#1

As an M.D. and Ph.D., I realized my lab results were alarming. Other patients might not

Last year, I joined the millions of American men now on testosterone therapy — a treatment whose use has quietly tripled over the past two decades, often at doses far above Endocrine Society guidelines.

Within weeks, I felt younger, stronger, and sharper. But within months, I was at serious risk of right-heart failure.

I didn’t come to testosterone casually. In 2022, I had surgery for chronic thromboembolic pulmonary hypertension — six hours on the table with my body cold and bloodless. Afterward, my oxygen saturations crept up from a pre-op 83% to about 94%-95%, which is close to normal, but my energy lagged. I’d seen so many men my age look younger, move better, and swear they “felt like themselves again” after starting testosterone. I wanted in.

The first clinic I visited promised to raise my testosterone from its very low 100 ng/dL to 1,200 — well above the normal range of 300-800 for healthy men, and far above the approximately 400-500 that’s typical for men my age. I passed.

Instead, I found an online provider who, after a brief video consult, prescribed 26 milligrams of testosterone daily. For context, the human body naturally produces the equivalent of about 4-7 mg per day. The Endocrine Society generally recommends replacement doses of 75-100 mg weekly for injections — not 182 mg weekly, which is what I was on.

With an M.D. and Ph.D. to my name, I thought I was pretty smart. I typically do literature searches for my patients. But I didn’t catch the magnitude of that difference right away.

…

But four months in, the warning signs appeared. My hematocrit, already slightly elevated at 48% post-lung surgery, shot up to 59.8%. Blood that thick strains the heart, especially the right side, which pumps through the lungs’ fragile vessels. Above 54%, pulmonary vascular resistance doesn’t just increase — it spikes. I’d been in right-heart failure three years earlier. I knew what that road looked like.

Read the full story: Testosterone made me feel 30 again — until it nearly broke my heart (Stat)

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#2

I think this pushes me into the ‘Ill accept my current testosterone levels’ camp.

I feel great enough as it is from all the other meds/supplements.

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#3

This seems a bit like unnecessary fear mongering though. His dose was evidently way too high for him, and yes of course you should monitor your HCT if you’re on TRT and stop or reduce the dose if it gets anywhere near that high

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#4

Kinda a silly article IMO. His HCT shot up because he was on too high a dose. Then he just quit, when there was a reasonable middle ground of just lowering the dose and dealing with the HCT by other means (such as blood donations, if needed)

Also, this part is also very silly. You will not see any differences 1 single day after injection. That’s just placebo effects.

After a month off, I had an important event coming up. I injected about a third of my old daily dose the day before. The next morning, I looked in the mirror and saw a confident, healthy-looking man. The day before, the reflection had been a pale, skinny version of my high-school self.

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#5

Not to mention this guy doesn’t seem to be all there. Who, much less a physician, is so sloppy and careless that they just inject stuff willy nilly without carefully checking the dose and doing considerable research… the average gym bro takes more care than this histrionic drama yama.

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#6

Perhaps… But I suspect most biohackers are not any more rigorous in their tracking of HCT numbers over months, and dosing levels vs baseline normal levels than this MD/PHD who works in medicine.

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#7

I always get HCT as part of the bloods.

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#8

182mg per week is not that high of a dose. 75mg would be too low and defeat the purpose of taking it to begin with. 100mg is the minimum dose anyone should be on but I still think that’s too low for most. It’s not a one size fits all approach but 150mg is usually a good sweet spot for a lot of people.

I’ve seen bodybuilders taking over 1000 mg a week with normal hematocrits. Yes, one gram, and it’s VERY common. I’ve seen a lot of lab work and discuss this with physicians who specialize in TRT.

I have a high hematocrit too and even when I lower the dose, it barely goes down at all. I’d like to know how hydrated he was before his lab draw and what other genetic factors came into play for him (Factor V and Jak2 should be mandatory to test before putting someone on TRT but no one does it). I have seen hematocrit drop by 6% in 24 hours just by being hydrated enough.

There are just too many variables. We don’t know how to draw a conclusions based on this one anecdote.

