Hematocrit: Natural vs Injectable

[DixieWrecked]

Have been searching for this data for a whle now but can't seem to find an answer. Does engenous production of testosterone cause a rise in hematocrit like injections would? Are 18 year old males wlaking around with elevated hematocrit? ANyone have any data?

@madman

 

[madman]

Have been searching for this data for a whle now but can't seem to find an answer. Does engenous production of testosterone cause a rise in hematocrit like injections would? Are 18 year old males wlaking around with elevated hematocrit? ANyone have any data?

@madman

Driven to the point of being too high.....no.

RBCs/hemoglobin/hematocrit increase during puberty to levels that would be considered healthy as androgens play a strong role.

Keep in mind that when using exogenous testosterone the 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).

.post #19

Considering starting TRT although levels are not "clinically low" Feedback would be appreciated

I'm new to the forum and would like to possibly get some opinions on my situation. I am 58 years old and have considered going on TRT for several years. Between reading lots of information, talking to several highly knowledgeable people and researching this forum for many years, I feel like I am...

www.excelmale.com

Frontiers | Androgens and Anemia: Current Trends and Future Prospects

www.frontiersin.org

Androgens and Erythropoiesis (2019)

Animal and human studies suggested a direct and indirect stimulatory effect of androgens on erythropoiesis, though the exact mechanism of such relation remains vaguely understood. Androgens administration results in an increase in the erythroid cell mass, the colony-forming units for erythrocytes (CFU-E), and the production and secretion of Erythropoietin (EPO) (6) while androgen deprivation causes a reduction in red blood cell indices due to reduced proliferation of marrow erythroid precursors (18).

Androgens are converted to 17-keto-steroids capable of increasing the synthesis of mRNA in the nucleus causing differentiation of bone marrow cells from EPO-non-responsive to EPO responsive (6). Moreover, androgens enhance the glucose uptake resulting in glycolysis and gene transcription, and mRNA synthesis in the erythroid (19–21).

T may increase Hct by inhibiting the secretion of hepcidin, the principal iron regulatory peptide, thereby leading to an increase in bioavailable iron (22) but may also enhance the incorporation of iron into the red blood cells (23) and improve red blood cells survival (24). Finally, the finding of raised insulin-like growth factor 1 (IGF-1) levels in those receiving androgens suggested a potential link between androgens and an IGF-1 driven erythroid progenitor cells proliferation and differentiation (25, 26).

The effect of T on erythropoiesis is most pronounced during puberty, with prepubertal Hb being similar in boys and girls, but increases in boys after age 13 years in tandem with increasing T concentrations (6, 27). Boys with delayed puberty have Hb levels similar to those of prepubertal boys and girls, and treatment with T normalizes hemoglobin levels to those observed in the late male puberty (28, 29).






Male puberty is followed by a 2-g/dL increase in blood hemoglobin concentration. The regulation of this acceleration in erythropoiesis has remained poorly understood, although it has been connected with the pubertal increase in serum testosterone (T) concentration.1,2 The rise in blood hemoglobin concentration, however, is slowly progressive and takes about 6 years, whereas serum T increases more rapidly and in a more linear fashion from the early puberty onward.3 This lack of synchronism between the changes in T and hemoglobin makes it difficult to explain the puberty-associated changes in erythropoiesis exclusively, as the effects of testosterone.





