Building a TRT protocol around hCG

FunkOdyssey

Seeker of Wisdom
Cortex released a video on this concept of using hCG and DHEA as the foundation of a protocol and then tailoring testosterone dose around that:

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I have kept going back and forth with hCG myself. I've noticed, now that I have some Janoshik-verified potent hCG (eutrig), if I take 250 iu EOD, after a few doses my libido goes from the usual dead state to pretty damn high. It is actually the most dramatic libido result I've experienced, besides an occasional blip after increasing testosterone dose. I'm realizing that finding a way to make hCG work is probably the only way I'm going to have a good libido on TRT. Bear in mind my libido pre-TRT was also nil, but among the many benefits I've derived from TRT, sustainably improved libido was not one of them.

It makes me think of Nelson, and how he basically turns on and off his libido like a light switch by adding or removing the 1000 iu hCG weekly from his baseline 100 mg weekly TRT protocol. He's been on TRT a VERY long time, and I wonder if that is the state that many men will reach eventually, where testosterone alone isn't able to support normal sexual desire anymore after many years of HPTA shutdown. I see themes like this on Reddit too.

I am inspired to try dropping my test cyp dose to ~100 mg weekly to give myself the E2 headroom for a longer-term trial of hCG. Dropping the TRT dose is painful because of how impactful that is on lifting and physique, but I think it's time to rip off that bandaid.

Anyone ever approached a protocol with this mindset before? Making a substantial dose of hCG the central non-negotiable pillar, and then letting testosterone have the remaining scraps of your capacity to handle e2?
 
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... He's been on TRT a VERY long time, and I wonder if that is the state that many men will reach eventually, where testosterone alone isn't able to support normal sexual desire anymore after many years of HPTA shutdown. I see themes like this on Reddit too.

I am inspired to try dropping my test cyp dose to ~100 mg weekly to give myself the E2 headroom for a longer-term trial of hCG. Dropping the TRT dose is painful because of how impactful that is on lifting and physique, but I think it's time to rip off that bandaid.
...

This is very much in line with my thinking, particularly the part about a longer HTPA shutdown being more problematic. In my case the addition of hCG was an improvement, but it never led to consistent libido and/or sexual function, and things still went downhill over the years. Dropping the hCG in favor of the enclomiphene/gonadorelin stimulation was a further improvement, but still ended up a bit short of where a guy would want to be. Interestingly, the switch to apparently ultra-low dose testosterone suspension has brought a consistency in libido and sexual function I hadn't seen in years. This is odd considering that serum testosterone appears to be barely above what it was when I developed hypogonadism—which was a miserable experience. It does align with the threshold effect mentioned in research. I think every guy who still has issues on TRT needs to "rip off that bandaid".
 
Cortex released a video on this concept of using hCG and DHEA as the foundation of a protocol and then tailoring testosterone dose around that:

To view this content we will need your consent to set third party cookies.
For more detailed information, see our cookies page.

I have kept going back and forth with hCG myself. I've noticed, now that I have some Janoshik-verified potent hCG (eutrig), if I take 250 iu EOD, after a few doses my libido goes from the usual dead state to pretty damn high. It is actually the most dramatic libido result I've experienced, besides an occasional blip after increasing testosterone dose. I'm realizing that finding a way to make hCG work is probably the only way I'm going to have a good libido on TRT. Bear in mind my libido pre-TRT was also nil, but among the many benefits I've derived from TRT, sustainably improved libido was not one of them.

It makes me think of Nelson, and how he basically turns on and off his libido like a light switch by adding or removing the 1000 iu hCG weekly from his baseline 100 mg weekly TRT protocol. He's been on TRT a VERY long time, and I wonder if that is the state that many men will reach eventually, where testosterone alone isn't able to support normal sexual desire anymore after many years of HPTA shutdown. I see themes like this on Reddit too.

I am inspired to try dropping my test cyp dose to ~100 mg weekly to give myself the E2 headroom for a longer-term trial of hCG. Dropping the TRT dose is painful because of how impactful that is on lifting and physique, but I think it's time to rip off that bandaid.

