When hemoglobin or hematocrit rise above the safe range, your blood becomes thicker. Testosterone tells your body to make more red blood cells. Monitoring hemoglobin is one of the most important parts of safe testosterone replacement therapy (TRT).
Evidence for occult iron deficiency was lacking in this population, as indicated by normal ferritin, serum iron and transferrin saturation, and normal mean corpuscular volume. Anemia is commonly seen in older adults; it is not known whether anemic participants respond differently to testosterone than nonanemic participants. However, serum interleukin-6 levels were similar between groups at baseline and did not change significantly in either group (Figure 4E). The changes in serum iron, total iron binding capacity, and transferrin saturation did not differ significantly between groups (data not shown). Serum sTR concentration reflects total erythroid activity in rats and humans and has been shown to reflect plasma iron turnover and erythroid transferrin uptake very closely if iron deficiency is not present (22). CONSORT Diagram depicting the flow of participants, treatment arms, and attribution of nonanemic and anemic participants. Compared with the testosterone group, slightly more participants in the placebo group were former smokers.
If hemoglobin or hematocrit becomes too high, therapeutic phlebotomy may be recommended. This is why it’s important to look at the whole picture, not just testosterone levels. Some people respond better to methods that provide steady hormone levels rather than sharp peaks.
Thus, increased hemoglobin and hematocrit would normally be expected to suppress serum EPO levels. The vertical shift in the top two panels indicates increased EPO per hemoglobin or hematocrit at end of testosterone treatment. Serum EPO levels trended toward baseline by 6 months in spite of continued testosterone administration, but remained nonsuppressed in spite of elevated levels of hemoglobin and hematocrit in testosterone-treated men.
Testosterone stimulates erythropoiesis through an initial rise in erythropoietin (EPO), the establishment of a new EPO/hemoglobin 'set point', and a parallel decrease in the master iron regulator protein hepcidin, as well as several other potential mechanisms. Erythrocytosis, or elevated hematocrit, is a common side effect of testosterone therapy (TTh) in male hypogonadism. What are the signs and symptoms of high hemoglobin/hematocrit? What are the potential risks of elevated hemoglobin/hematocrit?