26yo, 480 T, healthy LH. HCG vs troches as front-line — opinions?

newuser1002

New Member
Hey all, longtime lurker, first post. Looking for opinions before committing to a protocol with my clinic I found online (Defy).

Background​

  • 26M, 5'8", ~20-22% BF
  • UARS (Upper Airway Resistance Syndrome) for 7+ years — similar to sleep apnea, fragmented sleep / occasional hypoxia, no cure available short of major surgery (MMA/EASE). On ASV currently.
  • Result: chronic sleep deprivation, late chronotype (sleep 5-7 AM, wake 1-2 PM)
  • No AAS/PED history, lift 3x/week
  • Optimization-focused, not crisis treatment
  • Low-ish libido, tiredness and low energy, low concentration, lower drive

Longitudinal labs​

All draws at post-wake peak time relative to schedule.
Marker2022-102023-012026-04Reference
Total T (ng/dL)454636487264–916
LH (mIU/mL)6.05.41.7–8.6
FSH4.71.5–12.4
SHBG (nmol/L)26.827.516.5–55.9
E2 sensitive (pg/mL)66 (estrogens total)28.08–35
Prolactin (ng/mL)19.8 (HIGH)not tested4.0–15.2
IGF-1 (ng/mL)222166101–307
Vit D (ng/mL)28.541.229.530–100
Hct (%)41.841.743.437.5–51.0
Read: T has bounced around 454-636 over the years, currently settled ~490 across two recent draws. LH stable 5-6 throughout = pituitary signaling fine. IGF-1 also dropped (222→166), fits the sleep/GH connection.

Notable: vitamin D was adequate (41.2) in 2023 when T was peak (636). Currently refractory at 29.5 despite 5K IU/day for years + mag threonate.

What I'm considering​

  1. HCG monotherapyDefy will prescribe, planning 100 IU/day SQ microdose. Got this recommendation from Desmolysium, search up his "TRT lite" protocol.
  2. Troches as 4-week diagnostic trial first — reversible, HPTA preservation, tells me if elevated T actually addresses symptoms before committing. Got this idea from a post by @Cataceous on this forum.
Which do you think is a better idea to start with? Or something else entirely?

Questions​

  1. For those who tried short-acting T as a diagnostic before HCG/TRT — did the experience translate? Did feeling good on troches predict you'd do well on HCG, or did the kinetics feel too different?
  2. For HCG monotherapy users at similar baseline (T 450-550, healthy LH, high-ish E2) — at 50-100 IU/day microdose, did you see meaningful subjective benefits? Or need higher doses to feel anything? Is my E2 a concern - should I lower body fat first?
  3. 2023 prolactin at 19.8 was never followed up — should I retest before any protocol? Could elevated prolactin be contributing even with normal LH?
  4. Anything obviously missing in the workup before starting?

Thanks in advance!
 
Your Vermeulen calculated free testosterone is about 11 ng/dL, which is above what's considered borderline. Obviously I'm going to favor a trial with fast-acting testosterone; depending on the protocol, hCG can still be suppressive of the HPTA. The concept of trialing short-acting testosterone is fairly new, so that will limit the feedback on it. Do use the search function to look up some threads on using Natesto. I'd expect troches to be somewhat easier to sustain, though I can't comment from personal experience. My thought would be to start with the 2.5 mg troches twice a day, increasing to three if needed. If testing suggests poor absorption then you could jump up to the 5 mg size. But you're targeting absorption of only about one milligram of testosterone at a time, enough to push serum testosterone to upper-normal levels for short periods.

Starting out with higher estradiol and prolactin could make hCG use problematic. HCG is notorious for increasing estradiol, which in turn can raise prolactin. A prolactin of 20 ng/mL is already high enough to cause problems for some men. A retest could be worthwhile. If it's still this high then micro-dosing cabergoline might do more for you than directly raising testosterone. In fact, lowering prolactin can raise testosterone levels, though this is more common when dealing with much higher prolactin, as in prolactinomas.
 
While I agree with what Cat said, you might also investigate a low dose of thyroid (T3) and also consider a work-up from a good holistic/integrative doc who can check for nutrient issues and other possible issues like chronic infections. TSH should be under 2 from what I've heard recently, and if your thyroid is off, nothing else will work well as far as energy goes. That said, the sleep issue may be hard to overcome and it's not something I have any knowledge of although trying different sleep supps (e..g C B D, sleep breakthrough, vagus nerve stimulation, etc. ) obviously is worth a try.
 
Your Vermeulen calculated free testosterone is about 11 ng/dL, which is above what's considered borderline. Obviously I'm going to favor a trial with fast-acting testosterone; depending on the protocol, hCG can still be suppressive of the HPTA. The concept of trialing short-acting testosterone is fairly new, so that will limit the feedback on it. Do use the search function to look up some threads on using Natesto. I'd expect troches to be somewhat easier to sustain, though I can't comment from personal experience. My thought would be to start with the 2.5 mg troches twice a day, increasing to three if needed. If testing suggests poor absorption then you could jump up to the 5 mg size. But you're targeting absorption of only about one milligram of testosterone at a time, enough to push serum testosterone to upper-normal levels for short periods.

Starting out with higher estradiol and prolactin could make hCG use problematic. HCG is notorious for increasing estradiol, which in turn can raise prolactin. A prolactin of 20 ng/mL is already high enough to cause problems for some men. A retest could be worthwhile. If it's still this high then micro-dosing cabergoline might do more for you than directly raising testosterone. In fact, lowering prolactin can raise testosterone levels, though this is more common when dealing with much higher prolactin, as in prolactinomas.
In a TRT trial like this one where Natesto or troches are used, would it be expected that one could simply stop the therapy and quickly regain natural function, sans PCT and with minimal discomfort, even after a number of months?
 
In a TRT trial like this one where Natesto or troches are used, would it be expected that one could simply stop the therapy and quickly regain natural function, sans PCT and with minimal discomfort, even after a number of months?

