Dumbass q - how do you put together a cycle?

[Until_It_Sleeps]

What I mean is, how do people know what drugs work best with what? If all steroids will add mass with proper training and diet, why the need for stacks containing 3, 4 or more different things?

For example, one common recommendation I see is test/tren /win or test/deca /eq. What reason for these three together? What would happen if you ran test and tren by themselves, or if you ran test and tren with eq instead of win?

Are there drugs that almost always have to be stacked with something else; that just won't work alone? Are there injectables that should not be used with other injectables? And, is any of this determined in any way other than what people see their friends do?

Asking as someone with next to no knowledge of chemistry...

[t-dogg]

Pretty much all aas will shut a man down. So test should always be the base.

Certain aas work well for some and others not so much. You figure out stacks that work best for you or someone lays a blue print out for you.

[Bonaparte]

Note: all the stuff about test in here is for men. Women do not require a test base.

Well, you first want to pick a compound that will be the base of your cycle. The workhorse. The one that will best give the results you're looking for and that you can run at a solid dose. If that compound is test, things just got simpler.
Otherwise, you'll probably want to add some test to maintain proper male functioning.
Now if you want some extra benefits from the cycle that the base compound does not offer much of, you start adding a bit of this or that. Also, some drugs will help counteract the side effects of others, so stacking those is great (this will usually involve using a DHT analogue to help reduce the estrogen and bloat from a test derivative or nandrolone ).

But tell us about yourself. Are you trying to figure out what to AAS to run? Do you compete? What sides are you trying to avoid, and how much risk are you willing to take?

[Sworder]

All steroids will give you the mass that you need with proper training and diet!

The reasoning behind adding more compounds can be plenty. Certain steroids dry you out such as Winstrol , Masteron , and Primobolan . Other will give you a lot of bloat such as dianabol , nandrolone and testosterone .

It is a lot of personal preference when it comes to picking what steroids you include in your cycle. They are all slightly different, but all achieve the same goal, activating the androgen receptor.

The reason I start adding more compounds is to avoid having too much of one; side effects from one compound may pile up if using too much. For example: 1000mg Test E/week will give you bountiful estrogen conversion which may be difficult to manage. A better plan may be to do 500mg Test E and then adding an oral such as 100mg Anadrol /day.

Starting cycles should be 500mg Test, then if your growth starts to slow down using that amount(you should be by your natural limit at that point). You can bump it up and run another compound so you would be running 500mg Test and 400mg Deca . I don't like running Deca too high, makes me just feel weird.. So if I needed to bump it up even more I could do 500 Test, 400 Deca, and 60mg winstrol/day.

The reason for stacking is generally because you want to create a synergy(1+1=3) between the compounds. But! I believe there is a minimum you have to do of each compound to achieve the effect of it.
Because if you would want synergy wouldn't it make sense to run: 100mg EQ, 200mg Test, 100mg Deca, 100mg Tren , 100mg Mast, 100mg Primo, 20mg Dianabol/day, 50mg Anadrol/day the total sum of AAS would be 1190mg(I think). Now IMO! That would be a very sloppy cycle and it would be very difficult to "feel" each compound. 500mg Test 400mg Tren and 50mg Winny/day would be a better combo!

In reality, you don't need anything else than Test/Tren. Those two compounds will get you to any place you want to go! Then, once you are starting to plateau on AAS you can start adding insulin /hGH. So then you can run something like 700mg Test/600mg Tren/10iu slin/6iu hGH... *Note these doses are appropriate if you are trying to achieve a pro card..

It's all about what level your physique is at.

You can mix pretty much anything, you will always want something that will convert to estrogen though as you will feel like crap if you have 0 estrogen.

You can bulk or cut on anything. 500mg Test 400mg Deca can provide a good cut cycle depending on your diet and exercise. The bloat produced is, or should, be irrelevant as it is the body-fat you want to burn. Water retention/bloat will leave after your cycle.

The most common cut cycles will have testosterone/anavar . The cut cycles for competition will have some testosterone/tren/masteron(or primo/winny) the latter 3 for their ability to convert to DHT. DHT conversion is done heavily just below the skin via 5AR. This will cause and produce certain effects more acne, less fluid retention et cetera... There is a misconception that anavar is made for cutting, it is not! All AAS will do so you burn more fat. There are a lot of studies on anavar where body-fat has been reduced and I think that is where the notion is spawned from.

