The Truth About Erythrocytosis: What Men on TRT Need to Understand

[01dragonslayer]

These three conditions are all related to an increased number of red blood cells (RBCs) in the bloodstream, but they have different causes, risks, and implications—especially for men on TRT.

Erythrocytosis

Erythrocytosis refers to an elevated red blood cell count (or hematocrit) due to increased erythropoiesis (red blood cell production). This condition can be caused by testosterone therapy, as testosterone stimulates the production of erythropoietin (EPO), a hormone that signals the bone marrow to produce more RBCs.

• Key characteristics:
  • Common in men on TRT
  • Managed through dose adjustments, blood donation (therapeutic phlebotomy), and hydration
• Why it matters for TRT:
  • Unlike true polycythemia, erythrocytosis does not involve an overproduction of RBCs due to a bone marrow disorder.
  • TRT-induced erythrocytosis is not inherently dangerous if managed properly with regular bloodwork and monitoring.
  • Erythrocytosis has not been shown to increase the risk of blood clots when secondary to TRT.

Polycythemia Vera (PV)

Polycythemia Vera is a rare blood disorder caused by a genetic mutation (JAK2 mutation) that leads to uncontrolled red blood cell production by the bone marrow. This is a true disease rather than a reaction to external factors like TRT or low oxygen levels.

• Key characteristics:
  • Involves overproduction of RBCs, white blood cells, and platelets
  • Increases the risk of serious blood clots, strokes, and heart attacks
  • Requires ongoing treatment with blood thinners and bone marrow-suppressing medications
  • Not caused by TRT and should be ruled out in men with very high hematocrit levels

Secondary Polycythemia

Secondary polycythemia is an adaptive response to low oxygen levels (hypoxia), leading to an increase in red blood cell production. This occurs in response to conditions that reduce oxygen availability, such as:

• Chronic lung disease (COPD, sleep apnea)
• Living at high altitudes
• Kidney disease (which increases EPO production)
• Anabolic steroid or TRT use (mild cases related to erythrocytosis)
• Key characteristics:
  • Caused by an external trigger (not bone marrow dysfunction)
  • Can be reversed or managed by treating the underlying cause

Why This Distinction Matters for TRT Patients

• TRT-induced erythrocytosis is not the same as polycythemia vera. It is a reactive process, not a disease.
• Routine bloodwork (checking hematocrit, hemoglobin, and red blood cell counts) helps ensure safe TRT use.
• If hematocrit rises too much (>54%), interventions like blood donation may be necessary.

 

[propower]

These three conditions are all related to an increased number of red blood cells (RBCs) in the bloodstream, but they have different causes, risks, and implications—especially for men on TRT.

Erythrocytosis

Erythrocytosis refers to an elevated red blood cell count (or hematocrit) due to increased erythropoiesis (red blood cell production). This condition can be caused by testosterone therapy, as testosterone stimulates the production of erythropoietin (EPO), a hormone that signals the bone marrow to produce more RBCs.

• Key characteristics:
  • Common in men on TRT
  • Managed through dose adjustments, blood donation (therapeutic phlebotomy), and hydration
• Why it matters for TRT:
  • Unlike true polycythemia, erythrocytosis does not involve an overproduction of RBCs due to a bone marrow disorder.
  • TRT-induced erythrocytosis is not inherently dangerous if managed properly with regular bloodwork and monitoring.
  • Erythrocytosis has not been shown to increase the risk of blood clots when secondary to TRT.

Polycythemia Vera (PV)

Polycythemia Vera is a rare blood disorder caused by a genetic mutation (JAK2 mutation) that leads to uncontrolled red blood cell production by the bone marrow. This is a true disease rather than a reaction to external factors like TRT or low oxygen levels.

• Key characteristics:
  • Involves overproduction of RBCs, white blood cells, and platelets
  • Increases the risk of serious blood clots, strokes, and heart attacks
  • Requires ongoing treatment with blood thinners and bone marrow-suppressing medications
  • Not caused by TRT and should be ruled out in men with very high hematocrit levels

Secondary Polycythemia

Secondary polycythemia is an adaptive response to low oxygen levels (hypoxia), leading to an increase in red blood cell production. This occurs in response to conditions that reduce oxygen availability, such as:

• Chronic lung disease (COPD, sleep apnea)
• Living at high altitudes
• Kidney disease (which increases EPO production)
• Anabolic steroid or TRT use (mild cases related to erythrocytosis)
• Key characteristics:
  • Caused by an external trigger (not bone marrow dysfunction)
  • Can be reversed or managed by treating the underlying cause

Why This Distinction Matters for TRT Patients

• TRT-induced erythrocytosis is not the same as polycythemia vera. It is a reactive process, not a disease.
• Routine bloodwork (checking hematocrit, hemoglobin, and red blood cell counts) helps ensure safe TRT use.
• If hematocrit rises too much (>54%), interventions like blood donation may be necessary.

 

[propower]

Thanks for this info. I joined to research this very thing. My free testosterone levels are at 32 right now following my blood work. I'm finding it would be cheaper for me to handle it myself outside of my network of insurance. Just really don't know which way to go. I use to cycle about 15 years ago and had some stuff happen and never got the chance to do a pct after being in the middle of a very big and intense cycle and had to stop abruptly. If any one has any suggestions or opinions I'm all ears please.

