This is what makes AAS so complex. For example Anadrol; regarded as strongest oral. Has very weak affinity (if any), to the AR

However because classic AAS is more understood (decades of literature), we can make a more definitive assessment from anecdotal experience. That being said; I have plenty of anecdotal experience. This is why I usually hang out in the anabolics forum. However even with the literature; AAS will not always act the same in the body (with exception of T), as would be expected on paper (chemical structure, controlled studies, etc)

As for masteron; this question belongs in the anabolics forum. Masteron was initially developed for breast cancer, however later abandoned because IT WAS highly androgenic. Perfect example to concrete my above statement


Why wouldn't sub 1000mg be possible for mental effects? People have reported mood changes in their logs at way lower doses than that.
People meaning scientist? The internet is FULL of misinformation, and the industry will base write ups/ draw conclusions on highly questionable data. For example these self proclaimed SARMs guru's, that have no background in bodybuilding or powerlifting. These folks making definitive claims about SARMs and Andros are full of ****, and just making money off there vested interest

For exampe; I have been taking between 400 and 500 mg of androsterone (it is part of a blend with epiandro). And I would respectively disagree; that very little IF ANY crossing at the blood brain barrier takes place. If you could show me studies on humans (and not rats); please by all means educate me
 
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celc5

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Super subjective post here but I've tried quite a few of the compounds in this thread.

Furuza and prostan are not the same. Furuza was very mild, decent strength, and decent hardening. It gave mild aggression, strength, libido. It was non methylated so it was a nice boost to our dumb oral only cycles back then. It had to be dosed very high. The user who suggested 3 bottles is being conservative. 4 or 5 was necessary if u wanted to maximize benefit. I would purchase furuza again if were available and not cost prohibited.

Prostan was even weaker, had to be dosed even more aggressively, and always seemed harder to find. It was a waste imo.

I enjoy the mildness of epi andro and androstereone. I feel like androstereone is much more potent and cost effective transdermal. It makes me feel like working hard feels good. I can remember having to do push-ups to failure after waking up in the middle of the night. Probably just took it too late LOL Libido affect was even more pronounced than furaza, but I eventually became grumpy/irritable with a less smooth alpha feeling. Furuza stayed smooth and androstereone eventually makes me angry in comparison. I never experienced the gaba fog that is being discussed, but maybe I didn't dose it high enough? I'd probably use both of these if they fell into my lap, but imo cost outweighs benefit.

An interesting discussion might be to differentiate gaba fog vs uh oh endogenous test is shut the ef down fog.

Masteron is what it is. No need for me to rehash.
 
tubzy

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AAS binds to AR, DHT, IGF1, ER, PGR, etc. They all have different binding affinity for the receptor sites. This is what makes AAS so complex. For example Anadrol; regarded as strongest oral. Has very weak affinity (if any), to the AR

However because classic AAS is more understood (decades of literature), we can make a more definitive assessment from anecdotal experience. That being said; I have plenty of anecdotal experience. This is why I usually hang out in the anabolics forum. However even with the literature; AAS will not always act the same in the body (with exception of T), as would be expected on paper (chemical structure, controlled studies, etc)

As for masteron; this question belongs in the anabolics forum. Masteron was initially developed for breast cancer, however later abandoned because IT WAS highly androgenic. Perfect example to concrete my above statement



People meaning scientist? The internet is FULL of misinformation, and the industry will base write ups/ draw conclusions on highly questionable data. For example these self proclaimed SARMs guru's, that have no background in bodybuilding or powerlifting. These folks making definitive claims about SARMs and Andros are full of ****, and just making money off there vested interest

For exampe; I have been taking between 400 and 500 mg of androsterone (it is part of a blend with epiandro). And I would respectively disagree; that very little IF ANY crossing at the blood brain barrier takes place. If you could show me studies on humans (and not rats); please by all means educate me
I know how AAS work - I'll ask again...pls show me evidence of masteron binding to the DHT receptor and the potency at which it binds meaning in the muscle or prostate? :). I have not seen it unless you mean androgen receptor.




Anadrol being the strongest oral for what exactly?

