Thank you, I think this might be the way to go. What happens when these people came off the SERM therapy after a few months? Did test levels crash again or stabilize at the serm therapy levels?
I admit, I am very ignorant to the subject but is LH 3.1 really bad? What are the minimum reuirements LH and FSH for fertility potential.
Iâm no expert on this subject there is guys on here that know alot more about this then me.
But personally I tried a regular pct with nolva only which did nothing to me
Tried a little bit of clomid around march and was told by guys on here to quit so I did after like a week. I should have stayed on
I talked to a known bodybuilder was advised to do 1000 iu of hcg eod for 14 days
Clomid at 100mg a day I will do 50
And nolva at 20
Aromasin at 25mg a day
I will probably so 12.5 or aromasin
Will the levels stay who knows I hope they do
Dont stress over it bro. Itâs a slow road.
Plenty of guys that had decka dick and recovered just fine
Test will likely drop when you come off, but hopefully it will be higher than you are currently. It will be individual how much, or how long it may take (some claim elevated TT for 6 weeks after SERM administration, I donât have any clinical data to back that up though).
By running the SERM for extended time at low dose, you will likely get a bit of growth in your balls since you will have elevated LH and FSH from the SERM. Hopefully, when you drop the SERM your high functioning balls will make more Test with the lower LH and FSH levels. I would taper down the SERM, and get blood work each time you do. Stay at each dose for a couple months. That will give you a good idea of where you will be off of it.
This isnât terrible advice, but doing so will result in competing mechanisms one positive and one negative. Will the positive outweigh the negative for overall positive or not? The positive, is that it will likely get your balls larger and used to producing a lot of test. The negative is that it will slow down the pituitary and result in less LH. Then it will take time once you stop the HCG to get the pituitary to produce more LH (it will be faster with a SERM).
If LH is ~0 like right after your last pin in a cycle, then the HCG suppressing LH is no big deal (LH wonât really start coming back until the test clears anyways). In this case it makes a lot of sense to me to use HCG. If someone has already recovered LH / FSH, then I am not convinced on its use. Maybe it is more positive. I just donât know. A SERM can potentially get the balls to be larger and more productive as well, without the suppression of the pituitary. SERM only here is simpler too.
Yes you are correct about serm being alot easier. But Iâm hating myself for not running all 3 back in march
I would have known by now if I recovered or not.
My way of thinking is run all 3 see what happens, if not recovered atleast you will know you covered all bases
Donât run the HCG at the same time as the SERMS. HCG will suppress the pituitary while the SERM tries to increase its function.
Yes I will be doing 1000iu eod first 2 week then nolva clomid
I know it will be a roller coaster but this is my last resort
Ok, doing HCG first is fine.
Great explanation, thank you. I think that my next step will be to run clomid every day at 15 mg for 3 months, then get bloods done again. I
OVIDREL - choriogonadotropin alfa injection, solution
Easier site to read. See the clinical studies section.
@mnben87 has given you a lot to think about and sounds like youâve got a plan. So if you have plenty of time and youâd like to try and restore normal HPTA function before having kids this sounds good.
Just keep in mind the diagnostic utility of hCG or an hCG/FSH combo is to decouple the function of testicles from function (or limited function) of the pituitary. From the article I shared with you:
The vital role of testosterone in human spermatogenesis is partially elucidated by previously cited studies where it has been shown that spermatogenesis could be stimulated with the LH analog hCG in patients who had active spermatogenesis prior to pituitary suppression (13,31). More intimate knowledge of the intra-testicular hormonal milieu was deciphered through the development of a percutaneous approach to test intra-testicular hormones in humans (32). These studies led to the finding that intra-testicular testosterone was roughly ten times higher than circulating testosterone and that its inhibition was associated with significant declines in spermatogenesis. These findings led to the concept that preservation of intra-testicular testosterone is necessary for spermatogenesis and clinically translates into a potential cutoff in circulating testosterone below which deficits in intra-testicular testosterone (ITT) are suspected. It is apparent that intratesticular testosterone levels similar to normal circulating serum testosterone concentrations are insufficient to support normal spermatogenesis, but besides that observation, no studies in humans exists that defines a cutoff of intratesticular or serum testosterone that is necessary to maintain spermatogenesis adequate enough to maintain normal male fertility potential (32).
