1. Bhasin et al. (2008) – Testosterone Dose-Response Study in Healthy Men
• Source: Bhasin, S., et al. (2008). “Testosterone dose-response relationships in healthy young and older men.” Published in a journal cited by Canadian Medical Association Journal (2017) (Web ID: 10).
• Findings: This RCT examined hematocrit changes in healthy young (19–35 years) and older men (60–75 years) receiving graded doses of testosterone enanthate (25, 50, 125, 300, 600 mg weekly). Hematocrit increases were observed within 1 month, with peak increases by 3 months (12 weeks). At a 125 mg dose, 75% of older men and 42% of younger men reached peak hematocrit by 12 weeks, indicating stabilization within 3–6 months for most participants. The study noted dose-dependent increases, with stabilization occurring earlier at lower doses.
Coviello et al. (2013) – Testosterone and Erythropoiesis in Older Men
• Source: Coviello, A. D., et al. (2013). “Effects of graded doses of testosterone on erythropoiesis in healthy older men.” The Journals of Gerontology: Series A (Web ID: 10).
• Findings: This RCT studied older men (60–75 years, n=61) with mobility limitations receiving testosterone enanthate (25, 50, 125, 300 mg weekly). Hematocrit and hemoglobin increased significantly within 3 months, establishing a new erythropoietin/hemoglobin “set point” by this time. No consistent erythropoietin increase was observed after 20 weeks (5 months), confirming stabilization within ~3–6 months for most participants. The study highlighted that hematocrit plateaued as erythropoietin levels returned to baseline.
But even without sharing those studies, we can both see that I was actually correct in OP’s case. Like I said, he saw an initial jump of a few points, after which it stabilized. And that’s exactly what we should expect based on studies and countless anecdotal reports. So again, I was correct. But us sitting here arguing isn’t helping anyone(unless there are people who find it amusing), so at this point I’ll just say I accept your apology.
Your studies 2001, 2008 and 2013 end all be all right!
* indicating stabilization within 3–6 months for most participants.
As you say it is a given that the OPs levels have stabilized 3 months right LOL!
Let me get this out of the way first before I kill you off in 1 post!
Remember the OP has OSA and his hematocrit was already high-end pre-TTh and I would put money on it with his high stressed job and lack of. quality sleep that his blood pressure is not stellar!
Accept your apology.....LOL who you kidding here!
Again seeing as you are slow he never even stayed on 140 mg T long enough to truly see where his hematocrit would have ended up and it sure as hell not a given it has stabilized 3 months in.
He has tried numerous lower dosed protocols before recently jumping back on 140 mg T/week.
You nor anyone one here can say with certainty that his hematocrit stabilized 3 months in not a chance!
Let's get to the meat and potatoes here.
You not going to even look into the guidelines!
Let me guess need to rely on AI.
My gold mine of papers from the endless threads I have put up on here since 2016!
I will let you do the leg work and. find them or get them on your own time whatever suits your fancy CHAMP!
Most of them have been posted up on the forum over the years.
Have all the most updated medical texts for anything to do with testosterone therapy let alone fertility!
Like I said next time round paint the full picture here before dishing out half ass advice to to the OP about where his hematocrit sits you know 53.4% which could have easily been pushed above 54% if he stayed on the140 mg T/week long enough.
Again the first 6 months is critical and it is not a given hematocrit is stabilizing 3 months in whether starting TTh or tweaking a protocol (increasing dose of T)!
As I stated it is standard practice during the first year of therapy and depending on what guideline it is tested at 3, 6 and the 12 month mark or 3-6 months and 12 months then after the first year it is tested annually.
Why because there still can still be an increase after 3 months or even after 6 months better yet in some cases even longer during the first year of starting therapy plain and simple.
Look over the most recent EAU Guidelines 20f**King25 MAN!
The first 3-6 months is the most critical time period but even then it still needs to be tested thoroughly during the first year of starting therapy.
If you knew than you would have pointed it out to the OP let alone painted the full picture here instead of making it sound as if there is no worry about it rising further past the first 12 weeks of starting therapy.
Every guideline out there recommends testing hematocrit during the first year of starting therapy at the baseline, 3, 6 and 12 months or 3-6 and at 12 months in.
Again it is not a given that hematocrit stops rising or better yet has stabilized 3 months in LMFAO!
It's 2025 MAN!
EAU Guideline 2025.....
Any elevation above the normal range for haematocrit usually becomes evident between three and twelve months after testosterone therapy initiation.
