Primary Hypogonadism: Doctor wants to put me on 25mg of Testosterone enanthate per week

[PrimaryHypogonadismHell]

Hi everyone,

I have primary hypogonadism and need your help, i am less than 35 years old and no children so i would like to preserve the little sperm production i have.

My numbers for the 2 last years are similar to my last bloodwork and sperm test which are:

Total testosterone at 170 ng/dL
LH: 30
FSH: 24
Sperm count: 5 millions/ml

The doctor wants to start me at 25mg of TE per week, which i think is extremly low.

He says that since i am primary, this dosage will "add up" to my low natural production while preserving the remaining fertility. He says LH and FSH levels will much likely remain high even with low dose exogenous testosterone.

His goal is to improve metabolic health and bones/heart health while not hurting the residual fertility i currently have

He believe this low dosage will probably increase my test level to 300-400ng/dl while preserving fertility. He says that if 3 months after starting injections, my lh and fsh levels are still high enough and if sperm count has not decreased, we can increase the dosage to 37.5mg per week and aim for 500-600ng/dl test level. But he said that according to his experience, 50mg per week can decrease lh and fsh too much even in primary hypogonadism.

What do you think of this protocol? I am lost because i have never heard of this.Can you confirm that low dose exogenous testosterone will not decrease fsh and lh much for primary hypogonadism?

Thank you for your help!

 

[Cataceous]

You have a wise doctor. It's not common for guys with primary hypogonadism to get such good advice. All I would add is that dividing the dose into 2-3 injections per week is a good idea—if he didn't already suggest that.

It is correct that with primary hypogonadism, exogenous testosterone adds to natural production until you get close to normal levels of testosterone. You use LH/FSH measurements to tune your dose, just like he says. You're aiming to bring them down to normal from over-range/high-normal. The latter is a prominent feature of primary hypogonadism: It means that your brain is yelling at your testicles to make more testosterone, but they can't do it.

 

[PrimaryHypogonadismHell]

You have a wise doctor. It's not common for guys with primary hypogonadism to get such good advice. All I would add is that dividing the dose into 2-3 injections per week is a good idea—if he didn't already suggest that.

It is correct that with primary hypogonadism, exogenous testosterone adds to natural production until you get close to normal levels of testosterone. You use LH/FSH measurements to tune your dose, just like he says. You're aiming to bring them down to normal from over-range/high-normal. The latter is a prominent feature of primary hypogonadism: It means that your brain is yelling at your testicles to make more testosterone, but they can't do it.

Thank you for your answer, it awesome to know that this protocol is not stupid! He did not talk about increasing injection frequency for TE, but it is something i could do.

He also talked about another testosterone, Nebido, which has very long half life and is very popular in my country. But the issue is that it only comes in 4ml single usage , for a total 1000mg every 3 months. He suggested that we could split it in 25mg per week, but i dont understand how i could do split it since it is a single usage vial from what i have seen. Also, it does not seem to have any preservatives in it

Thanks again for your message, i am relieved that my doctor is not crazy. I looked on the web for such protocols, but i could not find anything

 

[Cataceous]

Nebido—testosterone undecanoate—is viable, but it's not ideal when you are still planning to make dose adjustments. Either testosterone cypionate or testosterone enanthate would be better, although these should be injected at least three times a week or every other day to smooth out levels. Once you have determined the correct dose—that yields good subjective results and normal testosterone/LH/FSH—then you could switch to testosterone undecanoate and cut the injection frequency to once a week or even once every 10 days. The shorter half-lives of cypionate/enanthate mean that dose changes stabilize over a period of a few weeks. With undecanoate, the stabilization period may be extended to months.

An advantage of injections is that you have a lot of precision in dose adjustments. For example, if the best dose for you happens to be 35 mg of testosterone enanthate per week then that is simple to achieve with EOD injections of 10 mg. You doctor undoubtedly understands how to convert this to injections of testosterone undecanoate, but here's the explanation: The enanthate is 72% testosterone, while the undecanoate is 63.2% testosterone. So the equivalent of 35 mg T enanthate per week is 35 * 72 / 63.2 = 40 mg T undecanoate per week.

