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Tamoxifen Blocks HCG Induced Leydig Cell Desensitization


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Tamoxifen Blocks HCG Induced Leydig Cell Desensitization
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 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 HCG does not increase T levels any more than HCG alone, even though the combination reduces desensitization.

Since we are trying to avoid this desensitization so when we quit the HCG our testes respond to our endogenous LH, it makes sense to always use nolvadex with 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.

drug A is synergestic with drug B, drug B increases the effiency of drug C, drug C decreases the side effects of drug A ,

then there is drug D that helps all of other drugs, drug E is waiting to be researched.

How many fucking drugs are we gonna use ?:biggrin::biggrin:
Im confused, you should or should not take nolva with HCG?

I say no.. Yes there may be some studies that show Tamoxifen Blocks HCG Induced Leydig Cell Desensitization, but who gives a shit.. Tamoxifen also lowers igf. It also causes estro rebound too.

If hcg is used right you should not have to worry about Desensitization.

Human Chorionic Gonadotropin (hCG) is a peptide hormone that mimics the action of luteinizing hormone (LH). LH is the hormone that stimulates the testes to produce testosterone. (1) More specifically LH is the primary signal sent from the pituitary to the testes, which stimulates the leydig cells within the testes to produce testosterone.

When steroids are administered, LH levels rapidly decline. The absence of an LH signal from the pituitary causes the testes to stop producing testosterone, which causes rapid onset of testicular degeneration. The testicular degeneration begins with a reduction of leydig cell volume, and is then followed by rapid reductions in intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3 (INSL3) – All important bio-markers and factors for proper testicular function and testosterone production. (2-6,19) However, this degeneration can be prevented by a small maintenance dose of hCG ran throughout the cycle. Unfortunately, most steroid users have been engrained to believe that hCG should be used after a cycle, during PCT. Upon reviewing the science and basic endocrinology you will see that a faster and more complete recovery is possible if hCG is ran during a cycle.

Firstly, we must understand the clinical history of hCG to understand its purpose and its most efficient application. Many popular “steroid profiles” advocate using hCG at a dose of 2500-5000iu once or twice a week. These were the kind of dosages used in the historical (1960’s) hCG studies for hypogonadal men who had reduced testicular sensitivity due to prolonged LH deficiency. (21,22) A prolonged LH deficiency causes the testes to desensitize, requiring a higher hCG dose for ample stimulation. In men with normal LH levels and normal testicular sensitivity, the maximum increase of testosterone is seen from a dose of only 250iu, with minimal increases obtained from 500iu or even 5000iu. (2,11) (It appears the testes maximum secretion of testosterone is about 140% above their normal capacity.) (12-18) If you have allowed your testes to desensitize over the length of a typical steroid cycle, (8-16 weeks) then you would require a higher dose to elicit a response in an attempt to restore normal testicular size and function – but there is cost to this, and a high probability that you won’t regain full testicular function.

One term that is critical to understand is testosterone secretion capacity which is synonymous to testicular sensitivity. This is the amount of testosterone your testes can produce from any given LH or hCG stimulation. Therefore, if you have reduced testosterone secretion capacity (reduced testicular sensitivity), it will take more LH or hCG stimulation to produce the same result as if you had normal testosterone secretion capacity. If you reduce your testosterone secretion capacity too much, then no amount of LH or hCG stimulation will trigger normal testosterone production – and this leads to permanently reduced testosterone production.

To get an idea of how quickly you can reduce your testosterone secretion capacity from your average steroid cycle, consider this: LH levels are rapidly decreased by the 2nd day of steroid administration. (2,9,10) By shutting down the LH signal and allowing the testis to be non-functional over a 12-16 week period, leydig cell volume decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to secrete testosterone decreases as much as 98%. (2-6)

Note: visually analyzing testes size is a poor method of judging your actual testicular function, since testicular size is not directly related to the ability to secrete testosterone. (4) This is because the leydig cells, which are the primary sites of testosterone secretion, only make up about 10% of the total testicular volume. Therefore, when the testes may only appear 5-10% smaller, the testes ability to secrete testosterone upon LH or hCG stimulation can actually be significantly reduced to 98% of their normal production. (3-5) The point here is to not judge testosterone secretion capacity by testicular size.