Yes, this should be the case. With limited HPTA suppression it's going to be easier and faster to bounce back to baseline. Full suppression is different in part because each link in the hormonal cascade must recover in sequence from atrophy. That is, the testicles need the LH/FSH signals to start recovery, which requires the pituitary to receive GnRH for sufficient time, which in turn requires the hypothalamus to have long enough exposure to kisspeptin activity. It's also presumed that recovery of each link from atrophy takes longer than from only slightly depressed activity; the low trough levels seen with fast-acting testosterone give the HPTA daily exercise.
 
...Result: chronic sleep deprivation, late chronotype (sleep 5-7 AM, wake 1-2 PM)

Although they would be treating the symptoms rather than the underlying condition, growth hormone secretagogues are something you could look into. In particular, ibutamoren or ipamorelin before bed might make you feel somewhat better, and possibly improve hormone levels in general
 
Yes, this should be the case. With limited HPTA suppression it's going to be easier and faster to bounce back to baseline. Full suppression is different in part because each link in the hormonal cascade must recover in sequence from atrophy. That is, the testicles need the LH/FSH signals to start recovery, which requires the pituitary to receive GnRH for sufficient time, which in turn requires the hypothalamus to have long enough exposure to kisspeptin activity. It's also presumed that recovery of each link from atrophy takes longer than from only slightly depressed activity; the low trough levels seen with fast-acting testosterone give the HPTA daily exercise.
Do you think it'd likely be a similarly easy recovery when utilizing oral testosterone for a trial? Some rough figures I've seen is ~45% suppression from Natesto and ~60% from oral TU. In your experience, does that extra bit make a sizable difference?
 
Do you think it'd likely be a similarly easy recovery when utilizing oral testosterone for a trial? Some rough figures I've seen is ~45% suppression from Natesto and ~60% from oral TU. In your experience, does that extra bit make a sizable difference?

I expect that for most it would be almost as easy to recover from oral TU. But with individual variability there would be some exceptions. Some AI commentary:

Natesto has stronger published data specifically touting HPTA/fertility preservation:​
  • In a prospective phase 4 study (n=40 evaluable hypogonadal men, 6 months), LH and FSH decreased significantly but remained in the normal range in most patients (~73–82% at 6 months). Total motile sperm count (TMSC) was preserved above the 5 million threshold in 88–94% of men. Only ~7.5% developed severe oligospermia and ~2.5% azoospermia (the latter recovered after stopping). Testis volume and intratesticular testosterone markers were also maintained.
  • Marketing and studies emphasize that its very short half-life and frequent dosing mimic natural pulsatility better, reducing the risk of losing endogenous production.
Oral TU shows similar qualitative behavior (partial, non-complete suppression with many men keeping detectable/non-zero gonadotropins and, in limited data, preserved semen parameters), but it lacks the same volume of dedicated fertility-focused prospective semen-analysis studies that Natesto has. No head-to-head trials directly compare the two on HPTA metrics. Both carry the standard TRT warning about potential spermatogenesis suppression (via FSH feedback), and neither is guaranteed to preserve fertility in every individual—monitoring LH/FSH ± semen analysis is recommended if fertility matters.​
Bottom line: Oral TU suppresses the HPTA noticeably but usually incompletely (similar in spirit to Natesto). Natesto’s more frequent dosing and dedicated fertility studies give it a slight edge in the “preserves own production/fertility” narrative, but both are far better options for fertility-conscious men than long-acting TRT. Individual response varies a lot, so lab monitoring (LH/FSH, semen if relevant) is key.​
 
Although they would be treating the symptoms rather than the underlying condition, growth hormone secretagogues are something you could look into. In particular, ibutamoren or ipamorelin before bed might make you feel somewhat better, and possibly improve hormone levels in general
Got it. Thanks for the response!

I also have really poor concentration. I think my REM sleep is getting affected worse than my deep sleep, as far as I can tell, based on looking at my sleep graphs. But I'm not 100% sure about this. So, do I really need more growth hormone? I'm not well-versed in the downstream effects of growth hormones at all.

Is it safe to take ipamorelin? I saw a YouTube video saying how it could potentially increase the risk of cancer. Although I haven't really done a deep dive into this, so my opinions are very, very low confidence.
 
Starting out with higher estradiol and prolactin could make hCG use problematic. HCG is notorious for increasing estradiol, which in turn can raise prolactin. A prolactin of 20 ng/mL is already high enough to cause problems for some men. A retest could be worthwhile. If it's still this high then micro-dosing cabergoline might do more for you than directly raising testosterone. In fact, lowering prolactin can raise testosterone levels, though this is more common when dealing with much higher prolactin, as in prolactinomas.
Thanks again for the response! I saw another person in the forum saying that cabergoline could cause bad long-term effects on depression and the dopamine system and potentially heart issues too. I'm not allowed to post links since my account is too new, but the names of the threads are:
- "cabergoline-and-depression"
- "cabergoline-improves-orgasms-in-two-thirds-of-men"

Looks like this person, @Pacman, also had a bad experience with it with a starting prolactin of 19.5 (very similar to mine) and only 3 doses of 0.25 mg: cabergoline-should-i-really-take-it-pros-vs-cons

Curious how to think about these long term downsides. I'm only 26, so I'm wondering if this is something I can microdose for the long run. Also curious if there's any other risks I should be aware of.

I'm generally a pretty risk-averse type of person, but I also really want to optimize and improve my living situation since I'm unsatisfied with it, which is kinda a bad combo haha. But I would love for this to be a great solution for me so I'm hoping that these downsides can be mitigated.

And finally, one other question: I saw recommended on Reddit that one should try P5P before trying cabergoline to reduce prolactin. Let me know what you think!
 
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I also have really poor concentration. I think my REM sleep is getting affected worse than my deep sleep, as far as I can tell, based on looking at my sleep graphs. But I'm not 100% sure about this. So, do I really need more growth hormone? I'm not well-versed in the downstream effects of growth hormones at all.