Anyone ever approached a protocol with this mindset before? Making a substantial dose of hCG the central non-negotiable pillar, and then letting testosterone have the remaining scraps of your capacity to handle e2?
I'm increasingly thinking, both from my own experience and observing others, that what you are describing makes the most sense, but with the addition of other targeted compounds to address specific issues. In your case, a moderate dose of Oxandrolone to replace the "lost" T seems logical (or perhaps short-acting Nandrolone). By modest I mean 10mg or so pre-workout no more than 4 times per week. If estrogen from the HCG is an an issue, then perhaps a low dose of Boldenone would be a better choice if you happen to be someone for whom Boldenone blocks the effects of estrogen
 
That "Janoshik-verified potent hCG" and the costs of hcg might be limiting for some men.
Cortex also often mentioned estrogen control as a key factor. Yet another protocol on which he feels great...

Good news if that hcg solves your libido problem!
 
Cortex released a video on this concept of using hCG and DHEA as the foundation of a protocol and then tailoring testosterone dose around that:

To view this content we will need your consent to set third party cookies.
For more detailed information, see our cookies page.

I have kept going back and forth with hCG myself. I've noticed, now that I have some Janoshik-verified potent hCG (eutrig), if I take 250 iu EOD, after a few doses my libido goes from the usual dead state to pretty damn high. It is actually the most dramatic libido result I've experienced, besides an occasional blip after increasing testosterone dose. I'm realizing that finding a way to make hCG work is probably the only way I'm going to have a good libido on TRT. Bear in mind my libido pre-TRT was also nil, but among the many benefits I've derived from TRT, sustainably improved libido was not one of them.

It makes me think of Nelson, and how he basically turns on and off his libido like a light switch by adding or removing the 1000 iu hCG weekly from his baseline 100 mg weekly TRT protocol. He's been on TRT a VERY long time, and I wonder if that is the state that many men will reach eventually, where testosterone alone isn't able to support normal sexual desire anymore after many years of HPTA shutdown. I see themes like this on Reddit too.

I am inspired to try dropping my test cyp dose to ~100 mg weekly to give myself the E2 headroom for a longer-term trial of hCG. Dropping the TRT dose is painful because of how impactful that is on lifting and physique, but I think it's time to rip off that bandaid.

Anyone ever approached a protocol with this mindset before? Making a substantial dose of hCG the central non-negotiable pillar, and then letting testosterone have the remaining scraps of your capacity to handle e2?
From the report, Eutrig is double dosed, so did you take that into account when mixing.
 
I've been on TRT for over 10 years. HCG has been the backbone of every one of my protocols. I started with 500 IU every 3 and 1/2 days and now 500 IU every 3rd day.

If you're one of them members that has anxiety issues. HCG may not work for you. But most do good with HCG.
 
In my case the addition of hCG was an improvement, but it never led to consistent libido and/or sexual function, and things still went downhill over the years. Dropping the hCG in favor of the enclomiphene/gonadorelin stimulation was a further improvement, but still ended up a bit short of where a guy would want to be. Interestingly, the switch to apparently ultra-low dose testosterone suspension has brought a consistency in libido and sexual function I hadn't seen in years. This is odd considering that serum testosterone appears to be barely above what it was when I developed hypogonadism—which was a miserable experience.
Very interesting result with the test suspension results. I think there are a percentage of men that do maintain long-term libido on testosterone alone, another group that maintains it long-term with hCG, and I would imagine the fraction that cannot maintain libido despite the combination is the smallest. ChatGPT estimated 50-60% of men maintain long-term function with T alone. That seems like it's probably accurate based on what I see on Reddit, comparing the number of people saying "yes, long-term libido loss is a thing" to those saying "I've been on 15 years of T monotherapy and have sex daily" and associated upvotes.

I know I'm not in the lucky 50-60% who will get away with T alone, but hopefully I'm in that large subgroup where TRT + hCG does the trick (like Nelson and Vince).

I'm increasingly thinking, both from my own experience and observing others, that what you are describing makes the most sense, but with the addition of other targeted compounds to address specific issues. In your case, a moderate dose of Oxandrolone to replace the "lost" T seems logical (or perhaps short-acting Nandrolone). By modest I mean 10mg or so pre-workout no more than 4 times per week. If estrogen from the HCG is an an issue, then perhaps a low dose of Boldenone would be a better choice if you happen to be someone for whom Boldenone blocks the effects of estrogen
Oxandrolone seems like the more attractive of these options to me. I've only tried nandrolone very briefly a couple times, but it seems to immediately tank my mood, and I'm pretty scared of its effects on the brain. Boldenone does not seem to inhibit aromatase but instead competes with testosterone for access to aromatase, and is aromatized into huge quantities of estrone (E1). I might consider experimenting with it if I could find a shorter ester version than the standard undecylenate.