The decreased testosterone secretion capacity caused by steroid use was well demonstrated in a study on power athletes who used steroids for 16 weeks, and were then administered 4500iu hCG post cycle. It was found that the steroid users were about 20 times less responsive to hCG, when compared to normal men who did not use steroids. (8) In other words, their testosterone secretion capacity was dramatically reduced because they did not receive an LH signal for 16 weeks. The testes essentially became desensitized and crippled. Case studies with steroid using patients show that aggressive long-term treatment with hCG at dosages as high as 10,000iu E3D for 12 weeks were unable to return full testicular size. (7) Another study with men using low dose steroids for 6 weeks showed unsuccessful return of Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of HCG treatment for 12 weeks (6) (INSL3 is an important biomarker for testosterone production potential and sperm production. 20)

These studies show that postponing hCG usage until the end of a steroid cycle increases your need for a higher dose of hCG, and decreases your odds of a full recovery. As a consequence to using a higher dose of hCG at the end of a cycle, estrogen will be increased disproportionately to testosterone, which then causes further HPTA suppression (from high estrogen) while increasing the risk of gyno. (11) For example, high doses of hCG have been found to raise estradiol up to 165%, while only raising testosterone 140%. (11) Higher doses of hCG are also known to reduce LH receptor concentration and degrade the enzymes responsible for testosterone synthesis within the testes (12,13,19 ) -- the last thing someone wants during recovery. While these negative effects of hCG can be partly mitigated by the use of a SERM such as tamoxifen, it will create further problems associated with using a toxic SERM (covered in another article).

In light of the above evidence, it becomes obvious that we must take preventative measures to avoid this testicular degeneration. We must protect our testicular sensitivity. Besides, with hCG being so readily available, and such a painless shot, it makes you wonder why anyone wouldn’t use it on cycle.

Based on studies with normal men using steroids, 100iu HCG administered everyday was enough to preserve full testicular function and ITT levels, without causing desensitization typically associated with higher doses of hCG. (2) It is important that low-dose hCG is started before testicular sensitivity is reduced, which appears to rapidly manifest within the first 2-3 weeks of steroid use. Also, it’s important to discontinue the hCG before you start PCT so your leydig cells are given a chance to re-sensitize to your body’s own LH production. (To help further enhance testicular sensitivity, the dietary supplement Toco-8 may be used)

A more convenient alternative to the above recommendation would be a twice a week shot of 200iu hCG, or possibly a once a week shot of 500iu. However, it is most desirable to adhere to a lower more frequent dose of hCG to mimic the body’s natural LH release and minimize estrogen conversion. If you are starting hCG late in the cycle, one could calculate a rough estimate for their required hCG ‘kick starting’ dosage by multiplying 40iu x days of LH absence, since the testes will be desensitized, thus requiring a higher dose. (ie. 40iu x 60 days = 2400iu HCG dose)

Note: If following the on cycle hCG protocol, hCG should NOT be used for PCT.

Recap –

For preservation of testicular sensitivity, use 100iu hCG ED starting 7 days after your first AAS dose. At the end of the cycle, drop the hCG two weeks before the AAS clear the system. For example, you would drop hCG about the same time as your last Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you would drop the hCG about 10 days before your last oral dose. This will allow for a sudden and even clearance in hormone levels, while initiating LH and FSH production from the pituitary, to begin stimulating your testes to produce testosterone. Remember, recovery doesn’t begin until you are off hCG since your body will not release its own LH until the hCG has cleared the system.

In conclusion, we have learned that utilizing hCG during a steroid cycle will significantly prevent testicular degeneration. This helps create a seamless transition from “on cycle” to “off cycle” thus avoiding the post cycle crash.

drug A is synergestic with drug B, drug B increases the effiency of drug C, drug C decreases the side effects of drug A ,

then there is drug D that helps all of other drugs, drug E is waiting to be researched.

