T Nation

Studies Pointing to Efficacy of HCG Post-TRT?

Hi all,

My endocrinologist believes I may have been misdiagnosed as primary Hypogonadism and wants me to come off TRT to see if we can restore my natural levels. I am a 28y.o male.

I was wondering if anyone can link me some literature which explains the benefits of using HCG/Clomid/ Nolva to stimulate endogenous testosterone production post trt. As my endo doesn’t believe there is evidence to suggest it is faster at stimulating natural production over going cold-turkey.

Thank you for your advice.

Pre TRT Bloods:

Testosterone: 7.2 nmol/L (6.0 - 28)

SHBG 16 nmol/L (15-50)

Free Testosterone 196 pmol/L (200-600)

Estradiol 60 pmol/L (<150)

FSH 14 IU/L (1-8)

LH 4 IU/L(2-8)

Prolactin 136 mIU/L (45 - 375)

TSH 1.46 mIU/L (0.50 - 5.00)

PSA 0.44 (<2.51)

This is secondary hypogonadism with a mixture of poor testicle response to stimulation and levels of a 90 year old man. I would tell your doctor thanks but you’re not interested. He will more than likely once you stop TRT claim you’re levels are normal after the restart not allowing you to go back on TRT, then you are screwed!

You do not recover natural optimal levels scoring in the 200 ranges, you are getting quacked by this endo, also very common. If you ask your endo what he considers normal levels for a guy your age, I bet the answer will allow you to see how unskilled your doctor really is.

He should want your Free T levels at the top of the reference ranges.

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Your doc is right and wrong, right because you were probably misdiagnosed with primary hypogonadism, it is extremely rare and extremely difficult to diagnose from labs. The only way to be sure is with a HCG stimulation test.

I agree with @systemlord that it is going to be tough for you to recover with really low levels like that.

But, if your low from AAS use recovery is possible, if you are low just because and not from a suppressive medication, chances are there is no chance of recovery.

The problem is even if you do recover, you may not be happy with what “recovery” is.

Hope this helps.

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Thank you, I do take on board what you are saying but I am confident he will be supportive of commiting long term to TRT if I am not able to recover to a more acceptable level; he just wants to make sure. And because I’ve had trouble feeling ’ right’ on TRT I think it is worth a try; I just need some references to show him so I can hopefully persuade him to prescribe HCG/Nolva to aid in recovery.

Cheers

Your endo is an idiot like my endo and most endos are bro. First accept this fact.
Yes, you may have been misdiagnosed with primary, but so what? I’m with secondary and guess what…there is not much difference.

Yes, you can try clomid and nova. But they have terrible side effects with most patients me included(i’ve tried only clomid in fact). Clomid in most cases will elevate your T levels but WILL NOT resolve your symptoms. You have high T on paper and continue to feel like shit or even worse. What I’ve heard of nova it is even worse because it will crash your estrogen.

HCG may work. I myself think to try it. But the best doctors that do hormone OPTIMIZATION and are not shitheads like this endo are very skeptical about HCG monotherapy. According to them it cannot bring the same symptom improvements like TRT.

Do you think you can take clomid/nolva/HCG for some time and your natural production becomes strong, you stop the medications and you remain in the top ranges? This will not happen man. YOu will get back to your shitty natural levels with all the symptoms. And do you believe it is better to take long-term this shit clomid thant TRT? Guess what…

The only thing you need to consider with TRT according to me is the fertility issue. I also do not have children and am afraid of that. So adding adequate amount of HCG to the cocktail to keep fertility and continuing TRT seems the best approach.

With all else you are gonna fuck yourself. And tell this endo that he has now idea what normal levels are and you don’t want to be in the shitty lab levels but you want to be optimal and feel optimal.

The aim of this study is to review four case-based scenarios regarding the treatment of symptomatic hypogonadism in men. The article is designed as a review of published literature. We conducted a PubMed literature search for the time period of 1989-2014, concentrating on 26 studies investigating the efficacy of various therapeutic options on semen analysis, pregnancy outcomes, time to recovery of spermatogenesis, as well as serum and intratesticular testosterone levels. Our results demonstrated that exogenous testosterone suppresses intratesticular testosterone production, which is an absolute prerequisite for normal spermatogenesis. Cessation of exogenous testosterone should be recommended for men desiring to maintain their fertility. Therapies that protect the testis involve human chorionic gonadotropin (hCG) therapy or selective estrogen receptor modulators (SERMs), but may also include low dose hCG with exogenous testosterone. Off-label use of SERMs, such as clomiphene citrate, are effective for maintaining testosterone production long-term and offer the convenience of representing a safe, oral therapy. At present, routine use of aromatase inhibitors is not recommended based on a lack of long-term data. We concluded that exogenous testosterone supplementation decreases sperm production. It was determined that clomiphene citrate is a safe and effective therapy for men who desire to maintain fertility. Although less frequently used in the general population, hCG therapy with or without testosterone supplementation represents an alternative treatment.

The use of testosterone replacement therapy (TRT) for hypogonadism continues to rise, particularly in younger men who may wish to remain fertile. Concurrently, awareness of a more pervasive use of anabolic-androgenic steroids (AAS) within the general population has been appreciated. Both TRT and AAS can suppress the hypothalamic-pituitary-gonadal (HPG) axis resulting in diminution of spermatogenesis. Therefore, it is important that clinicians recognize previous TRT or AAS use in patients presenting for infertility treatment. Cessation of TRT or AAS use may result in spontaneous recovery of normal spermatogenesis in a reasonable number of patients if allowed sufficient time for recovery. However, some patients may not recover normal spermatogenesis or tolerate waiting for spontaneous recovery. In such cases, clinicians must be aware of the pathophysiologic derangements of the HPG axis related to TRT or AAS use and the pharmacologic agents available to reverse them. The available agents include injectable gonadotropins, selective estrogen receptor modulators, and aromatase inhibitors, but their off-label use is poorly described in the literature, potentially creating a knowledge gap for the clinician. Reviewing their use clinically for the treatment of hypogonadotropic hypogonadism and other HPG axis abnormalities can familiarize the clinician with the manner in which they can be used to recover spermatogenesis after TRT or AAS use.