TRT in men with low SHBG

[BBC3]

BBC, I think you've got it wrong: the effectiveness of the "diabetes treatment" is not measured by how much your SHGB is lowered (I don't understand where you get this from??), but is measured by how much your overall blood glucose levels and insuline levels have dropped. By decreasing circulating insuline levels, your SHBG will probably rise slightly.

Yes I do understand that. I guess I am hung up on the fact that my SHBG just came in at 12 and I have that crazy high level of estradiol. I am not saying that I am going to measure the effectiveness of the insuline modulation by the change in SHBG. What I am saying is that I am hoping to raise that number by first normalizing insuline. The whole thing is that I would not have even allowed a drug for insuline response correction at this time in my life as it is really questionable as to whether this is really a problem. As I indicated my blood sugar may stay around 125 alot, BUT, it also does not rise past that with a stress test. So I am basically probably playing with a bigger fire than ever before by taking these meds at this time. The long and the short is that I do seem to find myself having an incredible affinity for simple sugar, and it does not take too much when combined with a stimulant or nasty like nicotine to give me a really cold feeling in my lower left leg. SO there must be something to my sugar issues. I am now betting there has to be. I am going to assume as my body may like to keep suger at 125 that this has to be incorrect, (just like my low test is incorrect). I simply think that at this juncture, it would be foolish to go on working with my hormones when I have not even made an attempt with an "easier to fix" problem like blood sugar. So hopefully after a few months of a lower level of blood sugar and better insuline response, I will find that SHBG has risen a few points.

You mentioned that you were not sure where i got this from. Isn't this the thread where the last few post just stated (even by yourself) that correcting insuline response is to correctly "fix the chicken", and not to try to treat the SHBG itself??

James, can you please chime back in. Am I totally on the wrong page?

 

[pcgizzmo]

OK,

I have been following this. I also have SHBG issues. Mine came back at 9. It seems everyone agrees about high insulin causing low SHBG but apparently lowring insulin wll not raise SHBG as readily as raising it lowers it.

Here is something to ponder. Low testosterone has been linked to Syndrome X (Insulin sensitivity/Pre-Diabetes) Raising testosterone is supposed to increase insulin sensitivity. So, it seems that adding testosterone would be the cure for what is causing the insulin sensitivity/low SHBG issue but I don't think it's that easy. Once your testosterone is low it's like a huge circle jerk. I think by frequent lower testosterone administration coupled with appropriate E2 management might over time solve the problem but I'm just speculating and have no proof.

Paul

 

[HeadDoc]

OK,

I have been following this. I also have SHBG issues. Mine came back at 9. It seems everyone agrees about high insulin causing low SHBG but apparently lowring insulin wll not raise SHBG as readily as raising it lowers it.

Here is something to ponder. Low testosterone has been linked to Syndrome X (Insulin sensitivity/Pre-Diabetes) Raising testosterone is supposed to increase insulin sensitivity. So, it seems that adding testosterone would be the cure for what is causing the insulin sensitivity/low SHBG issue but I don't think it's that easy. Once your testosterone is low it's like a huge circle jerk. I think by frequent lower testosterone administration coupled with appropriate E2 management might over time solve the problem but I'm just speculating and have no proof.

Paul

there are some small studies around that support the use of testosterone for type 2 diabetes.

 

[Axl]

OK,

I have been following this. I also have SHBG issues. Mine came back at 9. It seems everyone agrees about high insulin causing low SHBG but apparently lowring insulin wll not raise SHBG as readily as raising it lowers it.

Here is something to ponder. Low testosterone has been linked to Syndrome X (Insulin sensitivity/Pre-Diabetes) Raising testosterone is supposed to increase insulin sensitivity. So, it seems that adding testosterone would be the cure for what is causing the insulin sensitivity/low SHBG issue but I don't think it's that easy. Once your testosterone is low it's like a huge circle jerk. I think by frequent lower testosterone administration coupled with appropriate E2 management might over time solve the problem but I'm just speculating and have no proof.

