T Nation

Singhbuilder's Fertility Log

Even if he was only at 800 TT our bodies seem to know the difference between injected T and natural T. Injected T shuts you down and no amount of HCG fixes that. HCG only keeps one pathway open to your balls and as I understand it help you with PCT. It does not send any signals to make sperm.

For TRT guys it reduces testicle atrophy. In my case not by much. I have been taking 300-400IU’s of HCG for the last 7 years and my ball are half their normal size.

It does. It activates LH receptors directly. T in the blood does not matter at that point.

I’d maybe use hCG in combination with FSH for optimal results.

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Isn’t HMG just that combination, but a lot less money? I also see UGLs that have HMG, but I don’t know if I have ever seen FSH from a UGL.

Awesome clarification! Thank you.

Abstract

The relative roles of FSH and LH in the control of human spermatogenesis are not well established. We previously reported that supraphysiological doses of hCG can stimulate sperm production in gonadotropin-suppressed normal men despite prepubertal FSH levels. To determine whether more nearly physiological levels of human LH (hLH) also can stimulate spermatogenesis when FSH levels are suppressed, we administered hLH to normal men whose endogenous gonadotropin levels and sperm production were suppressed by exogenous testosterone enanthate (T). After a 3-month control period, 11 normal men received 200 mg T, im, weekly to suppress LH and FSH. T administration alone was continued for 3-4 months until 3 successive sperm concentrations (performed twice monthly) revealed azoospermia or severe oligospermia (sperm concentrations, less than 4 million/ml). Then, while continuing T, 4 of the 11 men (experimental subjects) simultaneously received 1100 IU hLH, sc, daily for 4-6 months to replace LH activity, leaving FSH activity suppressed. The effect on sperm production of the selective FSH deficiency produced by hLH plus T administration was determined. The remaining 7 men (control subjects) continued to receive T alone at the same dosage, without gonadotropin replacement, for an additional 6 months. In the four experimental subjects, sperm concentrations increased significantly from 0.7 +/- 0.7 million/ml (mean +/- SEM) during T treatment alone to 19 +/- 4 million/ml during hLH plus T administration (P less than 0.001). However, none of the men achieved sperm concentrations consistently in their own pretreatment range. Sperm motilities and morphologies were normal in all four subjects by the end of hLH plus T administration. In contrast, sperm concentrations in the seven control subjects remained suppressed (less than 3 million/ml) throughout the entire period of prolonged T administration alone. Serum LH bioactivity, determined monthly by in vitro mouse Leydig cell bioassay in all four experimental subjects, was markedly suppressed during T administration alone (120 +/- 10 ng/ml) compared to that during the control period (390 +/- 20 ng/ml; P less than 0.001). With the addition of hLH to T, LH bioactivity returned to control levels (400 +/- 40 ng/ml; P = NS compared to control value). Serum FSH levels determined monthly by RIA were reduced from 98 +/- 12 ng/ml during the control period to undetectable levels (less than 25 ng/ml) during the T alone and the hLH plus T periods (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Early Experience With hMG in Combination With hCG Therapy

FSH has been used successfully for infertility treatment of patients with hypogonadotropic hypogonadism for more than 50 years, initially with urinary menopausal gonadotropins having FSH activity. It is worth reading the initial reports of FSH therapy in hypogonadotropic patients. MacLeod and coworkers reported on the successful therapy with urinary menopausal gonadotropins of a 37-year-old patient who underwent complete hypophysectomy in 1963 (10, 11). The patient had provided a semen sample 1 day before the hypophysectomy that showed 576 million sperm per ejaculate and quite good sperm motility and morphology. After surgery, the ejaculate quality decreased significantly and, following several weeks after hypophysectomy, the patient was unable to provide semen samples any more. Approximately 14 weeks after hypophysectomy, a bilateral testicular biopsy was performed which showed involution of spermatogenesis to the level of spermatogonia and only few areas with primary spermatocytes. One day after the first testicular biopsy, treatment with hMG (human menopausal gonadotropin originating from human urine with mainly FSH and some LH activity) was initiated in the patient, at a dose of approximately 206 I.U. per day.