The more androgens you have in your system the greater your body recomp/fat burning will be. The body doesn't recognize individual drugs, they are all known as androgens to the body. Other wise it would be nice to add trenbolone to your natural testosterone production. But the body senses the androgen trenbolone and shuts down its own production of testosterone.

Then there is the ester aspect. The ester used is a reflection of the cycle length. Short esters for short cycles and long esters for longer cycles.

[Budly69]

All steroids will give you the mass that you need with proper training and diet!

The reasoning behind adding more compounds can be plenty. Certain steroids dry you out such as Winstrol , Masteron , and Primobolan . Other will give you a lot of bloat such as dianabol , nandrolone and testosterone .

It is a lot of personal preference when it comes to picking what steroids you include in your cycle. They are all slightly different, but all achieve the same goal, activating the androgen receptor.

The reason I start adding more compounds is to avoid having too much of one; side effects from one compound may pile up if using too much. For example: 1000mg Test E/week will give you bountiful estrogen conversion which may be difficult to manage. A better plan may be to do 500mg Test E and then adding an oral such as 100mg Anadrol /day.

Starting cycles should be 500mg Test, then if your growth starts to slow down using that amount(you should be by your natural limit at that point). You can bump it up and run another compound so you would be running 500mg Test and 400mg Deca . I don't like running Deca too high, makes me just feel weird.. So if I needed to bump it up even more I could do 500 Test, 400 Deca, and 60mg winstrol/day.

The reason for stacking is generally because you want to create a synergy(1+1=3) between the compounds. But! I believe there is a minimum you have to do of each compound to achieve the effect of it.
Because if you would want synergy wouldn't it make sense to run: 100mg EQ, 200mg Test, 100mg Deca, 100mg Tren , 100mg Mast, 100mg Primo, 20mg Dianabol/day, 50mg Anadrol/day the total sum of AAS would be 1190mg(I think). Now IMO! That would be a very sloppy cycle and it would be very difficult to "feel" each compound. 500mg Test 400mg Tren and 50mg Winny/day would be a better combo!

In reality, you don't need anything else than Test/Tren. Those two compounds will get you to any place you want to go! Then, once you are starting to plateau on AAS you can start adding insulin /hGH. So then you can run something like 700mg Test/600mg Tren/10iu slin/6iu hGH... *Note these doses are appropriate if you are trying to achieve a pro card..

It's all about what level your physique is at.

You can mix pretty much anything, you will always want something that will convert to estrogen though as you will feel like crap if you have 0 estrogen.

You can bulk or cut on anything. 500mg Test 400mg Deca can provide a good cut cycle depending on your diet and exercise. The bloat produced is, or should, be irrelevant as it is the body-fat you want to burn. Water retention/bloat will leave after your cycle.

The most common cut cycles will have testosterone/anavar . The cut cycles for competition will have some testosterone/tren/masteron(or primo/winny) the latter 3 for their ability to convert to DHT. DHT conversion is done heavily just below the skin via 5AR. This will cause and produce certain effects more acne, less fluid retention et cetera... There is a misconception that anavar is made for cutting, it is not! All AAS will do so you burn more fat. There are a lot of studies on anavar where body-fat has been reduced and I think that is where the notion is spawned from.

The more androgens you have in your system the greater your body recomp/fat burning will be. The body doesn't recognize individual drugs, they are all known as androgens to the body. Other wise it would be nice to add trenbolone to your natural testosterone production. But the body senses the androgen trenbolone and shuts down its own production of testosterone.

Then there is the ester aspect. The ester used is a reflection of the cycle length. Short esters for short cycles and long esters for longer cycles.

Repped for a bad ass post, very well done.

[Bonaparte]

The most common cut cycles will have testosterone /anavar . The cut cycles for competition will have some testosterone/tren/masteron(or primo/winny) the latter 3 for their ability to convert to DHT. DHT conversion is done heavily just below the skin via 5AR. This will cause and produce certain effects more acne, less fluid retention et cetera... There is a misconception that anavar is made for cutting, it is not! All AAS will do so you burn more fat. There are a lot of studies on anavar where body-fat has been reduced and I think that is where the notion is spawned from.

