HCG monotherapy

[chaos]

Does HCG monotherapy induce LH suppression? If so, is it to a lesser degree than exogenous testosterone?

It occurs to me that testosterone and estradiol/DHT are involved with negative feedback but HCG (LH mimic) would not be, at least directly.

If LH downregulated because of a secondary surge in T/E/DHT due to the HCG, wouldn’t it make sense that it’s lesser than exogenous testosterone?

Any clinical information to support this?

[DrMariano2]

@chaos 105 wrote:

Does HCG monotherapy induce LH suppression? If so, is it to a lesser degree than exogenous testosterone?

It occurs to me that testosterone and estradiol/DHT are involved with negative feedback but HCG (LH mimic) would not be, at least directly.

If LH downregulated because of a secondary surge in T/E/DHT due to the HCG, wouldn’t it make sense that it’s lesser than exogenous testosterone?

Any clinical information to support this?

HCG (chorionic gonadotropin) increases testosterone production. Generally, in monotherapy for hypogonadism, it is used in doses to reach an adequate target level of testosterone production – e.g. 650 ng/ml.

HCG also stimulates aromatase enzyme production. This increase the production of estradiol from testosterone. One of the problems in using HCG for testosterone replacement therapy is that excessive estradiol may result in some men – even in lose doses such as in Dr. Crisler’s protocol (250 IU twice a week, http://www.allthingsmale.com).

Estradiol is a stronger signal for reducing LH (lutenizing hormone) production than testosterone. The brain, in a way, places more importance on measuring estrogen than testosterone (which also requires progesterone in order to be sensed optimally by the brain).

The amount of estradiol formed from exogenous testosterone treatment depends on existing aromatase enzyme activity (which, could be increased, for example, in men with larger amounts of belly fat (visceral fat).

In both HCG monotherapy and exogenous testosterone treatment, the target level of testosterone is the same – generally about 650 ng/ml (halfway between the reference range of 300-1000, as per Endocrine Society guidelines for the treatment of hypogonadism).

Which form of therapy suppresses LH more will depend on which induces estradiol production more. This is difficult to predetermine since each man is different in aromatase enzyme activity and susceptibility to increase aromatase from HCG. Some men do very well on HCG monotherapy and do not have excessive estradiol production.

All things being equal, however, I would expect HCG monotherapy to cause more LH suppression since there would be more estradiol formed from increased aromatase enzyme production. Exogenous testosterone alone would not increase aromatase enzyme production.

[chaos]

If on IM injections, is that 650 in the middle?

I like the idea of using HCG because I’ve heard it maintains baseline function. Since I use an anti-estrogen (aromatase inhibitor) anyways, I was thinking maybe I could get by on HCG only.

It seems more natural to me. Don’t know if that’s good or bad. But it also seems like it would keep levels more stable. I have heard some are doing 100 iu per day.

But I’ve also heard mixed reviews on the effectiveness of monotherapy.

[DrMariano2]

@chaos 116 wrote:

If on IM injections, is that 650 in the middle?

I like the idea of using HCG because I’ve heard it maintains baseline function. Since I use an anti-estrogen (aromatase inhibitor) anyways, I was thinking maybe I could get by on HCG only.

It seems more natural to me. Don’t know if that’s good or bad. But it also seems like it would keep levels more stable. I have heard some are doing 100 iu per day.

But I’ve also heard mixed reviews on the effectiveness of monotherapy.

HCG is one option in maintaining testicular function and testosterone production.

Whether or not it would keep testosterone levels more stable is questionable. It probably does NOT given the much longer half-life of testosterone cypionate and enanthate (about 7 days on average) compared to testosterone (10-100 minutes).

I would generally prescribe a total of 3000 IU a week divided into 3 or 7 doses. This would give a testosterone level comparable to Testosterone Cypionate at 100 mg a week.

“Natural” is a questionably used term. HCG is not natural in men. The use of an aromatase inhibitor is also not natural. Nor is injecting something “natural”. But these options may be necessary or useful to improve function. One primarily needs to assess risk vs. benefit to help make their decision on the course of treatment.