Where is it a given that at the 3 month mark there is no further increase or levels have stabilized!
EAU Guidelines of Sexual and Reproductive Health (2025)
3.5 Safety and follow-up in hypogonadism management
3.5.6 Erythrocytosis
An elevated haematocrit is the most common adverse effect of testosterone therapy. Stimulation of erythropoiesis is a normal biological action that enhances delivery of oxygen to testosterone-sensitive tissues (e.g., striated, smooth and cardiac muscle).
Any elevation above the normal range for haematocrit usually becomes evident between three and twelve months after testosterone therapy initiation. However, polycythaemia can also occur after any subsequent increase in testosterone dose, switching from topical to parenteral administration and, development of co-morbidity, which can be linked to an increase in haematocrit (e.g., respiratory or haematological diseases).
There is no evidence that an increase of haematocrit up to and including 54% causes any adverse effects. If the haematocrit exceeds 54% there is a testosterone independent but weak associated rise in CV events and mortality [81, 182-184]. Any relationship is complex as these studies were based on patients with any cause of secondary polycythaemia, which included smoking and respiratory diseases.
There have been no specific studies in men with only testosterone-induced erythrocytosis.
As detailed, the TRAVERSE study, which had included symptomatic hypogonadal men aged 45-80 years who had pre-existing or a high risk of CVD, showed a mild higher incidence of pulmonary embolism, a component of the adjudicated tertiary end point of venous thromboembolic events, in the testosterone therapy than in the placebo group (0.9% vs. 0.5%) [78]. However, three previous large studies have not shown any evidence that testosterone therapy is associated with an increased risk of venous thromboembolism [185, 186]. Of those, one study showed that an increased risk peaked at six months after initiation of testosterone therapy, then declined over the subsequent period [187]. In one study venous thromboembolism was reported in 42 cases and 40 of these had diagnosis of an underlying thrombophilia (including factor V Leiden deficiency, prothrombin mutations and homocysteinuria) [188]. A meta-analysis of RCTs of testosterone therapy reported that venous thromboembolism was frequently related to underlying undiagnosed thrombophilia-hypofibrinolysis disorders [79]. In a RCT of testosterone therapy in men with chronic stable angina there were no adverse effects on coagulation, by assessment of tissue plasminogen activator or plasminogen activator inhibitor-1 enzyme activity or fibrinogen levels [189]. Similarly, another meta-analysis and systematic review of RCTs found that testosterone therapy was not associated with an increased risk of venous thromboembolism [169].
With testosterone therapy an elevated haematocrit is more likely to occur if the baseline level is toward the upper limit of normal prior to initiation. Added risks for raised haematocrit on testosterone therapy include smoking or respiratory conditions at baseline. Higher haematocrit is more common with parenteral rather than topical formulations. Accordingly, a large retrospective two-arm open registry, comparing the effects of long-acting testosterone undecanoate and testosterone gels showed that the former preparation was associated with a higher risk of haematocrit levels > 50%, when compared to testosterone gels [190].
In men with pre-existing CVD extra caution is advised with a definitive diagnosis of hypogonadism before initiating testosterone therapy and monitoring of testosterone as well as haematocrit during treatment.
Elevated haematocrit in the absence of comorbidity or acute CV or venous thromboembolism can be managed by a reduction in testosterone dose, change in formulation or if the elevated haematocrit is very high by venesection (500 mL), even repeated if necessary, with usually no need to stop the testosterone therapy.
Hematocrit (%) - Year 1 of treatment baseline, 3, 6 and 12 months
After year 1 of treatment annually
Endocrine Society Guidelines 2018.....
Men with elevated hematocrit should undergo further evaluation before considering T therapy. Clinicians should measure hematocrit at baseline, 3 to 6 months, and then annually after a patient begins T therapy.
Again where is the its a given at the 3 month mark there is no further increase or levels have stabilized!
Testosterone Therapy in Men With Hypogonadism: An Endocrine Society* Clinical Practice Guideline (2018)
Erythrocytosis
T administration increases hemoglobin and hematocrit (88, 89); these effects are related to T doses and circulating concentrations (89). I
n some men with hypogonadism, T therapy can cause erythrocytosis (hematocrit . 54%). The increase in hematocrit during T administration and the frequency of erythrocytosis is higher in older men than in young men (87). The commissioned meta-analysis showed that T treatment was associated with a significantly higher frequency of erythrocytosis vs placebo.