Only testosterone converts to DHT. Those are DHT-derivatives, in that they are modified DHT molecules that will act somewhat like DHT and not convert to estrogen.
And Tren is not even a DHT-derivative, but will not convert to estrogen nor undergo 5a-reductase because of it methyl groups at the 4 and 9 positions.

[Sworder]

Only testosterone converts to DHT. Those are DHT-derivatives, in that they are modified DHT molecules that will act somewhat like DHT and not convert to estrogen.
And Tren is not even a DHT-derivative, but will not convert to estrogen nor undergo 5a-reductase because of it methyl groups at the 4 and 9 positions.

For simplicity, I choose to word it like that. They are or their metabolites are subject to 5AR. In essence, it would be false to call them "DHT-derivatives" as well; "5 alpha reductase" would be the appropriate term. As they are not derived from DHT, for simplicity we choose this wording. 19-nortestosterone's(nandrolone ) metabolite 5α-dihydro-19-nortestosterone has already passed through that process. Although 19-nortestosterone wouldn't be considered a "DHT-derivative" it is indeed subject to 5AR. Winstrol , Primo, and winny, you included trenbolone although I said latter three. I don't "see" much 5AR activity with trenbolone which is why I didn't include it. Winstrol clearly has 5AR activity as you can tell visually, it would be an exercise in futility to have me name the metabolites which are subject to 5AR.

Yes, I am wrong in stating they convert to dihydrotestosterone, but they are subject to 5AR which in laymans terms is comparable to DHT.


Edit: Worthy of note, the reason why nandrolone isn't seen as a "DHT derivative" is because its 5AR form has a much weaker affinity to the AR than nandrolone.

[Bonaparte]

I have an exam tomorrow and don't feel like getting into this just now, but you are WAY off on the meaning of 5ar (which is an enzyme, not a class of hormone as you are painting it).

[austinite]

I have an exam tomorrow and don't feel like getting into this just now, but you are WAY off on the meaning of 5ar (which is an enzyme, not a class of hormone as you are painting it).

Damn it Bona. You just answered one of my Interview questions. Now I have to submit another.

[Sworder]

Yes, it's an enzyme. I am not classing it as a hormone. Certain steroids are subject to "aromatase", same as certain are subject to "5AR".

[Bonaparte]

Yes, it's an enzyme. I am not classing it as a hormone. Certain steroids are subject to "aromatase", same as certain are subject to "5AR".

Ok, I see what you're getting at, but:
You can say a hormone is 5a-reduced, and this means that it is already a DHT analogue and cannot undergo 5a-reductase or aromatase. This would include Winstrol , Primo, Var, etc.
Or you could say that a hormone is subject to 5a-r, but this would include test, Dbol , EQ, nandrolone , etc.
I think your wording is just throwing me off.

[Sworder]

Ok, I see what you're getting at, but:
You can say a hormone is 5a-reduced, and this means that it is already a DHT analogue and cannot undergo 5a-reductase or aromatase. This would include Winstrol , Primo, Var, etc.
Or you could say that a hormone is subject to 5a-r, but this would include test, Dbol , EQ, nandrolone , etc.
I think your wording is just throwing me off.

Correct!

[Metalject]

For simplicity, I choose to word it like that. They are or their metabolites are subject to 5AR. In essence, it would be false to call them "DHT-derivatives" as well; "5 alpha reductase" would be the appropriate term. As they are not derived from DHT, for simplicity we choose this wording. 19-nortestosterone's(nandrolone ) metabolite 5α-dihydro-19-nortestosterone has already passed through that process. Although 19-nortestosterone wouldn't be considered a "DHT-derivative" it is indeed subject to 5AR. Winstrol , Primo, and winny, you included trenbolone although I said latter three. I don't "see" much 5AR activity with trenbolone which is why I didn't include it. Winstrol clearly has 5AR activity as you can tell visually, it would be an exercise in futility to have me name the metabolites which are subject to 5AR.