The above mentioned gap in knowledge of what a ânormalâ testosterone is in patients being evaluated for infertility leads one to rely on more current studies on testosterone levels in young men. One recent study helped define testosterone ranges in young men by measuring sample testosterone levels obtained during the conduction of several large cohort studies in a central Centers for Disease Control and Prevention (CDC) lab (33). This study revealed that 303 ng/dL was the fifth percentile value among healthy non-obese patients between 19 and 39 years of age. Unfortunately without any access to semen analyses or other hormonal laboratories it is difficult to assess whether those in the fifth percentile or below had poorer semen quality. However, given these findings, it may not be unreasonable to treat certain patients with testosterone values less than 300 ng/dL and poor semen quality with agents that can increase ITT (34) Treatment strategies that may help increase ITT include the use of hCG injections or selective estrogen receptor modulators that block normal estrogen negative feedback leading to increase in endogenous FSH and LH (e.g., clomiphene citrate). It should be emphasized that trying to increase serum testosterone with exogenous testosterone will not help in this regard as it will decrease ITT by suppressing endogenous LH (as well as FSH) production due to negative feedback action on the hypothalamus and anterior pituitary. In fact, exogenous testosterone typically leads to a decline in spermatogenesis to the level of azoospermia in a majority of patients (35).
So you can give the SERM a try and if you canât get LH levels up high enough to induce fertility you can go back and diagnose an issue with the testicles using hCG or hCG/FSH treatment. The SERM treatment assumes you have a functional Pituitary. Clearly you are making some LH now. Lots of unknowns and assumptions in your case, especially since you used words like tren and deca where these compounds are highly suppressive and animal studies indicate potential physical damage (again, age dependent, lots of if and buts).
Finally, if youâd like even additional understanding of primary vs secondary HH, LH vs Testosterone levels:
Hypogonadotropic Hypogonadism (HH) and Gonadotropin Therapy
Take care.
This is good advice.
Understanding HPTA control loop should be a prerequisite for AAS use. If you understand how the loop works, diagnosing issues and making intelligent decisions becomes much easier.
It was mentioned earlier, Clomid monotherapy. Not as common but the results are usually pretty good. Low dose a few times a week can maintain good test levels. But itâs going to be just like testosterone in that when you stop using it your numbers will start to slip again. Without intervention youâll see a mean reversion.
So then you are basically saying it isnât even worth it, and I would have to be on it permanently to see lasting results?
Do you believe that if clomid therapy brought my levels up to ~500 from the current 177 ( just for example sake)⊠thenâŠ
Once I stop taking it, the âmean reversionâ you speak of will drag the levels back down to the 177 I am at now? You do not believe I could naturally be producing in the 300 range after stopping the clomid therapy or is it just completely unknown until tested?
If stopping clomid therapy, would my natural test levels crash below the 177 level it is at now? I canât handle another complete test crash, I would rather not even try the therapy.
I have found the main studies where this has been proven to work, but none of them mention testing levels once discontinuing the therapy. Can anyone find one if they are feeling up to it? Iâve found three so far, none of which test after discontinuation.
If 177 is your baseline then youâd likely return to somewhere around there. Possible you stay well above thatâlike in the 300âs as you mentionedâfor a while before nature takes over. I started trt because I was around 300, so itâs not like thatâs a number you want to shoot for. If that ends up being your best case scenario as a natty then youâll have to get to that point and then assess whether or not you can live that way. Maybe for you 300 ends up being not that bad? Hard to predict how individuals will respond to any of this.
Thanks for the response. I really donât feel âTHATâ bad at 177. My mood is good, not depressed, Maybe just slightly lower energy level than used to be. Really the only remaining differences I feel are a bit more lethargic, tad less motivation and concentration, but If I go to the gym everyday, seems to help. So I think if I could get back to 300, I would be very happy.
From all that I have read, you really only need to be around 300 to build and maintain muscle mass. So If my mood is good now, it should be even better at 300, and if I can build and maintain muscle even just a little at 300 I will be stoked. I used to be very big, but now I am ok with just being âFitâ and having some definition.
For me at least, the difference between high and low test is how much fat I hold to be at a certain muscularity. I can be leaner with the same muscle, when I cut, I keep a lot more muscle. When I gain more of it is muscle.
I was big and strong with test around 400 ng/dL, but I was also pretty fat.
I think clomid mono therapy might be a good option for you. It seems doses like 10-15 mg per day can have awesome results in many. There is a log you could dig up from a few years ago where a guy got his TT to 800ish with IIRC 12.5 mg per day. This individual found that increasing dose did not lead to higher TT, so he kept it at 12.5 mg/day.
I think a possibility is that you regain some ball function while on, and upon stopping you may get more out of your natural LH and FSH production. This is a possibility, not a certain at all.
At the same time, I am not sure if you will have any perceived negative side effects from clomid if the dose is low enough. Might be worth running long term. For some it loses effectiveness over time, so that is something to look out for.
