How to Lower Red Blood Cell Count on Steroids

Testosterone and other anabolic steroids reliably push red blood cell (RBC) counts upward, and the most effective way to bring those numbers back down involves a combination of strategies rather than a single fix. Adjusting the dose or delivery method, therapeutic phlebotomy, staying well hydrated, and treating conditions like sleep apnea that compound the problem can all help. The specifics matter, though, because the mechanisms behind steroid-driven RBC production go deeper than most people realize, and some popular internet remedies have weaker evidence than others.

Why Steroids Raise Red Blood Cell Count

Testosterone stimulates red blood cell production through at least two pathways working in tandem. First, it boosts erythropoietin (EPO), the hormone your kidneys release to signal your bone marrow to make more red blood cells. Second, it suppresses hepcidin, a liver protein that acts as the gatekeeper for iron absorption. When hepcidin drops, more iron becomes available for building hemoglobin, the oxygen-carrying molecule packed inside every red blood cell. Research in men given testosterone showed a roughly 7–10% increase in hemoglobin and hematocrit, along with significantly increased EPO and decreased hepcidin levels within the first one to three months of treatment.¹ A separate study found that over 12 months, testosterone increased RBC count by about 9%, hematocrit by 4%, and hemoglobin by 8%, while cutting hepcidin levels by more than half.²

What makes this tricky is that the body appears to establish a new “set point.” After about six months on testosterone, EPO and hepcidin levels tend to drift back toward baseline, but hemoglobin and hematocrit stay elevated.¹ Your body essentially recalibrates to a higher red blood cell mass and treats it as the new normal. This is partly why the problem does not resolve on its own even after your body adapts to the hormone, and why active management is often necessary.

Why Elevated Hematocrit Actually Matters

A hematocrit climbing above 50% is called erythrocytosis, and it is one of the most common side effects of testosterone therapy, reported in anywhere from 6% to 40% of patients depending on the study and the formulation used. The concern is not abstract. Thicker blood flows less easily, and elevated hematocrit has been linked to increased risks of blood clots and cardiovascular events. A large retrospective study of men on testosterone therapy found that those who developed polycythemia (hematocrit at or above 52%) had a meaningfully higher risk of major adverse cardiovascular events and venous thromboembolism compared to men who maintained normal hematocrit, with about 35% greater odds of these outcomes.³

That said, the research picture is not entirely settled. A systematic review of drug-induced erythrocytosis noted that most men who developed deep vein thrombosis while on testosterone had other identifiable risk factors, and none of them had erythrocytosis at the time of their clot diagnosis.⁴ The overall evidence linking testosterone-driven erythrocytosis specifically to thrombosis has been described as mixed.⁵ Still, current clinical guidelines generally recommend holding testosterone therapy if hematocrit exceeds 54%, and many clinicians begin closer monitoring or take action at lower thresholds around 50%.

Switch Your Delivery Method

If you are using injectable testosterone cypionate or enanthate, your delivery method is likely one of the biggest drivers of your high hematocrit. Not all testosterone formulations push red blood cells up equally. A systematic review and meta-analysis of randomized trials found that while every formulation raises hematocrit compared to placebo, intramuscular testosterone cypionate and enanthate produced a significantly larger increase than testosterone patches. Gels raised hematocrit by about 3%, patches by about 1.4%, and IM cypionate/enanthate by about 4%.⁶

The real-world data is even more striking. One registry study found that men receiving intramuscular testosterone undecanoate were far more likely to exceed a hematocrit of 50% than men using transdermal gel, roughly 23% versus 5%.⁷ Another study comparing gels, injections, and pellets found that erythrocytosis occurred in about two-thirds of men on injectable testosterone, compared to roughly 13% on gels and 35% on pellets.⁸

The likely reason: injections create a spike-and-trough pattern in blood testosterone levels, with supraphysiological peaks in the days after injection. Those peaks send a stronger erythropoietic signal than the steadier levels maintained by gels and patches. If your hematocrit keeps climbing on injections and switching to a gel or patch is feasible, this is one of the single biggest levers you can pull.

Lower the Dose or Increase Injection Frequency

Testosterone’s effect on red blood cell production is dose-dependent. Research using graded doses confirmed that hemoglobin and hematocrit increase in a linear fashion as the testosterone dose goes up, and this pattern holds for both younger and older men.⁹ So if your blood work is creeping toward the danger zone, reducing the dose is a straightforward option to discuss with your prescriber. Even a modest reduction can nudge hematocrit downward, though it may also reduce the therapeutic benefit you are getting from treatment.

For people on injectable testosterone who want to stay on injections, splitting the same weekly dose into two or more smaller injections (say, every 3.5 days instead of once weekly) can smooth out the hormone peaks. Less dramatic spikes in testosterone levels mean less dramatic stimulation of red blood cell production. This approach has become increasingly popular in testosterone replacement therapy circles, and while direct head-to-head trials on this specific question are limited, the rationale aligns with the well-established link between supraphysiologic testosterone peaks and erythrocytosis.