Yes, I am wrong in stating they convert to dihydrotestosterone, but they are subject to 5AR which in laymans terms is comparable to DHT.


Edit: Worthy of note, the reason why nandrolone isn't seen as a "DHT derivative" is because its 5AR form has a much weaker affinity to the AR than nandrolone.

Actually compounds like Winstrol, Primo and Tren are not metabolized by 5AR at at all. Neither is Anavar , Masteron , Anadrol . The only hormones affects by 5AR directly in a pronounced fashion are testosterone , methyletestosterone, nandrolone, fluoxymesterone and boldenone . However, there's while you can use related inhibitors with these hormones you rally can't with nandrolone as it converts to DHN and a 5AR would actually enhance the androgenicity. Then there are steroids like Dbol which while affected by 5AR it is very miniscule.

[Metalject]

What I mean is, how do people know what drugs work best with what? If all steroids will add mass with proper training and diet, why the need for stacks containing 3, 4 or more different things?

For example, one common recommendation I see is test/tren /win or test/deca /eq. What reason for these three together? What would happen if you ran test and tren by themselves, or if you ran test and tren with eq instead of win?

Are there drugs that almost always have to be stacked with something else; that just won't work alone? Are there injectables that should not be used with other injectables? And, is any of this determined in any way other than what people see their friends do?

Asking as someone with next to no knowledge of chemistry...

A simple way to look at it:

There are really only three primary hormones, testosterone , dihydrotestosterone and nandrolone , but even nandrolone and dihydrotestosterone can be traced back to testosterone. With each steroid , most all of which will derive from these three hormones, each one has been structurally altered, often very slightly in order to change the hormone's ratio of anabolic to androgenic effects. By picking the right hormones, you can maximize or minimize the particular anabolic or androgenic traits. The hormone in question will gauge how great this enhancement or minimization is.

With most female plans, the goal is normally to maximize anabolic effects with as little androgenic effects as possible due to virilization. However, when it comes to things like hardness and dryness, in some cases steroids that are more androgenic will promote a dryer, harder look. This is why men often choose combos like tren and halo at the end of a contest plan. How much androgenic action a woman can tolerate will be lower than a man but it will also vary greatly from one woman to the next.

Not sure if this helped but hope so.

[SBEONE]

Repped for a bad ass post, very well done.

^^ This

[Sworder]

Yes. I think I worded it awfully wrong. The 5AR activity was meant as these compounds strongly tend to have an affinity for type 1 5AR and type 2 5AR. Which is why you notice, these compounds right under the skin and that is why they exhibit their effects so strongly there. I don't know how to explain exactly how or why they are attracted to the 5AR enzymes so strongly but they seem to have an attraction to those regions. OR I could just be confused to the expression these drugs have after AR binding, but I don't think that is the case. They really seem to stay active in the skin, this is why these drugs increase sebaceous gland excretion so much... It seems unlikely that their expression would produce that effect if they weren't attracted to 5AR regions..

DHN enhances the "androgenicity" sure.. But it has a much lower AR affinity..

Edit: Are you sure trenbolone & metabolites are not subject to 5AR? I was told to look for the 4,5 double bond... Maybe I misinterpreted that..

[Bonaparte]

Yes. I think I worded it awfully wrong. The 5AR activity was meant as these compounds strongly tend to have an affinity for type 1 5AR and type 2 5AR. Which is why you notice, these compounds right under the skin and that is why they exhibit their effects so strongly there. I don't know how to explain exactly how or why they are attracted to the 5AR enzymes so strongly but they seem to have an attraction to those regions where 5AR enzymes are. OR I could just be confused to the expression these drugs have after AR binding, but I don't think that is the case. They really seem to stay active in the skin, this is why these drugs increase sebaceous gland excretion so much... It seems unlikely that their expression would produce that effect if they weren't attracted to 5AR regions..

DHN enhances the "androgenicity" sure.. But it has a much lower AR affinity..

And here is where all the confusion stems from. DHT-derivatives (or 5a-reduced compounds) seem more "active under the skin" because they share the anti-estrogenic properties of DHT. So they reduces estrogen levels, which reduces sub-Q water retention. They also encourage lipolysis. And the reason for the acne is because they bind tightly to the AR and are androgenic (if we're talking about the more androgenic ones, like masteron ), and increased sebum production is an androgenic side effect. They have NO affinity for the 5a-r enzyme and CANNOT interact with it.