The hematocrit level at which the risk of neuro-occlusive or cardiovascular events increases is not known. The frequency of neuro-occlusive events in men with hypogonadism enrolled in RCTs of T who developed erythrocytosis has been very low.
Clinicians should evaluate men who develop erythrocytosis during T-replacement therapy and withhold T-therapy until hematocrit has returned to the normal range and then resume T therapy at a lower dose. Using therapeutic phlebotomy to lower hematocrit is also effective in managing T treatment–induced erythrocytosis.
3. Monitoring of Testosterone-Replacement Therapy
3.1 In hypogonadal men who have started testosterone therapy, we recommend evaluating the patient after treatment initiation to assess whether the patient has responded to treatment, is suffering any adverse effects, and is complying with the treatment regimen. (Ungraded Good Practice Statement)
Technical remark
• Monitoring includes measuring testosterone and
hematocrit at 3 to 6 months (depending upon the formulation) and measuring testosterone and
hematocrit at 12 months and annually after initiating testosterone therapy.
Table 9. Monitoring Men Receiving T Therapy
Check hematocrit at baseline, 3–6 mo after starting treatment, and then annually. If hematocrit is .54%, stop therapy until hematocrit decreases to a safe level; evaluate the patient for hypoxia and sleep apnea; reinitiate therapy with a reduced dose.
Evidence
T administration in hypogonadal men is associated with a dose-dependent increase in hemoglobin concentrations (88); the increase in hemoglobin is greater in older men than in young hypogonadal men (89).
Baseline hematocrit . 48% and . 50% for men living at higher altitudes is a relative contraindication to T therapy because these men are more likely to develop a hematocrit .
54% when treated with T. Men with elevated hematocrit should undergo further evaluation before considering T therapy. Clinicians should measure hematocrit at baseline, 3 to 6 months, and then annually after a patient begins T therapy.
AUA Guideline 2018.....
During testosterone therapy, levels of Hb/Hct generally rise for the first six months, and then tend to plateau.
Again where is the its a given at the 3 month mark there is no further increase or levels have stabilized!
EVALUATION AND MANAGEMENT OF TESTOSTERONE DEFICIENCY:
AUA GUIDELINE (2018)
11. Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia. (Strong Recommendation; Evidence Level: Grade A)
Prior to commencing testosterone therapy, all patients should undergo a baseline measurement of hemoglobin/hematocrit. If the Hct exceeds 50%, clinicians should consider withholding testosterone therapy until the etiology is formally investigated. While on testosterone therapy, a Hct ≥54% warrants intervention, such as dose reduction or temporary discontinuation. While the incidence of polycythemia for one particular modality of testosterone compared to another cannot be determined, trials have indicated that injectable testosterone is associated with the greatest treatment-induced increases in hemoglobin/Hct.
22
11. Prior to offering testosterone therapy, clinicians should measure hemoglobin and hematocrit and inform patients regarding the increased risk of polycythemia. (Strong Recommendation; Evidence Level: Grade A)
Polycythemia, sometimes called erythrocytosis, is generally defined as a hematocrit (Hct) >52%. It is categorized into primary (life-long), often related to genetic disorders; and
secondary (acquired), which is attributed to polycthemia vera, living at high altitude, hypoxia (e.g., chronic obstructive pulmonary disease, obstructive sleep apnea, tobacco use), paraneoplastic syndromes, and testosterone therapy.187 188
P
rior to commencing testosterone therapy, all patients should undergo a baseline measurement of Hb/Hct (Appendix C). If the Hct exceeds 50%, clinicians should consider withholding testosterone therapy until the etiology of the high Hct is explained.187 While on testosterone therapy, a Hct ≥54% warrants intervention. In men with elevated Hct and high on- treatment testosterone levels, dose adjustment should be attempted as first-line management. In men with elevated Hct and low/normal on-treatment testosterone levels, measuring a SHBG level and a free testosterone level using a reliable assay is suggested. If SHBG levels are low/free testosterone levels are high, dose adjustment of the testosterone therapy should be considered. Finally, men with elevated Hct and on-treatment low/normal total and free testosterone levels should be referred to a hematologist for further evaluation and possible coordination of phlebotomy.
Androgens have a stimulating effect on erythropoiesis and elevation of Hb/Hct is the most frequent adverse event related to testosterone therapy.189-191 During testosterone therapy, levels of Hb/Hct generally rise for the first six months, and then tend to plateau.192, 193
