Testosterone Replacement Therapy and Secondary Polycythemia: Does a Rising Hematocrit Increase Cardiovascular and Blood Clot Risk?

Testosterone replacement therapy (TRT) can dramatically improve quality of life in appropriately selected men with testosterone deficiency. Improvements in energy, libido, sexual function, muscle mass, body composition, bone density, mood, and overall well-being can make testosterone an important therapy for men with clinically significant hypogonadism.

Testosterone also has a predictable effect that deserves considerably more attention: it stimulates the production of red blood cells.

For many men, this is not a problem. Hemoglobin and hematocrit may increase modestly while remaining within an acceptable range. In other patients, however, hematocrit continues climbing and eventually produces what is commonly called testosterone-induced erythrocytosis or secondary polycythemia.

For years, one of the major questions surrounding TRT has been whether this increase in hematocrit actually matters.

Does testosterone itself increase cardiovascular risk?

Does a higher hematocrit increase the risk of heart attack, stroke, or blood clots?

Or are these two separate questions that should not be confused?

Increasingly, the evidence suggests that the distinction matters.

The landmark TRAVERSE randomized controlled trial provided considerable reassurance regarding testosterone and major cardiovascular events overall. In men with hypogonadism who had established cardiovascular disease or substantial cardiovascular risk, appropriately monitored transdermal testosterone was noninferior to placebo for major adverse cardiovascular events (MACE).

That is important.

However, observational studies that specifically separate men who develop secondary polycythemia from men who do not tell a more nuanced story. Men whose hematocrit rises substantially during testosterone therapy appear to have a higher risk of cardiovascular and venous thromboembolic events than men taking testosterone whose hematocrit remains controlled.

In other words:

The important question may not simply be whether a patient takes testosterone. The important question may be what happens to his hematocrit after he starts testosterone.

That distinction has major implications for how TRT should be prescribed and monitored.

What Is Hematocrit?

Hematocrit is the percentage of your blood volume that consists of red blood cells.

If your hematocrit is 45%, approximately 45% of your blood volume consists of red blood cells, while the remainder consists primarily of plasma along with white blood cells and platelets.

Red blood cells are essential. They contain hemoglobin, which transports oxygen from the lungs to tissues throughout the body.

A higher red blood cell count is not inherently harmful. In fact, testosterone therapy can correct anemia in men who begin treatment with low hemoglobin.

The concern arises when red blood cell production becomes excessive.

As hematocrit rises, the cellular concentration of blood increases. At sufficiently high levels, blood viscosity can increase and circulation through small blood vessels may become less efficient.

This is why hematocrit is one of the laboratory values that should be monitored during testosterone therapy.

Erythrocytosis vs. Polycythemia: Are They the Same Thing?

These terms are often used interchangeably in conversations about testosterone, although they are not technically identical.

Erythrocytosis means an increased red blood cell mass or concentration.

Polycythemia is often used clinically to describe an abnormally elevated hemoglobin or hematocrit, but the term can also refer to disorders involving increased blood cell production.

The distinction becomes particularly important when discussing polycythemia vera.

Polycythemia vera is a myeloproliferative blood disorder, usually associated with a JAK2 mutation, in which the bone marrow produces blood cells abnormally.

That is very different from what usually happens during TRT.

Testosterone-related erythrocytosis is generally considered a form of secondary erythrocytosis or secondary polycythemia because something outside the bone marrow—testosterone exposure—is stimulating red blood cell production.

A patient with an elevated hematocrit during TRT should therefore not automatically be assumed to have polycythemia vera.

At the same time, an elevated hematocrit should not automatically be blamed on testosterone without considering other causes.

Why Does Testosterone Increase Hematocrit?

Testosterone stimulates red blood cell production through several complementary mechanisms.

Testosterone Increases Erythropoietin Signaling

Erythropoietin, commonly called EPO, is a hormone produced primarily by the kidneys.

Its job is essentially to tell the bone marrow:

Produce more red blood cells.

Testosterone can increase erythropoietic signaling and alter the relationship between EPO and red blood cell production.

Testosterone Suppresses Hepcidin

Hepcidin is one of the body's major regulators of iron metabolism.

Higher hepcidin levels restrict iron absorption and reduce the release of stored iron. Lower hepcidin levels make more iron available.

