I’m currently on cycle, want to keep LH/FSH pumping throughout.
Tren/test/eq;- 400/500/600mg.
Running HCG 500iu e2d. Running tamox 40mg every day.
Got blood panel back yesterday, 0 LH and FSH.
So the question then is, drop to tamox because it’s doing nothing, or increase the dose?
Does a SERM during cycle even have the intended effect?
The purpose of a SERM during cycle is to prevent gyno. That’s it. That’s all it can do. It absolutely will not maintain LH and FSH function. I don’t know why you think it would. The feedback mechanism that exists has been obliterated by exogenous hormones. It doesn’t return to normal until you’re no longer doing that.
Many people would disagree with you.
Have a flick through this thread (amongst others) The PCT SERM dosing in this forum is wrong
Many people are free to disagree. Some of them also believe the earth is flat. But the science is the science. HPTA is disrupted by exogenous hormones. It’s a fact. As long as that state is maintained then raising LH beyond a marginal level is not feasible. HCG is much better at that and even then we’re talking about LH going from 0.0 to 0.1 for most guys. I know this because that’s how it works with my (and many others’) trt treatments.
Additionally, PCT is very different from on cycle. Like, by definition they’re opposites. The conditions under which a drug works are contextual. I’m not sure why you brought that up within this discussion but I’m open to hearing what you have to say.
Brought up because although the thread is about PCT there is more discussed including things such as;
This relates to on cycle use.
I have also read that hpta suppression is based on estrogen levels rather than testosterone, in which case an argument for SERM use on cycle starts to make more sense.
By quoting a crackpot who’s no longer on here you’re kind of making my point for me. Part of what he said is common sense and true (do not use HCG for pct) but the rest is highly questionable.
LH is going to be at 0 when you are on. Period. I don’t care what else you’re taking, your body isn’t going to be easily convinced that you need more test when your T level is high.
Well there seems to be evidence from literature from those shutdown on trt that serms plus HCG resumes fertility, implying that lh and fsh production was resumed.
Exogenous testosterone inhibits spermatogenesis. Hypogonadal men wanting to preserve their fertility and at the same time benefiting from TRT effects can be prescribed selective oestrogen receptor modulators or testosterone plus low-dose human chorionic gonadotrophin (hCG).
Sorry didnt mean to flag that last post, trying to do things from phone.
Back to the topic however.
The HPT Axis is suppressed through exogenous testosterone, but only because it aromatises into estradiol which the hypothalamus uses to judge the level of testosterone. The male body doesnt produce estrogen itself, and instead converts testosterone. High levels of E then mean high levels of T and shutdown the HPTA.
Based on this, the use of a SERM on cycle should be just as effective as off-cycle into tricking the hypothalamus into believing there is very low E and thus starting to produce GnRH.
See studies such as;
" In men, peripheral estradiol levels directly reflect the action of estrogens at the hypothalamo-pituitary level to inhibit gonadotropin secretion."
Estradiol inhibits gonadotropin release in men by an action at the hypothalamus and pituitary. Because of the tissue-specific regulation of aromatase, peripheral estradiol levels may not reflect brain estradiol concentrations.
…We suppressed aromatase activity in 10 young healthy men with letrozole 2.5 mg once daily, restored plasma estradiol levels with estradiol patches (100 microg/d for the first week, 50 microg/d the second week, 25 microg/d the third week, and no estradiol patch the fourth week) and measured plasma testosterone, estradiol, LH, FSH, and SHBG levels… During letrozole use, the mean plasma estradiol level needed to restore testosterone, LH, and FSH levels to baseline levels was not significantly different from the baseline mean estradiol level.
Local aromatization of testosterone in the hypothalamo-pituitary compartment is not a prerequisite for expression of the inhibitory action of estrogens on gonadotropin secretion in men. Peripheral estradiol levels directly reflect the inhibitory tone exerted by estrogens on gonadotropin release and are a major determinant of peripheral testosterone, LH, and FSH levels…
Let me have my coffee before I dig into this. But this is a worthwhile conversation and I’m glad you put this thread up. Good value add to the forum.
The study concluded that serm plus HCG brought back sperm production. I believe that is true. What I don’t believe is that they significantly increased LH and FSH. HCG mimics LH, and can cause sperm production. My guess is that the serm had very little to do with the sperm production.
They’re not taking exogynous test in those studies, which is causing suppression. Your body does not rely on aromatised E2 for the feedback loop, there are men that cannot aromatise (genetic mutation - they can’t make the enzyme) and they don’t have run-away test levels.
Didn’t read the whole article. If not on AAS, then serm may help.
I think this is the most cogent point. While fascinating, if the subjects weren’t exposed to exogenous testosterone, then is it really applicable to the subject matter?
Many of these articles do refer to exogenous testosterone because the men are on TRT.
If you read the conclusions of the last article I linked it says
‘Conclusions
Exogenous testosterone inhibits spermatogenesis. Hypogonadal men wanting to preserve their fertility and at the same time benefiting from TRT effects can be prescribed selective oestrogen receptor modulators or testosterone plus low-dose human chorionic gonadotrophin (hCG).’