Bingo, completely agree. Anabolic potential for a low BF% is main pro of higher Test levels in my experience. At 8% BF, I can maintain FFMI of 23 with total T at 300 ng/dL. To get to FFMI of 27 at same BF%, not a chance.
This is dependent on his long term testicular function. Iâll review this in more detail since given all the effort @mnben87 has put in here, this thread should be a sticky instead of having a new HPTA/PCT post every day. There seems to be a lot of dudes that need to grasp these concepts.
To get a top quartile Test level with clomid (SERM) monotherapy, both the pituitary and testicles of @tripleanon have to function well. If heâs set on long term ânaturalâ HPTA mode of operation and wants no âexogenous helpâ in the long term, then this can be tried as a trial and heâll end up where he ends up as @iron_yuppie stated.
My attraction to a provocative hCG monotherapy trial for him at this point is he can quickly (4-16 week trial) ascertain his testicular function and find out best case scenario for his endogenous production. Then switch back to âPCTâ mode, get the Pituitary involved. Then finally remove all exogenous substances. Unless one methodically does it this way, he canât diagnose whether he may have a primary or secondary issue in the context of HH (assuming thatâs the case long term, but I hope it isnât). I can think of at least five simplified scenarios (below) that ignore the time dependency of all this (which makes it more complicated).
Scenarios
hCG trial, total T doesnât move (primary failure). Hence, little sense in continuing to SERM trial unless didnât try hCG long enough.
hCG trial, total T increases (primary system working!), drops hCG adds in SERM, total T drops back down (âsecondary failureâ as he canât get LH high enough)
hCG trial, total T increases (primary system working!), drops hCG adds in SERM, total T stays up at XX (back to âfunctionalâ at YY%)
tries SERM (no hCG trial), total T increases (back to âfunctionalâ at ZZ%)
tries SERM (no hCG trial), total T doesnât budge (WHY?). Measuring a low normal LH at this point (like he shared in the post above ainât going to tell you).
All this dependent on Total Test the OP wants long term and what intra-testicular testosterone level he needs to be fertile.
Given where heâs at presently, might as well collect the data methodically and learn something about himself (thatâs my bias). Scenarios 1-3 give you the functional capacity of testicles and pituitary.
In the context of scenario 5, you donât know the failure mode without hCG. I hope scenario 4 gives you what you want.
IF after removing SERM in scenarios 3 and 4 your test levels decline below where either
(1) you either want them in the normal range OR
(2) need them to be for fertility
you know your pituitary canât seal the deal without chemical assistance. Normal is subjective here of course as I donât know his pre AAS baseline.
Hope this helps and reinforces why you need to speak with a knowledgeable medical provider who has the clinical experience to help you.
EDIT: Iâll add in a 6th scenario that I donât quite comprehend but I guess anything is possible with the human body. Note the author invokes an explanation I donât understand. Perhaps someone can explain it to me (@lordgains, @unreal24278 if you guys donât have enough homework):
A Case Report
A 37 year old professional athlete and bodybuilder arrived in my office complaining of low testosterone symptoms of low libido, erectile dysfunction, chronic fatigue, and mood disorder. He admitted to anabolic steroid abuse in the past, and now sought medical intervention to ârestore his testosterone to normal.â
A few years ago, he had married and fathered a child, and he now wanted to devote more time to his family, but complained of a lack of energy to do so. He also wanted to preserve fertility, as he wanted more children. Previous medical doctorâs lab studies showed low testosterone levels, all below 300 ng/dl, and low FSH and LH levels as well.
Upper left image : cropped portions of an anonymous body builder, courtesy of wikimedia commons. This image is an illustration only, and not an actual patient in any clinic.
Diagnosis and Treatment
After our usual workup, and the obvious diagnosis of hyopogonadal hypogonadism, treatment was started with HCG (human chorionic gonadotropin), an LH analog which stimulates testicular testosterone production. The patient wished to retain fertility which contra-indicated the use of Testosterone preparations.
Shortly after starting the HCG injections, the patient reported an immediate improvement in mood and energy, lasting about one week. However, this improvement was short lived and lasted only one week, after which he reported a recurrence of more severe low testosterone symptoms, worse than before.
Paradoxical Response with Lower Testosterone Levels
Repeat labs at 6 weeks showed testosterone levels had actually dropped lower to the 150 ng/dl range. FSH and LH were undetectable. My diagnosis at this point was hypothalamic suppression, and the HCG was discontinued.
Switch to Clomiphene was Sucessful
Treatment with Clomid (clomiphene 25 mg tablet daily) was started. Six weeks later, the patient reported âfeeling like my old selfâ with improved energy, libido and mood. Repeat labs 6 weeks after starting the Clomid showed testosterone levels of 832 ng/dl, and LH and FSH had increased as well. Serum estrogen was quite high at 72 pg/ml. Anastrazole was added to the treatment program with follow up normalization of estrogen levels.