At a certain age, such as in one’s fifties, the testes become less sensitive to HCG. At this time, HCG will stop working and alternatives would have to be used. Too high a dose of HCG would hasten testicular insensitivity to HCG.

[hardasnails1973]

@DrMariano 118 wrote:

HCG is one option in maintaining testicular function and testosterone production.

Whether or not it would keep testosterone levels more stable is questionable. It probably does NOT given the much longer half-life of testosterone cypionate and enanthate (about 7 days on average) compared to testosterone (10-100 minutes).

I would generally prescribe a total of 3000 IU a week divided into 3 or 7 doses. This would give a testosterone level comparable to Testosterone Cypionate at 100 mg a week.

“Natural” is a questionably used term. HCG is not natural in men. The use of an aromatase inhibitor is also not natural. Nor is injecting something “natural”. But these options may be necessary or useful to improve function. One primarily needs to assess risk vs. benefit to help make their decision on the course of treatment.

At a certain age, such as in one’s fifties, the testes become less sensitive to HCG. At this time, HCG will stop working and alternatives would have to be used. Too high a dose of HCG would hasten testicular insensitivity to HCG.

There has been long argument of what is the dosage of HCG that can desensitize a person testicles. I have heard 500ius one time 1,000 another time. From my own clinical experience with this 1,000ius m,w,f took a young male to 1500 ng/dl of testosterone. The blood was drawn on the day before the injection to get a mid line reading. The clients e2 went up to 65 as well. The number one question is that why in some people that a person can take testosterone only to achieve a number of 600 TT with good e2, but the same person took only hcg and had TT of 500 but e2 of double then the testosterone at 600? What mechanism could be responsible for approximately same TT but 2 different e2 readings. Is there something that is occuring that some how the HCG is over stimulating the part of the testiculars responsible for aromatization?

[DrMariano2]

@hardasnails1973 119 wrote:

There has been long argument of what is the dosage of HCG that can desensitize a person testicles. I have heard 500ius one time 1,000 another time. From my own clinical experience with this 1,000ius m,w,f took a young male to 1500 ng/dl of testosterone. The blood was drawn on the day before the injection to get a mid line reading. The clients e2 went up to 65 as well. The number one question is that why in some people that a person can take testosterone only to achieve a number of 600 TT with good e2, but the same person took only hcg and had TT of 500 but e2 of double then the testosterone at 600? What mechanism could be responsible for approximately same TT but 2 different e2 readings. Is there something that is occuring that some how the HCG is over stimulating the part of the testiculars responsible for aromatization?

I don’t know. I ascribe it up to genetic differences between men. After all, HCG is a foreign, not natural, substance in a man.

One patient had excessive progesterone production, as an example of a different expression pathway, and normal estradiol production, in response to HCG treatment.

Perhaps, by stimulating steroid hormone formation, it stimulates precursors to testosterone, such as progesterone, which can also go through different pathways to reach estradiol rather than testosterone. For example, in the testes, progesterone is the main precursor for testosterone. Progesterone production has to ramp up for testosterone production. But progesterone can also be shunted to 17 hydroxy-progesterone to androstenedione to estrone to estradiol. Thus it would not just be aromatase enzyme that is stimulated, but all the other steroid pathyway enzymes.

Note that the production of estradiol is the primary reason for LH production. The hypothalamus and pituitary are much more sensitive to estradiol levels than testosterone levels. Having testosterone, in a way, is a side effect.

In development, if the fetus with XY chromosomes is insensitive to testosterone, it automatically develops into a female – though without ovaries or a uterus.

[chaos]

I understand.

I was diagnosed with hypogonadism by my PCP. My levels were just under normal (although interestingly, I was around 330, the reference range of that lab cut off the bottom at 350) and I had incredible fatigue and while I had a decent sex drive, erections were so-so, among other symptoms.

I had to make the risk-benefit analysis and the last thing I ever would have wanted was to be on a lifetime of medication. But I am glad to feel better.

As you read about the issue on the web (I’m kind of new to researching it), I have found a number of fascinating opinions, and want to treat it in a way which most closely mimics nature and is least obtrusive.