It is not too difficult to split Nebido, even if it comes in a single-use ampule instead of a multi-dose vial. Nebido contains a preservative, so you don't need to be too worried about microbial growth as long as you use good aseptic techniques. All you have to do is transfer the Nebido from the single-use container to a new sterile vial of suitable size, e.g. 5-10 mL. You would use a sterile syringe to do this transfer. Even better is to divide the 4 mL of Nebido into a few separate sterile vials so that no one vial is used/punctured excessively over time.

For subcutaneous administration your doses are then drawn from the reusable vial(s) with U-100 insulin syringes.

 

[PrimaryHypogonadismHell]

Nebido—testosterone undecanoate—is viable, but it's not ideal when you are still planning to make dose adjustments. Either testosterone cypionate or testosterone enanthate would be better, although these should be injected at least three times a week or every other day to smooth out levels. Once you have determined the correct dose—that yields good subjective results and normal testosterone/LH/FSH—then you could switch to testosterone undecanoate and cut the injection frequency to once a week or even once every 10 days. The shorter half-lives of cypionate/enanthate mean that dose changes stabilize over a period of a few weeks. With undecanoate, the stabilization period may be extended to months.

An advantage of injections is that you have a lot of precision in dose adjustments. For example, if the best dose for you happens to be 35 mg of testosterone enanthate per week then that is simple to achieve with EOD injections of 10 mg. You doctor undoubtedly understands how to convert this to injections of testosterone undecanoate, but here's the explanation: The enanthate is 72% testosterone, while the undecanoate is 63.2% testosterone. So the equivalent of 35 mg T enanthate per week is 35 * 72 / 63.2 = 40 mg T undecanoate per week.

It is not too difficult to split Nebido, even if it comes in a single-use ampule instead of a multi-dose vial. Nebido contains a preservative, so you don't need to be too worried about microbial growth as long as you use good aseptic techniques. All you have to do is transfer the Nebido from the single-use container to a new sterile vial of suitable size, e.g. 5-10 mL. You would use a sterile syringe to do this transfer. Even better is to divide the 4 mL of Nebido into a few separate sterile vials so that no one vial is used/punctured excessively over time.

For subcutaneous administration your doses are then drawn from the reusable vial(s) with U-100 insulin syringes.

Thank you for your help and for all this information.

I did my first injection subcutaneous of TE 2 days ago, 12.5mg injected with insulin seringe. Very easy and painless, no inflammation at injevtion site at all. Next injection is tomorrow. So 2x12.5mg per week. I did not tell yet my doctor that i am splitting the dose but i dont think he will be against it.

Right now i have a feeling that my testicles are tighter than usual, they sit higher. I hope that it is all in my head and that there is no significant suppression going on

Next bloodwork is in 5 weeks, I will keep you informed about the outcome

 

[t_spacemonkey]

the guy is retarded. there is a study, and i wont find the source now, measuring muscle building properties of test 50-600mg. the guys on 50mg/week was the only group which lost muscle. at that dose you be better of trying to raise it naturally. morons like this is why people are abandoning the medical system

 

[Guided_by_Voices]

the guy is retarded. there is a study, and i wont find the source now, measuring muscle building properties of test 50-600mg. the guys on 50mg/week was the only group which lost muscle. at that dose you be better of trying to raise it naturally. morons like this is why people are abandoning the medical system

It could have been a study with people who are secondary, not primary

 

[Nelson Vergel]

The doctor wants to start me at 25mg of TE per week, which i think is extremly low.

He says that since i am primary, this dosage will "add up" to my low natural production while preserving the remaining fertility. He says LH and FSH levels will much likely remain high even with low dose exogenous testosterone.

I would go to another doctor. TRT does not "add" testosterone to your baseline number. It completely replaces it from zero. 25 mg per week will probably bring you to 200 dg/dL. You need at least 100 mg/week, plus hCG 500 IU twice per week. Or 25 mg/day Clomid.

 

[Cataceous]

the guy is retarded. there is a study, and i wont find the source now, measuring muscle building properties of test 50-600mg. the guys on 50mg/week was the only group which lost muscle. at that dose you be better of trying to raise it naturally. morons like this is why people are abandoning the medical system

This study applied to men who had natural testosterone production completely suppressed by a GnRH agonist. It's an apples-to-oranges comparison. The OP's doctor has probably forgotten more about TRT than you'll ever know.