Paul

Please read the attachment I've posted in this thread. "Androgens Insuline Resistance and Vasular Disease in men". In the summary and on page 4 you'll find the following text:
Role of visceral fat in peripheral hyperinsulinaemia and systemic
insulin resistance: "[I]Increasing abdominal fat leads to liver being exposed to
higher concentrations of free fatty acids. The free fatty acids increase hepatic
glucose production and decrease hepatic insulin uptake. This results in
systemic hyperinsulinaemia and skeletal muscle insulin resistance, which in
turn causes further release of insulin by the islet cells."[/I] They describe a visious circle: once you're in it, it is difficult to stop the process.

So, Step 1 is proper diet to reduce visceral fat overall and free fatty acids in the bloodstream in particular. Second step is increasing muscular activity because it increase the insuline receptiveness of the cell, hence reducing the high glucose levels in the blldstream and reducing the free fatty acids in the blood. Step 3 is testosterone.

Summary
Type 2 diabetes mellitus is increasing globally and is an established
risk factor for the development of atherosclerotic vascular disease.
Insulin resistance is the hallmark feature of type 2 diabetes and is
also an important component of the metabolic syndrome. There is
evidence to suggest that testosterone is an important regulator of
insulin sensitivity in men. Observational studies have shown that
testosterone levels are low in men with diabetes, visceral obesity (which
is strongly associated with insulin resistance), coronary artery disease
and metabolic syndrome. Short-term interventional studies have
also demonstrated that testosterone replacement therapy produces
an improvement in insulin sensitivity in men. Thus hypotestosteronaemia
may have a role in the pathogenesis of insulin-resistant
states and androgen replacement therapy could be a potential treatment
that could be offered for improvements in glycaemic control
and reduction in cardiovascular risk, particularly in diabetic men.

 

[BBC3]

Man Axl, that font is killing me so I will have to read yours tomorrow.

Gizzmo, I can tell you that I have supp'd test to varying degrees over the past two years and it has not helped my insuline response (1) IODA. I dont measure every day, but it happens enough to guage with this response (at least for me.) ON this chicken or egg argument I am going to have to go with the egg. meaning that I have known for over 20 years that bodybuilders have been supping insuline on top of their testosterone to further muscle growth. Would they have needed to when they were already on test for starters?? Conciliator metioned a "U" shaped curve regarding insuline responce as related to testosterone dosing. I have found that interesting to say the least and feel it merits a bigger look from at least myself.

All in all, my bodybuilder anecdote does not hold all that much water because their whole idea is to increase insuline so they can process MORE food and faster. I mean when you eat 10,000 calories a day you ARE going to need a little extra insuline. I may even be a good idea in that it is sparing your pancreas from being overworked... HMMMM Just some thoughts.

OK,

I have been following this. I also have SHBG issues. Mine came back at 9. It seems everyone agrees about high insulin causing low SHBG but apparently lowring insulin wll not raise SHBG as readily as raising it lowers it.

Here is something to ponder. Low testosterone has been linked to Syndrome X (Insulin sensitivity/Pre-Diabetes) Raising testosterone is supposed to increase insulin sensitivity. So, it seems that adding testosterone would be the cure for what is causing the insulin sensitivity/low SHBG issue but I don't think it's that easy. Once your testosterone is low it's like a huge circle jerk. I think by frequent lower testosterone administration coupled with appropriate E2 management might over time solve the problem but I'm just speculating and have no proof.

Paul

 

[BBC3]

Please read the attachment I've posted in this thread. "Androgens Insuline Resistance and Vasular Disease in men". In the summary and on page 4 you'll find the following text:
Role of visceral fat in peripheral hyperinsulinaemia and systemic
insulin resistance: "[I]Increasing abdominal fat leads to liver being exposed to
higher concentrations of free fatty acids. The free fatty acids increase hepatic
glucose production and decrease hepatic insulin uptake. This results in
systemic hyperinsulinaemia and skeletal muscle insulin resistance, which in
turn causes further release of insulin by the islet cells."[/I] They describe a visious circle: once you're in it, it is difficult to stop the process.