Therapeutic Phlebotomy

Phlebotomy, the medical term for removing blood, is the fastest and most direct way to lower hematocrit. It works exactly the way you’d expect: remove some blood, and the concentration of red blood cells drops. Donating blood at a blood bank accomplishes the same thing and is how many men on testosterone therapy manage their hematocrit in practice. A standard donation removes about 450 to 500 mL, which typically reduces hematocrit by a few percentage points.

There is an ongoing debate about whether routine phlebotomy is truly justified for testosterone-induced erythrocytosis. A recent review in Endocrine Connections questioned whether the evidence linking testosterone-driven erythrocytosis to thrombotic events is strong enough to warrant phlebotomy as a blanket recommendation, particularly because the best available data is still mostly retrospective.¹⁰ The authors noted that the same large database study showing a 35% increased odds of cardiovascular events and blood clots is the strongest evidence to date, but it has limitations inherent to any retrospective analysis.

Regardless of the debate, if your hematocrit crosses 54%, most guidelines recommend at minimum holding testosterone therapy and performing phlebotomy. The practical downside of repeated phlebotomy is that it progressively depletes your iron stores. Over time, this can lead to iron deficiency, which brings its own symptoms including fatigue, brain fog, and exercise intolerance. Some men find themselves in an ironic cycle: taking testosterone to feel more energetic, getting phlebotomies to manage the erythrocytosis, and then feeling depleted because their iron is too low. If you are getting frequent phlebotomies, monitoring ferritin alongside hematocrit is worth discussing with your doctor.

Stay Hydrated

This one is deceptively simple but frequently overlooked. Hematocrit is a ratio: the percentage of your blood volume occupied by red blood cells. When you are dehydrated, plasma volume contracts and the same number of red blood cells gets squeezed into less liquid, artificially inflating your hematocrit reading. Drinking adequate water will not reduce your actual red blood cell mass, but it can prevent misleadingly high readings and reduce blood viscosity. Many clinicians advise patients to drink plenty of water in the 24 hours before a blood draw for this reason. If your hematocrit is borderline, the difference between being well hydrated and slightly dehydrated can be the difference between a normal result and one that triggers clinical action.

Research on blood collection has shown that even the time a tourniquet is applied during a blood draw can bump hematocrit by a couple of percentage points, which underscores how sensitive this measurement is to transient factors.¹¹ Prolonged tourniquet application of two minutes or more was enough to significantly affect hemoglobin and hematocrit values.¹² The takeaway: if your hematocrit reading seems surprisingly high, consider whether dehydration or a rough blood draw might have contributed before making treatment changes.

Treat Sleep Apnea If You Have It

Obstructive sleep apnea (OSA) is remarkably common in men on testosterone therapy, particularly those who are overweight. OSA causes intermittent drops in blood oxygen during sleep, and the body responds to this chronic low-oxygen state by producing more red blood cells. This means OSA and testosterone can pile onto each other, both independently pushing hematocrit upward. Research on hypogonadal men found that those with a concurrent diagnosis of sleep apnea had roughly double the odds of developing polycythemia compared to those without it, even after adjusting for age, BMI, and testosterone levels.¹³

If you are on testosterone and your hematocrit keeps climbing despite other adjustments, getting screened for sleep apnea is worthwhile. Treating OSA with a CPAP machine or other interventions removes one of the two stimuli driving your red blood cell production upward and can make the remaining hematocrit elevation from testosterone alone much more manageable.

The Iron Connection

Because testosterone works partly by unlocking iron stores for red blood cell production, some people wonder whether restricting dietary iron could slow the process. Animal research provides an intriguing clue here: in mice, testosterone increased red blood cell counts in iron-replete animals but actually worsened anemia in iron-deficient ones. The iron-deficient mice mounted a stress response to produce red blood cells, but without enough iron, the new cells were defective.¹⁴ Deliberately inducing iron deficiency to counteract testosterone-driven erythrocytosis is not a recommended strategy. It creates its own serious problems and can result in a paradoxical combination of high red blood cell turnover and functional anemia, leaving you worse off than where you started.

This is also why repeated phlebotomy eventually becomes counterproductive for some men. Each blood draw removes iron along with the red blood cells. Once iron stores are truly depleted, the bone marrow struggles to make healthy red blood cells regardless of how much testosterone is stimulating it. Monitoring ferritin alongside hematocrit gives your clinician a clearer picture of whether your iron balance is sustainable.

