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Sleep apneaSleep apnea is one of the strongest risk factors. Older adults may also have other health conditions that increase the effect. AgeOlder adults have a higher chance of developing high hemoglobin on TRT. Their risk level appears to fall between gels and injections. While the release is steady, pellets still raise hemoglobin in some users. Because of this, gels and patches have a lower chance of causing high hemoglobin compared to injections. This creates more stable hormone levels and fewer sharp peaks.
As a result, hemoglobin and hematocrit often rise, especially in the first year of treatment. When TRT is added, the stimulation of red blood cell production may cause hemoglobin to rise faster than expected. Testosterone can increase the brain’s drive to produce red blood cells, which makes the body react even more strongly to low nighttime oxygen.
What is the best treatment for erythrocytosis induced by testosterone replacement therapy? Hepcidin regulates iron utilization in the body and iron is a key component of red blood cells. There are several different theories how TRT causes an increase in red blood cell volume. To Learn more about the risk of blood clot formation on testosterone therapy Erythrocytosis and polycythemia should not be confused with Polycythemia Vera which is a type of cancer of the bone marrow resulting in an increase in all components of blood volume not only red blood cells.
Studies show that 10–20% of people on TRT develop elevated hemoglobin or hematocrit at some point during treatment. This increase can push hemoglobin and hematocrit above the normal range. When estradiol levels rise slightly during TRT, it can add to the stimulation of red blood cell production. Testosterone increases EPO levels, which raises hemoglobin even further. Each step explains why testosterone therapy often raises these blood values more than natural hormone levels do.
In light of this controversy, the American Urological Association (AUA) issued a policy statement stating that, based upon current evidence, definitive answers on the cardiovascular risks of TTh are not currently available . Extensive debate has surrounded high impact publications with questionable methodologies and controversial conclusions that suggested significant cardiovascular risk for men on TTh with alternative studies suggesting benefit 16–20. In an official statement, the organization proposed an algorithm for TTh in patients with AOH . Primary hypogonadism represents failure of testosterone production, characterized by low serum testosterone and elevated gonadotropins. A literature review was performed using PubMed for articles addressing TTh, erythrocytosis, and polycythemia.
While TRT can help with these symptoms, it also affects many systems in the body.
For example, Chuvash erythrocytosis is a congenital disorder caused by a missense mutation in the VHL gene. While not researched in humans, animal data show that the net result of these two competing mechanisms on tissue pO2 follows the direction of hematocrit change when hematocrit is in the range of 20 to 60% (49). As O2 is continuously consumed, there will be a steep pO2 gradient radially and longitudinally along the blood capillaries, with the highest value at the arterial and the lowest at the venous end (31, 32). The best available evidence evaluating the link between TTh–induced erythrocytosis and thrombosis to date is therefore is a retrospective cohort study (45). The TRAVERSE trial found a nonsignificant higher incidence of VTE events in the testosterone-treated group compared with placebo (HR 1.46, 95% CI 0.92–2.32) (23). A Danish prospective cohort study of the general population (the Copenhagen General Population Study) evaluated the association between hematocrit and both arterial and venous thrombosis (43).
At 6 months, EPO and hepcidin levels returned toward baseline in spite of continued testosterone administration, but EPO levels remained nonsuppressed even though elevated hemoglobin and hematocrit higher than at baseline, suggesting a new set point. TRT often increases hemoglobin because testosterone stimulates red blood cell production (erythropoiesis). Testosterone replacement therapy (TRT) can raise hemoglobin and hematocrit because it stimulates the body to make more red blood cells. When you start testosterone replacement therapy (TRT), your body responds by making more hemoglobin, hematocrit, and red blood cells. When red blood cells increase, hemoglobin and hematocrit rise as well. The question that remains is whether decreased tissue pO2 in response to therapeutic phlebotomy in TTh-induced erythrocytosis increases HIF activity sufficiently to also confer a thrombotic risk that might offset or override the potential benefit of correcting increased hematocrit. How does testosterone replacement therapy (TRT) cause an increase in red blood cell volume?