So, Step 1 is proper diet to reduce visceral fat overall and free fatty acids in the bloodstream in particular. Second step is increasing muscular activity because it increase the insuline receptiveness of the cell, hence reducing the high glucose levels in the blldstream and reducing the free fatty acids in the blood. Step 3 is testosterone.

Summary
Type 2 diabetes mellitus is increasing globally and is an established
risk factor for the development of atherosclerotic vascular disease.
Insulin resistance is the hallmark feature of type 2 diabetes and is
also an important component of the metabolic syndrome. There is
evidence to suggest that testosterone is an important regulator of
insulin sensitivity in men. Observational studies have shown that
testosterone levels are low in men with diabetes, visceral obesity (which
is strongly associated with insulin resistance), coronary artery disease
and metabolic syndrome. Short-term interventional studies have
also demonstrated that testosterone replacement therapy produces
an improvement in insulin sensitivity in men. Thus hypotestosteronaemia
may have a role in the pathogenesis of insulin-resistant
states and androgen replacement therapy could be a potential treatment
that could be offered for improvements in glycaemic control
and reduction in cardiovascular risk, particularly in diabetic men.

OK, I read it tonight. WOW "a vicious cycle" you aint just wistling Dixie. I have never allowed myself to get this fat (50lbs overweight), and I am finding this to be a SONOFABITCH!!! I always use to cycle myhealth. Get fat and take it all off in 3 months. There is always a point where you can feel yourself "turn the corner". Let me tell you that I am having to bust my ass this time, and I am just now finding a slight curve, the corner is not even yet in sight!!! But it is starting to turn. Thank God....

 

[James23]

I figured I'd provide my "story" to show how exceedingly difficult this problem may be to solve via natural means:

Last year, I was very, very thin. My bodyfat was 11%. I'd been eating large amounts of vegetables, avoiding meat, and avoiding all sources of sugar. Carbs were consumed in the form of fibrous legumes, oats, and occasional whole fruits (low GI only, and each of those categories only once per day.) I was in the gym for about an hour 2 - 3 times a week.

After a year and a half of this behavior, I had a bood test. Free and total testosterone were below the reference range and SHBG was "7" -- one point away from being out of the reference range. This was an identical scenario to when I was on HRT and eating with less restriction (I naively had one huge insulin spiking meal after working out and ate mostly fruit for breakast -- the rest of the day was chicken , vegetables and various fats.)

Honestly, I don't know if it would be possible to eat any less carbohydrate and maintain any sort of muscle mass -- or even to eat any healthier, for that matter. I didn't stray from my regimen for any reason. Not once. If soda were the only thing to drink, I simply did not drink; if my girlfriend drug me to a pizza restaurant, I just refused to eat, etc.

HRT (testosterone in the 800ng/dl range, rather than my measly natural 189ng/dl) did nothing to change my SHBG. When I was a few years younger and on Dr. John's protocol, it was 9-11. That's the highest I've ever seen it. However, those numbers don't mean that it improved. The range for the lab was just different than the one I used for my more recent test. Plus, he had me on no less than 4 medications, entirely ignorant of the fact that low SHBG was negating the work of any boost in hormone levels.

This is why I stress the need for medication in conjunction with healthy habbits. I would have to quit my day job to demonstrate behavior any more beneficial to my insulin levels. However, if someone's body were able to "fix itself" using the same regimen that I tried, I would certainly love to hear about it!

I am currently experimenting with regimen of "natural" blood sugar lowering supplemetns. I also use low levels of HCG to boost my testosterone because my natural levels leave me entirely impotent and unable to maintain mass (I lost 40lbs. of muscle after stoppping T.) We'll see how it goes...