After 64 days of menopausal gonadotropin treatment, another testicular biopsy only of the right testis revealed stimulated spermatogenesis, showing all stages of spermatogenesis including late elongated testicular spermatids. However, the restoration of spermatogenesis appeared only qualitatively normal, not quantitatively. As a patient was still unable to produce an ejaculate probably due to the insufficient low LH activity in the hMG preparation and therefore low testosterone serum levels, hCG therapy with 4000 I.U. on alternate days was added to stimulate testosterone production by the Leydig cells. At the same time the hMG dose of 206 I.U. was given no longer daily, but only every second day (alternating with hCG injections). With the combined therapy of hMG and hCG the patient regained the ability to produce an ejaculate that showed a total sperm count of several million with progressive sperm motility and normal sperm morphology, that were still decreased compared to the levels analyzed before hypophysectomy (11). Later the patient decided not to continue with hMG therapy and, unfortunately, no fertility data are available. However, this early comprehensive case report demonstrated clearly the principle of FSH therapy in combination with hCG for stimulation of spermatogenesis in patients with hypogonadotropic hypogonadism.

Sourcing and using gonadotropins from an UGL. Now that takes some balls.

Haven’t done it. Is it that much worse than something like Test?

Trusting some criminals to purify product from urine stream via chromatography vs dissolving testosterone in some oil and adding some preservative and a bacteriostat.

Probably not, the UGL probably sourcing some dubious batches of off-spec product or diverting some lyophilized powder finished product. It honestly must be rolling the dice.

I was just trying to make a bad joke. Sounded funny though…balls, gonadotropins.

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It wasn’t lost on me and I enjoyed it :joy:

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Thanks, I’m having a slow day. Sorry.

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Here’s a sobering article of contaminant analysis in Pharma hCG (u- and r-hCG). Who really knows what the long term effects of these proteins are in addition to the potential (although small) chance) of prion contamination.

Would be fun to do same analysis with your favorite UGL hCG/hMG :-). Oh well, we are all going to die of something.

r-hCG much cleaner than u-hCG but my experiments with both indicated r-hCG doesn’t have the same subjective benefit as u-hCG while on TRT. Just a qualitative observation. It was a bummer as I liked the purity profile with r-hCG but controlling for IU conversion left me underwhelmed.

Pregnyl (u-hCG) looks like a soup of human/other proteins but really does the job after 6 months running TRT solo. Libido, function and mood. YMMV.

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Many thanks for the studies! 1100iu hCG daily for 4 months! My dose suddenly doesn’t seem that high anymore.

Not sure if LH receptor downregulation/desensitisation is bro-science though, I’ve seen conflicting evidence.

I do have a few boxes of hMG I will start on next month, its just so damn expensive!

I have noticed my loads are massive now. Sorry about the detailed description.

Would adding a SERM be of any benefit?

SB

Yes, me too. In my opinion there is. It could be that some people can handle significantly more HCG than others, their receptors don’t desensitize as fast. But that’s just a guess for why the doses and frequency have such great disparity.

My eyes! My eyes!!

Can’t un-see that now

Have you had a sperm count yet?

A gym buddy of mine was/is a pretty big AAS user and he jumped off and ran hcg and his wife got pregnant pretty fast

@studhammer did he just jump off AAS use, staying on T, or did he jump off everything ran a PCT with HCG to get his LH and FSH working again? I don’t think you can make sperm with only one path open that being LH which is all HCG helps with.

Hahaha sorry brother! It’s progress so gotta report it.

I haven’t had a sperms count yet, the last 2 were azoo but that was pre hCG.

I’m also interested in what @hrdlvn is saying. I can’t see myself coming off TRT, that would be an absolute last resort.

SB

@Singhbuilder ((( 1100iu hCG daily for 4 months ))) OMG. There was a weight loss fad going around a year or so ago suggesting these levels but I have never heard of that much to keep your LH going. I copied this from my TRT prescription plan (HCG 400 iu SQ two times a week - current dose) I go to a pretty expensive TRT/antiaging doctor so I did not pick this dose out of the air. I would find it hard to believe you would need more than 800IU’s per week to atleast get your LH producing. One thing is forsure you can blood test for LH and FSH so you might consider buy a mini blood test to see if the HCG is working.

I’m pretty sure hCG doesn’t show up as LH on blood tests.

The blood results there show no LH so I’m unsure what you were referring to?

SB

I was just showing you there are tests for LH and FSH.
My bloods of course are shutdown this was my first blood test with my PCP on T gel only.
This was before I moved to a proper HRT clinic and was put on HCG and anastrozole.

I did not know HCG replaced LH. I thought it trigger the natural production.
So it is tricking your balls and does not sending you real luteinizing hormone. I wonder how that helps with PCT if your body is not making natural LH and FSH?

I think he stopped cold and went on HCG until he got his wife pregnant. He is a powerlifter who cycles pretty hard. He’s about 38.

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