Question about ultradrol and pct

[Smitch]

I'm not sure why he's so argumentative on here.

His posts over on UK-M were not normally as aggressive, he gave out some pretty good info and i read quite a bit of it when i was looking at PH's last year.

 

[Con]

TBH I read the forum he moderates on and his attitude is poor over there also.
He's now banned, for many of you this will be a pleasing thing but I am sure some of you will be sad at this tragic loss.
Fear not though as I am sure you can find this good fellow spamming his garbage on many other sites.
Lets keep this one in check, super egos are not welcome.

 

[Little Simon]

I'm not sure why he's so argumentative on here.

His posts over on UK-M were not normally as aggressive, he gave out some pretty good info and i read quite a bit of it when i was looking at PH's last year.

To put it simply, he didn't get his own way so started acting the asshole about it.

He's now the ProHormone Troll of TM.

 

[kuju]

Hmmm - it does seem odd, he was always pretty sound as I remember him - we both contributed a lot to a thread about those dodgy Recov Bipeptides and he seemed fairly even handed (or i'm conveniently forgetting stuff..who knows). It's a shame in some ways because he knows his stuff - but seems to have forgotten how to convey it in an even handed, calm and concise manner.



I think he made some very good points in this thread - just perhaps...not particularly well.

 

[Rusty76]

All that being said, I'm still curious about the OP's original question. What is the point of taking a SERM after a cycle of an AAS that does not aromatize? The way I see it, a nonaromatizable compound will first decrease one's natural testosterone production, of course. Testosterone is the precursor for Estradiol and the other estrogens, so estrogen levels will decrease as well. After the cycle ends, the pituitary and the hypothalamus respond positively to low levels of both testosterone and estrogen and will produce more GnRH and LH respectively. It is typically said that the main point of SERMs is to block the hypothalamus and pituitary from the negative feedback of estrogen. But if estrogen is already low, even lower than it would be naturally, is it really necessary to take a SERM? I understand that it would still be mildly beneficial since there is still some endogenous estrogen, but is it worth the side effects the SERM can produce? I've even heard the SERMs are carcinogenic.

Anyway, alternative mechanisms of action I've heard are that Nolva and Clomid can actually directly stimulate the Hypothalamus and Pituitary to release their hormones through an unknown mechanism. Hackskii also mentioned that Clomid can potentially increase the sensitivity of the pituitary to GnRH without the influence of estrogen. Has anyone else heard of any other possibilities?

In general, it seems to me that the use of SERMs with nonaromatizable compounds is based mostly on tradition. However, I am not certain. Tradition is often there for a reason. I was just wondering if anyone could provide some insight on SERMs and nonaromatizables, so I asked my brother to post this thread. Thanks to Jethro52185 for agreeing to help his kid brother.

Hi , new to the board here. I would like to bump Jonny's question here. You seem like you have done quite a bit of research on Ultradrol as well Jonny and your question about the neccessity for a SERM is one I have wondered about as well. Obviously there is no direct aromatization to estrogen, so that imbalance may not be the sticking point. Maybe the value in the SERM is kickstarting test production quickly again? Please forgive my lay terms here because I am not an expert, but I believe that Clomid does this by tricking the production of test again by lowering the amount of estrogen able to bind in the body and so tricking the body into thinking it needs to produce more test to reach the proper balance. There obviosly is a negative feedback that would occur when the free (and I guess technically unreproted to the body) estrogen in the body would start to cause problems. If this is completely wrong sorry for the incorrect analysis, but I am wondering just like Jonny is, what is the value of a SERM when using Ultradrol in specific, after looking at its sides and type of delivery.

 

[hackskii]

From my perspective I think it is the SERMS cause the receptors in the pituitary to be more sensitive to GnRH.
I personally feel clomid works best for any single SERM.

 

[Jonny784]

Hi , new to the board here. I would like to bump Jonny's question here. You seem like you have done quite a bit of research on Ultradrol as well Jonny and your question about the neccessity for a SERM is one I have wondered about as well. Obviously there is no direct aromatization to estrogen, so that imbalance may not be the sticking point. Maybe the value in the SERM is kickstarting test production quickly again? Please forgive my lay terms here because I am not an expert, but I believe that Clomid does this by tricking the production of test again by lowering the amount of estrogen able to bind in the body and so tricking the body into thinking it needs to produce more test to reach the proper balance. There obviosly is a negative feedback that would occur when the free (and I guess technically unreproted to the body) estrogen in the body would start to cause problems. If this is completely wrong sorry for the incorrect analysis, but I am wondering just like Jonny is, what is the value of a SERM when using Ultradrol in specific, after looking at its sides and type of delivery.