This is important because the hypothalamus is looking to regulate the bodies hormones, and in the case of sex hormones (supposedly) is searching for estrogen levels (estradiol), and not excess testosterone.
SERMs effects the hypothalamus by making it think there is less E in the body than there should be, and therefore assuming low testosterone, and it messages the next part down the chain to release GnRH.
HCG alone cannot fully restore testicular function. In the testicles are two primary cells, leydig and sertoli, you need a combination of both LH and FSH to have live sperm, and HCG can only do one half of this.
When the article says they brought back sperm production, this means then they must have successfully resumed GnRH production.
Look at this additional article, and the bits I have selected.
“For men of reproductive age who suffer from hypogonadal symptoms, preservation of fertility is an important aspect of their treatment paradigm. Treatment with human chorionic gonadotropin (hCG) has shown the ability not only to reverse azoospermia brought on by testosterone supplementation therapy but also to help maintain elevated intratesticular testosterone levels. In addition, selective estrogen receptor modulators, often used with hCG have been shown both to elevate total testosterone levels and to maintain spermatogenesis in hypogonadal men…
…The purpose of this review is two-fold. First is to evaluate the potential therapies that could help restore sperm production in those men who have infertility resulting from exogenous testosterone use and a second is to look at therapies that may allow a hypogonadal man to concurrently maintain spermatogenesis as well as receive TST and thus preserve the ability to initiate a pregnancy…
…In those patients desiring to establish a pregnancy within 6–12 months, testosterone therapy can be continued with 500 IU hCG every other day ± clomiphene citrate. Those patients desiring to establish a pregnancy after more than 12 months should cycle off testosterone every 6 months with a 4 week cycle of 3000 IU hCG every other day.”
This study shows how applying estradiol suppresses the HPTA
Amongst other things, it states;
“Our study shows that the male HPG axis is very sensitive to circulating estradiol levels. The relationship between estradiol and testosterone or gonadotropin levels was nonlinear. Higher estradiol levels have increasingly less effect on circulating LH, FSH, and testosterone levels. Varying peripheral estradiol concentrations in the male physiological range resulted in testosterone levels in the low-normal to high-normal range. Although testosterone has an estradiol-independent effect on gonadotropin release (18, 19), high testosterone levels did not prevent gonadotropins from increasing in response to low estradiol levels….
…This raises an intriguing question: is the male HPG axis primarily driven by circulating testosterone or by estradiol? The results of the present study make a good case for estradiol. However, the increased gonadotropin and testosterone levels in the presence of normal estrogen levels in adult androgen-insensitive subjects indicate that there must be a contribution of an androgen-receptor-mediated effect (23). Also, Hayes et al . (24) demonstrated an estradiol-independent effect of testosterone on LH but not on FSH release by the pituitary. Nevertheless, it remains to be determined whether the circulating testosterone, when varied within the male physiological range, has an estradiol-independent, clinically relevant effect on gonadotropin release in men.”
And why do I/should anyone care?
And what do I want to know;
This is an excellent point, but what is their baseline test levels, presumably there is a ceiling as to the amount of GnRH the body would produce in the absence of E2. Do these mean have higher than average, average or lower levels of testosterone compared to the wider population. Also, are there any contraindications with their disorders and otherwise normal HPTA function, or do these people suffer any other hormone or other issues because of their inability to aromatise E2.
They suffer from low E2, which brings a host of problems.
In regards to aromatase deficiency, initially looking from wiki’
“Aromatase deficient males experience a normal growth into adulthood. With a very low level of circulating estrogen (<7pg/mL), resulting in a higher level of FSH and LH in the blood.”
It would appear that this is also consistent with the hypothalamus measuring estradiol, resulting in higher levels of released GnRH.
Similarly, in this article discussing men with aromatase deficiency; 'LH, FSH and testosterone levels in both aromatase-deficient patients were markedly elevated. ’
This only seems to strengthen the argument for HPTA being E2 driven, and thus for the possible use of SERMs on cycle.
Edit,
Further evidence that in this population LH and FSH are not only elevated but are quite significantly so. In this study, for one individual, prior to E2 treatment LH registered at 9.7iU/L (ref range 0.2-6.5) and FSH registered at 27.5iU/L (ref range 0.5-8.0).
I run a serm on cycle for gyno prevention. All I know is if I go off it whilst on cycle, I notice my balls get achy and start to shrink. So whilst it might not keep you fertile on cycle I believe it is somehow stimulating the balls activity, meaning they will be in better shape when you go on PCT. Not scientific proof by any means
With your cycle I personally wouldn’t drop the serm, as you are on a1500mg/ wk, some you will probably need it to stop gyno. Your HCG might not be legit. How is the size of your balls?
If they haven’t atrophied much the serm/hcg might still be keeping them in decent shape for when your cycle finishes.