Testosterone suppresses hepcidin.

That means more iron becomes available to the bone marrow for hemoglobin synthesis and red blood cell production.

This combination—greater erythropoietic signaling plus increased iron availability—helps explain why hematocrit frequently increases after testosterone therapy begins.

The response is dose- and concentration-dependent. The Endocrine Society notes that testosterone increases hemoglobin and hematocrit and that these effects are related to testosterone dose and circulating concentrations.

Why Some Men Develop High Hematocrit and Others Do Not

Two patients can receive testosterone and have very different hematocrit responses.

That variability is important.

Factors that can increase the likelihood or magnitude of erythrocytosis include:

• Higher testosterone doses
• Higher peak testosterone concentrations
• Injectable testosterone formulations
• Older age
• Obstructive sleep apnea
• Smoking
• Chronic lung disease
• Chronic hypoxia
• Living at higher altitude
• Dehydration or reduced plasma volume
• Individual differences in erythropoietic response

This is why a rising hematocrit should not simply trigger the instruction to "donate blood."

The better question is:

Why is this patient's hematocrit increasing?

Sometimes the testosterone protocol is the primary driver.

Sometimes testosterone is amplifying an underlying problem such as sleep apnea or hypoxia.

Frequently, several factors are working together.

Is Testosterone Replacement Therapy Cardiovascularly Dangerous?

This question has generated controversy for decades.

The strongest randomized evidence to date provides considerable reassurance.

What the TRAVERSE Trial Found

The TRAVERSE trial was specifically designed to examine cardiovascular safety.

Researchers enrolled 5,246 men between 45 and 80 years of age who had symptoms of hypogonadism, two fasting testosterone concentrations below 300 ng/dL, and either established cardiovascular disease or a high cardiovascular risk.

Participants received either transdermal 1.62% testosterone gel or placebo. Testosterone dosing was adjusted to maintain concentrations between 350 and 750 ng/dL.

The primary endpoint included:

• Cardiovascular death
• Nonfatal myocardial infarction
• Nonfatal stroke

The result was reassuring.

Major adverse cardiovascular events occurred in 7.0% of the testosterone group and 7.3% of the placebo group, producing a hazard ratio of 0.96 (95% CI 0.78–1.17).

Testosterone was therefore noninferior to placebo for the primary cardiovascular outcome.

That is powerful evidence against the simplistic claim that medically supervised testosterone therapy inherently causes heart attacks and strokes.

But it does not end the discussion.

Testosterone Therapy and Blood Clots: What Did TRAVERSE Show?

The venous thromboembolism findings deserve separate consideration.

Venous thromboembolism, or VTE, primarily includes:

• Deep venous thrombosis (DVT)
• Pulmonary embolism (PE)

In TRAVERSE, venous thromboembolic events occurred in:

Testosterone: 44 patients, or 1.7%

Placebo: 30 patients, or 1.2%

The hazard ratio was 1.46, with a 95% confidence interval of 0.92–2.32.

Because that confidence interval crossed 1.0, the result did not establish a statistically significant increase in overall VTE.

However, pulmonary embolism occurred in 24 testosterone-treated patients versus 12 placebo-treated patients, and the investigators reported a higher incidence of pulmonary embolism in the testosterone group.

That finding deserves attention without overstating what it proves.

TRAVERSE tells us that testosterone did not increase the trial's primary MACE endpoint.

It does not prove that every man receiving testosterone has identical thrombotic risk regardless of his hematocrit response.

That requires a different type of analysis.

The More Important Question: What Happens When Hematocrit Actually Rises?

This may be where the conversation becomes much more clinically useful.

Rather than comparing everyone taking testosterone with everyone not taking testosterone, researchers have asked:

Among men taking testosterone, do those who develop secondary polycythemia experience more cardiovascular and thromboembolic events than those whose hematocrit remains controlled?

The answer from observational evidence is concerning.

The 2022 Study That Changed the Conversation

A 2022 study published in The Journal of Urology examined a multi-institutional database containing approximately 74 million patients.

Researchers identified men with low testosterone who received testosterone therapy and divided them according to whether they developed secondary polycythemia.

For this study, polycythemia was defined as:

Hematocrit ≥52%.

After propensity matching, researchers compared 5,842 testosterone-treated men who developed polycythemia with 5,842 testosterone-treated men who did not.