Also, I adamantly believe that a high hematocrit without high platelets and high blood pressure is not a big risk factor for anything. There is only one study showing a slight short term increased risk of MACE among TRT users with hematocrits above 52% (5.15% increase compared to 3.87% in normal hematocrit people). The study makes no mention of their genetic clotting risk factors or platelets though, which is very important information. Secondary Polycythemia in Men Receiving Testosterone Therapy Increases Risk of Major Adverse Cardiovascular Events and Venous Thromboembolism in the First Year of Therapy - PubMed

I know multiple guys walking around with 60% hematocrits for years and years with absolutely no problems and everything else is healthy, and I’m talking about bodybuilders, not people living in the Andes who all have hematocrits of 60% with no issues (some even with 70% in the highest altitude of Peru whose blood was LESS likely to clot).

If platelets are high, then it’s really time to worry. Testosterone does not increase platelets though.

As far as I’m concerned, this story is no better than Bryan Johnson’s reasons for stopping Rapamycin. A 10% increase in hematocrit after going on TRT is incredibly rare.

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#9

Do you know the SNPs associated with Jak2 and Factor V?

#10

I’m not sure. You can add those to your next blood draw though to see whether you’re positive or negative.

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#11

Factor V (F5)
• Factor V Leiden (R506Q): F5 rs6025 (c.1601G>A; p.Arg534Gln). Heterozygosity raises venous thromboembolism (VTE) risk; homozygosity raises it substantially. This is the Factor V variant clinicians test for inherited thrombophilia.

https://www.snpedia.com/index.php/Rs6025

JAK2
• JAK2 V617F: rs77375493 (c.1849G>T; p.Val617Phe). A somatic (acquired) mutation that essentially defines most polycythemia vera (PV) and many related MPNs; PV is a classic cause of high hematocrit. If TRT is followed by unexpected erythrocytosis, testing for V617F (and EPO level, ± JAK2 exon 12 panel if V617F–) helps distinguish secondary erythrocytosis from PV.

https://www.snpedia.com/index.php/Rs77375493

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#12

I think he mentioned heart failure though and not MACE.

#13

Testosterone-induced erythrocytosis does not equal polycythemia!!! Totally different conditions and very commonly conflated unfortunately. People living in Denver etc with high hemoglobin/crit from the reduced oxygen partial pressure don’t see an increase in risk - different cause but same end result of increased RBC production by the marrow. Polycythemia is spontaneously-occurring (not caused by testosterone) and causes increased clot risk due to the increase in platelets

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#14

I’m not a doctor, just an interested reader. I’m not familiar with testosterone-induced erythrocytosis. Would you agree with this ChatGPT summary?

Testosterone-induced erythrocytosis refers to the abnormal increase in red blood cell (RBC) mass and hematocrit that can occur in men receiving testosterone therapy. It is the most common dose-limiting side effect of testosterone replacement, particularly with certain formulations.

Mechanism

  • Androgen receptor stimulation in bone marrow directly promotes erythropoiesis.
  • Increased erythropoietin production (via renal stimulation).
  • Suppression of hepcidin (the master regulator of iron metabolism), leading to increased iron availability for RBC production.
  • Enhanced sensitivity of progenitor cells in bone marrow to erythropoietin.

Risk Factors

  • Testosterone formulation: Short-acting intramuscular injections (e.g., testosterone cypionate/enanthate) produce supraphysiologic peaks and are most strongly associated. Transdermal gels/patches and long-acting injectables have lower risk.
  • Dose: Higher testosterone doses correlate with higher risk.
  • 年龄: Older men are more susceptible.
  • Baseline hematocrit: Elevated or high-normal levels before therapy predispose to erythrocytosis.
  • Comorbidities: Hypoxia (sleep apnea, COPD, smoking, high altitude residence) increases risk.

Incidence

  • Reported rates vary 5–66%, depending on formulation and monitoring.
  • Intramuscular injections: highest (up to 40%+ in some series).
  • Transdermal: ~5–15%.
  • Oral undecanoate: intermediate.

Clinical Concerns

  • Erythrocytosis raises blood viscosity, which may increase risk of thrombosis, stroke, myocardial infarction, and venous thromboembolism, although the exact risk magnitude is debated.
  • Symptomatically, patients may develop headaches, dizziness, flushing, pruritus, or visual disturbances—but many remain asymptomatic until hematocrit is markedly high.

Monitoring & Thresholds

  • Guidelines (Endocrine Society, AUA):

    • Check hematocrit before starting, then at 3–6 months, and at least annually.
    • Hematocrit >54% → therapy should be reduced, paused, or discontinued.
    • Hematocrit >50–52% → many clinicians begin dose adjustments or closer monitoring.