 

[pcgizzmo]

I figured I'd provide my "story" to show how exceedingly difficult this problem may be to solve via natural means:

Last year, I was very, very thin. My bodyfat was 11%. I'd been eating large amounts of vegetables, avoiding meat, and avoiding all sources of sugar. Carbs were consumed in the form of fibrous legumes, oats, and occasional whole fruits (low GI only, and each of those categories only once per day.) I was in the gym for about an hour 2 - 3 times a week.

After a year and a half of this behavior, I had a bood test. Free and total testosterone were below the reference range and SHBG was "7" -- one point away from being out of the reference range. This was an identical scenario to when I was on HRT and eating with less restriction (I naively had one huge insulin spiking meal after working out and ate mostly fruit for breakast -- the rest of the day was chicken , vegetables and various fats.)

Honestly, I don't know if it would be possible to eat any less carbohydrate and maintain any sort of muscle mass -- or even to eat any healthier, for that matter. I didn't stray from my regimen for any reason. Not once. If soda were the only thing to drink, I simply did not drink; if my girlfriend drug me to a pizza restaurant, I just refused to eat, etc.

HRT (testosterone in the 800ng/dl range, rather than my measly natural 189ng/dl) did nothing to change my SHBG. When I was a few years younger and on Dr. John's protocol, it was 9-11. That's the highest I've ever seen it. However, those numbers don't mean that it improved. The range for the lab was just different than the one I used for my more recent test. Plus, he had me on no less than 4 medications, entirely ignorant of the fact that low SHBG was negating the work of any boost in hormone levels.

This is why I stress the need for medication in conjunction with healthy habbits. I would have to quit my day job to demonstrate behavior any more beneficial to my insulin levels. However, if someone's body were able to "fix itself" using the same regimen that I tried, I would certainly love to hear about it!

I am currently experimenting with regimen of "natural" blood sugar lowering supplemetns. I also use low levels of HCG to boost my testosterone because my natural levels leave me entirely impotent and unable to maintain mass (I lost 40lbs. of muscle after stoppping T.) We'll see how it goes...

I think there must be more going on that we don't understand. Possibly genetics play a role as well. My SHBG is 9 and I have ton's of muscle mass even w/low T. I can't put much more on but I don't lose it either. My T Dr. also said that the T I used would be used more efficiently due to the low SHBG. I realize that more frequent dosing might be required to counteract the lack of SHBG to buffer the T.

 

[BBC3]

I think there must be more going on that we don't understand. Possibly genetics play a role as well. My SHBG is 9 and I have ton's of muscle mass even w/low T. I can't put much more on but I don't lose it either. My T Dr. also said that the T I used would be used more efficiently due to the low SHBG. I realize that more frequent dosing might be required to counteract the lack of SHBG to buffer the T.

Isn't he referring to the obvious fact that your Free testosterone levels are higher with low SHBG. I think our problem is that most of us are also finding high E2 associated with this. WHICH will completely negate many testosterone qualities we a looking for.

Are you taking something to control Estrogens?? I am sorry I am not familiar with you. Are you natural or HRT?

 

[James23]

pcgizzmo,

Is it possible that your muscle mass is mostly attributable to your hormone replacement therapy?

Low SHBG is not "more efficient" as your doctor states. Healthy males have a huge buffer of bound testosterone which can be unbound due to metabolic requirements and different steroid molecules. It is not being "inefficiently" utilized, it is being "appropriately buffered." Therefore, unnaturally low levels of SHBG are in no way a blessing.

---

The problem with low SHBG, in a natural context, is that the excess of free testosterone blunts LH output. Therefore, one will often have a "normal" level of free testosterone while maintaining a very low "store" of bound testosterone.

We have a generally constant, low level of SHBG that can only bind a generally constant, low level of testosterone. When we circumvent the HPTA by adding exogenous testosterone, we grossly upset the balance of free testosterone vs testosterone that the body is able to bind. Since we have low SHBG, our bodies simply cannot do anything but let any excess testosterone roam free in the blood.