You're absolutely right in your analysis. First off, UD does not aromatize, so an Antiaromatase wouldn't help much. Here's the way I envisioned the benefits of the SERM in this case. At the end of your UD cycle, your test levels will be low and your Estrogen will be about average or slightly low. However, even though both hormones are low, the Testosterone to Estrogen ratio at the end of the cycle is much lower than it normally is. So the estrogen will still have a relatively significant and noticeable effect on your system. There will still be some estrogen limiting the release of GnRH from the Hypothalamus and LH and FSH from the pituitary. Therefore, the SERM will still have a beneficial effect on allowing the HPG Axis to return to normal functionality as quickly as possible. One can still eventually recover their Testosterone production without a SERM, but at the cost of potentially losing gains since the process will take much longer. Long story short, I'll be using a SERM for PCT on my UD cycle.

 

[Jonny784]

From my perspective I think it is the SERMS cause the receptors in the pituitary to be more sensitive to GnRH.
I personally feel clomid works best for any single SERM.

Good post. You are correct. It inspired me to do some serious researching on the subject. Here is one of particular interest.


Effects of Estradiol and Some Antiestrogens
(Clomiphene , Tamoxifen, and Hydroxytamoxifen) on
Luteinizing Hormone Secretion by Rat Pituitary Cells
in Culture*)
G. E m o n s , O. O r t m a n n , Sabine Thi e s s en, and R . K n u p p e n
link: SpringerLink - Archives of Gynecology and Obstetrics, Volume 237, Number 4


This is an in vitro study with isolated rat pituitary cells. You're totally right in that SERMs can have a direct effect on the pituitary to release FSH and LH without the presence of estrogen. However, it turns out from this study and several others that estrogen itself, the thing we are trying to block, has an even more potent positive effect on releasing LH and FSH than any of the SERMs do. So estrogen can be beneficial in the pituitary in increasing the sensitivity to GnRH. This result really got me confused, so I did some more digging. It turns out the regulation of this system is more complicated than I ever imagined. Estrogen can have mixed effects. Estrogen has a strong inhibitory effect on the release of GnRH from the hypothalamus, so overall, estrogen is negative. SERMs can also have a positive and negative effect on the pituitary. It all depends on timing, dosing, the state of the body's hormones, sensitivity, etc., etc., etc.... Most of the studies are in vitro, as in a petri dish, to isolate the effects in specific environments. Since it's so damn complicated, it's easier to just look at human in vivo studies, as in an actual person, so that all the complications are taken into account. Specifically, for post-cycle body builders, we can look at hypogonadal and oligozoospermic men whose HPG axis is below normal levels. All we want to see is if on a SERM, the Testosterone, LH, and FSH levels are increased within the ~4 weeks time a traditional PCT lasts. I found one study that studied this general concept.

Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development. SERMs definitively increase LH, FSH, and Test. This happens through a ridiculously complicated positive and negative feedback pathway which is still not fully understood. Also, they help to reduce gynecostemia, so it's always good to have on hand in case symptoms flair up. After all my research, the topic is still debatable to me, but the evidence seems to suggest that a PCT would still be useful in a nonaromitzable cycle whether it directly effects the pituitary or indirectly prevents the hypothalamus's inhibition by estrogen. Anyway I'm still planning Tamoxifen as PCT for four weeks. Better to have it and not need it than to need it an not have it. This post was not a direct reply to anyone's post specifically, but more of just me ranting in general about the complications of SERMs, their effects, and whether they're needed in the first place.

 

[Rusty76]

Great posts, thanks so much for some of the insight. How about aromatase inhibitors during the PCT? I think I may be leaning toward Clomid like hackskii is; think this would need an AI like Arimidex? Any AI at all? Obviously estrogen would be low but any test kicked up by the clomid could aromatise more than we want correct? You planning on an AI Jonny?

 

[Jonny784]

Great posts, thanks so much for some of the insight. How about aromatase inhibitors during the PCT? I think I may be leaning toward Clomid like hackskii is; think this would need an AI like Arimidex? Any AI at all? Obviously estrogen would be low but any test kicked up by the clomid could aromatise more than we want correct? You planning on an AI Jonny?

Personally I won't be taking an AI. I would only recommend an AI with compounds that aromatize. For these aromatizable compounds, an AI will block your exogenous (from outside of the body) steroid from turning into super high and unnatural levels of estrogen. With a nonaromatizable cycle this is not an issue, and the SERM as PCT effectively blocks estrogen everywhere it can have a negative impact. Some estrogen is actually beneficial for arousal and sex drive so you don't want to totally block it. SERMs (Selective Estrogen Receptor Modulators) block it in the breast tissue and hypothalamus where it's negative, but not in other places where it serves some good. I'll use Nolva after my cycle as PCT and have it in case some gyno symptoms flare up (which is unlikely with a nonaromatizable)

Also I started my UD cycle today. I'm taking detailed notes and will post a full summary when the cycle is over.

 

[hackskii]

I have alot of studies on clomid, some of them even with hypogonadal men.
If you like I can post them here.
Endo doctors use clomid to determine if one is secondary aquired hypogonadism, and the typical response from 100mg of clomid a day for 5 to 7 days is doubling of LH output and an increase of FSH by up to 50%.

It would make sense.

That study comparing clomid to nolva is old, and I use both, this for some reason I find some synergistic effect.