Population of Normal Adolescent Boys

During the 5 years of follow-up, from the average age of 11.7 years up to 16.6 years, there was a 2.1-g/dL increase in blood hemoglobin concentration (Table III). The blood hemoglobin concentration did not increase significantly until the average age of 13.6 years (Table III). At that age, the mean testicular volume was 10.0 mL (range, 2.2 to 25.6 mL) and the serum T concentration was 2.1 ng/mL (range, 0.1 to 9.4 ng/ mL). Using a cutoff point of 4 mL for testicular volume, 10% of the boys were prepubertal at the average age of 13.6 years. The first significant annual increment in hemoglobin concentration occurred at the average age of 14.6 years when the mean hemoglobin was 13.6 g/dL, the testicular volume was 14.2 mL (range, 3.4 to 29.4 mL), and the serum T concentration was 2.7 ng/mL (range, 0.1 to 6.2 ng/mL). Most of the increase in hemoglobin took place at late puberty, between the ages of 14.6 and 16.6 years, when the hemoglobin concentration increased by 1.6 g/dL in 2 years (Figure 4). During those 2 years, the serum T concentration increased to 5.7 ng/mL (range, 3.6 to 11.7 ng/mL) and the testicular volume increased to 19.8 mL (range, 12.4 to 26.7 mL). The change in RBC was more linear and increased steadily throughout puberty (Figure 4). The serum ferritin decreased during the first year of follow-up, reaching the nadir at the average age of 13.6 years (Table III). Thereafter, the serum ferritin concentration increased.

At the average age of 11.7 years, the blood hemoglobin concentration correlated with the serum IGF-I concentration (r = 0.36, P = .008) but not with the serum T concentration.15 Thereafter, the serum T concentration correlated with the blood hemoglobin concentration at the average ages of 13.6 years (r = 0.35, P < .01) and 14.6 years (r = 0.27, P < .05). At these two ages, there was a close correlation between the blood hemoglobin concentration and the FAI (r = 0.50, P < .001 and r = 0.50, P < .001, respectively). The correlations between T and hemoglobin and between FAI and hemoglobin failed to reach significance at the average ages of 12.6 and 16.6 years.




Iron and Hematological Status among Adolescent Athletes Tracked through Puberty (1995)

This study assessed change in hematological status among physically active children as they progressed through puberty. Values for serum ferritin, hemoglobin, and hematocrit at all stages of puberty were within the normal range of reference values. Significant changes in serum ferritin were not detected in the different pubertal stages, although serum ferritin was highest in prepubertal boys and girls. There were no significant differences in marginal or deficient iron stores between the sexes at any pubertal stage, suggesting that gender was not predisposing for iron deficiency; however, girls had a greater overall incidence for both measures. With more children under consideration, these trends may have reached significance. Boys in TS4 and TS5 had higher hemoglobin and hematocrit compared with earlier stages of puberty and compared with girls at the same stages of puberty. This can be explained by testosterone production in boys. Among girls, pubertal progression had no significant effect on hemoglobin or hematocrit. In the absence of controls, there was no direct evidence that involvement in sports had an adverse effect on iron status.





Androgens and erythropoiesis: Past and present (2009)

*Initial human studies showed that adult men have higher hemoglobin and red cell count than adult women (4, 5). Interestingly, this difference in blood parameters between the two genders is not apparent before puberty, and only after the pubertal spurt, men gain an edge over women in their erythropoietic machinery (6).

 

[madman]

Underlying medical conditions/lifestyle factors could cause elevated hematocrit in young males.

 

[DixieWrecked]

I was looking for a post you had, madman. It had a study showing the rise in hematocrit for each type of T administration. The study showed injections caused the greatest increase.

 

[madman]

I was looking for a post you had, madman. It had a study showing the rise in hematocrit for each type of T administration. The study showed injections caused the greatest increase.

Yes as I stated in a previous thread.

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 TT/FT levels will have a stronger impact on driving up HCT.

Although injectables have been shown to have a greater impact on HCT you can see even when using a transdermal formulation that maintains stable serum concentrations that the impact it has on HCT is DEPENDANT ON THE DOSE AND SERUM LEVEL OF T.

Using higher doses of transdermal T and achieving higher TT/FT levels will have a great impact on HCT levels.

 

[Warrior]

I just had my yearly labs, HCt is always around 51ish, 10yr +TRT user. No sides, 30mg x 3 in 9 days.
Troughed for 5 days prior to labs, normal then is 500ish. Added a larger amount of water pre test, 24hrs of hydration. Normal fast for bloodwork, no diet changes, HCT was 49.
Lowest it's ever been! Guess the hydration works.