[Metalject]

Yes. I think I worded it awfully wrong. The 5AR activity was meant as these compounds strongly tend to have an affinity for type 1 5AR and type 2 5AR. Which is why you notice, these compounds right under the skin and that is why they exhibit their effects so strongly there. I don't know how to explain exactly how or why they are attracted to the 5AR enzymes so strongly but they seem to have an attraction to those regions. OR I could just be confused to the expression these drugs have after AR binding, but I don't think that is the case. They really seem to stay active in the skin, this is why these drugs increase sebaceous gland excretion so much... It seems unlikely that their expression would produce that effect if they weren't attracted to 5AR regions..

DHN enhances the "androgenicity" sure.. But it has a much lower AR affinity..

Edit: Are you sure trenbolone & metabolites are not subject to 5AR? I was told to look for the 4,5 double bond... Maybe I misinterpreted that..

I'm positive Tren isn't metabolized by the 5AR enzyme. Obviously this doesn't mean it doesn't have strong androgenic effects.

[Sworder]

And here is where all the confusion stems from. DHT-derivatives (or 5a-reduced compounds) seem more "active under the skin" because they share the anti-estrogenic properties of DHT. So they reduces estrogen levels, which reduces sub-Q water retention. They also encourage lipolysis. And the reason for the acne is because they bind tightly to the AR and are androgenic (if we're talking about the more androgenic ones, like masteron), and increased sebum production is an androgenic side effect. They have NO affinity for the 5a-r enzyme and CANNOT interact with it.

I was thinking they did some how, as when a 5AR inhibitor is used; the androgenic effects seem to diminish in the skin and scalp. Not saying they are binding, but attracted lmao...

[Bonaparte]

I was thinking they did some how, as when a 5AR inhibitor is used; the androgenic effects seem to diminish in the skin and scalp. Not saying they are binding, but attracted lmao...

Only if you're using test as well. Otherwise, 5a-r inhibitors have no effect.

[Sworder]

No, I think you are wrong!
3-alpha hydroxysteroid dehydrogenase is the enzyme used to metabolize the "DHT derivatives" and it is heavily concentrated in the skin, more accurately sebaceous glands as well as the prostate!! I think that is the reason why it is "attracted" there and why it is considered "androgenic ".

[Metalject]

The strong binding to the androgen receptor does enhance Tren 's androgenicity, that's definitely true. The boucle delta bond at 9 an 11 increases it even more. It does this despite 5AR metabolism. Further, there is no DHT component in trenbolone . Its structural nature is what provides it androgenicity, and the lacking %AR interaction protects it.

[Swifto]

Your making a habit of being incorrect now aren't your Sworder.

Keep copy, pasting and googling and the cracks will show - and they are.

[panntastic]

Your making a habit of being incorrect now aren't your Sworder.

Keep copy, pasting and googling and the cracks will show - and they are.

This is all serious science stuff and way way over my head here your guys knowledge is far superior than what mine or the average joes will ever be.
When it comes to advice on this board there are some heavy hitters I seriously trust down to the final word
Sheven (lab)
Bonaparte (lab)
Swifto (read your original hcg post years ago)
Marcus (probably calmest member ever)
Austinite
Times roman
Lunk
Farfrommassive
And there are others (apologise if not mentioned)

Every once in a while I see members come out of nowhere with masses of advice like sworder and think wow asset to the board.

I've been here a few years now and only chime in when I think I can give a appropriate answer based on my experiences and very very limited knowledge.

Could somebody not get hurt of this copy and paste attitude that some folks have

All in all this board is amazing and full of volumes of information that I am slowly digesting but sometimes I do worry about incorrect advice and theories having a effect on younger members.

[Swifto]

This is all serious science stuff and way way over my head here your guys knowledge is far superior than what mine or the average joes will ever be.
When it comes to advice on this board there are some heavy hitters I seriously trust down to the final word
Sheven (lab)
Bonaparte (lab)
Swifto (read your original hcg post years ago)
Marcus (probably calmest member ever)
Austinite
Times roman
Lunk
Farfrommassive
And there are others (apologise if not mentioned)

Every once in a while I see members come out of nowhere with masses of advice like sworder and think wow asset to the board.

