T Nation

Effect of AAS Use on Fat Distribution?

In my quest to help understand AAS better and it’s effects, I recall reading in some of the stickies that gear use causes a more “male body fat distribution” within the body. What does this exactly mean? Does this mean that if someone carries most of their fat in places that are linked to high estrogen (glutes, thighs, etc.), that a shift takes place? Is it permanent or will the body return back to it’s original tendencies to store fat once natural hormonal levels return? I wasn’t really sure because the fact was vaguely listed.

[quote]Droogan Leader wrote:
In my quest to help understand AAS better and it’s effects, I recall reading in some of the stickies that gear use causes a more “male body fat distribution” within the body. What does this exactly mean? Does this mean that if someone carries most of their fat in places that are linked to high estrogen (glutes, thighs, etc.), that a shift takes place? Is it permanent or will the body return back to it’s original tendencies to store fat once natural hormonal levels return? I wasn’t really sure because the fact was vaguely listed.[/quote]

heres my theory,take it for what it is please.

a person is always burning and storing fat
fat distribution is an ongoing thing and when you up the male hormones then you start to store the fat in male patterns.

when your hormones shift again to more female dominant then you will start to store them in female patterns again.
my theory anyways I know i may be off but this is what I think.

It is actually this simple in my mind too - hormones are messenger chemicals, and one of the messages that is given is to store or burn fat (estrogens tends to stimulate storage of fat due to the need for women to carry more fat on their bodies and androgens tend to stimulate lipolysis in adipose tissue when they attach to the receptors there)

This isnt to say that some steroids are cutting drugs, except maybe the 5x as androgenic as testosterone, trenbolone. It is just saying that AAS have a positive nutrient partitioning effect, that is, with the calories one eats more will go to anabolism in the muscles and less will go to anabolism in the adipose tissue.

This often changes after discontinuation as the levels of testosterone drop and the increase in estrogen are left dominating the testosterone.
With the accurate use of HCG, AI’s and SERM’s this shound be a non-issue (in a perfect world).

Brook

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does this mean that the majority of users will never return back to pre-cycle levels? to my understanding, the amount of E in the body is somewhat regulated by the amount of aromatose u have in the body, which in turn is corelated to the amount of body fat one carries.

so in theory, shouldnt the level of T be higher and E lower at homeostasis than before if say precycle u carried 15%bf and post u are carrying 10%?

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[quote]bushidobadboy wrote:
malty_goodness wrote:
does this mean that the majority of users will never return back to pre-cycle levels? to my understanding, the amount of E in the body is somewhat regulated by the amount of aromatose u have in the body, which in turn is corelated to the amount of body fat one carries.

so in theory, shouldnt the level of T be higher and E lower at homeostasis than before if say precycle u carried 15%bf and post u are carrying 10%?

What you say makes sense of course, but assumes complete recovery of natural hormone profile. Often this is not the case, especially in those with a ‘fragile’ HPTA, i.e. those who may be borderline hypogonadal in the first place.

There have been quite a few posts from AAS users who simply have not returned to pre-cycle ‘normal’ function, whether they did actually do a PCT or simply waited for time to sort things out. Libido seems to be the most common complaint, along with erectile dysfunction.

BBB[/quote]
and this is where I believe the use of an AI like arimidex off cycle can come in handy.
regulating the aromatase off cycle and helping to keep the ratio of T-E in favor of higher test levels.

[quote]MaddyD wrote:
bushidobadboy wrote:
malty_goodness wrote:
does this mean that the majority of users will never return back to pre-cycle levels? to my understanding, the amount of E in the body is somewhat regulated by the amount of aromatose u have in the body, which in turn is corelated to the amount of body fat one carries.

so in theory, shouldnt the level of T be higher and E lower at homeostasis than before if say precycle u carried 15%bf and post u are carrying 10%?

What you say makes sense of course, but assumes complete recovery of natural hormone profile. Often this is not the case, especially in those with a ‘fragile’ HPTA, i.e. those who may be borderline hypogonadal in the first place.