Is it safe to take ipamorelin? I saw a YouTube video saying how it could potentially increase the risk of cancer. Although I haven't really done a deep dive into this, so my opinions are very, very low confidence.

Both ibutamoren and ipamorelin seem pretty safe in the short-term. There's probably not enough data to say much about long-term use. I haven't seen anything so far to suggest there are risks beyond the effects on GH and IGF-1. In your case IGF-1 is below average for your age. Therefore you have some room to increase these, and the GH secretagogues often help with sleep, which in turn might improve other parameters. It's one of various things you can try.

Thanks again for the response! I saw another person in the forum saying that cabergoline could cause bad long-term effects on depression and the dopamine system and potentially heart issues too. I'm not allowed to post links since my account is too new, but the names of the threads are:
- "cabergoline-and-depression"
- "cabergoline-improves-orgasms-in-two-thirds-of-men"

Looks like this person, @Pacman, also had a bad experience with it with a starting prolactin of 19.5 (very similar to mine) and only 3 doses of 0.25 mg: cabergoline-should-i-really-take-it-pros-vs-cons

I'd go into a trial of cabergoline with the idea that it's more about characterizing your problem than necessarily being a long-term solution. I'd consider even 0.25 mg to be somewhat large for starting out. When I tried it I used 0.125 mg/week, which I split into two doses. You'd be looking to push prolactin down to around 5-10 ng/mL to see if it helps. If it does and estradiol is still somewhat high in range then you might consider ways to reduce aromatization, as bringing down estradiol can also lower prolactin. If you have any extra pounds then losing them is the healthiest way. Other options are less attractive. Micro-dosing an aromatase inhibitor would be effective, and would also raise testosterone, but the long-term safety is not firmly established.

With either cabergoline or an AI, if you had good and sustainable results with micro-dosing then it's likely that the small risks of long-term use would be worth it if there were no other easy way to achieve those results.

And finally, one other question: I saw recommended on Reddit that one should try P5P before trying cabergoline to reduce prolactin. Let me know what you think!

I've been a bit biased against P5P because of the high doses required and less targeted effectiveness, But it appears to be the safer option. AI summary:

Head-to-head relative safety summary
  • P5P is relatively safer for mild, symptomatic hyperprolactinemia: lower absolute risk (vitamin vs. potent agonist), no cardiac concerns, easier reversibility, and supportive (though limited) trial data showing comparable short-term efficacy with zero significant sides in direct comparison. Use the P5P form specifically to minimize any neuropathy potential.
  • Cabergoline micro-doses are still quite safe but carry a small incremental risk profile (rare valvular changes debated but minimal; dopaminergic side effects) that makes them better reserved for cases where P5P is insufficient or prolactin is more significantly elevated/persistent. They are more predictably effective.
  • Practical approach: For "somewhat above-range," many clinicians might trial lifestyle factors + P5P (under guidance) before escalating to cabergoline. Both are far safer than untreated symptomatic hyperprolactinemia (e.g., hypogonadism, infertility risks). Always confirm etiology first and avoid self-treatment.
 
Your total testosterone seems to track well with your vitamin D levels. Perhaps boosted up to 80 and see what happens. A ketogenic carnivore diet wouldn’t hurt either. Throw in some gym time and you’ve got a solid chance.
 
My physician (a nurse practitioner who, based on a 30 min call, I don't think cares too much or has that much expertise), responded to me by saying:

"if you take the testosterone troche more than once a day you can shut down your production of testosterone. how often were you looking to take it?"

Curious your thoughts on this. I guess it would depend on the dosage as well.

My plans as of now are:
0. Increase my vitamin D intake from 5k IU daily to 10k. Not sure why my vit D has not been increasing despite taking this daily for years. I only go outside like once per day during weekdays so that makes sense; however, I used to take 5k IU daily back a few months in 2022-2023 under similar conditions and that increased my vit D higher during that period of time.
1. Get prolactin and related bloods tested again
2. If it tests high again (which I expect), then get a prolactinoma screening
3. Regardless of the above result, go on P5P or cabergoline. My gut somewhat leans towards p5p right now but I haven't thought about this much yet
4. If I still feel unsatisfied with my energy levels, then going on troches 2-3x per day to test what high T feels like.
5. If it feels good, then I could just stay on troches long term? Any downsides of that?
6. If it doesn't feel good (not sure why this would be the case), then not sure what happens here.

- I guess, at this point there's no point in going on HCG? If troches is truly better at preserving baseline endocrine system function, then it seems like a strictly worse option than long term troches.
- Perhaps worth adding ipamorelin at some point in this sequence? I want to build muscle and I wonder if my low IGF reading is impacting that. I also saw ppl on reddit saying HGH > ipamorelin in general, curious your thoughts on that
- One other thing I haven't mentioned before is that my mom's side has a history of type 2 diabetes. My mom, despite being ~100 pounds, has it too, and her doctor said she was the skinniest person that they've ever seen has diabetes. My glucose levels were at the high range of normal, but I've noticed that when I skip breakfast and eat a big lunch, I get this massive headache that I think is blood sugar related. Not sure if this has any relationship with everything else but worth mentioning in case it is

Let me know if that sounds reasonable. Thanks again for your help!
Both ibutamoren and ipamorelin seem pretty safe in the short-term. There's probably not enough data to say much about long-term use. I haven't seen anything so far to suggest there are risks beyond the effects on GH and IGF-1. In your case IGF-1 is below average for your age. Therefore you have some room to increase these, and the GH secretagogues often help with sleep, which in turn might improve other parameters. It's one of various things you can try.



I'd go into a trial of cabergoline with the idea that it's more about characterizing your problem than necessarily being a long-term solution. I'd consider even 0.25 mg to be somewhat large for starting out. When I tried it I used 0.125 mg/week, which I split into two doses. You'd be looking to push prolactin down to around 5-10 ng/mL to see if it helps. If it does and estradiol is still somewhat high in range then you might consider ways to reduce aromatization, as bringing down estradiol can also lower prolactin. If you have any extra pounds then losing them is the healthiest way. Other options are less attractive. Micro-dosing an aromatase inhibitor would be effective, and would also raise testosterone, but the long-term safety is not firmly established.