I've been here a few years now and only chime in when I think I can give a appropriate answer based on my experiences and very very limited knowledge.

Could somebody not get hurt of this copy and paste attitude that some folks have

All in all this board is amazing and full of volumes of information that I am slowly digesting but sometimes I do worry about incorrect advice and theories having a effect on younger members.

What do you mean?

The copy and pasting is done mostly be repeating others articles and theory's and when they are wrong, so is the copy and paster. Sworder is a member of another board and repeats Michael Scally's and Bill Roberts hard work. It makes him sound intelligent here, but he's written f*ck all himself. I have a fair amount of experience with his type, its nothing new.

NO ONE is always right, we all make mistakes along the line. There are only a select few that havent in my experience on these boards, one of them is no longer alive (Nandi - Karl Hoffman).

[songdog]

We got some guys here that are true lab rats.These guys know their stuff.And I really respect their knowledge and love it when they show it off.Now just try to find this somewhere else.

[Sworder]

Your making a habit of being incorrect now aren't your Sworder.

Contribute instead Swifto! Lets hear about the DHT receptors

Yes, 99% of the things I know are due to Michael Scally MD and Bill Roberts, I will always give them credit for my knowledge base. I haven't written any book nor attended Steroid Pharmacology 101. So...?

I am often wrong in my interpretations of data or in my theories, which I don't mind at all!

The interesting thing about the DHT derivatives is their concentration in different skin regions. If you would measure the metabolic enzyme (3-a hydroxysteroid dehydrogenase) in different areas you might find some interesting data and, it could be an explanation to the steroid induced acne distribution. I will look into this further...

[Bonaparte]

Contribute instead Swifto! Lets hear about the DHT receptors

Yes, 99% of the things I know are due to Michael Scally MD and Bill Roberts, I will always give them credit for my knowledge base. I haven't written any book nor attended Steroid Pharmacology 101. So...?

I am often wrong in my interpretations of data or in my theories, which I don't mind at all!

The interesting thing about the DHT derivatives is their concentration in different skin regions. If you would measure the metabolic enzyme (3-a hydroxysteroid dehydrogenase) in different areas you might find some interesting data and, it could be an explanation to the steroid induced acne distribution. I will look into this further...

http://en.wikipedia.org/wiki/3-beta-HSD
http://www.ncbi.nlm.nih.gov/pubmed/2243100
From what I can find, 3-beta-HSD is mainly responsible for the conversion of all hormonal precursors into more active hormones in the adrenal glands.
What does this have to do with the actions or metabolism of DHT-analogues (5a-reduced steroids )?

[Sworder]

3 Alpha, not beta!

[Bonaparte]

3 Alpha, not beta!

Ohhhh, now I see what you're getting at!
This is the enzyme that deactivates DHT in skeletal muscle (where it is concentrated).
But here's the problem: that only affects DHT, not masteron and other DHT derivatives, which were modified specifically to avoid deactivation by 3-a hydroxysteroid dehydrogenase, so that they could remain active in skeletal muscle and thus have have an anabolic effect.

So no...that's not it either. They just cause acne (if highly androgenic ), lipolysis, and reduce estrogen because they share some properties of DHT.

[Sworder]

I will have to present it more thoroughly later. Before that, can we agree that "AAS acne" has a certain distribution?

What do you mean by "androgenic "? Having a high affinity for the AR? Having a "strong" expression when bound in the ligand? <- This is unknown as is the duration of binding, actually I remember seeing a paper which showed expression duration in different ligands. Never saved it but I will try to find it again.

I know it may be a difficult question to accurately answer but I would like to see what your response is. Androgenic/anabolic ratios have been thrown out, not very applicable...

[fit2bOld]

Lost me at post 3 but I'm ok with that.....