I agree though, that adjusting testosterone to produce optimal E2 and then filling in any anabolic deficit with a non-aromatizing androgen makes sense and should provide a great combination of anabolism and well-being, if perhaps not being as optimal for long-term health as leaving out the additional androgen.

That "Janoshik-verified potent hCG" and the costs of hcg might be limiting for some men.
Cortex also often mentioned estrogen control as a key factor. Yet another protocol on which he feels great...
Access to inexpensive, high potency hCG has never been better than it is today. 5,000 iu (apparently really 10,000 iu) vials of Eutrig are only $10 each: https://pricelist.cosmicpct.com/pricelist-february-2025.pdf

On estrogen control, we aren't doing that here, because inhibiting aromatase in the brain often kills libido and is totally counterproductive, in addition to the other health risks associated with aromatase inhibition.

You have a bucket that represents your capacity to handle E2 without adverse effects or loss of symptomatic benefit. Instead of filling that bucket with testosterone, and then pouring hCG on top until the bucket overflows, we're going to start with the hCG, and then see how much testosterone we can fit in the bucket afterwards. It isn't estrogen control - it's experimentally determining how much E2 you can handle, while giving top priority to the hCG.

From the report, Eutrig is double dosed, so did you take that into account when mixing.
I'm aware of it, but the doses I reported above were the labelled doses, so where I said 250 iu, it was probably more like 500 iu.
 
Do you know "your capacity to handle E2 without adverse effects or loss of symptomatic benefit."?
In my case, and with my current SHBG of high 30's (as critical for context when interpreting E2 as it is for T), I think that translates to an e2 of less than 40. You don't actually need any labwork to determine that though.

You would simply start with hCG at a target dose, start with testosterone at a dose too low to cause 99% of people problems, and bring up the T slowly until things go to shit. You'll know when you've gone too far. To use myself as an example, some of my telltale high E2 symptoms include GERD/LPR, acne, high BP, crying too easily at TV/movies/anything emotional, and brain fog. Erections and libido will begin suffering at some point also.
 
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Don't get me wrong. It's great if HCG works for you, in whatever combination.
I'm just sceptical when people seem to jump to conclusions and generalize them (sometimes Nelson did it when it comes to estrogen or hcg).

Regarding Anastrozole and the brain or brain blood barrier:
Here are key references documenting anastrozole concentrations in cerebrospinal fluid (CSF) compared to serum/plasma in humans, supporting its ability to cross the blood-brain barrier (BBB):

1. **Salmaggi A. et al. (2011)**
*Study:* "Anastrozole Concentrations in Brain Metastases and Normal Brain Tissue of Breast Cancer Patients."
*Journal:* **Neuro-Oncology**
*Findings:* Measured anastrozole levels in brain metastases, normal brain tissue, CSF, and serum. Found CSF concentrations were approximately **10-15% of serum levels**. This provided direct evidence of CNS penetration.
*DOI:* [10.1007/s11060-011-0573-x](https://doi.org/10.1007/s11060-011-0573-x)

2. **Pilleron S. et al. (2013)**
*Study:* "Pharmacokinetics of Anastrozole in Plasma and Cerebrospinal Fluid of Breast Cancer Patients."
*Journal:* **Clinical Cancer Research**
*Findings:* Quantified anastrozole in paired CSF and plasma samples. Reported a **median CSF/plasma ratio of 0.14 (14%)**, confirming limited but consistent BBB penetration.
*DOI:* [10.1158/1078-0432.CCR-13-1892](https://doi.org/10.1158/1078-0432.CCR-13-1892)

3. **Bhardwaj A. et al. (2018)**
*Study:* "Anastrozole brain pharmacokinetics in breast cancer patients: A pilot study."
*Journal:* **Cancer Chemotherapy and Pharmacology**
*Findings:* Measured anastrozole in plasma and CSF. Found **CSF concentrations ranged from 7.7% to 19.8% of plasma concentrations**, reinforcing earlier studies.
*DOI:* [10.1007/s00280-018-3662-0](https://doi.org/10.1007/s00280-018-3662-0)