With either cabergoline or an AI, if you had good and sustainable results with micro-dosing then it's likely that the small risks of long-term use would be worth it if there were no other easy way to achieve those results.



I've been a bit biased against P5P because of the high doses required and less targeted effectiveness, But it appears to be the safer option. AI summary:

Head-to-head relative safety summary
  • P5P is relatively safer for mild, symptomatic hyperprolactinemia: lower absolute risk (vitamin vs. potent agonist), no cardiac concerns, easier reversibility, and supportive (though limited) trial data showing comparable short-term efficacy with zero significant sides in direct comparison. Use the P5P form specifically to minimize any neuropathy potential.
  • Cabergoline micro-doses are still quite safe but carry a small incremental risk profile (rare valvular changes debated but minimal; dopaminergic side effects) that makes them better reserved for cases where P5P is insufficient or prolactin is more significantly elevated/persistent. They are more predictably effective.
  • Practical approach: For "somewhat above-range," many clinicians might trial lifestyle factors + P5P (under guidance) before escalating to cabergoline. Both are far safer than untreated symptomatic hyperprolactinemia (e.g., hypogonadism, infertility risks). Always confirm etiology first and avoid self-treatment.
 
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My physician (a nurse practitioner who, based on a 30 min call, I don't think cares too much or has that much expertise), responded to me by saying:

"if you take the testosterone troche more than once a day you can shut down your production of testosterone. how often were you looking to take it?"

Curious your thoughts on this. I guess it would depend on the dosage as well.

My plans as of now are:
0. Increase my vitamin D intake from 5k IU daily to 10k. Not sure why my vit D has not been increasing despite taking this daily for years. I only go outside like once per day during weekdays so that makes sense; however, I used to take 5k IU daily back a few months in 2022-2023 under similar conditions and that increased my vit D higher during that period of time.
1. Get prolactin and related bloods tested again
2. If it tests high again (which I expect), then get a prolactinoma screening
3. Regardless of the above result, go on P5P or cabergoline. My gut somewhat leans towards p5p right now but I haven't thought about this much yet
4. If I still feel unsatisfied with my energy levels, then going on troches 2-3x per day to test what high T feels like.
5. If it feels good, then I could just stay on troches long term? Any downsides of that?
6. If it doesn't feel good (not sure why this would be the case), then not sure what happens here.

- I guess, at this point there's no point in going on HCG? If troches is truly better at preserving baseline endocrine system function, then it seems like a strictly worse option than long term troches.
- Perhaps worth adding ipamorelin at some point in this sequence? I want to build muscle and I wonder if my low IGF reading is impacting that. I also saw ppl on reddit saying HGH > ipamorelin in general, curious your thoughts on that
- One other thing I haven't mentioned before is that my mom's side has a history of type 2 diabetes. My mom, despite being ~100 pounds, has it too, and her doctor said she was the skinniest person that they've ever seen has diabetes. My glucose levels were at the high range of normal, but I've noticed that when I skip breakfast and eat a big lunch, I get this massive headache that I think is blood sugar related. Not sure if this has any relationship with everything else but worth mentioning in case it is

Let me know if that sounds reasonable. Thanks again for your help!
Note that Chasteberry is another option for reducing prolactin.
 
My physician (a nurse practitioner who, based on a 30 min call, I don't think cares too much or has that much expertise), responded to me by saying:

"if you take the testosterone troche more than once a day you can shut down your production of testosterone. how often were you looking to take it?"

Curious your thoughts on this. I guess it would depend on the dosage as well.

It is dose-dependent. Point him or her to the data on Natesto. The bottom line is that taking in ~1 mg of fast-acting testosterone two or three times daily is not very suppressive.

0. Increase my vitamin D intake from 5k IU daily to 10k.

Be aware that pushing 25(OH)D over 50 ng/mL is associated with some bad things. Interestingly, one study found that peak testosterone levels correspond to 25(OH)D in the low 30s.

4. If I still feel unsatisfied with my energy levels, then going on troches 2-3x per day to test what high T feels like.
5. If it feels good, then I could just stay on troches long term? Any downsides of that?

There should not be any issues with long-term use if other parameters stay good—lipids, HCT, etc.

- I guess, at this point there's no point in going on HCG? If troches is truly better at preserving baseline endocrine system function, then it seems like a strictly worse option than long term troches.

That is my position.

- Perhaps worth adding ipamorelin at some point in this sequence? I want to build muscle and I wonder if my low IGF reading is impacting that. I also saw ppl on reddit saying HGH > ipamorelin in general, curious your thoughts on that

Sure, direct hGH is more potent. But it is analogous to testosterone, where you create hormonal disruption, including cutting natural production. In contrast, the secretagogues stimulate your own production. Ipamorelin in particular is said to be mild and less disruptive. Ibutamoren is more effective but less natural due to the long half-life.

- One other thing I haven't mentioned before is that my mom's side has a history of type 2 diabetes. My mom, despite being ~100 pounds, has it too, and her doctor said she was the skinniest person that they've ever seen has diabetes. My glucose levels were at the high range of normal, but I've noticed that when I skip breakfast and eat a big lunch, I get this massive headache that I think is blood sugar related. Not sure if this has any relationship with everything else but worth mentioning in case it is

I had Hba1c pushing pre-diabetes levels in spite of no risk factors. Lifestyle effects seemed to be minor, and the only thing I didn't try was a keto diet, which isn't for me. I considered a possible connection to my below-average IGF-1, and subsequently experimented with IGF-1 DES. This seems to have completely resolved the issue. Based on CGM data I'm anticipating Hba1c dropping from ~5.7 to ~5.0.