I have, at times during the 3 years I’ve been on therapy had times when I wanted to stop therapy to see if I could somehow raise my own production normally or with HCG by itself. But I am afraid to crash.

I guess I like the idea of HCG monotherapy because I’ve read where it can induce normal rhythms of testosterone in using it as a replacement. I’d also love not to have to use an anti-estrogen, like you say, it’s not natural. I figure the least medication the better.

[DrMariano2]

@chaos 123 wrote:

I guess I like the idea of HCG monotherapy because I’ve read where it can induce normal rhythms of testosterone in using it as a replacement. I’d also love not to have to use an anti-estrogen, like you say, it’s not natural. I figure the least medication the better.

Whatever method for testosterone replacement is used, when testosterone is kept at a stable and not excessive level, estradiol production is minimized. Thus with HCG, the more frequent the dosing, the better. With testosterone cypionate injections, the shorter the half-life for testosterone cypionate, the shorter the intervals should be between injections.

[pmgamer18]

Just to give an example of how men react to TRT or HCG only. I have been on TRT 27 yrs now for the first 23 yrs I was told I am Primary meaning my tesits don’t work. I have been on every kind of TRT out there I ended up doing shots was up to 150 mgs of Depo T a weeks the best I could get my levels were between 550 to 600. Estradiol for me was a bigger problem on gels then it was on shots. After reading Dr. John’s HCG update he posted to me to help me get my Dr. to let me add HCG. Here is a cut and paste of what he said.
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He probably feels that since you suffer primary hypogonadism (I am guessing) there is no use in adding HCG to your protocol. There are several reasons why this is not so. First, you have not lost all Leydig cells, so any HCG you take will stimulate those who still function to produce endogenous testosterone.

This will support testicular size. We should not ignore this aesthetic consideration.

Next, if he reads my work, he will learn that HPTA-suppressed (as all TRT patients are to some extent) also suffer decreased pregenenolone levels, which is the first step after CHOL in all three hormonal pathways which begin with CHOL. HCG increases pregnenolone production, and therefore restores a more natural balance of our hormones.

Next, nearly all TRT patients who add in HCG to their regimens report an increased sense of well-being and also libido. These are genuine quality of life issues.

Finally, I just instinctively do not want all those LH receptors (including those we have yet to discover and appreciate) unstimulated.
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My Dr. did not follow Dr. John’s form of treatment he had me doing 500 IU’s 3x’s a weeks after the 15 shot we did labs and my labs doubled the lab we used was here in MI. There top of range for Total T was 1572. On the HCG my labs went to 1000 and I never felt this good. We did an MRI on my Pituitary nothing showed up. But before I got sick 27 yrs ago I had a bad head injury do to an auto accident. We looked back at my lags I had copys of all of them and they were screaming I was Hypopituitary.

My estradiol leveled became a bigger problem doing this so after reading on the forums form one of Dr. Shippens men he was treating him self doing shots of T every 3 days subq.

I got my Dr. to let me do this because Dr. Shippen felt doing less T more offten helps keep Estradiol levels down. My Dr. would not let me do subQ shots but let me do them with a 27g 1ml. x 1/2″ lg. needle into my thigh for both T and HCG shots

Doing this helped with keeping me more leveled and I was able to go from 1mg of Arimidex every other day to .25 mgs every other day to keep my estradiol down. I feel it’s a small price to pay taking arimidex to keep E2 down and feeling this good.

So today I do 70 mgs of 200mgs/ml. of Depo T every 3 days and shoot 400 IU’s of HCG the 2 days each in between my T shots. When I first started on HCG my testis were the size of small grapes not today they are normal size.

I tried HCG 100 IU’s everday no T shots and did this for 6 months I did not feel as good as doing both. And doing this drive my estradiol nuts.
Phil

[chaos]

@pmgamer18 127 wrote:

I tried HCG 100 IU’s everday no T shots and did this for 6 months I did not feel as good as doing both. And doing this drive my estradiol nuts.
Phil

Great post, PM.

Were you taking arimidex when you did the 100 iu HCG ED?

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