Help/Advice Interpreting My Labs? Fertility After Blast/Cruise

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. I’ll 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 he’s set on long term “natural” HPTA mode of operation and wants no “exogenous help” in the long term, then this can be tried as a trial and he’ll 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 “PCT” mode, get the Pituitary involved. Then finally remove all exogenous substances. Unless one methodically does it this way, he can’t diagnose whether he may have a primary or secondary issue in the context of HH (assuming that’s the case long term, but I hope it isn’t). I can think of at least five simplified scenarios (below) that ignore the time dependency of all this (which makes it more complicated).


  1. hCG trial, total T doesn’t move (primary failure). Hence, little sense in continuing to SERM trial unless didn’t try hCG long enough.

  2. hCG trial, total T increases (primary system working!), drops hCG adds in SERM, total T drops back down (“secondary failure” as he can’t get LH high enough)

  3. hCG trial, total T increases (primary system working!), drops hCG adds in SERM, total T stays up at XX (back to “functional” at YY%)

  4. tries SERM (no hCG trial), total T increases (back to “functional” at ZZ%)

  5. tries SERM (no hCG trial), total T doesn’t budge (WHY?). Measuring a low normal LH at this point (like he shared in the post above ain’t 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 he’s at presently, might as well collect the data methodically and learn something about himself (that’s my bias). Scenarios 1-3 give you the functional capacity of testicles and pituitary.

In the context of scenario 5, you don’t 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 can’t seal the deal without chemical assistance. Normal is subjective here of course as I don’t 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: I’ll add in a 6th scenario that I don’t quite comprehend but I guess anything is possible with the human body. Note the author invokes an explanation I don’t understand. Perhaps someone can explain it to me (@lordgains, @unreal24278 if you guys don’t 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 “restore his testosterone to normal.”

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 doctor’s 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 “feeling like my old self” 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 don’t get into the particulars of using hCG with vs without Clomid. They throw in the whole kitchen sink.

Recovery of spermatogenesis following testosterone replacement therapy or anabolic-androgenic steroid use

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 × 106 ml-1 sperm in 3–6 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 4–5 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 (500–2500 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 don’t think it’s you. The explanation is clearly without any sense. There’s no need for endogenous LH production when you supplement HCG (exogenous “LH”). 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. There’s two possibilities:

  1. It was just way too much hCG or
  2. There was too high a level hCG in the blood over time

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 I’ll 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

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I like it. After my long screed, I figured I’d outsource this to you. I hit the character limit :-). So the hypothesis is the Doc blew out the Leydig cells with hCG (no dosage given) but then another 6 weeks with “reasonable” Clomid dosing came with reversing LH receptor sensitivity and improvement in Test levels. I can buy that. I like that graph, thank you. Maybe that’s why the doc didn’t mention the hCG dosage given.

To the OP, good example of why you should start low with hCG although Fertility doctors usually much more aggressive on hCG dosage so this example just another example of individual variation which is critical to the discussion.

I think he didn’t know but he knew instinctively it was too much.

One question came to mind as I read the article. Is the doc right about the E receptors in the hypothalamus being the only receptors for the feedback loop?
I did my own research months ago and read a few studies that suggested that there are T receptors responsible for the feedback, too.
Just wanted to get your opinion on this.

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Not my active area of research but I would agree with you. That diagram ain’t correct.

This human investigative model employing sex steroid ablation and selective physiological sex steroid add-back in healthy and GnRH-deficient men provides novel insights into the study of LH regulation in men. These data suggest a model of sex steroid feedback whereby 1) T and E2 have independent effects on LH secretion, 2) inhibition of LH by T requires aromatization for its pituitary but not its hypothalamic effects, and 3) E2 has dual sites of feedback, but its predominant effect is at the hypothalamus.