 

[01dragonslayer]

Thanks for this info. I joined to research this very thing. My free testosterone levels are at 32 right now following my blood work. I'm finding it would be cheaper for me to handle it myself outside of my network of insurance. Just really don't know which way to go. I use to cycle about 15 years ago and had some stuff happen and never got the chance to do a pct after being in the middle of a very big and intense cycle and had to stop abruptly. If any one has any suggestions or opinions I'm all ears please.

Glad I could help you brotha. Welcome to the family brotha. Never hesitate to ask questions. We are all here to help.

 

[johnjuanb1]

These three conditions are all related to an increased number of red blood cells (RBCs) in the bloodstream, but they have different causes, risks, and implications—especially for men on TRT.

Erythrocytosis

Erythrocytosis refers to an elevated red blood cell count (or hematocrit) due to increased erythropoiesis (red blood cell production). This condition can be caused by testosterone therapy, as testosterone stimulates the production of erythropoietin (EPO), a hormone that signals the bone marrow to produce more RBCs.

• Key characteristics:
  • Common in men on TRT
  • Managed through dose adjustments, blood donation (therapeutic phlebotomy), and hydration
• Why it matters for TRT:
  • Unlike true polycythemia, erythrocytosis does not involve an overproduction of RBCs due to a bone marrow disorder.
  • TRT-induced erythrocytosis is not inherently dangerous if managed properly with regular bloodwork and monitoring.
  • Erythrocytosis has not been shown to increase the risk of blood clots when secondary to TRT.

Polycythemia Vera (PV)

Polycythemia Vera is a rare blood disorder caused by a genetic mutation (JAK2 mutation) that leads to uncontrolled red blood cell production by the bone marrow. This is a true disease rather than a reaction to external factors like TRT or low oxygen levels.

• Key characteristics:
  • Involves overproduction of RBCs, white blood cells, and platelets
  • Increases the risk of serious blood clots, strokes, and heart attacks
  • Requires ongoing treatment with blood thinners and bone marrow-suppressing medications
  • Not caused by TRT and should be ruled out in men with very high hematocrit levels

Secondary Polycythemia

Secondary polycythemia is an adaptive response to low oxygen levels (hypoxia), leading to an increase in red blood cell production. This occurs in response to conditions that reduce oxygen availability, such as:

• Chronic lung disease (COPD, sleep apnea)
• Living at high altitudes
• Kidney disease (which increases EPO production)
• Anabolic steroid or TRT use (mild cases related to erythrocytosis)
• Key characteristics:
  • Caused by an external trigger (not bone marrow dysfunction)
  • Can be reversed or managed by treating the underlying cause

Why This Distinction Matters for TRT Patients

• TRT-induced erythrocytosis is not the same as polycythemia vera. It is a reactive process, not a disease.
• Routine bloodwork (checking hematocrit, hemoglobin, and red blood cell counts) helps ensure safe TRT use.
• If hematocrit rises too much (>54%), interventions like blood donation may be necessary.

This is some excellent information and relevant to my current situation. Thank you very much for your detailed post!
I can tell you first hand, if you let your hematocrit and hemoglobin get out of range you’ll feel like crap! You’ll feel like you’ve been poisoned 24/7, plus extreme fatigue! Do quarterly bloodwork, and donate if your hemo numbers get out of range. Word on the street is taking 10,000+FU Nattokinase daily and 500mg Naringin twice a day helps keep hemoglobin/hematocrit down. Studies on Nattokinase with aspirin grip clean plaque out of the arteries, as well.

Effects of nattokinase, a pro-fibrinolytic enzyme, on red blood cell aggregation and whole blood viscosity​

Eszter Pais et al. Clin Hemorheol Microcirc.2006.
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Abstract PubMed PMID
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Abstract​

The vegetable cheese-like food, natto, is extremely popular in Japan with a history extending back over 1000 years. A fibrinolytic enzyme, termed nattokinase, can be extracted from natto; the enzyme is a subtilisin-like serine protease composed of 275 amino acid residues and has a molecular weight of 27.7 kDa. In vitro and in vivo studies have consistently demonstrated the potent pro-fibrinolytic effect of the enzyme. However, no studies to date have evaluated the effects of nattokinase on various hemorheological parameters and thus we have begun to assess the effects of the enzyme on RBC aggregation and blood viscosity. Blood samples were incubated with nattokinase (final activities of 0, 15.6, 31.3, 62.5 and 125 units/ml) for 30 minutes at 37 degrees C. RBC aggregation was measured using a Myrenne MA-1 aggregometer and blood viscosity assessed over 1-1000 s(-1) with a computer controlled scanning capillary rheometer (Rheolog). Our in vitro results showed a significant, dose-dependent decrease of RBC aggregation and low-shear viscosity, with these beneficial effects evident at concentrations similar to those achieved in previous in vivo animal trials. Our preliminary data thus indicate positive in vitro hemorheological effects of nattokinase, and suggest its potential value as a therapeutic agent and the need for additional studies and clinical trials.