HCG: And You

HCG is a big subject - by necessity, this article will be specific to men only as its function in men and women are different. It’s also not related in any way to the HCG diet, which you may have heard of in the past. In this context, we’re talking about the injectable form, generally subcutaneous (subq) i.e. injected into fat. Injections are done with a very small needle (‘slin pins’) that many users may find a lot less intimidating, and are commonly used by diabetics.

HCG (human chorionic gonadotropin) is a hormone produced by the placenta. HCG is an analog for luteinizing hormone (LH) and produced from the pee of pregnant and post-menopausal women.

>hcg comes from women’s pee

>pee comes from women’s urethra

>urethra is close to the vagina

>injected hcg

>basically had sex

Later virgins.

LH is produced in the pituitary. When exogenous test is present, a feedback loop shutdowns LH production. This is the implication of AAS use, turning off the production (or at least significantly reducing) the amount of LH being produced, and is the main difference in my mind between being ‘shutdown’ or ‘suppressed’. Non testosterone derived PEDs do not have this effect (SARMs), so may suppress but as LH is not impacted normal levels of testosterone will be restored without intervention once you discontinue SARM use.

While I said HCG is an analog for LH, they’re not identical and may have secondary smaller functions in the body that do not overlap. Otherwise, HCG is commonly used to stimulate leydig cells, just like LH does, which produce testosterone when they receive LH, and is an important function in the production of sperm. Without LH, the guys downstairs stop their production of testosterone. And also you’re likely temporarily infertile.

SERM + SARM use v HCG + SARM use

We (the PEDsR community) have some blood test data that indicates that running a SERM alongside a SARM reduces suppression. The challenge is in explaining this, because it doesn’t really make sense. It could be our sample size is too small (n=3) and that a SERM does not reduce suppression at all, or that there is something else at work here: SARMs have a suppressing effect on testosterone without impacting LH, which implies that SARMs suppresses test through an as of yet not understood action (perhaps due to its impact on SHBG as we previously discussed, but probably not). Despite the lack of understanding as to the ‘why’ or ‘how’, I’ve allowed for the possibility given peoples bloodwork and anecdotes.

HCG & SARMs on the other hand is something I speculate about here. My rationale at the time was since HCG and SERMs accomplish the same task of increasing LH, then perhaps either could be both used while on a SARM only cycle. As limited as the data we have on SERM + SARMs is, we have ZERO bloods from folks on HCG + SARM. And I just finished saying that SERMs must have a different action that increases testosterone, separate from LH (since that remains in range on SARM only cycles). So with that said I’d stay away from running a HCG + SARM cycle unless you really want to for some reason, or your doctor has you on HCG monotherapy. In both cases, please share your blood work!

HCG Monotherapy

HCG is successfully used to increase fertility in the gonad-aly challenged or those injecting testosterone, 2. It can also be used to restore testosterone to normal levels: a 3-month trial of bi-weekly 5000 IU units of HCG in 40 men had an average baseline testosterone level of 320 ng/dl. By the end of the study, the average testosterone level was 778 ng/dl. Considering also that the average age was 67, this is a pretty significant result, and it’s clear to me that HCG monotherapy can be used in lieu of other compounds with undesirable side effects (specifically Clomid) where someone has legitimate hypogonadism, and just wants to return testosterone levels to normal and is OK running it forever.

Cycling & Dose

When I was trying to get my wife pregnant, I was told by my TRT doc at the time to cycle HCG 8 weeks on, 4 weeks off. Once she was pregnant, it went to 4 weeks on and 4 weeks off. It was explained to me that long term HCG use can desensitize the leydig cells. That seems to be correct, with a study running 4500 iu’s ew for 2 years reducing testicular response to the HCG.

This sales rep reckons the injected dose should be no more than 0.6cc’s, and that the weekly dose should not exceed 1000 iu’s ever. I don’t often take cycle data from shills, but I was surprised to see that her advice was less than the studies I’ve looked at, so hey I’ll give her some credit for recommending minimally effective doses for once, instead of trying to pump up her sales volume.

She also has some really solid advice:

HCG is suppressive! Since we know that hCG mimics LH, then we know that in the presence of exogenous LH, the pituitary gland will not produce LH. Hang on a minute!.. Why on earth would you want to suppress your pituitary with hCG when you're trying to recover?!

So don’t run HCG post-cycle as a recovery. It really doesn’t make any sense at all.


Useful when fertility matters, especially on cycle. No evidence to suggest that HCG + SARM works in minimizing suppression side effects (but if you try it, lmk). Useful also for hypogonadal men seeking to return testosterone levels to normal. Don't run it as a PCT.