I would go to another doctor. TRT does not "add" testosterone to your baseline number. It completely replaces it from zero. 25 mg per week will probably bring you to 200 dg/dL. You need at least 100 mg/week, plus hCG 500 IU twice per week. Or 25 mg/day Clomid.

You are thinking about secondary hypogonadism. With primary the exogenous testosterone is additive until you get close to the brain's natural set point.

 

[Nelson Vergel]

This study applied to men who had natural testosterone production completely suppressed by a GnRH agonist. It's an apples-to-oranges comparison. The OP's doctor has probably forgotten more about TRT than you'll ever know.



You are thinking about secondary hypogonadism. With primary the exogenous testosterone is additive until you get close to the brain's natural set point.

That statement is wrong - or at least oversimplified to the point of being misleading.

Here's why:

The Negative Feedback Still Works

Even in primary hypogonadism, exogenous testosterone suppresses LH/FSH through negative feedback at the hypothalamus and pituitary. This happens at any dose, not just when you approach some "set point."
The brain doesn't wait until you hit a threshold before it starts responding to testosterone - the feedback is continuous and dose-dependent.

What May Create This Misconception:
The confusion might come from the fact that in primary hypogonadism:

LH/FSH are already elevated, they're high because the brain is trying hard to compensate for failing testes
The testes can't respond well, so even with high gonadotropin drive, testosterone production is poor
Initially, small doses might not fully suppress , you might see some reduction in LH/FSH but not complete suppression immediately

However, this doesn't mean the testosterone is "additive" in a simple sense. You're still suppressing whatever marginal endogenous production exists, even if it's minimal.

With primary hypogonadism, even low doses of exogenous testosterone will begin suppressing LH/FSH. The "additive" concept would only be truly accurate if the HPT axis didn't respond to exogenous testosterone until some threshold - but that's not how the negative feedback loop works.
The net testosterone level is a combination of (reduced endogenous + exogenous), not a simple addition of the two independent of each other. I doubt that a low dose to try to preserve fertility will provide any quality of life benefits since T will never be high enough.

He should probably try a short acting formulation like Natesto or oral testosterone undecanoate.

 

[Cataceous]

From the Grok AI:

The premise—that low-dose exogenous testosterone, titrated gradually, can normalize serum testosterone levels in primary hypogonadism while reducing initially elevated LH and FSH back to normal ranges without full suppression—aligns with physiological reasoning rooted in the dynamics of the hypothalamic-pituitary-testicular axis (HPTA), particularly when considering the heightened sensitivity of gonadotropin responses in primary cases, variable suppression profiles across TRT formulations, and the distinction from secondary hypogonadism. While large-scale studies are lacking, and standard literature often reports overall gonadotropin suppression during TRT, the mechanics suggest this approach could work in select patients with intact pituitary function, avoiding the over-suppression seen with conventional dosing. Below, I'll break down the reasoning step by step.

1. Understanding the HPTA Feedback Loop in Primary vs. Secondary Hypogonadism

• In a eugonadal (normal) man, the pituitary gland senses serum testosterone (and its metabolite estradiol) levels via negative feedback. When testosterone is in the mid-normal range (e.g., 450-600 ng/dL), it maintains LH and FSH at normal levels (typically 1.5-8.6 IU/L for LH and 1.5-12.4 IU/L for FSH), which in turn support endogenous testosterone production and spermatogenesis in responsive testes.
• Primary hypogonadism (e.g., due to testicular failure like Klinefelter syndrome or damage) features low endogenous testosterone (often <300 ng/dL) despite an intact pituitary-hypothalamic axis. This lack of feedback drives LH and FSH to elevated levels (e.g., >10-20 IU/L) in a compensatory effort to stimulate the unresponsive testes. The axis is "hyperactive" but ineffective at the testicular level.
• Secondary hypogonadism (hypogonadotropic, due to pituitary or hypothalamic issues) involves low or inappropriately normal LH/FSH from the start, leading to low testosterone. The axis is inherently impaired, often described as more "sensitive" to feedback inhibition because the baseline signaling is already disrupted—any exogenous testosterone can rapidly reinforce suppression, as the pituitary may over-respond or fail to rebound due to underlying pathology.
• Key difference: In primary, the HPTA is fully functional upstream (hypothalamus and pituitary), so feedback responses are robust and potentially titratable. In secondary, the impaired axis leads to more profound or "hyper-suppression" with exogenous testosterone, as you noted, making it harder to avoid dropping LH/FSH to subnormal or undetectable levels.