So, when we add exogenous testosterone, as BBC has pointed out -- we create an unnaturally high level of free testosterone which now readily aromatizes into E2, metabolizes to DHT, etc. Our bodies keep our testosterone low to prevent this very scenario.

In a healthy male, SHBG production is not limited and can respond appropriately to exogenous testosterone.

 

[pcgizzmo]

I have always had good muscle mass. Even on low T. I do have Arimidex. I guess I don't see the problem as long as someone uses an AI which most would need to anyway. If anything we could get away with a lower does of T as well as probably do more frequent dosing.

What other drawbacks besides conversion to E and possibly fast metabolism?

Paul

 

[James23]

pcgizzmo,

Keep in mind that E2 is only one specific form of estrogen, and if your AI is Arimidex, it's only blocking that one specific form of estrogen. Your total estrogens will be too high.

Don't forget about the excess DHT, zeroed FSH, LH, etc...

If you have low SHBG, your free testosterone could be as high as 4-5% of your total testosterone rather than the "healthy" 1-2%. Therefore, your free testosterone levels are most likely perfectly normal before you add any HRT. Since free testosterone is normal, so will be E2, DHT, etc. The only symptom you started out with should have been low total testosterone.

If your free testosterone, E2, and DHT is normal, and free testosterone is apparently all with which you are concerned, then why are you adding any testosterone at all?

 

[BBC3]

James, you brought another question. Say Arimidex for example. It is blocking aromatization at the "p450 Cytochrome and others", or something like that, as I am not that technical. The question is exactly what is being blocked by that drug.?

a) Any change in testosterone period.
b) allows testosterone to aromatize to DHT, andrio, angrodens only, etc..
c) allows testosterone to also aromatize to estrogen, estrone, but not estradiol.
d) not really sure but it does stop estrogen aromatization entirely or up to 80%.
e) stops all estrogen (of most) aromatization and may even hender aromatization to DHT, etc.

Forgive my ignorance. I am just taking any chance I can get to learn more about AI's.

 

[Axl]

pcgizzmo,

Is it possible that your muscle mass is mostly attributable to your hormone replacement therapy?

Low SHBG is not "more efficient" as your doctor states. Healthy males have a huge buffer of bound testosterone which can be unbound due to metabolic requirements and different steroid molecules. It is not being "inefficiently" utilized, it is being "appropriately buffered." Therefore, unnaturally low levels of SHBG are in no way a blessing.

---

The problem with low SHBG, in a natural context, is that the excess of free testosterone blunts LH output. Therefore, one will often have a "normal" level of free testosterone while maintaining a very low "store" of bound testosterone.

We have a generally constant, low level of SHBG that can only bind a generally constant, low level of testosterone. When we circumvent the HPTA by adding exogenous testosterone, we grossly upset the balance of free testosterone vs testosterone that the body is able to bind. Since we have low SHBG, our bodies simply cannot do anything but let any excess testosterone roam free in the blood.

So, when we add exogenous testosterone, as BBC has pointed out -- we create an unnaturally high level of free testosterone which now readily aromatizes into E2, metabolizes to DHT, etc. Our bodies keep our testosterone low to prevent this very scenario.

In a healthy male, SHBG production is not limited and can respond appropriately to exogenous testosterone.

Good post! I agree with you 100%.

Just one remark. You said: "With low SHBG, our bodies simplie cannot do anything but let any excess testosterone roam free in the blood".
This is true, but the consequneces of this fact differ for each person, I think.
- people with a lot of androgen receptors (AR) can take make maximal use of the free unbound testosterone. The free T binds to the cell receptors.
- in people that are AR deficinient, the free unbound T circulates in the blood without further use. The free T metabolises (the half life of T is about 1 week or so) and is secreted out of the bloodstream. All this unbound T is lost. (This is the case with James23 and myself, I think)
- other people are more pre-destined t aromatise T to E2, 5-alpha reductise it to DHT, or convert it to Androstanedione via 17-beta hydroxistroid dehydrogenase. The effects depend on the number of specific receptors you have. (This is the case with BBC3, I guess).