However even with the literature; AAS will not always act the same in the body (with exception of T), as would be expected on paper (chemical structure, controlled studies, etc)

That is my point. Testosterones, DHT, androsterone, epiandrosterone are all natural occurring bioidentical hormones. So your point in using proviron or masteron to compare androsterone or DHT is not accurate. Synthetic AAS that are altered from their parent hormone behave differently than bioidentical hormones do.

As for masteron; this question belongs in the anabolics forum. Masteron was initially developed for breast cancer, however later abandoned because IT WAS highly androgenic. Perfect example to concrete my above statement

You are incorrect. Not only that masteron was shown to be less virializing in comparison to test prop and we obviously known DHT is much more virializing than test. DHT is more androgenic than masteron.







You can see the androgenic ratios between DHT and masteron below:

DHT



Masteron




For exampe; I have been taking between 400 and 500 mg of androsterone (it is part of a blend with epiandro). And I would respectively disagree; that very little IF ANY crossing at the blood brain barrier takes place. If you could show me studies on humans (and not rats); please by all means educate me

You asked for evidence and I showed you a study and now you want a human study. Seems like you keep moving the goal post but there is more evidence supporting that is does cross the brain barrier. So the burden is on you to prove it doesn't cross if that is what you believe.

Increase your dosage. If you take blends you will actually feel less of an effect mentally since androsterone and epiandrosterone have opposite effects. Androsterone is a GABA agonist while Epiandrosterone is a GABA antagonist so they can actually cancel each other out which is why some people like taking the blend since the epi will help overcome the lethargy from androsterone.

There is almost a 100 page thread of people using small amounts of androsterone (milligrams) and getting effects mentally
 

Dmzjne

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I know how AAS work - I'll ask again...pls show me evidence of masteron binding to the DHT receptor and the potency at which it binds meaning in the muscle or prostate? :). I have not seen it unless you mean androgen receptor.




Anadrol being the strongest oral for what exactly?

However even with the literature; AAS will not always act the same in the body (with exception of T), as would be expected on paper (chemical structure, controlled studies, etc)

That is my point. Testosterones, DHT, androsterone, epiandrosterone are all natural occurring bioidentical hormones. So your point in using proviron or masteron to compare androsterone or DHT is not accurate. Synthetic AAS that are altered from their parent hormone behave differently than bioidentical hormones do.

As for masteron; this question belongs in the anabolics forum. Masteron was initially developed for breast cancer, however later abandoned because IT WAS highly androgenic. Perfect example to concrete my above statement

You are incorrect. Not only that masteron was shown to be less virializing in comparison to test prop and we obviously known DHT is much more virializing than test. DHT is more androgenic than masteron.







You can see the androgenic ratios between DHT and masteron below:

DHT



Masteron




For exampe; I have been taking between 400 and 500 mg of androsterone (it is part of a blend with epiandro). And I would respectively disagree; that very little IF ANY crossing at the blood brain barrier takes place. If you could show me studies on humans (and not rats); please by all means educate me

You asked for evidence and I showed you a study and now you want a human study. Seems like you keep moving the goal post but there is more evidence supporting that is does cross the brain barrier. So the burden is on you to prove it doesn't cross if that is what you believe.

Increase your dosage. If you take blends you will actually feel less of an effect mentally since androsterone and epiandrosterone have opposite effects. Androsterone is a GABA agonist while Epiandrosterone is a GABA antagonist so they can actually cancel each other out which is why some people like taking the blend since the epi will help overcome the lethargy from androsterone.

There is almost a 100 page thread of people using small amounts of androsterone (milligrams) and getting effects mentally
Actually affinity for DHT receptors is irrelevant! I'm the guy here answering the questions; your the guy asking. Tell me your AAS experience, again 🤔 bodyweight?? squat/ bench/ deadlift numbers?

Your list of bio identical hormones is irrelevant. Both DHT and estrogen are converted directly from total T. You can add exogenous DHT all you want; if total T is low, adding stanalone would do nothing. This is why, like I said, its preferable to use masteron/ proviron over bioidentical downstream hormones
 
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Dmzjne

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That is my point. Testosterones, DHT, androsterone, epiandrosterone are all natural occurring bioidentical hormones. So your point in using proviron or masteron to compare androsterone or DHT is not accurate. Synthetic AAS that are altered from their parent hormone behave differently than bioidentical hormones do.