This is something to be aware of if you decide to push up hGH. It can raise or lower glucose depending on the relative responses to higher hGH and IGF-1.

Let me know if that sounds reasonable. ...

Yes, I think you will gain some useful information from this plan.
 
Be aware that pushing 25(OH)D over 50 ng/mL is associated with some bad things. Interestingly, one study found that peak testosterone levels correspond to 25(OH)D in the low 30s.
What are the bad things and what's the evidence? My understanding is that "bad things" happen when D is taken without K2, but not with. Further there were some studies that came out during covid that showed that 50 and above were where the biggest immune system benefits were found, which is what I would think we would want to prioritize since there are other ways to raise T, if that correlation is even valid.
 
What are the bad things and what's the evidence? My understanding is that "bad things" happen when D is taken without K2, but not with. Further there were some studies that came out during covid that showed that 50 and above were where the biggest immune system benefits were found, which is what I would think we would want to prioritize since there are other ways to raise T, if that correlation is even valid.

Below I'll resuscitate one of Curt Moyer's articles from PeakTestosterone.com on the subject. It's a little dated and overstated in some places, but still makes it look dubious to supplement excessively, especially in light of a current AI summary:

Question to AI:
Regarding supplementation with vitamin D in the absence of severe deficiency, is the evidence for effects on health overall positive, neutral or negative?​

Answer:
Neutral.​
High-quality evidence from large randomized controlled trials (RCTs) and systematic reviews shows that vitamin D supplementation in vitamin D-replete adults (those without severe deficiency, typically with baseline 25-hydroxyvitamin D levels >50 nmol/L or ~20 ng/mL) has no demonstrable overall benefits for major health outcomes, nor does it cause meaningful harm at standard doses (e.g., 800–2000 IU/day). Benefits are largely limited to correcting deficiency, not adding extra vitamin D on top of sufficiency.​

---------

The Dangers of High Vitamin D by Curt Moyer​
It is now fairly well-known in the men's health community that correcting a vitamin D deficiency can increase testosterone, something I cover in my page on Testosterone and Vitamin D. I have seen men on the Peak Testosterone Forum increase their testosterone with this simple supplement. However, I have also seen other men jump on this and assume, therefore, that the more vitamin D taken, the better. Below I make the case that this is likely an unwise assumption and even show potential risks of driving your vitamin D levels too high.​
Measuring your vitamin D level is a simple, inexpensive blood test that you can order yourself (here in the U.S.) at any one of these Inexpensive Testosterone Self-Testing Labs. The test is called "25-Hydroxy" and measures a metabolite of vitamin D. Taking this test is a good idea, because abundant research shows that a vitamin D deficiency is likely NOT a good thing and has been tied to literally dozens of chronic and​
autoimmune diseases and conditions. A deficiency is usually defined as 25-hydroxy levels below 30 ng/ml. And, as mentioned above, low vitamin D can in turn lower testosterone levels. I take vitamin D every day and am personally targeting 40-50 ng/ml 25-hydroxy levels, but you'll have to study the​
research and talk to a good doc and decide for yourself of course.​
I also recommend that you look at the Six Potential Dangers of Increasing Your Vitamin D Levels Above ~50 ng/ml that I have listed below:​
Please support the site and check out Lee Myer's two popular books: Natural Versus Testosterone Therapy and The Peak Erectile Strength Diet​
1. Decreased Fertility. When I first started understanding the importance of vitamin D, I listened to a vitamin D supplement representative claiming that 25-hydroxy levels above 140 are common in some indigenous cultures exposed to direct sunlight. He was clearly arguing for supplementation to very high levels. Like many men, I assumed that I would need to really boost my vitamin D levels to achieve maximum benefits. However, one of the first clues that there was more to the story came from hearing about high vitamin D levels actually lowering male fertility. One study found that "Sperm concentration, sperm progressive motility, sperm morphology, and total progressively motile sperm count were lower in men with '25OHD=50 ng ml(-1)' when compared to men with '20 ng ml(-1)=25OHD<50 ng ml(-1)'." [1]​
This showed the obvious: all hormones have a "good" range and vitamin D is no exception. (Vitamin D is considered a hormone by many experts, because it affects so many tissues and systems.) CAUTION: One study showed that lower levels of vitamin D likely lower fertility and stated that "the pregnancy rates per patient and per cycle and delivery rates per patient and per cycle were all significantly higher in couples with normal Vit D levels." [4] This argues again for a "sweet spot."​
2. Increased Estradiol. While it is true that some hypogonadal men are low in estradiol, the high prevalence of overweight and obese men often leads to unnecessarily high estradiol levels and "estrogen dominance" if you will. Men in this category do not need more estradiol, and it turns out that vitamin D is one of the controllers of estradiol levels in both males and females. Men get their estradiol via the aromatase-enzyme conversion of testosterone, and vitamin D governs the aromatase enzyme. One study on mice with deficient vitamin D levels found greatly reduced aromatase-enzyme levels. Estradiol levels were reduced correspondingly by almost 40%. [2][3] Going back to #1, this may explain the decreased fertility in men who take too much vitamin D: higher levels of estradiol actually worsen sperm parameters.​
3. Poor Study Outcomes. There have been literally dozens of studies testing the effects of vitamin D supplementation on people. If raising vitamin D to higher levels were beneficial then arguably it should have shown up already in the research. However, the studies have actually shown the opposite, i.e. that going above 50 ng/ml either provides no additional benefits or, in some cases, even makes things worse. This journal summary says it all:​
"Even if 25(OH)D values above 50 ng/mL, or even above 100 ng/mL, are unlikely to cause acute toxicity, achieving 25(OH)D values above 50 ng/mL has not been found to be beneficial, especially for the general population." [6]​
4. Increased Mortality Rates. One study showed that death rates increased at either low or high serum levels of vitamin D. The authors wrote that "analysis of 24,094 adult patients showed that 25(OH)D levels less than 20 ng/mL and 60 ng/mL or greater before hospitalization were associated with an increased odds of 90-day mortality. Although previous reports have suggested an association between low vitamin D status and mortality, these data raise the issue of potential harm from high serum 25(OH)D levels, provide a rationale for an upper limit to supplementation, and emphasize the need for caution in the use of extremely high doses of vitamin D among patients." [5]​
By the way, this verified what an earlier study had found:​
"In this study from the general practice sector, a reverse J-shaped relation between the serum level of 25(OH)D and all-cause mortality was observed, indicating not only a lower limit but also an upper limit. The lowest mortality risk was at 50-60 nmol/liter. The study did not allow inference of causality, and further studies are needed to elucidate a possible causal relationship between 25(OH)D levels, especially higher levels, and mortality." [7]​
5. Higher Cardiovascular Disease Rates. A 2009 study found that vitamin D levels in non-institutionalized seniors had an inverse association with cardiovascular disease risk. In other words, the lower the vitamin D levels, the lower the risk of heart disease! [8] It is hard to know the cause for this, but remember that vitamin D controls the body's calcium levels and, therefore, potentially vitamin D could push calcium into soft tissues. Yes, arterial plaque is calcium, so perhaps this is the mechanism.​
6. Increased Pancreatic Cancer Risk. There is a recent study that shows 5000 IU of vitamin D regressed prostate cancer. However, yet another study found that going too high seemed to increase risk:​
"No significant associations were observed for participants with lower 25(OH)D status. However, a high 25(OH)D concentration (> or =100 nmol/L) was associated with a statistically significant 2-fold increase in pancreatic cancer risk overall (odds ratio = 2.12, 95% confidence interval: 1.23, 3.64). Given this result, recommendations to increase vitamin D concentrations in healthy persons for the prevention of cancer should be carefully considered.." [9]​
CONCLUSION: We now have several studies, some even large and recent, that show that raising 25-hydroxy serum levels above 50 (or perhaps 60) ng/dl is risky and associated with increased risk of chronic disease. Results seem to indicate that there is an optimal zone for Vitamin D.​
 
