How to Come Off TRT Without Destroying Your Hormones | Weekly Q&A #1

Watch the full video on Rumble: https://rumble.com/v7fsovm-how-to-come-off-trt-without-destroying-your-hormones-weekly-q-and-a-1.html

I posted in the men's group asking what people wanted covered. And before I took the post down, just over a couple of days, it ended up having like over 300 comments.

So what we did is we took those 300 comments and we distilled them down to 28 total questions and the way we distilled them was we removed all the stuff that we've previously touched on before, removed all the specific, detailed protocol questions and just took the questions out where we could provide educational content, talking about mechanisms of how things work.

If this is something that you guys think is valuable, I think one of the things that we can do is we can look at doing this Q and a once per week, post the full length video on YouTube, and then we'll take the clips and we'll also put those on the short form platforms like tick tock and Instagram, obviously over 300 questions.

The biggest one, by volume, was about getting off testosterone.

Before anything else, you need the whole chain in your head, because every intervention in this article plugs into one specific point on it. Your hypothalamus releases a signaling hormone called GnRH, which travels a short distance to the pituitary. The pituitary responds by releasing luteinizing hormone, or LH, into the bloodstream. LH reaches the Leydig cells in your testicles, and those cells make testosterone. Testosterone circulates, some of it converts to estrogen, and that estrogen travels back up to the hypothalamus where it tells the brain to ease off, which is the whole loop working like a thermostat that reads the room and adjusts the heat accordingly.

Break the chain at the bottom and you have primary hypogonadism. Break it higher up, at the brain or the pituitary, and you have secondary hypogonadism. I cannot point you to a study that cleanly maps those two categories onto the anatomy the way I just described it, so treat that as the working model I use with clients rather than something the literature has settled.

The distinction matters because it decides your treatment. TRT is the appropriate approach for somebody who has primary hypogonadism, since the factory itself is broken and no amount of signal will restart it. For secondary hypogonadism, most of the time you can intervene upstream with something like enclomiphene or HCG to turn testosterone production back on.

Clinics rarely bother separating the two categories before they treat you. They see a low number, they write a prescription, and once you are on it, it is treated as a lifetime decision.

Here is the part that makes it a lifetime decision. When you put exogenous testosterone into your body, your own production winds down, and the Leydig cells in your testicles atrophy because nothing is calling on them. The research hasn't given me a clean number for how universal or how complete that shutdown is across different doses, so I am telling you what I see with clients.

Recovery is slow and the literature backs that up. In men coming off long term testosterone undecanoate injections, LH and FSH recovery ran on a timeline of months, not weeks, and full endocrine normalization stretched well past the point most people expect (Handelsman 2022). The fertility literature says the same thing from a different angle, describing exogenous testosterone as a preventable cause of male infertility precisely because the suppression is not instantly reversible (Crosnoe 2013).

However, there is a way that you can turn that back on, uh, but it may take up to six or even 12 months for your body to resume production and maybe put you into a position where you can pursue, we'll say less invasive methods for improving your testosterone, uh, for longevity and long-term use.

You're going to start with HCG at between five and 1500, I use either three times a week or every other day and do that for two to four weeks.

HCG works because it looks like LH to the receptor, landing as a direct knock on the testicle door rather than traveling down through the brain first, which is exactly what you want when the Leydig cells have gone quiet. You are waking up the factory before you bother rebuilding the phone line to it.

And once you start to see a response from the testicles and your testosterone levels start to increase by using the HCG therapy, then you can introduce a CIRM like in clomophene or tamoxifen, which is basically what it's going to do is it's going to block the estrogen receptors in the hypothalamus to tell your brain to send more GNRH down to the pituitary.

Estrogen is what tells the hypothalamus the room is warm enough, and once you blind that thermostat to the reading, the hypothalamus keeps calling for more heat, which means more GnRH, more LH, more testosterone from the testicles you just spent a month waking up.

So we're intervening the, we'll say upstream or the suppression that occurs when your body actually starts producing testosterone and that's going to trick your brain into telling your body to produce more.