How many fucking drugs are we gonna use ?:biggrin::biggrin:

ALL of them. :evil:
If your running HCG in post cycle and not at low dose on cycle then the inclusion of Tamoxifen may be of benefit based on above or where your hitting up high doses of HCG as you already have hypogonadotropic hypogonadism and attempting to alleviate it otherwise this is another reason why low dose HCG on cycle is the better option when comes to recovery.
From's HCG profile:-

As regards HCG´s use of Post-Cycle-Therapy (PCT), smaller and more frequent doses after a cycle of AAS would give the best results with the least amount of side effects. A dose of 250iu to 500iu everyday (ed) for 2 to 3 weeks is plenty and should very little from person to person (3). The Physicians Desk Reference recommends 500iu/day, as did the late, great, Dan Duchaine. The smaller doses are sufficient enough to begin reversal of testicular atrophy and used in conjunction with nolvade, will help the already present problem of recovery without raising the levels of estrogen to high and increasing the risk of gynecomastia in the user. Lower doses of 250iu to 500iu also avoid the further risk of down regulating LH receptors in the testes. The old saying more is better definitely does not apply to the use of HCG. You don´t want to finish PCT after using too much HCG only to find out your back at the beginning again. Your best bet is to start at 250iu or 500iu ed for 5 or 6 days, and if you don´t notice anything happening (nuts dropping and getting bigger) up the dose slightly. Small doses like 500iu two days a week isn´t going to cut it like some people think. The only thing small doses of HCG ay be useful (sublingually) for is reducing symptoms of benign prostatic hyperplasia (7). Yeah, that´s right, you can probably reduce some symptoms of an enlarged prostate with the use of small doses of HCG.

As stated above the cycles of HCG should be in the 2 to 3 week range with a least one month off in between, you could stretch your cycle out to four weeks without any major concern if you are using lower doses. One should however take care when using HCG as prolonged use could repress the body´s natural production of gonadotropins permanently, but this is mostly just pure speculation as it does not have yet to be reported nor has there been a case of an overdose. To be on the safe side shorter cycles of HCG seem to be that of the norm. Most users cycle HCG near the end of a steroid cycle, you should start your HCG therapy on the last week of your cycle. For best results you should also run nolva while you run HCG as taking HCG by itself will do little to nothing and gyno even though rare may also flair up. Once the HCG cycle is finished you continue with your usual clomid or nolvadex (preferably the latter) for pct as it is more effective when used in conjunction HCG for pct. With an AAS cycle of 6 to 10 weeks HCG may not be necessary unless extreme doses of AAS were used or there is an existing problem of testicular atrophy or you are running a heavy oral only cycle. AAS cycles of 12 or more weeks should have HCG as a part of post cycle plan.

Since HCG is used to stimulate testosterone production, side effects can be the same as those associated with AAS, although gyno may be more common. Possible side effects of HCG use are water and sodium retention after higher doses are used. This is usually a result of higher androgen production. It may cause gyno (again if doses are too high). Any athletes worried about failing urine test because of low levels of epitestosterone may find that using a dose of 500iu of HCG will increase epitestosterone levels. However the problem with HCG is that it is also banned by the IOC and can also be detected in a urine test, the half life of HCG is approximately 4 to 5 days. Another possible downside to HCG is that it to can be suppressive to natural testosterone because it takes the place of LH. Since LH is manufactured in the pituitary because of the response of GnRH (gonadotropin releasing hormone) which in turn is secreted by the hypothalamus. Because the HCG mimics LH and is being supplied exogenously the hypothalamus will be given a signal to still stop producing GnRH, so no natural LH will be produced (5). This is why it should always be used with a compound such as nolvadex. So although HCG is essential after long or heavy cycles, it should not be used without an ancillary such as (specifically) nolva. Also HCG therapy should be discontinued at least 2 weeks prior to stopping the use of nolva, or it may suppress natural testosterone itself (5). This should not be a problem if you are running it towards the end of your cycle of AAS and before pct.

I agree with this 100% i have always run nolva alongside HCG post cycle and would never EVER run a cycle without either drug ready for PCT.
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if your running hcg in post cycle and not at low dose on cycle then the inclusion of tamoxifen may be of benefit based on above or where your hitting up high doses of hcg as you already have hypogonadotropic hypogonadism and attempting to alleviate it otherwise this is another reason why low dose hcg on cycle is the better option when comes to recovery.

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