Typical med school diagrams circa 2019:

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This is nice! Thanks for the input, that’s what I came around to when I researched it but I read other studies so thanks for the support

Sure. Just for fun…these folks really exceeded expectations on their study:

Although this study really belongs over in the TRT forum given the range on the dose response curve:

In summary, pulsatile T is less effective as a negative-feedback signal on LH secretion than continuous T administration, as demonstrated by two independent methods. This difference in feedback strength occurs, probably in part, at the pituitary level, but the data do not exclude hypothalamic involvement. Visceral and total abdominal fat by CT correlated negatively with basal and total LH secretion but not with pulsatile secretion. Feedback strength decreased with higher BMI, both without and with exogenous GnRH stimulation. These data could indicate that physiologically pulsatile and pharmacologically continuous T feedback has unequal, suppressive effects on the central gonadal axis in men.

Good demonstration of how Natesto can be used to control Hct and have minimal negative feedback on HPG axis.

Hat tip to at madman at the other forum.

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This natesto seems like it could be a revolutionary step in TRT practice! I’m stunned by the fact that the feedback doesn’t get inhibited (as strongly) by pulsatile administration but since GnRH receptors work the same it’s not that outlandish a thought.

(i) pulsatile T is less effective than continuous T delivery in suppression of LH secretion, (ii) T feedback is reduced by BMI, and (iii) basal and total, but not pulsatile, LH secretion, estimated by deconvolution analysis is negatively correlated to visceral fat and total abdominal fat area, calculated from a single CT slice at L3-L4.

That’s what the study found. I like it, but we always gotta keep statistics in mind. Deconvolution is not the best way of getting data.

What’s also interesting was that free T and LH secretion correlated negatively with BMI (I think we knew that) which shows us again that fat people are hormonally fucked.

This might be a compensatory mechanism to decreased LH secretion in severe obesity

I’m surprised they got this approved by an ethics committee cause I wouldn’t be excited about getting 800 mg of Ketoconazole orally haha!
The discussion in the end about glucocorticoids and emotions is definitely a topic for another day.

A major discovery recently is that the pulsatility of cortisol is required for normal emotional and cognitive responses in man [42]

To the OP: I think you got some really good input here, I wish you and your family the best and report back how your fertility and T levels are going!
Also OP, maybe your Willy grows on HCG:

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Interesting mechanistic study from a while back. Great conversation @lordgains, thanks for your time.

Credit to @cataceous at the other place.

Nice find. It seems to be way more difficult to apply HCG right than we thought. I saw studies where people are given 3000 IU (I recently saw one with 5000 IU ED) hCG for a few weeks which should definitely be enough to suppress T production but it didn’t happen (at least not in that limited time frame, think it was 3-4 weeks). As I stated above: the effect is highly individual which shows is again how important bloods are.

If we are on the topic of hCG, there’s one thing I want to point out/discuss.
I repeatedly saw the mantra “AIs won’t stop the aromatization induced by hCG” on this forum and I’d like to get a rationale for that as I couldn’t verify this and my understanding would suggest otherwise. I’ll give my opinion:

HCG increases E2 before it increases T. Several studies show that E2 is highest 24 h after HCG dosing and T 72 h. (Won’t link that) Here you can see an example of acute stimulation of aromatization by hCG in Leydig cells independent of T production:

This could mean that the LH receptor regulates aromatase expression and voila, it does:

With 50 ng/ml oLH, a large augmentation (twofold) of the P450arom mRNA level either without or with testosterone was observed.

With that in mind the only question becomes if AIs get into the Leydig cells (primary T and E2 producers in man) so they can inhibit the aromatase there.
Since the next study shows that non-steroidal AIs readily cross the blood brain barrier, it’s safe to assume they pass the blood testis barrier. They are lipophilic and only anastrozole gets actively transported out of the brain. (I couldn’t find studies about the concentration measured in the testis)

All this info leads me to believe that AIs do

  1. Get into the Testis and Leydig cells
  2. Inhibit the aromatase there
  3. Therefore inhibit aromatization by hCG

Finally this paper shows that AIs do prevent the increase of E2 caused by hCG

In the hCG group, the rate of testicular aromatase activity and testicular E2 level were higher and the diameter of seminiferous tubules was smaller than in the control group. However, these changes were not observed in the hCG+A.I. group

If some of you have evidence suggesting the contrary I’m open to change my opinion.

@readalot I learned a lot too, thanks!