Incorrect. Not all bioidentical hormones are master hormones. Downstream intermediate hormones arent even close to the role of T, DHT, and PGR.

Tell me again how well you understand AAS?
 
tubzy

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Actually affinity for DHT receptors is irrelevant! I'm the guy here answering the questions; your the guy asking. Tell me your AAS experience, again 🤔 bodyweight?? squat/ bench/ deadlift numbers?

Your list of bio identical hormones is irrelevant. Both DHT and estrogen are converted directly from total T. You can add exogenous DHT all you want; if total T is low, adding stanalone would do nothing. This is why, like I said, its preferable to use masteron/ proviron over bioidentical downstream hormones
So if it not relevant why did you even bring up DHT's affinity in the first place in your quote below? Seems a bit of backtracking now as you don't want to talk about it and have yet to provide any research to back up your claim :rolleyes:.

Agreed. But masteron and proviron are classic AAS, and they can't be counted out. IMO they have a higher affinity for dht receptors in the body/
work more efficiently at raising dht levels, compared to androsterone

I hope you understand there is no such term as a DHT receptor. You keep referring as DHT receptor and Androgen Receptor as two different receptors. There is an androgen receptor in which DHT (or any androgen) binds too and expresses it androgenic ligand stronger than testosterone does. That is why if you use a topical androgen receptor blocker like RU58841 you can stop or reverse hair loss since you stop DHT along with all androgens (i.e. testosterone) from binding to the AR not the "DHT receptor".

Tell me your AAS experience, again 🤔 bodyweight?? squat/ bench/ deadlift numbers?

So now you want to leverage anecdotal evidence only when it is convenient for you. I have plenty experience with DHT derivatives and hair loss drugs. You can read my post history from this very forum 11 years ago in which my first thread here was my superdrol cycle and hair loss from it.


Your list of bio identical hormones is irrelevant. Both DHT and estrogen are converted directly from total T. You can add exogenous DHT all you want; if total T is low, adding stanalone would do nothing. This is why, like I said, its preferable to use masteron/ proviron over bioidentical downstream hormones

Are you familiar with the backdoor pathway? It seems you are just parroting the same mainstream bro science talking points about AAS without actually researching it. You can get DHT conversion without being directly converted from total T through the backdoor pathway - see below.

I have no issue with your comment about using synthetic AAS for HRT/TRT uses at all if someone wants to do that. But I never once discussed anything about using bioidentical hormones for low T or HRT use at all in this thread.

 

Dmzjne

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Tell me your AAS experience, again 🤔 bodyweight?? squat/ bench/ deadlift numbers?
Keep avoiding this question; maybe out of embarrassment?? The better understanding and experience with AAS = more muscle. Do you even lift?

Are you familiar with the backdoor pathway? It seems you are just parroting the same mainstream bro science talking points about AAS without actually researching it. You can get DHT conversion without being directly converted from total T through the backdoor pathway - see below.
Once again. In order to reach supra physiological levels of ANY hormone in the body; Total T is required to be sky high. The only proven and effective method is taking exogenous T (not punative downstream hormones; albeit bio identical)

This is why Stanolone was discontinued. It may raise DHT levels in the body AT first, but eventually will become inefficient and wreak havoc inside the body. This is why test boosters only work for a short period of time!


So if it not relevant why did you even bring up DHT's affinity in the first place in your quote below? Seems a bit of backtracking now as you don't want to talk about it and have yet to provide any research to back up your claim :rolleyes:.
I stated that AAS like Masteron have a higher affinity to DHT.; meaning once activated at the AR, they produce more DHT when compared to punative downstream hormones.

The androgen receptor IS the DHT receptor. They are one in the same. Once again; masteron/ proviron are more efficient at raising DHT levels in the body AND keeping them raised. As for literature; once again masteron was discontinued in medicine. Not to mention it was ONLY researched for breast cancer in females; IMO the literature is completely unrelated for what is being discussed. This is why I ask your AAS experience? Anecdotal experience with AAS will trump medical literature 99 percent of the time. We cannot draw conclusions based off the literature alone!
 