During the first year of therapy, combined MACE/VTE occurred in:

Polycythemia group: 5.15%

Normal-hematocrit group: 3.87%

That corresponded to an odds ratio of 1.35 (95% CI 1.13–1.61).

Put into patient-friendly terms, the group that developed hematocrit of at least 52% experienced about a 35% higher relative odds of the combined cardiovascular or venous thromboembolic outcome during the first year.

The absolute difference was approximately 1.28 percentage points.

Both numbers matter.

Relative risk communicates the strength of the association. Absolute risk provides perspective regarding its magnitude.

Here Is the Particularly Interesting Part

The researchers performed another comparison.

They examined hypogonadal men without polycythemia and compared those who received testosterone with those who did not receive testosterone.

They did not identify an increased MACE/VTE risk associated with testosterone therapy in that comparison.

This observation raises an important possibility:

Testosterone exposure itself may not be the primary problem. Developing secondary polycythemia during testosterone therapy may identify the subgroup in whom risk increases.

That is not proof of causation.

The study was observational, not randomized according to hematocrit response. Men who develop erythrocytosis could differ from men who do not in other clinically meaningful ways.

Nevertheless, it is a signal that should not be dismissed.

A Second Study Strengthens the Association

A 2024 retrospective cohort analysis published in The Journal of Urology approached the question differently.

Rather than defining a single polycythemia threshold, investigators asked whether the change in hematocrit after starting testosterone predicted cardiovascular outcomes.

The study used the TriNetX Research Network and examined men who had hematocrit measurements before and after beginning testosterone therapy.

After matching, researchers compared 10,511 men whose hematocrit increased after starting testosterone with an equal number whose hematocrit did not increase.

Men who experienced an increase in hematocrit had a significantly greater risk of MACE, defined as myocardial infarction, stroke, or death, at follow-up.

This adds an important dimension to the discussion.

Risk may not depend exclusively on crossing a magical laboratory cutoff.

The trajectory of hematocrit may matter as well.

A man whose hematocrit increases substantially from his baseline may deserve closer attention even before reaching 54%.

Does This Prove That High Hematocrit Causes Heart Attacks and Blood Clots?

No.

And this distinction is important.

Observational studies can demonstrate an association, but they cannot definitively establish that testosterone-induced erythrocytosis directly caused each cardiovascular event.

There are several possible explanations.

Elevated hematocrit itself could contribute to risk.

Alternatively, patients who develop erythrocytosis may have underlying characteristics—such as sleep apnea, smoking, hypoxia, metabolic disease, or different testosterone exposure—that independently increase cardiovascular risk.

Both could also be true.

The 2026 New England Journal of Medicine review on sex hormones and thrombotic risk emphasizes that the effect of testosterone on VTE remains incompletely understood. Randomized trials have relatively few thromboembolic events, while observational studies have produced inconsistent estimates.

That uncertainty should lead to careful monitoring, not panic and not complacency.

Why Would High Hematocrit Increase Risk?

There is a plausible physiological explanation.

Red blood cells are essential, but increasing their concentration changes the physical characteristics of blood.

As hematocrit rises, blood viscosity increases.

Think of the difference between moving water through a narrow tube and moving a more concentrated fluid through the same tube. The analogy is imperfect, but it illustrates why excessive cellular concentration can alter flow.

Higher viscosity may influence:

• Microvascular blood flow
• Vascular resistance
• Platelet interactions
• Endothelial shear stress
• Thrombus formation

Testosterone's effects on coagulation and thrombosis are more complicated than hematocrit alone, which is another reason that we should avoid reducing the entire cardiovascular discussion to one laboratory number.

Still, hematocrit is both measurable and modifiable, making it an especially important safety marker.

What Hematocrit Is Too High on Testosterone?

This is where patients often expect a simple number.

Unfortunately, biology does not provide one.

The Endocrine Society explicitly notes that the hematocrit level at which neuro-occlusive or cardiovascular risk increases is not known.

That does not mean guidelines ignore hematocrit.

A commonly used intervention threshold is:

Hematocrit ≥54%

At that point, major guidelines generally recommend intervention rather than continued observation.

