Tamoxifen Blocks Human Chorionic Gonadotropin (HCG) Induced Leydig Cell Desensitization

[ready2explode]

Tamoxifen Blocks HCG Induced Leydig Cell Desensitization

I found this running a search in the cuttingedgemuscle search engine...It was Posted by Nandi12 the admin over there...thought it would be an interesting read

Nandi12
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Tamoxifen Blocks Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) Induced Leydig Cell Desensitization
Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) induced testicular desensitization seems to be a hot topic. There are a number of studies showing that concomitant use of Nolvadex ameliorates this. The first abstract suggests that Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) at least partially blocks the conversion of 17 alpha-hydroxyprogesterone (17 OHP), a testosterone precursor, to testosterone. This effect is suppressed by Nolvadex.

The second abstract seems to indicate that estrogen may not be the only culprit, since Nolvadex plus Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) does not increase T levels any more than Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) alone, even though the combination reduces desensitization.

Since we are trying to avoid this desensitization so when we quit the Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) our testes respond to our endogenous LH, it makes sense to always use nolvadex with Human Chorionic Gonadotropin ( Human Chorionic Gonadotropin (HCG) ) to at least help the problem, if not solve it completely.


J Clin Endocrinol Metab 1980 Nov;51(5):1026-9

Tamoxifen suppresses gonadotropin-induced 17 alpha-hydroxyprogesterone accumulation in normal men.

Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg PW.

Intramuscular administration of 1500 IU hCG daily for 3 days induced a transient accumulation of 17 alpha-hydroxyprogesterone (17 OHP) relative to testosterone (T) in normal men, reaching its maximum 24 h after the first injection (17 OHP to T ratio, 1.7 +/- 0.3 times baseline; P < 0.01). Simultaneous administration of hCG and the estrogen antagonist tamoxifen (20 mg twice daily) almost completely abolished the hCG-induced steroidogenic block localized between 17 OHP and T (17 OHP to T ratio at 24 h, 1.1 +/- 0.1 times baseline; P < 0.01 vs. hCG alone). These data indirectly suggest that, in man, the hCG-induced steroidogenic lesion might be mediated through its estrogen-stimulating effect.



Andrologia 1991 Mar-Apr;23(2):109-14

Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.

Levalle OA, Suescun MO, Fiszlejder L, Aszpis S, Charreau E, Guitelman A, Calandra R.

Division Endocrinologia, Hospital Carlos Durand, Instituto de Biologia y Medicina Experimental, Buenos Aires, Argentina.

The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men. An hCG test (5000 IU hCG) was performed before, after two months of hCG administration (2000 IU hCG three times weekly) and after two months of hCG + Tx (2000 IU hCG three times weekly plus 20 mg/day of tamoxifen). Blood samples were obtained before and following 24 and 72 h of every test to determine T, E, 17OHP and SHBG. T increased only in HH with both treatments (X +/- SEM: Basal: 97.9 +/- 19.7; hCG: 237.7 +/- 43.2; hCG +/- Tx: 204.7 +/- 10.7 ng/100 ml). 17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization. However, the association of Tx does not improve T serum levels, suggesting that E might not be the unique factor involved in the mechanisms for testicular desensitization.
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[BiggieSwolls]

Its an interesting read. But I will say that this issue of optimal post cycle recovery will continue to be debated on the boards for years. Hell, its been going on for almost 2 decades already.

 

[warlord]

ok so in english is that saying that you should not use nolvedex with hcg?!?!

w

 

[ready2explode]

No...in english...use nolva with hcg...its a good thing

 

[bigjim33]

No...in english...use nolva with hcg...its a good thing

thanks for the translation

 

[LAWNSAVER]

I would never recomend Human Chorionic Gonadotropin (HCG) post cycle! Human Chorionic Gonadotropin (HCG) should only be used in small doses during a cycle as a preventitive measure against testicular atrophy. Too many people who cycle get this confused!

HCG will not restore ones HPTA.

The use of Human Chorionic Gonadotropin (HCG) in small doses during a cycle will prevent any atrophy from setting in. The small dose will also not allow any desensitization from occuring! N-dex in small doses while the Human Chorionic Gonadotropin (HCG) is active could help, but I dont think its needed.

Now, if you take it for 2-3 weeks straight at 500-1000ius per day, n-dex will be needed.

Think of Human Chorionic Gonadotropin (HCG) as a prevention, not something to fix a problem!

 

[ready2explode]

Why not use it post cycle lawnsaver? You never gave a reason...

 

[LAWNSAVER]

Because it is suppressive! It would only suppress your HPTA even more!

HCG does nothing to restart your natural test production. It should only be used to prevent testicular atrophy brought on when the testicle do not receive any signal from the LH. If you take small doses of Human Chorionic Gonadotropin (HCG) during your cycle, there will always be a LH signal, thus preventing atrophy from setting in.

 

[ready2explode]

Hcg suppresses your nat test because it elevates androgen and estrogen levels...androgen levels will fall pretty fast after its discontinuance and using nolva will block estrogen...hcg its any more suppressive than most other steriods and if you ran it like this:

Weeks 1-10: test
weeks 10-12: hcg
weeks 10-15: nolva

It would not take you any longer to get yourself back to normal than without its use...if you were to use it in the middle of that same cycle it would still take you the same amount of time (15 weeks in my example) to be back up and running...the bonus of running it at the end of your cycle is to make sure your testes are FULLY capable to produce the max amount of testosterone once the body produces LH...if you were to use in the middle of a cycle, after its dicontinuance one's testes MAY atrophy once again...

 

[rj420]

just use it throughout the whole cycle at small doses. I know a few bros who used 500-1000iu every 5-7 days, and they say that it always keeps their boys from atrophy. They also say they have no problems getting back to normal post-=cycle.

 

[SWALE]

A few thoughts: LH has effects that are stimulatory upstream in the testosterone pathway, so perhaps Human Chorionic Gonadotropin (HCG) does as well. That may account for the increase in the testosterone precursor, without an increase in the velocity of the enzyme that converts 17-OHP into T. If "Nolvadex plus Human Chorionic Gonadotropin (HCG) does not increase T levels any more than Human Chorionic Gonadotropin (HCG) alone, even though the combination reduces desensitization", by what measure are we assessing inhibition of converstion from 17-OHP into testosterone? It would seem the elevation in T is the same with, or without, Nolvadex. Also, the SERMs act as estrogen agonists (meaning "like estrogen") in some places, but block estrogen in others. At this point, we do not know the direction the Nolvadex is taking at that particular point in the testosterone pathway. And, once again, they are using Human Chorionic Gonadotropin (HCG) doses in excess of what we now recommend, even in overcoming the complete inhibition of the HPTA during a heavily androgenic Anabolic Androgenic Steroids (AAS) cycle.