2. Why Low-Dose Titration Could Normalize Testosterone While Bringing LH/FSH to Normal (Not Below)

• The pituitary adjusts LH/FSH based on total serum testosterone, regardless of source (endogenous or exogenous). In primary hypogonadism, starting with very low exogenous doses (e.g., 25-50 mg/week of short-acting formulations like intranasal or low-dose gels) and slowly increasing allows incremental rises in serum testosterone. This provides partial negative feedback, gradually reducing the hyper-elevated LH/FSH without overwhelming the system.
  • For example: Baseline in primary might be testosterone ~200 ng/dL with LH ~15 IU/L and FSH ~20 IU/L. A small exogenous dose raises testosterone to ~300-400 ng/dL, which the pituitary senses as "less deficient," dialing down LH/FSH to ~8-12 IU/L (still above subnormal but lower than baseline).
  • Continued slow titration (e.g., over weeks/months, monitoring levels) could reach normal testosterone (500 ng/dL) while LH/FSH settle at eugonadal ranges (3-7 IU/L), as the feedback loop equilibrates to mimic a healthy state. This avoids supraphysiological peaks that drive LH/FSH to <1 IU/L (common with higher or fluctuating doses).
• Evidence from suppression variability supports this: Studies show gonadotropin suppression is dose- and formulation-dependent, not all-or-nothing. Short-acting TRT (e.g., intranasal) reduces LH/FSH by only 37-47% on average, compared to 59-86% with longer-acting injectables or gels. From a high primary baseline, a 40% reduction could land in the normal range, whereas the same in secondary (from already low baseline) pushes to undetectable. Clinical data also indicate LH suppression is "variable" across patients, with not all reaching <1 IU/L even on standard TRT. This variability likely reflects individual HPTA sensitivity, supporting titration to a "sweet spot" in primary cases.

3. Role of Heightened Gonadotropin Sensitivity in Primary Hypogonadism

• The referenced observation—that increases in LH/FSH are more sensitive to decreases in testosterone delivery (e.g., following implant extrusion or dose reduction)—highlights the robust responsiveness of the intact axis in primary hypogonadism. When exogenous testosterone is reduced or removed, LH/FSH "bounce back" rapidly and strongly because the pituitary isn't pathologically impaired; it's been in overdrive mode and quickly resumes compensation for any perceived deficiency.
• This sensitivity works in reverse for suppression: Small exogenous testosterone increments can elicit proportionally larger LH/FSH decreases from their elevated baseline, allowing normalization without needing full replacement doses that cause over-suppression. In contrast, secondary hypogonadism's "hypersensitivity" (as you phrased it) means even low exogenous doses can trigger rapid, deeper suppression due to the dysfunctional axis, which struggles to modulate or rebound.
• Avoiding "hyper-suppression": Traditional TRT often uses doses that achieve upper-normal testosterone (for symptom relief), leading to unnecessary HPTA shutdown, testicular atrophy (from lost LH stimulation), and infertility (from FSH drop). Low-dose titration sidesteps this by maintaining partial axis activity—enough LH/FSH to prevent full atrophy while normalizing testosterone—especially if residual testicular function exists (common in milder primary cases).

4. Why This Avoids Issues Like Atrophy, Infertility, and Hormonal Disruption

• Testicular atrophy and infertility: Full HPTA suppression removes LH/FSH drive, shrinking testes and halting spermatogenesis (often to azoospermia). Keeping LH/FSH in normal ranges preserves some intratesticular testosterone and sperm production, mitigating these risks. In primary, where testes are already compromised but the axis is intact, this partial stimulation could maintain baseline fertility potential better than high-dose TRT.
• Broader hormonal disruption: Over-suppression can exacerbate estrogen imbalances, mood issues, or bone density loss tied to extreme gonadotropin lows. Titration to normal LH/FSH maintains a more physiological balance, reducing these.
• In secondary, low doses often fail because the impaired axis suppresses quickly, requiring alternatives like hCG (which mimics LH but is less effective in primary due to testicular non-responsiveness).