Below I'll resuscitate one of Curt Moyer's articles from PeakTestosterone.com on the subject. It's a little dated and overstated in some places, but still makes it look dubious to supplement excessively, especially in light of a current AI summary:

Question to AI:
Regarding supplementation with vitamin D in the absence of severe deficiency, is the evidence for effects on health overall positive, neutral or negative?​

Answer:
Neutral.​
High-quality evidence from large randomized controlled trials (RCTs) and systematic reviews shows that vitamin D supplementation in vitamin D-replete adults (those without severe deficiency, typically with baseline 25-hydroxyvitamin D levels >50 nmol/L or ~20 ng/mL) has no demonstrable overall benefits for major health outcomes, nor does it cause meaningful harm at standard doses (e.g., 800–2000 IU/day). Benefits are largely limited to correcting deficiency, not adding extra vitamin D on top of sufficiency.​

---------

The Dangers of High Vitamin D by Curt Moyer​
It is now fairly well-known in the men's health community that correcting a vitamin D deficiency can increase testosterone, something I cover in my page on Testosterone and Vitamin D. I have seen men on the Peak Testosterone Forum increase their testosterone with this simple supplement. However, I have also seen other men jump on this and assume, therefore, that the more vitamin D taken, the better. Below I make the case that this is likely an unwise assumption and even show potential risks of driving your vitamin D levels too high.​
Measuring your vitamin D level is a simple, inexpensive blood test that you can order yourself (here in the U.S.) at any one of these Inexpensive Testosterone Self-Testing Labs. The test is called "25-Hydroxy" and measures a metabolite of vitamin D. Taking this test is a good idea, because abundant research shows that a vitamin D deficiency is likely NOT a good thing and has been tied to literally dozens of chronic and​
autoimmune diseases and conditions. A deficiency is usually defined as 25-hydroxy levels below 30 ng/ml. And, as mentioned above, low vitamin D can in turn lower testosterone levels. I take vitamin D every day and am personally targeting 40-50 ng/ml 25-hydroxy levels, but you'll have to study the​
research and talk to a good doc and decide for yourself of course.​
I also recommend that you look at the Six Potential Dangers of Increasing Your Vitamin D Levels Above ~50 ng/ml that I have listed below:​
Please support the site and check out Lee Myer's two popular books: Natural Versus Testosterone Therapy and The Peak Erectile Strength Diet​
1. Decreased Fertility. When I first started understanding the importance of vitamin D, I listened to a vitamin D supplement representative claiming that 25-hydroxy levels above 140 are common in some indigenous cultures exposed to direct sunlight. He was clearly arguing for supplementation to very high levels. Like many men, I assumed that I would need to really boost my vitamin D levels to achieve maximum benefits. However, one of the first clues that there was more to the story came from hearing about high vitamin D levels actually lowering male fertility. One study found that "Sperm concentration, sperm progressive motility, sperm morphology, and total progressively motile sperm count were lower in men with '25OHD=50 ng ml(-1)' when compared to men with '20 ng ml(-1)=25OHD<50 ng ml(-1)'." [1]​
This showed the obvious: all hormones have a "good" range and vitamin D is no exception. (Vitamin D is considered a hormone by many experts, because it affects so many tissues and systems.) CAUTION: One study showed that lower levels of vitamin D likely lower fertility and stated that "the pregnancy rates per patient and per cycle and delivery rates per patient and per cycle were all significantly higher in couples with normal Vit D levels." [4] This argues again for a "sweet spot."​
2. Increased Estradiol. While it is true that some hypogonadal men are low in estradiol, the high prevalence of overweight and obese men often leads to unnecessarily high estradiol levels and "estrogen dominance" if you will. Men in this category do not need more estradiol, and it turns out that vitamin D is one of the controllers of estradiol levels in both males and females. Men get their estradiol via the aromatase-enzyme conversion of testosterone, and vitamin D governs the aromatase enzyme. One study on mice with deficient vitamin D levels found greatly reduced aromatase-enzyme levels. Estradiol levels were reduced correspondingly by almost 40%. [2][3] Going back to #1, this may explain the decreased fertility in men who take too much vitamin D: higher levels of estradiol actually worsen sperm parameters.​
3. Poor Study Outcomes. There have been literally dozens of studies testing the effects of vitamin D supplementation on people. If raising vitamin D to higher levels were beneficial then arguably it should have shown up already in the research. However, the studies have actually shown the opposite, i.e. that going above 50 ng/ml either provides no additional benefits or, in some cases, even makes things worse. This journal summary says it all:​
"Even if 25(OH)D values above 50 ng/mL, or even above 100 ng/mL, are unlikely to cause acute toxicity, achieving 25(OH)D values above 50 ng/mL has not been found to be beneficial, especially for the general population." [6]​
4. Increased Mortality Rates. One study showed that death rates increased at either low or high serum levels of vitamin D. The authors wrote that "analysis of 24,094 adult patients showed that 25(OH)D levels less than 20 ng/mL and 60 ng/mL or greater before hospitalization were associated with an increased odds of 90-day mortality. Although previous reports have suggested an association between low vitamin D status and mortality, these data raise the issue of potential harm from high serum 25(OH)D levels, provide a rationale for an upper limit to supplementation, and emphasize the need for caution in the use of extremely high doses of vitamin D among patients." [5]​