There have been quite a few posts from AAS users who simply have not returned to pre-cycle ‘normal’ function, whether they did actually do a PCT or simply waited for time to sort things out. Libido seems to be the most common complaint, along with erectile dysfunction.

BBB
and this is where I believe the use of an AI like arimidex off cycle can come in handy.
regulating the aromatase off cycle and helping to keep the ratio of T-E in favor of higher test levels.

[/quote]

The goal should never be to dependent on a drug for long term. Exemestane would be much more effective during PCT and would not need to be used indefinately the way anastrozole would. Long term off cycle dosing of ana would negatively affect blood lipid profile which is obv not desired.

[quote]egnatiosj wrote:
The goal should never be to dependent on a drug for long term. Exemestane would be much more effective during PCT and would not need to be used indefinately the way anastrozole would. Long term off cycle dosing of ana would negatively affect blood lipid profile which is obv not desired. [/quote]

…It would only negatively effect lipid profiles if dosed incorrectly.

and exemestane would need to be used indefinitely to have a long term effect.

It does destroy the receptors but they grow back.

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[quote]Westclock wrote:
…It would only negatively effect lipid profiles if dosed incorrectly.
[/quote]
This notion is correct only when consistent, accurate doses are provided. This is not the case with the average steroid user who;

-Does not get regular blood tests to confirm the desired E range
-Does not use pharmaceutically prepared medications
-Does not take consistent, regular doses.

I guarantee most steroid users do not do get blood tests. They are expensive and are usually not covered by insurance (in the states). Dosing is also very specific on a number of factors that influence the aromatase activity including age, obesity, insulin, gonadotropins , alcohol, prolactin, and smoking. The simplified instructions of start at .25mg/EOD and “keep it there if your head is not fuzzy and libido is in check” simply does not work.

Steroid users are also NOT likely to use pharmaceutically prepared aromatase inhibitors, but are more likely to use company prepared preparations that GREATLY vary amongst bottle to bottle and company to company. I will not go into defending this statement, as I am sure you will agree on it.

This is not specific to steroid users, MOST people forget regular medications here or there which will effect plasma levels. There can also be interactions with other drugs takin, including certain sulphamides. There is no reason to use a drug long term- when it is completely feasible to use a type 1 AI.

[quote]
and exemestane would need to be used indefinitely to have a long term effect.

It does destroy the receptors but they grow back.[/quote]

Completely wrong on both a practical and conceptual level.

[quote]bushidobadboy wrote:
Westclock wrote:
It does destroy the receptors but they grow back.

I think it actually binds to the aromatase enzyme irreversably (hence the term ‘suicide’ aromatase inhibitor). New aromatase will be produced though eventually.

BBB[/quote]

I was under the impression that the receptors die eventually and are replaced by new ones.

hence permenantly blocking one only works until it dies.

Regardless, the effect isnt permanent, taking a high dose will not prevent estrogen in your body forever.

2X on MaddyDs and Brooks posts. Made perfect sense.

Thanks for the excellent, informative responses so far guys. A lot of the facts and theories posted are still WAY over my head, but I think I get the gist of the answer to my original question. So, with a proper PCT executed, once (and if I read what some wrote correctly) hormone levels return to pre-AAS cycle levels, the partitioning of nutrients that would go towards anabolism within muscles primarily while using gear, go back to how the body previously operated (which includes fat storage tendencies and distribution patterns).

PLEASE correct me if I am wrong. Lots of good stuff here!

[quote]Westclock wrote:

I was under the impression that the receptors die eventually and are replaced by new ones.

hence permenantly blocking one only works until it dies.

[/quote]

Enzymes have active sites, exemestane acts as a false substrate for the aromatase enzyme, and is metabolized to an intermediate that binds irreversibly to the active site of the aromatase enzyme causing its inactivation. It does not “die” and thus can not “grow back.”

[quote]
Regardless, the effect isnt permanent, taking a high dose will not prevent estrogen in your body forever.[/quote]

No of course the medication would not cause PERMANENT changes, after cessation, few do! Why would we even want that? An increased concentration of substrate, in this case testosterone (while on cycle), would cause increased activity in aromatase. Exemestane would decrease this activity and allow the body to re-regulate itself based on current levels of available substrate, along with the other factors, noted in a previous post.

