testosterone level or Androstanediol-gluc

[1ainslie]

My T levels are at max range or over and my DHT is 2 to 3 times max level, however my Androstanediol-gluc level is only 1/3 up range. My doc says to take a lot more T as and the high DHT is not a problem because the Androstanediol-gluc is the metabolite of testosterone and is the more important level to get in the upper third, does anyone know about this?

[Axl]

Originally Posted by 1ainslie

My T levels are at max range or over and my DHT is 2 to 3 times max level, however my Androstanediol-gluc level is only 1/3 up range. My doc says to take a lot more T as and the high DHT is not a problem because the Androstanediol-gluc is the metabolite of testosterone and is the more important level to get in the upper third, does anyone know about this?

I thought that Androstandediol glucuronide is (most prominently) a metabolite of DHT, not T???

There is 3-Alpha Androstandediol glucuronide and 17-Beta Androstandediol glucuronide. I think the major pathway is T -> DHT -> DHT gluceronide (metabolisation)... if I understand it correctly. But I can be wrong; I'm no expert.

See this link for more info.

iHOP - Origin of plasma androstanediol glucuronide in men.

Origin of plasma androstanediol glucuronide in men.

Moghissi E, Ablan F, Horton R


The role of testosterone (T) and dihydrotestosterone (DHT) as precursors of the peripheral metabolite androstanediol glucuronide (3 alpha diol G) in plasma from normal men was studied. An apparent steady state of both putative precursors and the steroid glucuronides were attained by 8-h constant iv infusions of 3H-labeled steroid after a loading dose. The unconjugated steroids and the steroid glucuronides (after beta-glucuronidase hydrolysis) with 14C indicator were purified by serial microcolumn and paper chromatography steps previously reported to achieve radiochemical purity. The specific activities of 3 alpha diol and 3 alpha diol G in plasma were widely different in each subject, confirming our earlier suggestion that the two peripheral metabolites are formed in different pools. The conversion ratios (CRPre-Prod BB) varied widely. The CRT-3 alpha diol G was generally less than 5%, while the CRDHT-3 alpha diol G was 10 times higher. These results are compatible with the expected model, T----DHT----3 alpha diol G. In some of the studies, T glucuronide (TG) and DHT glucuronide (DHTG) were isolated after T infusions, and DHTG was isolated after DHT infusion. The major conversion product of blood T was DHTG, not TG, and the major conversion product of DHT was 3 alpha diol G. This suggests that metabolism proceeds through a steroid reduction step and glucuronidation. The peripheral pathway to 3 alpha diol G may involve formation of DHTG and then 3 alpha-reduction to 3 alpha diol G. This may also explain why blood levels of unconjugated 3 alpha diol have not been helpful in elucidating disorders of androgen formation, as this androgen mostly arises from sites different from 3 alpha diol G.

J. Clin. Endocrinol. Metab. (1984)
PMID: 6746859

[1ainslie]

Originally Posted by Axl

I thought that Androstandediol glucuronide is (most prominently) a metabolite of DHT, not T???

There is 3-Alpha Androstandediol glucuronide and 17-Beta Androstandediol glucuronide. I think the major pathway is T -> DHT -> DHT gluceronide (metabolisation)... if I understand it correctly. But I can be wrong; I'm no expert.

See this link for more info.

iHOP - Origin of plasma androstanediol glucuronide in men.

Origin of plasma androstanediol glucuronide in men.

Moghissi E, Ablan F, Horton R



The role of testosterone (T) and dihydrotestosterone (DHT) as precursors of the peripheral metabolite androstanediol glucuronide (3 alpha diol G) in plasma from normal men was studied. An apparent steady state of both putative precursors and the steroid glucuronides were attained by 8-h constant iv infusions of 3H-labeled steroid after a loading dose. The unconjugated steroids and the steroid glucuronides (after beta-glucuronidase hydrolysis) with 14C indicator were purified by serial microcolumn and paper chromatography steps previously reported to achieve radiochemical purity. The specific activities of 3 alpha diol and 3 alpha diol G in plasma were widely different in each subject, confirming our earlier suggestion that the two peripheral metabolites are formed in different pools. The conversion ratios (CRPre-Prod BB) varied widely. The CRT-3 alpha diol G was generally less than 5%, while the CRDHT-3 alpha diol G was 10 times higher. These results are compatible with the expected model, T----DHT----3 alpha diol G. In some of the studies, T glucuronide (TG) and DHT glucuronide (DHTG) were isolated after T infusions, and DHTG was isolated after DHT infusion. The major conversion product of blood T was DHTG, not TG, and the major conversion product of DHT was 3 alpha diol G. This suggests that metabolism proceeds through a steroid reduction step and glucuronidation. The peripheral pathway to 3 alpha diol G may involve formation of DHTG and then 3 alpha-reduction to 3 alpha diol G. This may also explain why blood levels of unconjugated 3 alpha diol have not been helpful in elucidating disorders of androgen formation, as this androgen mostly arises from sites different from 3 alpha diol G.

J. Clin. Endocrinol. Metab. (1984)
PMID: 6746859

Interesting info, it was Dr Hertoghe who told me AC was a metabolite or T and DHT, I assumed he knew but maybe not?

[Axl]

Dr Herthoghe is right. He really knows his stuff. Maybe I wasn't clear enough when trying to explain my point: my bad. What I was trying to say: it is a metabolite of both T and DHT: please re-read the text:

"The CRT-3 alpha diol G was generally less than 5%, while the CRDHT-3 alpha diol G was 10 times higher"

- CRTestosterone- 3 alpha diol G = less than 5%
- CR DHT - 3 alpha diol = 10 times higher (....means about 50%)

...But you can see that DHT metabolises ten times more to Andro-gluc than T.

I can't understand why your DHT is so high and, at the same time, your androstan-gluc is low. That puzzles me a bit.

A very high DHT is no problem if you are already bold or when you have very little androgen receptors. In this case, the DHT cannot bind to the AR-receptors in your scalp to initiate hairloss. Maybe you are in one of these two situations, and maybe that's why dr Hertoghe does not mind having your DHT in 2x above max level?? DHT is very important for virilisation: do you notice extra hair on your arms, face, chest?

[1ainslie]

Originally Posted by Axl

Dr Herthoghe is right. He really knows his stuff. Maybe I wasn't clear enough when trying to explain my point: my bad. What I was trying to say: it is a metabolite of both T and DHT: please re-read the text:

"The CRT-3 alpha diol G was generally less than 5%, while the CRDHT-3 alpha diol G was 10 times higher"

- CRTestosterone- 3 alpha diol G = less than 5%
- CR DHT - 3 alpha diol = 10 times higher (....means about 50%)

...But you can see that DHT metabolises ten times more to Andro-gluc than T.

I can't understand why your DHT is so high and, at the same time, your androstan-gluc is low. That puzzles me a bit.

A very high DHT is no problem if you are already bold or when you have very little androgen receptors. In this case, the DHT cannot bind to the AR-receptors in your scalp to initiate hairloss. Maybe you are in one of these two situations, and maybe that's why dr Hertoghe does not mind having your DHT in 2x above max level?? DHT is very important for virilisation: do you notice extra hair on your arms, face, chest?

NO change on chest arms, face, I was taking quite a lot DHEA 100mg per day so maybe thats why T and DHT was so high but the AC was only 1/2 way up range