5. Caveats and Why It's Not "Standard" Yet

• This relies on precise monitoring (frequent bloodwork for testosterone, LH/FSH) and patient-specific factors like residual testicular function or axis sensitivity. Short-acting formulations minimize fluctuations, supporting less suppression. However, if doses are too low, symptoms persist; too high, suppression ensues.
• Literature gaps: Most studies report aggregate data on mixed hypogonadism types, focusing on symptom relief rather than gonadotropin optimization. Primary-specific trials are rare, and suppression is often described as "expected" without nuance for low-dose approaches. Unpublished case studies, as you mention, may demonstrate this anecdotally (e.g., in clinical practice with careful titration), but peer-reviewed evidence is emerging slowly, likely due to fertility not being a priority in primary hypogonadism guidelines.

In summary, the premise holds logically because primary hypogonadism's intact, sensitive HPTA allows low-dose exogenous testosterone to provide just enough feedback to normalize levels without the full shutdown seen in higher doses or secondary cases. This preserves axis function, avoiding unnecessary complications. Always consult an endocrinologist for tailored implementation, as individual responses vary.

 

[Cataceous]

...
However, this doesn't mean the testosterone is "additive" in a simple sense. You're still suppressing whatever marginal endogenous production exists, even if it's minimal.
...

I was defining suppression as being below normal baseline levels. It's just semantics. If you want to say that hyper LH/FSH levels are being suppressed back to normal that's fine. But while that's happening serum testosterone is rising to normal levels—before suppression of endogenous testosterone production becomes significant, which means the exogenous testosterone is effectively adding to endogenous levels. The treatment is viable and preferred to the risks in traditional TRT with its complete HPTA suppression.

There are already individuals out there who are doing this successfully. It should be the first approach for treating primary hypogonadism.

 

[Nelson Vergel]

There are already individuals out there who are doing this successfully. It should be the first approach for treating primary hypogonadism.

I do not know anyone using low dose long acting T formulations like testosterone enanthate or cypionate successfully to improve QOL and retain fertility. Not one in over 30 years.

 

[Cataceous]

I do not know anyone using low dose long acting T formulations like testosterone enanthate or cypionate successfully to improve QOL and retain fertility. Not one in over 30 years.

There were two guys with primary hypogonadism on the old PeakTestosterone forum using this kind of treatment. I thought I might have discussed it with a different guy here as well. Consider the relative rarity of guys with primary hypogonadism—I recall Dr. Saya commenting on how infrequent these cases are relative to secondary. So given this dearth of cases and the lack of widespread knowledge about this kind of treatment, I am not surprised that it has not been on your radar. I have been promoting these ideas whenever one of these opportunities comes up.

 

[EVERYBODY_RUN]

Maybe this is a stupid question, but have you been checked for varicocele? Don't want to blast a bunch of medical jargon on my first post, but there have been a number of cases in which varicocele induced hypogonadism & issues with fertility due to impaired leydig cell function. Also if the case is that you're primary & wanting to have children at some point, I would think the first order of business would be to salvage and store as many healthy sperm as you can. After that, just moving to a trt protocol that would effectively manage your symptoms without having to jump through experimental hoops.

 

[FunkOdyssey]

He should probably try a short acting formulation like Natesto or oral testosterone undecanoate.

Oral testosterone would be my vote for this guy. Equalized for a target LH / FSH level, you'll be able to hit high peak levels with oral testosterone, whereas your non-fully-suppressive dose of injections will probably produce peak levels that are on the low side of the normal range.

Either option would be better than where you sit now though. Definitely do something.

 

[PrimaryHypogonadismHell]

Maybe this is a stupid question, but have you been checked for varicocele? Don't want to blast a bunch of medical jargon on my first post, but there have been a number of cases in which varicocele induced hypogonadism & issues with fertility due to impaired leydig cell function. Also if the case is that you're primary & wanting to have children at some point, I would think the first order of business would be to salvage and store as many healthy sperm as you can. After that, just moving to a trt protocol that would effectively manage your symptoms without having to jump through experimental hoops.