By the way, this verified what an earlier study had found:​
"In this study from the general practice sector, a reverse J-shaped relation between the serum level of 25(OH)D and all-cause mortality was observed, indicating not only a lower limit but also an upper limit. The lowest mortality risk was at 50-60 nmol/liter. The study did not allow inference of causality, and further studies are needed to elucidate a possible causal relationship between 25(OH)D levels, especially higher levels, and mortality." [7]​
5. Higher Cardiovascular Disease Rates. A 2009 study found that vitamin D levels in non-institutionalized seniors had an inverse association with cardiovascular disease risk. In other words, the lower the vitamin D levels, the lower the risk of heart disease! [8] It is hard to know the cause for this, but remember that vitamin D controls the body's calcium levels and, therefore, potentially vitamin D could push calcium into soft tissues. Yes, arterial plaque is calcium, so perhaps this is the mechanism.​
6. Increased Pancreatic Cancer Risk. There is a recent study that shows 5000 IU of vitamin D regressed prostate cancer. However, yet another study found that going too high seemed to increase risk:​
"No significant associations were observed for participants with lower 25(OH)D status. However, a high 25(OH)D concentration (> or =100 nmol/L) was associated with a statistically significant 2-fold increase in pancreatic cancer risk overall (odds ratio = 2.12, 95% confidence interval: 1.23, 3.64). Given this result, recommendations to increase vitamin D concentrations in healthy persons for the prevention of cancer should be carefully considered.." [9]​
CONCLUSION: We now have several studies, some even large and recent, that show that raising 25-hydroxy serum levels above 50 (or perhaps 60) ng/dl is risky and associated with increased risk of chronic disease. Results seem to indicate that there is an optimal zone for Vitamin D.​
Ok, thanks. First, I would be willing to bet that ALL of the risk of higher Vitamin D levels comes from supplementing D without Vitamin K2, since all studies I can recall had this blatant flaw. As the above points out, supplementing D without K2 can cause calcium dis-regulation which is certainly bad but does not at all mean that high levels of D are bad. Unfortunately, the importance of K2 with D and K2 in general has not made it into the mainstream yet but should hopefully be standard for people here, so this issue likely applies to observational as well as intervention studies.

I did not know that D increased E2 (for me that's a good thing) however it could partially explain why recent studies have found that higher D levels seem to link to lower risk of bad outcomes from infections since E2 is IIRC very supportive of anti-infection immune function. For me, and I would assume for most people reading this, the single biggest risk is likely to be pneumonia so I'm going to continue to believe that D levels in the 50-60 range are a good target. If fertility ever becomes a priority for me I'll have to dig deeper on that topic.

On a loosely related note, I would think that people with teenage children (especially daughters) would want to make sure that they are erring on the high side with K2 and D since those are so important for proper bone development.
 
Ok, thanks. First, I would be willing to bet that ALL of the risk of higher Vitamin D levels comes from supplementing D without Vitamin K2, since all studies I can recall had this blatant flaw.

Whereas I would expect other interactions as well, leading to some risks that are independent of K2. AI summary: "K2 is a smart cofactor with supportive (but not conclusive) evidence for synergy—not a complete safeguard against higher vitamin D risks."

... Unfortunately, the importance of K2 with D and K2 in general has not made it into the mainstream yet but should hopefully be standard for people here, ....

I learned about this at PeakTestosterone and have been supplementing ever since.

...
I did not know that D increased E2 (for me that's a good thing) however it could partially explain why recent studies have found that higher D levels seem to link to lower risk of bad outcomes from infections since E2 is IIRC very supportive of anti-infection immune function. For me, and I would assume for most people reading this, the single biggest risk is likely to be pneumonia so I'm going to continue to believe that D levels in the 50-60 range are a good target. If fertility ever becomes a priority for me I'll have to dig deeper on that topic.

Actually, the aromatization link is one of the things that appears to be overstated. It primarily holds only in comparison to deficiency. Otherwise it is more complex. AI Summary:

No, it is not generally true that vitamin D increases aromatization (the conversion of androgens to estrogens via the aromatase enzyme, CYP19A1) or circulating estradiol levels. The relationship is complex, tissue-specific, context-dependent, and often the opposite of a simple “increase.” Evidence comes from animal models, in vitro studies, observational data, and randomized controlled trials (RCTs) in humans. There is no consistent support for vitamin D supplementation broadly elevating estradiol in non-deficient adults.​
On a loosely related note, I would think that people with teenage children (especially daughters) would want to make sure that they are erring on the high side with K2 and D since those are so important for proper bone development.