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JKVol

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I interrupt this intellectual battle to inform everyone that I am willing to do a 100 unit run of Androsterone (250mg x 60 capsules). Cost would be $90-100 per bottle before discounts. So basically $80 average

Let me get a sound off and if you are down for a presale.
I believe this post got lost ITT.
 
tubzy

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Keep avoiding this question; maybe out of embarrassment?? The better understanding and experience with AAS = more muscle. Do you even lift?



Once again. In order to reach supra physiological levels of ANY hormone in the body; Total T is required to be sky high. The only proven and effective method is taking exogenous T (not punative downstream hormones; albeit bio identical)

This is why Stanolone was discontinued. It may raise DHT levels in the body AT first, but eventually will become inefficient and wreak havoc inside the body. This is why test boosters only work for a short period of time!




I stated that AAS like Masteron have a higher affinity to DHT.; meaning once activated at the AR, they produce more DHT when compared to punative downstream hormones.

The androgen receptor IS the DHT receptor. They are one in the same. Once again; masteron/ proviron are more efficient at raising DHT levels in the body AND keeping them raised. As for literature; once again masteron was discontinued in medicine. Not to mention it was ONLY researched for breast cancer in females; IMO the literature is completely unrelated for what is being discussed. This is why I ask your AAS experience? Anecdotal experience with AAS will trump medical literature 99 percent of the time. We cannot draw conclusions based off the literature alone!
Keep avoiding this question; maybe out of embarrassment?? The better understanding and experience with AAS = more muscle. Do you even lift?

Lol - you're obviously trolling but nice pivot but I would too after realizing I just the lost the actual argument. My actual personal stats mean nothing in reference to if DHT is more androgenic than masteron. I presented actual evidence both on paper and clinically and you just ignore and give your opinion without any evidence behind which means nothing.

Not only is masteron weaker than DHT on paper but it was even shown to be less virilizing than test propionate in clinical practice :ROFLMAO::ROFLMAO:. You not only lost your initial argument of masteron being more powerful androgenically than pure DHT but even testosterone showed stronger androgenic properties than it.


Once again. In order to reach supra physiological levels of ANY hormone in the body; Total T is required to be sky high. The only proven and effective method is taking exogenous T (not punative downstream hormones; albeit bio identical)

Obviously, you can't use any DHT hormones or synthetic derivatives as HRT solely without test as your estrogen function would be tanked long term. I don't understand why you keep bringing up HRT - pls stop pivoting. No one in this thread is talking about using these bioidentical hormones for HRT purposes. I'm talking about cycling which is what everyone in this thread is talking about.


This is why Stanolone was discontinued. It may raise DHT levels in the body AT first, but eventually will become inefficient and wreak havoc inside the body. This is why test boosters only work for a short period of time!

They still prescribe DHT gel today in other countries. Again, I could care less for HRT purposes, but if you were going to use DHT for HRT purposes would you do exogenous test + exogenous DHT that way you still have estrogen flowing but still maintain androgenic.


I stated that AAS like Masteron have a higher affinity to DHT.; meaning once activated at the AR, they produce more DHT when compared to punative downstream hormones.

The androgen receptor IS the DHT receptor. They are one in the same. Once again; masteron/ proviron are more efficient at raising DHT levels in the body AND keeping them raised. As for literature; once again masteron was discontinued in medicine. Not to mention it was ONLY researched for breast cancer in females; IMO the literature is completely unrelated for what is being discussed. This is why I ask your AAS experience? Anecdotal experience with AAS will trump medical literature 99 percent of the time. We cannot draw conclusions based off the literature alone!


Again - I will ask for the third time since you seem to keep giving me your baseless opinion. Please present evidence that masteron has higher affinity to DHT than actual DHT itself.

I already told you my AAS experience in my last post. Also, I have been watching Dylan Gemelli videos close to a decade now which automatically puts me above you.
 
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