Hello, yes i have varicocele. No i did not treat them as treating them often does not improve fertility

I will also never let a surgeon touch me unless my life is at stake. Surgeons destroy too much lives. I know too much people whi got their lives destroyed by surgeons

 

[Cataceous]

Oral testosterone would be my vote for this guy. Equalized for a target LH / FSH level, you'll be able to hit high peak levels with oral testosterone, whereas your non-fully-suppressive dose of injections will probably produce peak levels that are on the low side of the normal range.

Either option would be better than where you sit now though. Definitely do something.

Though I can't be definitive, I suspect low and steady exogenous testosterone may provide better results in these cases. The idea is to provide a fixed base level of testosterone and then let the HPTA do the fine-tuning. Faster-acting testosterone such as oral or nasal products produce high peaks that get into suppressive territory. This is tolerable when treating secondary hypogonadism because of the relatively short duration of the peaks. But with primary it seems unnecessary to interfere with the functional hypothalamic-pituitary part of the axis when you can instead just fill in for the testicular insufficiency.

It may also depend on the severity of the testicular insufficiency. If there's little endogenous production left to work with then it's plausible that the benefits of higher testosterone peaks could outweigh a reduction is the more limited endogenous fine-tuning.

 

[madman]

Though I can't be definitive, I suspect low and steady exogenous testosterone may provide better results in these cases. The idea is to provide a fixed base level of testosterone and then let the HPTA do the fine-tuning. Faster-acting testosterone such as oral or nasal products produce high peaks that get into suppressive territory. This is tolerable when treating secondary hypogonadism because of the relatively short duration of the peaks. But with primary it seems unnecessary to interfere with the functional hypothalamic-pituitary part of the axis when you can instead just fill in for the testicular insufficiency.

It may also depend on the severity of the testicular insufficiency. If there's little endogenous production left to work with then it's plausible that the benefits of higher testosterone peaks could outweigh a reduction is the more limited endogenous fine-tuning.

Some important points to keep in mind here!


* Patients with residual testosterone production may not require a full maintenance dose, e.g. Klinefelter patients in an early phase of testosterone deficiency.


* However, in the most frequent form of primary hypogonadism, i.e. in patients with Klinefelter syndrome, LH and FSH often do not show significant suppression during testosterone substitution. Moreover, oral or transdermal testosterone may have only little effect on gonadotropins. Therefore LH is not a good indicator of sufficient TRT.

Clinical use of testosterone in hypogonadism and other conditions (Chapter 14) - Testosterone

Testosterone - July 2012

www.cambridge.org

Clinical use of testosterone in hypogonadism and other conditions (2012)
Eberhard Nieschlag and Hermann M. Behre


Patients with residual testosterone production may not require a full maintenance dose, e.g. Klinefelter patients in an early phase of testosterone deficiency. In these cases injection intervals of testosterone esters may be extended; these cases may also be suited for low-dose testosterone undecanoate therapy (i.e. 40 mg once or twice daily) or intermittent transdermal treatment (e.g. every second or third day).This dose does not entirely suppress the residual endogenous testosterone production and supplements the lacking hormone.



14.1.3.8 Gonadotropins

The determination of LH and FSH plays a key role in establishing the diagnosis of hypogonadotropic (i.e. secondary) or hypergonadotropic (i.e. primary) hypogonadism. However, during surveillance of testosterone therapy they are of less importance. Negative-feedback regulation between hypothalamus, pituitaryand testes causes negative correlation between serum testosterone and LH, as well as to some extent to FSH levels in normal men.

In cases with primary hypogonadism (e.g. intact hypothalamic and pituitary function), FSH and in
particular LH increase with decreasing testosterone levels and may normalize under testosterone treatment. This is especially the case in patients with acquired anorchia (e.g. due to accidents or iatrogenic castration). However, in the most frequent form of primary hypogonadism, i.e. in patients with Klinefelter syndrome, LH and FSH often do not show significant suppression during testosterone substitution. Moreover, oral or transdermal testosterone may have only little effect on gonadotropins. Therefore LH is not a good indicator of sufficient TRT.

 

[Guided_by_Voices]

As with so many things, the answer seems to be to experiment and see what happens, using the least invasive, lowest risk approach first. It would seem that if total shutdown can be avoided then that would have the least chance of side effects and if it doesn't work, then more T can always be added.