Would do you think? Does this seem logical?

@BBC3: take a look at the map on the URL below. Everything marked with an "A" (aromitase) are substances that can aromitase. An AI Inhibitor like Arimidex inhibits the aromitase process by blocking the aromitase enzyme.
http://www.ceri.com/steroid.gif

 

[pcgizzmo]

Good post! I agree with you 100%.

Just one remark. You said: "With low SHBG, our bodies simplie cannot do anything but let any excess testosterone roam free in the blood".
This is true, but the consequneces of this fact differ for each person, I think.
- people with a lot of androgen receptors (AR) can take make maximal use of the free unbound testosterone. The free T binds to the cell receptors.
- in people that are AR deficinient, the free unbound T circulates in the blood without further use. The free T metabolises (the half life of T is about 1 week or so) and is secreted out of the bloodstream. All this unbound T is lost. (This is the case with James23 and myself, I think)
- other people are more pre-destined t aromatise T to E2, 5-alpha reductise it to DHT, or convert it to Androstanedione via 17-beta hydroxistroid dehydrogenase. The effects depend on the number of specific receptors you have. (This is the case with BBC3, I guess).

Would do you think? Does this seem logical?

@BBC3: take a look at the map on the URL below. Everything marked with an "A" (aromitase) are substances that can aromitase. An AI Inhibitor like Arimidex inhibits the aromitase process by blocking the aromitase enzyme.
http://www.ceri.com/steroid.gif

My free and total T are all below normal. In the 8 years I have know I had low T and not on HRT I have never had free or total T above normal.

If free T in the blood gets bound to androgen receptors it doesn't stay there forever. I assume it gets used and the more free T gets bound. If it's not bound by SHBG I have to agree it gets converted to something and yes these things aren't always beneficial at high levels like E and DHT. Forgive me this is a little beyond me and any research I have done. I have looked for articles on SHBG but there aren't many that you don't have to join a journal for.

So, my SHBG level is 9. Not much lower than normal but still below. Why is it guy's that do steriod doses are always wanting lower SHBG? Where is the fine line? 9 is closer to normal than say the top of the normal range (forgive me I don't have them in front of me now) At what point do you worry about low SHBG and at what point are you happy it's not high because you can take advantage of the higher levels of free T? Where is the sweet spot?

Why would my Dr. tell me my levels will take advantage of the T? He has been doing T thereapy for a while and seems to know what he is doing more than any other Dr. I have seen.

I tend to agree w/Axl. I also think I may be one of the people w/higer AR. If I could drop 35 lbs I would 5'10 210 and about 6% body fat. The rest would be muscle and that's w/low T for 8 years.

Paul

 

[BBC3]

I believe I can answer one of those questions. Guys that do steroids usually want lower SHBG because they don't know what the hell they are doing. It is just another examply of information misused and blindly accepted as the gospel (like "do your pct"). I know because I am/was one of them. I have learned 10 times more over here than in the steroid section. The more I learn from you guys over here, the more I see how poorly they are utilizing testosterone. It is only the top competitors out there that have managed to combine knowledge of HRT and the full gammit of the endocrine system with bodybuilding. When I was younger and natural in the gym, I would hear about world class bodybuilders utilizing things like insulin, thyroid, and estrogen controls while on cycle. It sounded like ludicrous abuse to me back then, but now I am beginning to have some understanding of how advanced their use of medical knowledge was.

With that said keep in mind that I also know Professional bodybuilders that dont give a crap about tweeking to this degree. They also think an off-cycle TRT dose is 500mgs/week and have been doing so for 20+ years. Just another 2 cents to the pot..

My free and total T are all below normal. In the 8 years I have know I had low T and not on HRT I have never had free or total T above normal.

