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).
hCG trial, total T doesn’t move (primary failure). Hence, little sense in continuing to SERM trial unless didn’t try hCG long enough.
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)
hCG trial, total T increases (primary system working!), drops hCG adds in SERM, total T stays up at XX (back to “functional” at YY%)
tries SERM (no hCG trial), total T increases (back to “functional” at ZZ%)
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.