Options may include:

• Reducing the testosterone dose
• Temporarily holding therapy
• Changing testosterone formulation
• Investigating hypoxia and sleep apnea
• Using therapeutic phlebotomy when appropriate

However, the 2022 observational study identified increased risk beginning with its definition of secondary polycythemia at 52%, which raises a reasonable question about whether waiting for 54% in every patient is ideal.

A cutoff should therefore be viewed as an action threshold, not necessarily a line below which risk suddenly disappears.

What About a Hematocrit of 50%?

Context matters enormously.

A hematocrit of 50% in a patient whose baseline was 49% is different from a hematocrit of 50% in someone whose baseline was 42% three months earlier.

Likewise, 50% in a well-hydrated nonsmoker without sleep apnea may deserve different interpretation from 50% in someone who smokes and has untreated nocturnal hypoxia.

This is why good testosterone management requires looking at:

The number + the trend + the patient.

Baseline Hematocrit Matters

Hematocrit should be checked before testosterone therapy begins.

A patient who already has an elevated hematocrit needs evaluation before adding another strong erythropoietic stimulus.

Potential causes include:

• Obstructive sleep apnea
• Smoking
• Chronic pulmonary disease
• High-altitude exposure
• Dehydration
• Kidney disease or tumors producing EPO
• Other causes of secondary erythrocytosis
• Polycythemia vera or another hematologic disorder

Starting testosterone without understanding an unexplained elevated baseline hematocrit can compound the problem.

Monitoring Hematocrit During Testosterone Therapy

Hematocrit should not be something that gets checked once and forgotten.

The Endocrine Society recommends monitoring hematocrit during therapy, and the development of erythrocytosis warrants evaluation and treatment modification.

A practical framework includes checking a CBC:

• Before starting TRT
• During the first several months after initiation or significant dose changes
• Periodically once therapy and hematocrit have stabilized
• More frequently when hematocrit is trending upward

The first year deserves particular attention because observational evidence linking testosterone-induced polycythemia with MACE and VTE specifically identified excess events during this period.

Testosterone Formulation Matters

Not every testosterone delivery method produces the same pharmacokinetic profile.

Injectable testosterone cypionate and enanthate can create relatively high serum peaks, particularly when larger doses are administered at longer intervals.

Those peaks can strongly stimulate erythropoiesis.

Transdermal preparations generally create smoother testosterone exposure and have historically been associated with less erythrocytosis than short-acting injectable regimens.

This distinction is also relevant when interpreting TRAVERSE.

TRAVERSE studied transdermal testosterone gel, with doses adjusted to maintain testosterone between 350 and 750 ng/dL.

Its cardiovascular safety findings therefore should not automatically be extrapolated to every possible testosterone regimen, particularly protocols producing sustained supraphysiologic concentrations or extreme peaks.

More Testosterone Is Not Necessarily Better Testosterone Therapy

One of the easiest ways to create unnecessary erythrocytosis is to overtreat.

The goal of TRT should be to restore physiologic testosterone exposure and improve symptoms, not to produce the highest laboratory testosterone concentration possible.

When hematocrit begins climbing, clinicians should reconsider:

• Total weekly dose
• Peak testosterone exposure
• Injection frequency
• Route of administration
• Actual clinical need for the current dose

Sometimes a relatively modest dose reduction substantially improves hematocrit without sacrificing the benefits of therapy.

Do Not Miss Sleep Apnea

Obstructive sleep apnea deserves special emphasis because it can independently stimulate erythropoiesis through intermittent hypoxia.

Now add testosterone.

The patient has two signals encouraging red blood cell production:

Hypoxia + testosterone.

That combination can produce a much greater hematocrit response than testosterone alone.

Patients with unexplained or disproportionate erythrocytosis should therefore be evaluated for symptoms such as:

• Loud snoring
• Witnessed apnea
• Morning headaches
• Daytime sleepiness
• Resistant hypertension
• Nocturnal oxygen desaturation

Correcting the oxygen problem addresses the physiology rather than repeatedly removing blood.

Smoking, Vaping, and Lung Disease Also Matter

Anything that chronically reduces oxygen delivery can encourage erythropoiesis.

That includes:

• Cigarette smoking
• Some forms of vaping exposure
• COPD
• Restrictive lung disease
• Chronic hypoxemia

A rising hematocrit should therefore prompt a broader medical assessment rather than an automatic assumption that testosterone is the only cause.