Medications That May Help

A few pharmaceutical options have been studied for their effects on erythrocytosis, though none are specifically approved for managing testosterone-induced high hematocrit. Losartan, an angiotensin receptor blocker commonly prescribed for high blood pressure, has been shown to lower hematocrit in patients with post-transplant erythrocytosis. In one study, hematocrit dropped from about 52.7% to 48.7% over eight weeks on losartan, and the drug appeared to work partly by reducing EPO levels in patients who had elevated baseline EPO.¹⁵ Whether this translates directly to testosterone-induced erythrocytosis is not well established, but some clinicians do prescribe ARBs off-label for this purpose in patients who also have hypertension.

Grapefruit juice and naringin (a compound found in grapefruit) are sometimes mentioned in bodybuilding forums as ways to lower hematocrit. The theoretical mechanism involves naringin’s mild inhibition of EPO production. The evidence for this in humans is thin, and the effect size, if real, is likely small. It would also interact with a long list of medications, so it is not a free lunch even as a supplement.

What About Nattokinase and Blood Viscosity

Nattokinase, an enzyme derived from fermented soybeans, has gained popularity as a supplement in the testosterone community for its purported blood-thinning properties. Lab research has shown that nattokinase can reduce red blood cell aggregation (the tendency of red blood cells to clump together) and lower blood viscosity in a dose-dependent way.¹⁶ A systematic review and meta-analysis of randomized controlled trials echoed these findings, concluding that nattokinase positively affected various blood flow parameters and could be considered a candidate for improving blood rheology.¹⁷

There is an important distinction here, though. Improving blood flow characteristics is not the same as lowering your red blood cell count. Nattokinase may make your blood flow more smoothly even at a higher hematocrit, which could theoretically reduce clotting risk, but it will not show up as a lower number on your blood work. And a randomized controlled trial found no significant effect of nattokinase supplementation on any standard laboratory measurements.¹⁸ If your concern is specifically about high hematocrit numbers, nattokinase is not the tool for the job. If your concern is more broadly about blood viscosity and cardiovascular protection, the evidence is more interesting but still preliminary.

Genetic Variation in Susceptibility

Not everyone on the same dose of testosterone develops erythrocytosis, and genetics likely play a role. Preliminary research has explored whether a polygenic risk score for polycythemia could predict who is most vulnerable. In one study, about 30% of men on testosterone therapy had their highest recorded hematocrit exceed 51%, compared to roughly 13% of untreated men. Men with a high genetic predisposition score (top 10%) showed a trend toward greater risk of exceeding that threshold, but the association did not reach statistical significance.¹⁹ The science here is early, but it confirms what many prescribers already notice clinically: some men are much more prone to erythrocytosis than others at equivalent doses, and a portion of that variability is probably baked into their DNA.

If you have a family history of polycythemia or high hemoglobin, or if you developed erythrocytosis quickly even at a low dose, you may simply be someone whose erythropoietic system is more sensitive to androgens. For these individuals, the strategies above become more important, and combination approaches (a lower dose, delivered by gel, with more frequent monitoring) are often necessary rather than relying on any single intervention.

SARMs and the Question of Alternatives

Some people who have struggled with erythrocytosis on testosterone have turned to selective androgen receptor modulators (SARMs) in hopes of getting anabolic benefits without the blood-thickening effect. There is a grain of rationale here. In early clinical trials of the SARM LGD-4033, participants showed increases in lean body mass with no significant changes in hemoglobin at low doses.²⁰ SARMs were originally designed to deliver tissue-selective effects, building muscle and bone while sparing the prostate, liver, and blood. In practice, the long-term safety data is sparse, SARMs suppress natural testosterone production, and many products sold online as SARMs contain mislabeled or adulterated ingredients. Trading a well-characterized risk (erythrocytosis on prescribed testosterone) for poorly characterized risks (unregulated SARMs with unknown purity) is a gamble most clinicians would advise against.

Putting a Practical Plan Together

If you are on testosterone and your hematocrit is trending upward, the interventions roughly stack in this order of impact and practicality:

Switch formulation: Moving from intramuscular injections to a transdermal gel or patch often produces the single biggest drop in hematocrit risk.
Reduce dose: The relationship between testosterone dose and red blood cell production is linear, so even modest reductions help.
Increase frequency: If staying on injections, splitting into more frequent, smaller doses smooths hormone peaks.
Phlebotomy: The fastest direct intervention when hematocrit is acutely high, but not sustainable long-term without monitoring iron.
Hydration: Will not change your true RBC mass but prevents artificially inflated readings and reduces viscosity.
Treat OSA: If present, treating sleep apnea removes a compounding stimulus for red blood cell production.
Medications: ARBs like losartan may offer modest benefit, particularly in patients who also need blood pressure management.

The key point is that these approaches work best in combination. A man who switches from biweekly injections to daily gel application, lowers his dose slightly, treats his sleep apnea, and stays well hydrated is going to have a dramatically different hematocrit trajectory than someone who changes nothing and relies on quarterly phlebotomies alone. Regular blood monitoring, typically every three to six months once stable, gives you the feedback loop to know whether your current combination of strategies is working or needs adjustment.