@Stpfan
I would not be too concerned with running higher-end levels (low 50s) if you are not experiencing any symptoms let alone feel well overall.
Once levels approach 54-55% most would recommend addressing the issue whether through blood donations or in many cases lowering the dose of T.
Need to keep in mind where your hematocrit sat pre-trt.
Some men are naturally on the higher-end pre-trt whereas many others fall well within range and there are also the ones with borderline/low levels due to underlying issues/anemia.
Come to your own conclusion!
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EVALUATION AND MANAGEMENT OF TESTOSTERONE DEFICIENCY: AUA GUIDELINE (2018)
Adjunctive Testing
6. In patients with low testosterone, clinicians should measure serum luteinizing hormone levels. (Strong Recommendation; Evidence Level: Grade A)
7. Serum prolactin levels should be measured in patients with low testosterone levels combined with low or low/ normal luteinizing hormone levels. (Strong Recommendation; Evidence Level: Grade A)
8. Patients with persistently high prolactin levels of unknown etiology should undergo evaluation for endocrine disorders. (Strong Recommendation; Evidence Level: Grade A)
9. Serum estradiol should be measured in testosterone deficient patients who present with breast symptoms or gynecomastia prior to the commencement of testosterone therapy. (Expert Opinion)
10. Men with testosterone deficiency who are interested in fertility should have a reproductive health evaluation performed prior to treatment. (Moderate Recommendation; Evidence Level: Grade B)
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)
12. PSA should be measured in men over 40 years of age prior to commencement of testosterone therapy to exclude a prostate cancer diagnosis. (Clinical Principle)
GUIDELINE STATEMENTS
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 polycythemia vera, living at high altitude, hypoxia (e.g., chronic obstructive pulmonary disease, obstructive sleep apnea, tobacco use), paraneoplastic syndromes, and testosterone therapy.187 188
Prior 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 an 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
Among 5 randomized, placebo-controlled trials that evaluated Hb and Hct levels in men (mean baseline testosterone <300 ng/dL) using either gel, solution, or IM testosterone therapy for 12 weeks to 1 year, a significant increase in the incidence of elevated Hct was observed in those using testosterone (OR=6.46; CI: 1.86, 22.40) compared to those on placebo.194-201 The calculated odds ratio belies the number of polycythemia events in absolute terms; 19 events in 1,094 patients occurred in the treatment arm as compared to 1 event in 1,093 patients in the placebo group.
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 Hb/Hct. In the current meta-analysis of RCTs, long-acting IM testosterone resulted in a mean increase in Hb levels of 1.4 mg/dL compared to 1.6 mg/dL with short-acting IM testosterone, 0.9 mg/dL with transdermal preparations, and 0.7 mg/dL with topical patches.150, 182, 194-196, 201-218
This is likely due to the high and sometimes supra-physiological levels of testosterone that occur in the early days after injection.219 A retrospective comparative series involving 175 men with testosterone deficiency who used different modalities of testosterone therapy reported that 19% of men receiving IM testosterone experienced polycythemia compared to 12.5% with testosterone pellets and 5.4% with gels.220
It is unclear if the risk of polycythemia is greater in men with comorbid disorders that predispose to hypoxia, such as chronic obstructive pulmonary disease or obstructive sleep apnea.188 It is also currently unknown if rates of polycythemia are associated only with short-acting injectable agents or occur with equal frequency when using the longer-acting testosterone undecanoate.221
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The use of exogenous T will result in driving up RBCs/hemoglobin/hematocrit within the first month of starting trt and can take up to 9-12 months to reach peak levels.
In many cases, levels can stabilize in due time but many will also struggle with high levels and try to manage with frequent blood donations.
In most cases running too high TT/FT levels will result in
high hematocrit.
My reply from another thread:
Daily Injection Experiment
Injectable T has been shown to have a greater impact on increasing HCT compared to transdermal T.
3–18% with transdermal administration and up to 44% with injection.
In most cases when using injectable T high supra-physiological peaks post-injection and overall T levels (running too high TT/FT level) will have a big impact on increasing HCT.
Manipulating injection frequency by injecting more frequently using lower doses of T resulting in minimizing the peak--->trough and maintaining more stable levels may lessen the impact on HCT but it is not a given.
As again
running very high FT levels will have a stronger impact on driving up HCT.
T formulation, the dose of T, genetics (polymorphism of the AR), age all play a role in the impact a trt protocol will have on blood markers (RBCs/hemoglobin/hematocrit).
Other factors such as sleep apnea, smoking can have a negative impact on hematocrit.