[Sworder]

Answering my own question, to make it clearer where I am going with this. You can't say that a steroid is highly "androgenic ", I understand what you mean but I believe that wording is poor. What pathways do the androgenic steroids follow? A "androgenic" steroid is going to follow a similar metabolic pathway or expression as others. This is what I am getting at, I think it has something to do with 3-A HSD for the DHT derivatives. If you say that a steroid is androgenic you should be able to state the properties which make it so. The metabolites, enzymes and expressions they posses. This is not the easiest task, I have honestly no clue.

I will get back to that later, still have shaving cream on my head and I gotta be out of the door in 20.

[Bonaparte]

Normally, when I say "androgenic ", I mean that it exerts strong androgenic effects in vivo (acne, aggression, rapid strength increase, hairloss on head, hair growth on body).

Careful, you're starting to pull a Lemonada here and make this more complicated than it is.

[Sworder]

Normally, when I say "androgenic ", I mean that it exerts strong androgenic effects in vivo (acne, aggression, rapid strength increase, hairloss on head, hair growth on body).
Careful, you're starting to pull a Lemonada here and make this more complicated than it is.

Sure, I agree that those are androgenic effects but my notion is how they are expressed. They have to have a certain pathway and that is what I am getting at with the 3a HSD theory. Did you agree with me about the AAS acne distribution?

[t-dogg]

So back on topic now... lol

[warmouth]

This post has been great! I have learned alot from both sides. OP, you got more of an answer than you bargained for I suppose. I am not taking sides, as I think both you guys are 100X smarter than me. I will say though that I wish I was Bonaparte! Coolest member on the site! Sworder, nothing against you at all. You have helped me tremendously several times, and I am thankful to have members like you on here. Thanks to both of you.

[Sworder]

3-alpha hydroxysteroid dehydrogenase is an enzyme that converts DHT ->5α-androstan-3α,17β-diol. I haven't actually checked if the other AAS that are considered DHT derivatives would be subject to this enzyme, given their similar structure I would assume they are!

Ok, so what's my point and what am I saying? I am saying that the distribution of the enzyme causes DHT derivative steroids to be more active in certain tissues such as the skin and prostate. Producing what you call "androgenic " effects. This is the reason to why acne is more prominent with certain steroids because they have different tissue distribution. I do not believe in the notion that all DHT derivative steroids are producing their effects because of their "anti-estrogenic properties" as you are calling it. They compete at the estrogen receptor, sure but I don't think this would cause the "androgenic effects" seen by DHT.

It is well known that 5AR enzymes are heavily under the skin, wouldn't it make sense that 3a HSD enzymes would be close by and that is what is causing these effects?


What do you think? Is this plausible? If not, why?

Keep in mind, it's just a theory! Mindful that there may be something to it and would be great if you could provide some substrate to eradicate it. Please and thank you.


Edit: "(DHT derivatives) were modified specifically to avoid deactivation by 3-a hydroxysteroid dehydrogenase" I didn't know that... Hmm, know what they do? If that's the case I guess I am wrong

I included some information from a paper I found to be interesting and applicable to the topic.

Human Types 1 and 3 3α-Hydroxysteroid Dehydrogenases: Differential Lability and Tissue Distribution
http://jcem.endojournals.org/content/86/2/841.full
RNA expression analysis indicates that human type 1 3α-HSD is expressed exclusively in the liver, whereas type 3 is more widely expressed and is found in the liver, adrenal, testis, brain, prostate, and HaCaT keratinocytes.

Type 3 3α-HSD is more widely expressed than type 1 3α-HSD. This enzyme is found in many peripheral tissues that produce active steroids, such as the prostate, the skin, the adrenals, and the brain. It is, thus, likely that type 3 3α-HSD plays a role in the intracrine control of active hormone levels in these tissues, especially DHT in the prostate.

This hypothesis is in agreement with the hypothesis being presented here, that type 3 3α-HSD is unique to human and that its role is to control the intracellular level of active steroids in peripheral target tissues.

[Sworder]

So back on topic now... lol

We are on-topic, t-dogg. Don't you want to know why you should avoid DHT derivatives if you have skin and prostate issues?

[t-dogg]

We are on-topic, t-dogg. Don't you want to know why you should avoid DHT derivatives if you have skin and prostate issues?

LOL, thread starter asked how to stack. Dont think she will have prostate issues.