I got a few things I’d like to discuss in the near future: Glucucorticoids (find them extremely interesting and complicated, also in combination with androgens) and then a smaller one would be thyroid hormones (here we could also discuss differences with synthetic and swine derived (I heard it’s a difference but I didn’t research yet, don’t know what it contains right now). I’ll open up new threads then and I’d appreciate your opinion there too.


My understanding was that the increase of e2 by HCG wasn’t via aromatase, so an AI wouldn’t be able to control it. The studies you linked show that’s not the case, so very interested to learn more about this. I’m one of those guys that doesn’t take HCG regularly for fear of higher e2

I tried to find an answer to that question too but it was difficult. One study wrote “all E2 from the Testis gets created through the aromatase enzyme complex” and others just used the higher aromatase activity as a reason.

Im skeptical myself because a few studies showed an increase in E2 after 1 hour with the peak at 24 h which seems a bit fast for an up regulation of the expression (takes a day usually so 24h makes sense).
It was also difficult to find studies linking LH to an upregulation of aromatase but the one I found supports it.

So we’re left with this non conclusive area. But if my hypothesis is wrong there are many questions:

  1. What means a higher activity of aromatase if not an increase in expression? It could be that aromatase enzymes are inactive in the cell per example as vesicles because it is an ER associated enzyme.
  2. If the AIs don’t block the aromatization, it shouldn’t happen through aromatase so what way is there to synthesize E2 in the testis without aromatase? (I touched on it in another lengthy post but I don’t think these ways happen in the testis on a large scale)
  3. Why does an AI seem to suppress the increase in E2 caused by hCG in some studies?

The easiest thing would be if we guys on here reported their blood results and experiment next time they PCT or are on TRT+hCG. Our own independent, no conflict of interest, crossover study.

I think the evidence I provide is the best we have right now. Let’s see if somebody finds additional knowledge.

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Thanks for this post. Very nice points. This is THE if not one of THE main posts that drove this narrative:

I’ll make some comments in the following days. I think the concern expressed is the relative concentration of competitive AI like anastrozole inside the testicles vs the intratesticular concentration of testosterone caused by hCG. Since the inhibition is competitive, we have to look at the relative concentration of testosterone and competitive AI inside the testicles as well as the respective binding affinities. I don’t think there is any concern that non-steroidal AI can’t get into the Leydig cells. I can share multiple research papers that shows this happens easily.

I’ll get back on this later @lordgains. I’m impressed with your research and cognitive abilities.

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More to come with some discussion.

This paper supports everything we wrote about down regulation of LH receptors. It even hints at upregulation (indirectly through T administration).
I’m out for today and I’m excited to read your input tomorrow!


I looked into the intratesticular T concentrations a bit and that’s what I came up with:

LH and FSH were profoundly suppressed to 5% and 3% of baseline, respectively, and ITT was suppressed by 94% (1234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group [all every other day], and 26% greater than baseline in the 500 IU hCG group.

Which leads me to believe, if you inject 500 IU two times weekly your intratesticar T levels are most likely within normal range (if you’re shut down and you inject more, you should also not get crazy high levels otherwise why inject that much when you respond well?) which means even a competitive AI will do it’s job.

For more info on competitive AIs see my Independence Day post here:

Now, even if a competitive AI like anastrozol doesn’t work, you’d always have the option of Exemestane to inhibit Aromatase which has different kinetics (see post) and simply doesn’t care about T level that much.

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Very nice follow up and post from July 3. Here’s another small (small) case study by a very smart clinician showing the effect of 150 IU vs 500 IU injection:

A relevant note for consideration in comparison of quantitative serum beta hCG concentrations with endogenous luteinizing hormone (LH) concentrations is that the typical “normal” range for endogenous LH is 1.7 – 8.6 mIU/mL. As noted, half-life differences (of large magnitude) are present, but this offers some perspective with the comparison.