If free T in the blood gets bound to androgen receptors it doesn't stay there forever. I assume it gets used and the more free T gets bound. If it's not bound by SHBG I have to agree it gets converted to something and yes these things aren't always beneficial at high levels like E and DHT. Forgive me this is a little beyond me and any research I have done. I have looked for articles on SHBG but there aren't many that you don't have to join a journal for.

So, my SHBG level is 9. Not much lower than normal but still below. Why is it guy's that do steriod doses are always wanting lower SHBG? Where is the fine line? 9 is closer to normal than say the top of the normal range (forgive me I don't have them in front of me now) At what point do you worry about low SHBG and at what point are you happy it's not high because you can take advantage of the higher levels of free T? Where is the sweet spot?

Why would my Dr. tell me my levels will take advantage of the T? He has been doing T thereapy for a while and seems to know what he is doing more than any other Dr. I have seen.

I tend to agree w/Axl. I also think I may be one of the people w/higer AR. If I could drop 35 lbs I would 5'10 210 and about 6% body fat. The rest would be muscle and that's w/low T for 8 years.

Paul

 

[BBC3]

Axl, I just checked out that "Juice Tree". Thanks thats pretty neat visual for dummys like me.... Does that mean that in the body Progesterone is a produced as a precurser to testosterone. I really need to do some more reading if so....

 

[BBC3]

Here is an interesting thought. I wonder if once the body has detected supesaturated levels of T (this applies especially to guys not genetically inclined to convert E2), will it actually just leave it in deposit untouched for extended periods. Because I have often wondered where it goes when you megadose (1000mgs/wk) and do not get a corrolating response. I have also been suspicious that this exact situation causes post cycle problems and delayed "normalization" issues?......

Good post! I agree with you 100%.

Just one remark. You said: "With low SHBG, our bodies simplie cannot do anything but let any excess testosterone roam free in the blood".
This is true, but the consequneces of this fact differ for each person, I think.
- people with a lot of androgen receptors (AR) can take make maximal use of the free unbound testosterone. The free T binds to the cell receptors.
- in people that are AR deficinient, the free unbound T circulates in the blood without further use. The free T metabolises (the half life of T is about 1 week or so) and is secreted out of the bloodstream. All this unbound T is lost. (This is the case with James23 and myself, I think)
- other people are more pre-destined t aromatise T to E2, 5-alpha reductise it to DHT, or convert it to Androstanedione via 17-beta hydroxistroid dehydrogenase. The effects depend on the number of specific receptors you have. (This is the case with BBC3, I guess).

Would do you think? Does this seem logical?

@BBC3: take a look at the map on the URL below. Everything marked with an "A" (aromitase) are substances that can aromitase. An AI Inhibitor like Arimidex inhibits the aromitase process by blocking the aromitase enzyme.
http://www.ceri.com/steroid.gif

 

[Axl]

Here is an interesting thought. I wonder if once the body has detected supesaturated levels of T (this applies especially to guys not genetically inclined to convert E2), will it actually just leave it in deposit untouched for extended periods. Because I have often wondered where it goes when you megadose (1000mgs/wk) and do not get a corrolating response. I have also been suspicious that this exact situation causes post cycle problems and delayed "normalization" issues?......

A T depot is released at a relatively constant pace and is not influenced by the body itself, so the body cannot decide to leave it in depot or not.
If you inject megadoses and if your body cannot use the T well, the testosterone-ester will be in your blood stream, it will de-esterify to normal T, and after a few hours (when it's not bound to Albumine or attached to a Androgen Receptor) it will be broken down (metabolised) by the body into a harmless substance and this substance will be evacuated out of the body.
See link below for more info.
Steroid . com - Anabolic steroids half life information

 

[pcgizzmo]

I've heard the term "hypermetabolizer". This is usually someone that has low SHBG. So, is a "hypermetabolizer" so is everyone w/low SHBG considered this or is there some other charecteristic that goes along w/it? Is it even a valid term? I haven't seen any studies that state anything regarding rapid metabolization of T.

Paul