Erthrocytosis vs polycythemia
See second reference in thread below (June 2022).
Kaplan-Marans, Elie. āSecondary Polycythemia in Men Receiving Testosterone Therapy Increases Risk of Major Adverse Cardiovascular Events and Venous Thromboembolism in the First Year of Therapy. Letter.ā The Journal of Urology (2022): 10-1097.ā
From the first reference above:
Cervi A, Balitsky AK. Testosterone use causing erythrocytosis. CMAJ. 2017;189(41):E1286-E1288. doi:10.1503/cmaj.170683
@mnben87
Thanks for this.
It would be wise to keep a close eye on blood viscosity while in TRT, or at least the measurable symptoms of it.
Make sure you understand your own unique situation with inflammation, plasma viscosity before hand waving that elevated Hct is harmless. Devil is in the details and still much remains to be uncoveredā¦
Blood viscosity and its determinants in the highest city in the world
Haemorheology
Paradoxically, although high altitude residents are known to experience profound haematological changes such as hypoxia-induced polycythaemia (Beall, 2007), very few data are available regarding their blood rheological characteristics. Kametas et al. (2004) previously reported lower blood viscosity in Andean women at 4800 m than those found in our study. However, the authors made an estimation of blood viscosity and did not measure it directly, making the comparison with our study difficult. Moreover, at sea level, women usually have lower blood viscosity than men (Gudmundsson & Bjelle, 1993; Kameneva et al. 1999) and one could speculate that this difference persists at high altitude. More recently, Tremblay et al. (2018) measured blood viscosity in Sherpa on ascent to 5050 m and also found lower values compared to the values observed in the present study but this finding may be attributable to their rather low haematocrit values and also to the lack of change during the ascension (44 Ā± 3% at 1400 m and 44 Ā± 2% at 5050 m). Moreover, the authors measured blood viscosity only at 225 sā1 while measurements were performed at 11.25, 22.5 and 45 sā1 in the present study using the same viscometer as Tremblay et al. (2018). Because blood is a shear thinning fluid, as well as because of important phenotypic differences between Andeans and Sherpas (Beall, 2007), comparisons of values from Tremblay et al. and the present study are rather difficult. However, it is likely that blood viscosity was significantly higher in our population since measurements were not possible at 225 sā1 because the percentage of torque obtained on the viscometer was higher than 100% at shear rates higher than 90 sā1. In the present study, as expected, Andean highlanders chronically exposed to hypoxia exhibited higher blood viscosity compared to individuals living at sea level, and these effects were not related to BMI or age differences (parameters known to potentially affect blood viscosity; Brun et al. 2011; Simmonds et al. 2013). In support of this, chronic hypoxic exposure in rat models was shown to increase haemoglobin concentration, haematocrit and blood viscosity (Yelmen et al. 2011; Pichon et al. 2012).
At 5100 m, blood viscosity measured at native haematocrit and at the two highest shear rates was higher in highlanders with moderate-to-severe CMS than in highlanders without CMS, suggesting that blood viscosity could also play a role in the development of CMS. A rise in blood viscosity has previously been observed in Andeans with EE (Tremblay et al. 2019) but the relationship between CMS symptoms and blood viscosity has not yet been studied. Surprisingly, blood viscosity measured at the lower shear rate (i.e. 11.5 sā1) was not different between the three groups living in La Rinconada, despite the higher haematocrit and haemoglobin observed in both groups with CMS compared to highlanders without CMS. Blood viscosity depends on RBC aggregation, plasma viscosity and haematocrit at low shear rate, while haematocrit exerts less influence at high shear rate. A loss of RBC deformability may also profoundly affect blood viscosity (Cho & Cho, 2011; Nader et al. 2019). RBC aggregation was lower in highlanders with moderate-to-severe CMS compared to individuals without CMS, which could have partly offset the effects of the increased haematocrit and haemoglobin levels on blood viscosity measured at the lowest shear rate. The reasons for the lower RBC aggregation found in individuals with moderate-to-severe CMS are unknown and need to be explored further but several mechanisms such as lower plasma fibrinogen, thrombospondin, von Willebrand factor concentrations (plasma factors) or difference in RBC membrane sialic contents (cellular factors) (Baskurt & Meiselman, 2013; Nader et al. 2017; Gondelaud et al. 2020) could be involved. At higher shear rates, blood viscosity was higher in the most severe group compared to highlanders without CMS but no significant difference in blood viscosity was noted between the mild CMS group and healthy highlanders despite the fact that haematocrit and haemoglobin concentration were higher in the two groups with CMS. Nevertheless, the multivariate analysis showed that blood viscosity was independently associated with the CMS score, emphasizing that blood viscosity may play a role in CMS severity. Altogether, these results suggest that RBC deformability could be severely impaired in the most severe CMS group, which, in association with the high haematocrit/haemoglobin levels, could lead to a further rise in blood viscosity. When measured at corrected haematocrits, highlanders with moderate-to-severe CMS maintained a very high blood viscosity in comparison to individuals with no CMS (+100% at 22.5 sā1) and also compared to highlanders with mild CMS (+70% at 22.5 sā1). This further supports the idea that RBC deformability was different between highlanders with moderate-to-severe CMS and the two other groups. In contrast, the mild group had only a slightly higher blood viscosity than the group with no CMS (+20%), which suggests that RBC deformability, and perhaps plasma viscosity, was not dramatically different between these two groups. Unfortunately, it was not possible to measure these two parameters in the present study, nevertheless it has been shown that RBCs stimulated by altitude hypoxia in highlanders from the Tibetan plateau have an increased osmotic fragility and higher haemolytic rate, suggesting a loss of deformability (Zhong et al. 2015). Whether these data from Tibetans apply to Andean populations remains hypothetical. Therefore, further studies are required to better understand the relationship between polycythaemia and blood viscosity at high altitude. Other specific hemorheological parameters (plasma viscosity and red blood cell deformability, as well as its determinants, i.e. RBC internal viscosity, RBC membrane deformability and RBC surface-to-volume ratio) should be investigated to elucidate the mechanisms involved in CMS.