This data indicates that there is indeed a drastic difference in quantitative serum beta hCG concentrations achieved following a single hCG injection of 150iu vs 500iu. More interesting is the fact that this dose-response relationship does NOT appear to be linear based on this limited data. The serum beta hCG concentration following a single hCG injection of 150iu appears to peak at ~1mIU/mL at 8 hours and has retreated to baseline prior to 24 hours after the injection. On the contrary, the serum beta hCG concentration following a single hCG injection of 500iu attains a level of 2mIU/mL at 8 hours and subsequently INCREASES to 3mIU/mL at 24 hours and 48 hours, before retreating to 1mIU/mL at 72 hours (still has not declined to baseline

According to this data, it would appear that a hCG dosage of 150iu would have to be administered on AT LEAST a daily basis (if not more frequently) to allow continual stimulation of the leydig cells of the testes. Further, with an apparent maximal serum concentration from a hCG dosage of 150iu reaching a peak of ~1mIU/mL, this may prove to be insufficient stimulation for SOME patients to achieve consistent testicular activity and prevent the aforementioned side effects of testicular deactivation/dormancy. Certainly one could debate the relative need for continual stimulation of the testes, however this may offer a clue for dosage adjustments for patients that either experience poor results, poor fertility, or continued decrease in testicular volume at lower hCG dosages.

A single dosage of 500iu of hCG appears to exert a much more prolonged (and pronounced) increase in serum beta hCG concentrations, likely coinciding with a more prolonged and pronounced biological effect. Once again, whether this is beneficial or detrimental, can certainly be debated and will often hinge on many factors on an individualized case by case basis. It does appear obvious from the data that a dosage of 500iu of hCG will maintain levels >1mIU/mL for up to 3 days (72 hours) following a single injection. Thus, it would seem a direct conclusion to state that an hCG injection of 500iu every 3.5 days (twice weekly) would provide relatively continual stimulation of the leydig cells of the testes (concentration >1mIU/mL), and injections of this magnitude in dosage would NOT be needed any more frequently than that.

My clinical mind and instincts suggest that the “ideal” hCG dosage likely lies in between these two extremes (150iu vs 500iu) and ideal frequency will hinge upon ideal dosage (with 150iu or less dosages likely requiring daily or even more frequent injections) and larger dosages (500iu, possibly even slightly smaller) requiring no more frequent than twice weekly injections, but this conclusion simply cannot be made concretely from this limited data. Furthermore, dosage decisions and frequencies are always individualized case-by-case based on many variables specific to the individual (fertility considerations, injection compliance, complicating factors such as SHBG levels, current/prior response to hCG, estradiol levels, testicular health, etc). Without specific data on other dosages (which I would like to obtain), these patterns suggest that a dosage regimen of hCG 250iu-350iu on an every other day (QOD) schedule would likely offer an alternative regimen for relatively steady and consistent testicular stimulation, although these conclusions are only speculative and cannot be drawn definitively from this limited data.

The argument that competitive AI will not reduce estradiol levels is not based on the data or the theoretical and constitutive framework we have in hand. Futhermore, don’t go crazy with the hCG dosage and 500 IU 3x weekly seems like plenty (especially if you are using hCG proactively while using exogenous T). Your point on irreversible AI is spot on. Great job @lordgains for the detailed review. The forum needs more of this along with relevant anecdotal and clinical experiences instead of hand waving. Thank you.

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There is a blood barrier that prevents AI’s from passing to the testes, thus being unable to inhibit aromatase there. HCG stimulates production there, so AI’s cannot stop the aromatization effected by HCG. In short, it suppresses aromatisation everywhere except where it is happening. That being said, if Ksman wrote the post, you should assume it’s incorrect and work out from there. I would be interested in reading the studies he claims exist in that post, I haven’t found them and he doesn’t actually reference them. I am leaning towards the opnion that they have never existed at all and he is just making stuff up.

See my post above, I addressed this. My research and knowledge leads me to believe otherwise.
This also stands in stark contrast to @readalot ‘s comment.

I just saw you yourself (@hardartery) wrote you couldn’t find them and it’s probably incorrect. My point is: if non steroidal AIs pass the blood brain barrier which has a significantly higher integrity and more proteins which transport molecules out, then they should easily be able to pass through the blood testis barrier. I think it’s very unlikely they don’t get into the nuts. @readalot could you point us in the right direction?