Could Dehydration Make Hematocrit Look High?

Absolutely.

Hematocrit is a concentration.

When plasma volume falls, the percentage of blood represented by red cells can increase even if total red blood cell mass has not changed substantially.

Potential contributors include:

• Dehydration
• Heavy sweating
• Diuretics
• Acute illness
• Excessive alcohol consumption
• Poor fluid intake

An unexpected CBC should sometimes simply be repeated when the patient is normally hydrated before major treatment decisions are made.

What Should Be Done When Hematocrit Starts Rising?

The best strategy is usually to identify and correct the drivers rather than automatically prescribing repeated phlebotomy.

A rational approach may include:

1. Confirm the elevation. Repeat the CBC when appropriate and make sure the patient is adequately hydrated.
2. Review the testosterone regimen. Look at dose, route, injection frequency, peak exposure, and actual testosterone concentrations.
3. Evaluate oxygenation. Screen for obstructive sleep apnea, smoking, pulmonary disease, and other causes of hypoxia.
4. Reduce excessive testosterone exposure. A modest dose adjustment may be sufficient.
5. Consider changing delivery. Smoother testosterone exposure may reduce erythropoietic stimulation.
6. Investigate unexplained or persistent erythrocytosis. Not every elevated hematocrit in a testosterone-treated patient is caused by testosterone.
7. Use phlebotomy selectively. Therapeutic phlebotomy can rapidly lower hematocrit when necessary, but it should not automatically replace correction of the underlying driver.

Why Routine Phlebotomy Should Not Be the Entire Strategy

Phlebotomy works.

Removing red blood cells lowers hematocrit.

But that does not necessarily mean scheduled blood removal is the ideal long-term solution for every patient.

Repeated phlebotomy can reduce iron stores and eventually produce iron deficiency, which may contribute to:

• Fatigue
• Reduced exercise tolerance
• Restless legs
• Impaired cognition
• Microcytosis

If a patient repeatedly requires blood removal because the testosterone regimen repeatedly drives hematocrit back upward, it is reasonable to ask whether the treatment protocol itself should be changed.

Phlebotomy can be an important tool.

It should not become a substitute for thoughtful TRT management.

Does Aspirin Fix the Problem?

No.

Aspirin does not lower hematocrit.

It inhibits platelet aggregation, which is an entirely different process.

There is not sufficient evidence to recommend aspirin simply because a patient on testosterone develops erythrocytosis. Aspirin also carries real risks, particularly gastrointestinal and other bleeding.

The decision to use aspirin should therefore be based on the patient's broader cardiovascular indications and risk-benefit profile rather than as a substitute for correcting elevated hematocrit.

What About Blood Clotting Disorders?

Hematocrit is not the only determinant of thrombosis.

Patients with underlying thrombophilia may have additional risk.

Examples include:

• Factor V Leiden
• Prothrombin gene mutation
• Antiphospholipid syndrome
• Previous unprovoked DVT or pulmonary embolism
• Strong family history of venous thrombosis

The 2026 New England Journal of Medicine review emphasizes that hormone-associated thrombosis must be considered within the broader context of formulation, previous thrombosis, thrombophilia, and individual clinical risk factors.

A history of thrombosis deserves individualized consideration rather than reliance on hematocrit alone.

How Should We Reconcile Apparently Conflicting Testosterone Studies?

This is perhaps the most important lesson.

The studies may not actually conflict as much as they initially appear to.

TRAVERSE asked:

Does appropriately managed testosterone gel increase overall MACE compared with placebo in men with hypogonadism and cardiovascular risk?

Its answer was essentially no.

The Ory study asked:

Among men receiving testosterone, do those who develop hematocrit ≥52% experience more MACE/VTE than those who do not?

Its answer was yes, there was a significant association.

The Kohn study asked:

Does a rise in hematocrit after starting testosterone identify men with greater subsequent MACE risk?

Again, the answer was yes, an association was observed.

Those findings can coexist.

Testosterone therapy may be cardiovascularly acceptable overall while poorly controlled erythrocytosis identifies a subgroup with greater risk.

That is a much more useful interpretation than either extreme:

"Testosterone causes heart attacks."

or

"Testosterone is completely cardiovascularly risk-free."

Neither statement adequately reflects the evidence.