4. **Lønning P.E. et al. (2011)** - *Indirect Evidence*
*Study:* "Estrogen suppression and breast cancer prevention."
*Journal:* **Pharmacology & Therapeutics**
*Context:* Discusses CNS effects/side effects of aromatase inhibitors (AIs), implying BBB penetration. While not reporting direct CSF ratios, this review supports the clinical relevance of CNS exposure inferred from CSF studies.
*DOI:* [10.1016/j.pharmthera.2011.01.009](https://doi.org/10.1016/j.pharmthera.2011.01.009)

**Key Takeaways from these Studies:**
- **Consistent Penetration:** All human studies detected anastrozole in CSF.
- **CSF/Serum Ratio:** Typically **~10-20%**, indicating partial BBB penetration.
- **Therapeutic Relevance:** CSF concentrations are sufficient to inhibit brain aromatase, explaining CNS efficacy (against metastases) and side effects (e.g., cognitive changes, fatigue).

**Limitations:**
- Studies involve cancer patients (often with brain metastases), not healthy volunteers.
- BBB integrity may vary between patients.
- Small sample sizes are common (pilot/exploratory nature).

These references provide direct experimental evidence for anastrozole's BBB penetration in humans. For mechanistic insights (e.g., P-glycoprotein transport), preclinical models (e.g., *Yamasaki et al., J Pharmacol Exp Ther, 2012*) are often cited, but the above focus on human CSF data as requested.


Details matter. Inter-person variability matters.

What you or cortex call low dose T, for me 125mg TU weekly results in 750 TT.
If I add oxandrolone or a sarm, then it feels like I need more T. What I mean to say: for me the idea of anabolic add-ons does not work. I have to balance the whole stack. On T only I didn't observe any physical benefit of 250mg over 125mg per week (muscle building, fat loss).
Yes, anastrozole crosses the BBB but it seems to be less dramatic as suggested by some people. Again, inter-person variability.
 
These references provide direct experimental evidence for anastrozole's BBB penetration in humans.
I don't understand how anastrozole brain penetration is relevant to our discussion, which has not been focused at all on anastrozole. What point were you trying to make?

What you or cortex call low dose T, for me 125mg TU weekly results in 750 TT.
If I add oxandrolone or a sarm, then it feels like I need more T. What I mean to say: for me the idea of anabolic add-ons does not work. I have to balance the whole stack. On T only I didn't observe any physical benefit of 250mg over 125mg per week (muscle building, fat loss).
This approach to TRT protocol design is meant to optimize sexual function, not anabolism / body composition. Much higher doses of testosterone, using either AIs or additional androgens for estrogen control, are what you want to optimize for anabolism.

I'm getting a sense that you find something about the hCG centric concept offensive but I'm not sure why.
 
I don't understand how anastrozole brain penetration is relevant to our discussion, which has not been focused at all on anastrozole. What point were you trying to make?


This approach to TRT protocol design is meant to optimize sexual function, not anabolism / body composition. Much higher doses of testosterone, using either AIs or additional androgens for estrogen control, are what you want to optimize for anabolism.

I'm getting a sense that you find something about the hCG centric concept offensive but I'm not sure why.

It was in response to the following:
"On estrogen control, we aren't doing that here, because inhibiting aromatase in the brain often kills libido and is totally counterproductive, in addition to the other health risks associated with aromatase inhibition."

"I agree though, that adjusting testosterone to produce optimal E2 and then filling in any anabolic deficit with a non-aromatizing androgen makes sense and should provide a great combination of anabolism and well-being, if perhaps not being as optimal for long-term health as leaving out the additional androgen."

I speculate that controlled AI dosage can remove the brain fog. Valuable tool if one is an 'over-aromatizer'.

I wanted to emphasize the concept of balancing hormones.
 
Yes, that sounds plausible that it could, but inhibiting aromatase will not optimize for libido or health if these are important goals.
Imo this is a over simplification and generalization.
I believe we don't have proof for that if applied in the context of TRT within physiological range.
Details matter. Dosage matters.
 

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