Management

  1. Adjust testosterone regimen:

    • Lower dose.
    • Switch to a formulation with more stable serum levels (e.g., gel, patch, long-acting undecanoate).
    • Extend injection interval.

  2. Therapeutic phlebotomy: Used when hematocrit remains high despite dose changes.

  3. Address comorbidities: Treat sleep apnea, stop smoking, reduce alcohol, evaluate for other causes of secondary polycythemia.

  4. Temporary discontinuation: If hematocrit remains above thresholds despite intervention.

:white_check_mark: Summary: Testosterone-induced erythrocytosis is a predictable, dose-dependent effect of androgen therapy, especially with injectable formulations. It requires regular monitoring of hematocrit, and management includes dose modification, formulation change, or phlebotomy to minimize thrombotic risk.

Full Testosterone Guidelines: Testosterone Deficiency Guideline - American Urological Association

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#15

This part is barbaric. The fact the guidelines still say in the year 2025 say you need to discontinue TRT once the hematocrit % reaches the magic number of 54% is a disastrous medical practice, especially since it’s more than likely because the doctor didn’t tell the patient that he needed to drink water before the blood draw.

Now men who feel great all of a sudden will go back to feeling like crap because of a little to no risk number.

This is why it’s a good thing more advanced TRT clinics exist who are staunch advocates against this heinous practice of taking men off TRT when hematocrit hits a certain %. The guidelines not only do this, but they tell men to use the ridiculously long syringes instead of insulin syringes to inject, and they still tell patients that they can inject once every two weeks. It’s a complete disaster.

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#16

I asked Google “Is heart failure one of the elements of MACE in cardiology”. Here is part of the answer I got.

Yes, heart failure is often included as one of the elements of Major Adverse Cardiovascular Events (MACE) in cardiology. The exact components of MACE can vary between different clinical studies, but heart failure is a common and serious outcome frequently monitored.

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#17

We should generally prefer to understand clinically meaningful health outcomes rather than surrogate markers such as bloodwork.

Here we have an explanation of a syndrome defined by the surrogate marker hematocrit. The clinical concerns section of the AI description says “Erythrocytosis […] may increase the risk of [important health outcomes we actually care about], although the exact risk magnitude is debated.”

We really need a more robust understanding of the relationship between increased hematocrit levels associated with exogenous testosterone supplementation and poor health outcomes.

If the increase risk is low enough, and there are enough other benefits of using testosterone, it may be wise to continue its use. If the risks are high enough and the benefits low enough, discontinuation or dose reduction would be indicated.

It is not clear to me that we have the answers to these questions yet…

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#18

Indirectly, you remind me of a study I shared on X, as the majority of studies focus on total testosterone due practicality and influencers replicate that. If it helps some reader here: while useful, TOTAL testosterone can be misleading in conditions altering SHBG, including obesity and diabetes, where FREE testosterone better correlates with muscle status, physical performance, or sexual symptoms. Saying that, Qin et al. (2025) highlight SHBG as a novel, sex-consistent low muscle mass (LMM) risk factor and underscores sex-specific hormone roles, informing endocrine-targeted sarcopenia prevention: https://onlinelibrary.wiley.com/doi/pdf/10.1002/jcsm.70056

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#19

Yea, it’s a pity there are providers who treat secondary erythrocytosis from TRT the same way they treat people with polycythemia vera, a rare and dangerous blood marrow disease. They sure as heck aren’t telling people living at high altitude to donate blood every month and give them an iron deficiency for no reason. It’s starting to get better but it’s going to take a while before it becomes universally accepted.

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#20

In general it annoys me that our current medical practice waits for signs of disease to react. I like the idea of treating the underlying causes of progression toward disease to prevent or delay its occurrence.

However, I think it is challenging to put that into practice when individual mechanisms do not always map cleanly. This hematocrit discussion is one such example.

I have been following along with interest. My hematocrit is on the high end of the range. My platelets, however, run at the very bottom end of the range and sometimes even dip below it. It have checked with my siblings and two of them report the same phenomenon—so it’s clearly genetic.

But I have never had an issue with bleeding, wound healing, etc. I never would have had an inkling anything was going on with respect to high hematocrit or low platelets outside of blood tests.

Does that mean these (and countless other unobserved) factors are in balance in my body? I have to concede this particular situation to the wait-until-disease camp pending a more sophisticated model linking these disparate elements.

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