Association Does Not Equal Causation—but It Still Matters Clinically

We should be careful with language.

Current observational evidence does not prove that lowering a testosterone-treated patient's hematocrit from 52% to 49% will necessarily reduce his cardiovascular risk by a specific percentage.

We do not yet have a randomized trial assigning men with testosterone-induced erythrocytosis to different hematocrit targets and measuring subsequent MACE and VTE.

That trial would provide much stronger causal evidence.

Until then, we have several pieces of information:

• Testosterone predictably increases hematocrit.
• The response is dose- and concentration-related.
• Randomized evidence does not show an overall increase in MACE with appropriately managed transdermal TRT.
• Observational evidence associates testosterone-induced hematocrit ≥52% with increased first-year MACE/VTE.
• Additional observational evidence associates rising hematocrit after TRT initiation with greater MACE risk.
• The exact hematocrit at which cardiovascular risk begins to rise remains uncertain.

That is enough evidence to take hematocrit seriously.

It is not enough evidence to frighten every patient away from testosterone.

What Patients Should Understand About Secondary Polycythemia

The practical message is actually reassuring.

Developing secondary polycythemia does not necessarily mean testosterone therapy must permanently stop.

It means the treatment deserves attention.

In many cases, hematocrit can be controlled by addressing:

• Testosterone dose
• Testosterone peaks
• Route of administration
• Injection schedule
• Sleep apnea
• Smoking
• Hypoxia
• Hydration
• Other secondary causes

The goal is not merely to produce a desirable testosterone laboratory result.

The goal is to achieve the benefits of hormone replacement while maintaining physiologic and cardiovascular safety.

The Bigger Lesson: TRT Safety Is About How Testosterone Is Managed

The cardiovascular debate around testosterone has historically focused on a binary question:

Is testosterone safe or dangerous?

That question is too simplistic.

A better question is:

How do we deliver testosterone in a way that restores normal physiology while minimizing preventable adverse effects?

Hematocrit provides an excellent example.

A man taking a physiologic testosterone dose with stable blood pressure, appropriate testosterone concentrations, normal oxygenation, and hematocrit of 46% is not physiologically equivalent to a man receiving large injectable doses who repeatedly reaches hematocrit of 55%.

Both are technically "on testosterone."

Their treatment protocols and risk profiles may be very different.

The Bottom Line

Testosterone replacement therapy does not appear to increase overall major cardiovascular events when appropriately prescribed and monitored, based on the best randomized evidence currently available.

The TRAVERSE trial found virtually identical primary MACE rates between testosterone and placebo: 7.0% versus 7.3%, respectively.

But that is not the end of the story.

Men who develop significant secondary polycythemia during testosterone therapy appear to represent an important subgroup.

In a large observational study, men who reached hematocrit ≥52% while taking testosterone had a 5.15% first-year incidence of MACE/VTE compared with 3.87% among testosterone-treated men without polycythemia.

A second large observational analysis found that increases in hematocrit after testosterone initiation were associated with greater subsequent MACE risk.

These studies do not prove that erythrocytosis directly causes cardiovascular events. The precise hematocrit threshold at which risk increases also remains uncertain.

But they give us a clinically important message:

Hematocrit should not be treated as an irrelevant laboratory side effect of testosterone therapy.

Nor should an elevated hematocrit automatically mean abandoning TRT.

It should prompt clinicians to investigate why it is happening and correct the modifiable drivers.

Monitor the CBC.

Watch the trend.

Use physiologic testosterone dosing.

Avoid unnecessary peaks.

Look for sleep apnea and hypoxia.

Investigate unexpected elevations.

Intervene when hematocrit becomes excessive.

The emerging evidence supports a more sophisticated view of testosterone safety:

Testosterone itself may not be the cardiovascular problem for most appropriately treated men. How an individual patient's physiology responds to testosterone—including his hematocrit response—may matter considerably more.

Scientific References

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3. Kohn TP, Agrawal P, Ory J, Hare JM, Ramasamy R. Rises in Hematocrit Are Associated With an Increased Risk of Major Adverse Cardiovascular Events in Men Starting Testosterone Therapy: A Retrospective Cohort Claims Database Analysis. J Urol. 2024;211(2):285-293. doi:10.1097/JU.0000000000003786.
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