Estrogen is approx 200 times more suppressive than testosterone.

Nolva actually helps lipid profiles post cycle, but long term use tends to elevate SHBG and lower IGF-1, so short runs ok, longer, I have an issue with.
For one, long term use of nolva puts uterine cancer at risk, beings the prostate and uterus has the same developmental cells I would not want to run that long term.

As a stand alone SERM, clomid hands down wins IMO, but together with nolva, I find works very well.

 

[Jonny784]

@hackskii Yes if you would post the title of one or two of your favorite studies on this subject, I'd definitely look them up and read them. Always looking to expand my understanding. Thanks man.

But yea I'll be using Nolva over Clomid for one simple reason: Dolla Bills. For me it was readily accessible and half the price of Clomid (per amount needed for a PCT.) That's the only reason.
For short term, the type of SERM should not make a huge difference, so Tamoxifen will suffice for my purposes. Thanks for the info.

 

[hackskii]

Here's a study showing low-dose Clomid therapy (25mg ED) boosts testosterone by 250% in 4-6 weeks:

Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism, Shabsigh A, Kang Y, Shabsign R, Gonzalez M, Liberson G, Fisch H, Goluboff E. Department of Urology, NY Presbyterian Medical Center, New York, NY, USA. J Sex Med. 2005 Sep;2(5):716-21.

AIM: Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio. METHODS: Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed.

RESULTS: The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 +/- 39.8 ng/dL and 32.3 +/- 10.9, respectively. By the first follow-up visit (4-6 weeks), the mean testosterone level rose to 610.0 +/- 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P < 0.001). There were no side effects reported by the patients.

CONCLUSIONS: Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estradiol ratio in men with hypogonadism.This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway.

​

Study showing a hypogonadic 30-year old male, suffering permanent shutdown from steroid abuse, fully recovered natural hormone levels and HPTA function from 2 months of 100mg Clomid therapy:

Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse, Tan RS, Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA.

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male.

INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months.

MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH.

RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis.

CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.

​

Here's another study showing only 7 days of Clomid therapy increased total testosterone by 100% and, more importantly, free testosterone by over 300% in young men:

The effects of aging in normal men on bioavailable testosterone and luteinizing hormone secretion: response to clomiphene citrate, J Clin Endocrinol Metab. 1987 Dec;65(6):1118-26.

Geriatric Research, Education, and Clinical Center, Veterans Administration Medical Center, Seattle, Washington.

Serum testosterone (T) levels in men decline with age while serum LH levels, as measured by RIA, increase. To assess if the decline in serum T levels in healthy aging men is paralleled by an age-related decline in the bioavailable non-sex hormone-binding globulin (SHBG)-bound fraction of T and to determine whether there are age-related changes in LH secretion or LH control of T production, we studied 29 young (aged 22-35 yr) and 26 elderly (aged 65-84 yr) healthy men. All men had single random blood samples drawn, and 14 men in each age group underwent frequent blood sampling for 24 h, both before and after 7 days of clomiphene citrate (CC) administration. Both mean 24-h serum total T levels and non-SHBG-bound T were reduced in elderly men compared to those in young men (P less than 0.05), while estradiol and SHBG levels were similar in the 2 age groups. Serum FSH determined by RIA and LH by RIA and bioassay were higher in the elderly men compared to those in young men (P less than 0.05), but the ratios of LH bioactivity to immunoreactivity and the LH pulse frequency and amplitude were similar. After CC administration, mean serum total T and non-SHBG-bound levels in young men increased by 100% and 304%, respectively, while in older men these values increased by only 32% and 8%, respectively. However, CC-stimulated LH pulse characteristics and serum levels of estradiol, SHBG, FSH, and bioactive and immunoreactive LH were similar in the 2 groups. Thus, both at baseline and after CC stimulation, elderly men had significantly lower serum total T and non-SHBG-bound (bioavailable) T levels than did young men, despite similar or increased levels of bioactive LH and similar bioactive to immunoreactive LH ratios and LH pulse characteristics. These results suggest that major age-related changes in the hypothalamic-pituitary-testicular axis occur at the level of the testes and are manifested by decreased responsiveness to bioactive LH. Administration of CC to young and elderly men resulted in similar changes in LH pulse characteristics and LH bioactivity and immunoreactivity, suggesting preserved hypothalamic-pituitary responsiveness in the elderly.

View attachment 023.guay.cc&testosterone-(3).pdfView attachment 22.2003. guay et al. clomiphene & hh.pdf

​

I have a bunch more of the clomid in pdf but for some reason I am not getting it in there.
You get the picture.
Again, nolva alone in my opinion is worthless, I failed a PCT using nolva alone, and also failed with aromasin and nolva.

 

[Rusty76]

@hackskii Would you recommend an AI while running a short cycle of Clomid during PCT? Not necessary since UD doesnt aromatise?

 

[kuju]

NIce work @hackskii!! Always love getting new papers and i hadn't looked at Clomid that closely before. INteresting stuff!! Thank you!