[quote]Droogan Leader wrote:
Thanks for the excellent, informative responses so far guys. A lot of the facts and theories posted are still WAY over my head, but I think I get the gist of the answer to my original question. So, with a proper PCT executed, once (and if I read what some wrote correctly) hormone levels return to pre-AAS cycle levels, the partitioning of nutrients that would go towards anabolism within muscles primarily while using gear, go back to how the body previously operated (which includes fat storage tendencies and distribution patterns).

PLEASE correct me if I am wrong. Lots of good stuff here![/quote]

There are a lot of variables at play determining fat/protein ‘storage’ post cycle.

For example, in a healthy male with a fully functioning and ‘strong’ HPTA, once they come off and recover from the suppression, they can expect that the muscle mass gained on cycle to help to maintain a lower fat physique, due to the metabolism of the tissue. As long as full effort is applied to maintain it.

The body has a distinct desire for 1) Homeostasis and 2) Energy efficiency. Homeostasis is a baseline natural steady state, and if one changes their body too fast in too short a timeframe, then the body will attempt to restore to its former condition harder than if slow steady gains are made - which leads on to the second point; energy efficiency. Muscle is metabolic and consumes calories at complete rest, so if this muscle is not deemed ‘necessary’ by the body, then it will catabolise it to a) use the muscle as energy to reduce the need for feeding - possibly storing the converted aminos to glucose as fat, and b) reduce the bodies metabolic rate, making it more efficient at running on a lower amount of calories.
This is the main problem of the bodybuilder, not just gaining muscle but ensuring that the body becomes ‘used’ to it, this is achieved by regular lifting of weights relative to the size of the muscle in you personally (which is difficult post cycle as often strength decreases), adequate calories to feed the metabolism and time at the weight gained.

Diet and training are going to massively help the maintenance of the new muscle/composition.

On the other hand, one may have a PCT that either wasnt effective in restoring the HPTA, due to either lack of effort/knowledge or a HPTA that simply wont restore to its former operation (which can happen to anyone - and the ability of the HPTA or any one of its 3 components to recover post shutdown is genetic and cannot be judged beforehand other than the possibility of a low test level to begin with), making the maintenance of the gains really quite hard… if not impossible.

Plus if estrogen is not controlled, when the exogenous test levels drop estrogen will become the dominant hormone. This will lead to further suppression of the HPTA, and visual physical estrogenic effects.

There is more but this post is too long and cutting into my day too much! I need to train this morning…

Brook

[quote] Brook wrote:
Droogan Leader wrote:
the partitioning of nutrients that would go towards anabolism within muscles primarily while using gear, go back to how the body previously operated (which includes fat storage tendencies and distribution patterns).

PLEASE correct me if I am wrong. Lots of good stuff here!

There are a lot of variables at play determining fat/protein ‘storage’ post cycle.

For example, in a healthy male with a fully functioning and ‘strong’ HPTA, once they come off and recover from the suppression, they can expect that the muscle mass gained on cycle to help to maintain a lower fat physique, due to the metabolism of the tissue. As long as full effort is applied to maintain it.

Diet and training are going to massively help the maintenance of the new muscle/composition.

Brook[/quote]

To answer the OP, estrogen and testosterone are the dominant hormones effecting fat distribution. This is because estrogen lowers the lipolytic response in subQ fat depot by increasing the number of antilipolytic 2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot.Estrogen Receptor-alpha, also plays a role in regulating food intake and energy expenditure which (may) affect body composition.

Testosterone, on the other hand stimulates catecholamine-induced lipolysis by increasing the number of beta-adrenoceptors as well as the activity of adenylate cyclase. Anecdotal evidence would also suggest that it increases insulin sensitivity; atleast in IDDM patients. There are also the indirect effects of T on body composition via, increased muscle mass, nitrogen retention, and metabolic demand.