If you're on the in clomophene, you would start at 12 and a half milligrams to go for six to eight weeks and make sure that you don't skip this step because the sequencing actually does matter here.

Run the SERM first and you are shouting down a phone line into a factory with no workers. The brain sends the signal, the atrophied Leydig cells cannot answer it, and you burn weeks getting nothing while convincing yourself the protocol failed. The case literature on treating hypogonadotropic hypogonadism follows the same logic of restoring testicular responsiveness before layering on central stimulation (Crosnoe-Shipley 2015).

And one thing that you can add, if your hypothalamus quiets down and stops firing that signal on its own, meaning the GNRH isn't getting released and LH production drops off with it, you can add Kispeptin for four to six weeks at 250 micrograms every other day, which will mimic that GNRH signal from your hypothalamus down to the pituitary.

You wake the testicle first, then the thermostat, then the brain itself, in that order, because skipping a rung just wastes months. Plan on a minimum of six months before things fire normally, and understand that none of this applies if your problem was primary to begin with.

Second most common question was visceral fat, and specifically tesamorelin.

Tessamerelin was developed to help with patients who had HIV related lipodystrophy, which is a condition where the drugs from HIV treatment cause you to store fat in abnormal places on your body.

Because that was the population, visceral fat was the endpoint the trials measured. That is the entire reason it wears the visceral fat label. It is not better than the other growth hormone secretagogues at the job, it just got measured doing the job.

Growth hormone drives the whole effect. When you are fasted and growth hormone is moving through your bloodstream, it triggers lipolysis, and there are more growth hormone receptors sitting on visceral fat than on subcutaneous fat. The tissue is simply more responsive to the signal.

Now there's also one thing to note, increasing your IGF 1 levels and increasing your growth hormone levels above baseline to we'll say super physiological levels also creates insulin resistance and increased insulin resistance causes visceral fat storage.

So the thing you took to burn visceral fat starts building it back, which is a closed loop you can ride all the way into disease.

And this is exactly why you see professional bodybuilders who are using doses of 10 IU or greater of growth hormone also have to supplement with insulin because their insulin resistance is so high that they actually have turned themselves into type two diabetics by abusing the growth hormone.

That bulging gut isn't just enlarged organs, it's fat wedged into every gap between them, filling space that shouldn't hold fat at all.

On loose skin, the skin behaves like a rubber band. Past a certain stretch it does not snap back.

Collagen peptides at 10 to 15 grams a day with vitamin C probably have the highest evidence of increasing the elasticity of your skin. GHK-Cu helps with collagen reconstruction, topical vitamin E manages stretch marks, and none of it does much past a hundred pounds lost.

So if you're obese and you went from three, 400 pounds down to a healthy 180, 200 pounds, you lost a lot of weight. At that point surgery is the answer and everything else is maintenance.

There is a lot more of this inside the free community, and it is genuinely free, so if you want somewhere to ask the follow-up question the men's group is here: https://www.skool.com/jh-iron-forge-brotherhood/about

Research: Handelsman DJ et al., Eur J Endocrinol 2022; Crosnoe LE et al., Transl Androl Urol 2013; Crosnoe-Shipley LE et al., World J Nephrol 2015.

References:

Crosnoe LE, Grober E, Ohl D et al.. Exogenous testosterone: a preventable cause of male infertility. Transl Androl Urol. 2013. https://pubmed.ncbi.nlm.nih.gov/26813847/

Crosnoe-Shipley LE, Elkelany OO, Rahnema CD et al.. Treatment of hypogonadotropic male hypogonadism: Case-based scenarios. World J Nephrol. 2015. https://pubmed.ncbi.nlm.nih.gov/25949938/

Handelsman DJ, Desai R, Conway AJ et al.. Recovery of male reproductive endocrine function after ceasing prolonged testosterone undecanoate injections. Eur J Endocrinol. 2022. https://pubmed.ncbi.nlm.nih.gov/35000898/