Some clinical perspective here:
Note these guys are trying to get the guy fertile so donât get into the particulars of using hCG with vs without Clomid. They throw in the whole kitchen sink.
Infertile male with a recent history or current use of TRT and/or AAS
A patient who presents for treatment of male factor infertility, indicated by oligospermia or nonobstructive azoospermia, who either reports a recent history or current use of TRT and/or AAS is a common scenario faced by a male fertility specialist. Several options could be discussed depending on the severity of his hypogonadal symptoms, timing in which he and his partner wish to achieve pregnancy, and assuming there is no clinical evidence of primary hypogonadism.
If the patient and his partner are willing to wait and his hypogonadal symptoms are manageable without TRT or AAS, the patient could simply discontinue the use of TRT or AAS to allow spontaneous recovery. Data from the male contraception literature indicate a reasonable probability of recovery in 67%, 90%, 96%, and 100% of men at 6, 12, 16, and 24 months, respectively, with a median time to recovery of 20 Ă 106 ml-1 sperm in 3â6 months.13,30,31 Yet, many men will not tolerate discontinuation either due to severe hypogonadal symptoms, uncertainty of recovery, and/or timing issues, and these men may require some form of alternate androgen supplementation. Therefore, one could administer gonadotropin analogs similar to those implemented in patients with HH. Assuming there is no major component of primary hypogonadism, this option is safe, would treat hypogonadal symptoms, and would hasten the time to recovery. It is reasonable to start with hCG 3000 IU subcutaneous injection 3 times weekly for 3 months with additional titration pending interim serum testosterone levels although the optimal hCG dose has not been clearly established. If at 3 months seminal parameters have not improved, one could add FSH. A typical starting dose is rFSH 75 IU subcutaneous injection 3 times weekly.
During gonadotropin therapy, adjunctive treatments with AIs or SERMs are typically implemented. Such an approach has demonstrated excellent results on average within 4â5 months.59 CC 25 mg daily or 50 mg every other day, titrated up to 50 mg daily, may demonstrate improvement in seminal parameters in as little as 3 months for men with HH. CC is cost effective and has been more effective as a combined therapy in this setting, with less extensive data to support it as a monotherapy.80 If the patient exhibits a low T/E ratio, an AI could be prescribed, with anastrozole 1 mg oral twice weekly is a reasonable starting dose that may be titrated up or down according to the response.
Maintenance of spermatogenesis before beginning or during TRT or AAS use
A second scenario is a patient who wishes to preserve existing spermatogenesis before beginning TRT or AAS use. Maintenance of normal ITT levels is critically necessary to maintain spermatogenesis. hCG has proven to maintain ITT levels with doses as low as 500 IU every other day.56,57 Clinical data evaluating higher doses of hCG given as monotherapy (500â2500 IU twice weekly), or low-dose hCG (500 IU every other day) in combination with TRT, have demonstrated satisfactory results for maintaining spermatogenesis,57,58 and either would be a good choice as recommended by these authors.
Alternatively, CC is commonly used as an alternative to TRT to treat hypogonadism in men wishing to preserve spermatogenesis. The ability to take an oral medicine that is relatively inexpensive and has good long-term safety data and is clinically efficacious at ameliorating hypogonadal symptoms is clearly advantageous.69,71 However, data are currently not available specifically evaluating CC in this manner, and randomized controlled trials are needed. The newer SERM on the horizon, EC, has been studied in the phase II clinical trial setting specifically demonstrating preservation of spermatogenesis on semen analysis while satisfactorily improving hypogonadal symptoms and serum testosterone levels, and phase III data is pending.82,84 Finally, AIs such as anastrozole or letrozole may be helpful in this clinical scenario for patients who are obese and/or exhibit a low T/E ratio <10:1.
I donât think itâs you. The explanation is clearly without any sense. Thereâs no need for endogenous LH production when you supplement HCG (exogenous âLHâ). The explanation must be wrong. I think the solution could be a desensitization of the LH receptors as happens with leuprorelin administration on the GnRH receptors. Thereâs two possibilities:
And it took me a bit but I found this study supporting my theory:
The testosterone response to hCG in vitro was completely inhibited for about 3 days, then rose to the control level at 5 days, when only a small proportion of the original receptor sites and cyclic AMP response had begun to return
Since I know you love graphs Iâll include this one
Edit: I should note that the response to hCG With functioning testicles is highly individual and the dose-response relationship is not linear