Even so, there's no data-driven reason to exceed 50 ng/mL. Of course this is really true for the US average of ~30 ng/mL as well. AI:

Evidence on Health Implications
  • IOM position (widely referenced): ≥20 ng/mL (50 nmol/L) is sufficient for most people for bone health and overall needs in healthy individuals. Levels of 12–20 ng/mL indicate potential inadequacy for some, and <12 ng/mL clear deficiency risk (e.g., rickets, osteomalacia). The US average exceeds this.
  • Large RCTs in replete/insufficient populations (e.g., VITAL, ViDA): Achieved levels around or above the US average showed no meaningful reductions in cancer, CVD, fractures, diabetes, or mortality from further supplementation. Benefits are clearest when correcting severe deficiency.
  • Observational data: Low levels correlate with worse outcomes, but causation is weak once above ~20 ng/mL; reverse causation and confounders (e.g., obesity, illness) play roles.
  • Recent Endocrine Society (2024): Healthy adults <75 years are unlikely to benefit from more than IOM-recommended intakes (600–800 IU/day). They no longer strongly endorse specific high cutoffs like 30 ng/mL for routine use and advise against broad screening.
Higher targets (e.g., 30–40+ ng/mL) are promoted by some for potential extra-skeletal benefits, but RCTs have not consistently supported them in non-deficient people, and pushing levels higher carries small lab risks (e.g., hypercalciuria).​
 
It is dose-dependent. Point him or her to the data on Natesto. The bottom line is that taking in ~1 mg of fast-acting testosterone two or three times daily is not very suppressive.



Be aware that pushing 25(OH)D over 50 ng/mL is associated with some bad things. Interestingly, one study found that peak testosterone levels correspond to 25(OH)D in the low 30s.



There should not be any issues with long-term use if other parameters stay good—lipids, HCT, etc.



That is my position.



Sure, direct hGH is more potent. But it is analogous to testosterone, where you create hormonal disruption, including cutting natural production. In contrast, the secretagogues stimulation your own production. Ipamorelin in particular is said to be mild and less disruptive. Ibutamoren is more effective but less natural due to the long half-life.



I had Hba1c pushing pre-diabetes levels in spite of no risk factors. Lifestyle effects seemed to be minor, and the only thing I didn't try was a keto diet, which isn't for me. I considered a possible connection to my below-average IGF-1, and subsequently experimented with IGF-1 DES. This seems to have completely resolved the issue. Based on CGM data I'm anticipating Hba1c dropping from ~5.7 to ~5.0.

This is something to be aware of if you decide to push up hGH. It can raise or lower glucose depending on the relative responses to higher hGH and IGF-1.



Yes, I think you will gain some useful information from this plan.

Hey Cataceous, thanks again for the detailed thoughts last round on troches and the prolactin angle. The cabergoline retest is in the pipeline (Defy is ordering prolactin + macroprolactin in my next draw before any treatment decisions).

In the meantime, I've been digging through the forum and the pattern I keep running into is a long-term fade in efficacy across short-acting T forms after some months in. Not sure if "tachyphylaxis" is technically the right word given the timeline, or if this is better characterized as chronic tolerance / receptor adaptation.

Some specific examples giving me pause:
  • ZALEMAX in excelmale.com/threads/anyone-have-experience-using-natesto.30452/ — 2 years on Natesto, escalated 2→3 pumps daily, "body acclimated" at ~6 months and switched to Zyosted. "My body acclimated and I was not feeling that it was working anymore."
  • BigBeard411 in excelmale.com/threads/my-notes-on-empower-nasal-t-gel-experiment.25326/ — felt incredible weeks 1-3, then "the positive effects diminished. I feel the same as when I first began, and maybe even worse." His FSH dropped 4.9 → 2.3 mIU/mL, which suggests accumulating HPTA suppression despite the brief-peak design.
  • Wolfieb on r/Testosterone (reddit.com/r/Testosterone/comments/1f9ppwe/my_journey_with_testosteronetroches/) — 10mg troches BID + tadalafil. T at 1250 at month 4, felt great. By month 10 "felt like crap" — sleep terrible, weight gain, mood crashed — despite labs still looking fine. Quit and is starting over.
  • Honeymoon-then-fade pattern named explicitly in excelmale.com/threads/scrotal-t-cream-chasing-the-honeymoon.19582/ — applies to scrotal cream too, with users developing on/off cycling strategies to "reset" the response.
It seems some Natesto fade reports turn out to be product QC issues (excelmale.com/threads/natesto-large-shards-update-batch-is-all-bad.28153/). But ZALEMAX's 6-month gradual adaptation and BigBeard411's documented FSH drop seem like genuine biological adaptation, not drug failure.

This doctor on youtube is also saying that troches could have a negative impact on the liver and is inferior to injections (though of course, I don't want to shut down my HPA axis): youtube.com/watch?v=BPJOVlGLZxc

A few specific questions if you have time:
  1. At lower troche doses (your 2.5mg BID vs Wolfieb's 10mg BID), does the fade pattern still apply, or does the lower dose preserve long-term responsiveness?
  2. Is there a sustainable long-term short-acting T protocol you're aware of, or do all options eventually require escalation / cycling / switching to longer-acting?
  3. If I do a 4-6 week diagnostic troche trial and feel real benefit, should I assume the benefit will fade by month 6, or is there reason to think early benefit predicts sustained benefit?

I did some more research on troches, and for some reason, most of the anecdotal reports on Reddit were from women. I was only able to find a few reports but they weren't positive. I also did a lot of searching on this site.

Overall, my impression is that it feels theoretically sound but for some reason, not as effective in practice. Does this align with what you've seen? I'm new to this site and I used AI to help me search, so you'll have definitely seen more anecdotal reports than me.

Given my situation (UARS-driven low T, healthy LH, 26yo, optimization not crisis), I'm trying to figure out whether short-acting T is even worth pursuing as anything beyond a brief diagnostic, given the apparent ceiling on long-term effectiveness.

Appreciate your time as always!
 
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