Limitations
The potential impact of toxic exposure in mining facilities remains unclear and difficult to evaluate. Previous studies suggested an effect of increased blood concentrations of zinc, lead and cobalt on red blood cell production and haematocrit (Hutchison & Stark, 1961; Jefferson et al. 2002; Gonzales et al. 2011). In La Rinconada, mercury is used to extract gold and represents the main risk of contamination, but its potential impact on blood viscosity remains unknown. Mining at altitude has also been reported to accelerate pulmonary disease, like silicosis and other pneumoconiosis, known to worsen hypoxaemia and to affect cardiopulmonary function (Vearrier & Greenberg, 2011). The pathogenic role of environmental factors on blood viscosity and CMS onset probably is insufficiently considered and should therefore be investigated in future studies.
Conclusions
The present study investigated for the first time blood viscosity and some of its determinants (RBC aggregation and haematocrit) in the highest city in the world (5100 m), in highlanders chronically exposed to severe hypobaric hypoxia with or without CMS. Living at high altitude resulted in an increase in haemoglobin concentration, haematocrit and blood viscosity. At 5100 m, highlanders with CMS had higher blood viscosity mainly at high shear rate and even at corrected haematocrit, with a lower red blood cell aggregation, suggesting that lower red blood cell deformability might promote increased blood viscosity and contribute to the occurrence of CMS symptoms. Further studies are required to clarify the relationship between chronic hypoxic exposure, red blood cell deformability and other determinants of blood viscosity.
I tried to read as much of this as my brain could handle but it got so overloaded with new acronyms I got lost. I came here because I absolutely experience issues from high hematocrit and RBC directly associated with TRT. I do not even require a test to know it is high although I do get them, my body feels absolutely awful when itās at 50+ (Hemoglobin and RBC are also high as well as MCV MCH MCHC RDW and MPV are all touching the high end of the spectrum) but SHBG is only 18 with total T of only 562 and free T at 152. My T dosage is down to 0.3 ml twice a week. I cannot breathe at all. Itās awful. One step on a stair and Iām sucking wind. My athletic ability is nil. After a phlebotomy I am back to being able to do jiu-jitsu.
So whatās the plan if lots of blood donations arenāt a great idea? An aspirin? I see you used something you refer to as āTCā but I canāt find the actual name unless youāre referring to cypionate, which is what I do (60ml/wk split into 2 doses). Thanks.
I recall a doctor talking about a patient who had been on TRT for many years, went to high elevation (13,500 ft) and was out of breath, tingling in his hands and face with a hematocrit at 52%.
His doctor knew exactly where to look and knew it wasnāt going to be good. He had left anterior descending artery or 75% blockage.
My point is if you canāt handle hematocrit above 50%, and have problems breathing, itās very possible something is wrong with you. My advice, donāt brush it off, find out why!
Iāve had my hematocrit at 57% and no symptoms.
What are the symptoms?
Cuz i have had it high as fuck and besides the labs, i never felt any difference.
You said you were sucking wind, it doesnt make sense as cardio athletes use blood doping to increase the RBC count because RBC carries oxygen so i would be under the impression that if something, it increases endurance. Therefore EQ is popular for endurance, and it is known to increase hematocrit and rbc more than any other drug - it is a drug for race horses and very popular for crossfit and MMA.
Also, do you test hematocrit in early morning or in the evening?
See your doctor.
Same as they list for anyone. Fatigue, labored breathing, sleep sweats, light headedness, etc. Athletes that abuse EPO are endurance athletes, if they donāt perform that incredibly high level of work rate they risk serious complications including death. I realize that sounds backwards given the reason they use EPO but thems the facts. EPO is sort of like a fuel that is so high test if you donāt burn it fast it will eat through your tank.
Oh for the love of god you actually posted that? As if I havenāt spoken to my doctor already?
What did your doc suggest?
This is the same for me. Once Iām up and moving Iām fine, but if Iām on the couch and get up I feel like shit. Hard to explain but just off. Blood pressure rises and I have a light but constant headache. As soon as I drop below 50 I feel more energetic and better in general, and blood pressure returns to normal.
As far as I know I do not have further issues. I have gone through an ekg or ecg (canāt remember which) and the doc said Iām borderline for left ventricular hypertrophy, but also suggested wall thickness is likely from a lifetime of sports and weight training. All other cardio markers are great, with stage one HBP well controlled via medication.
My non-med professional take is that we all have veins capable of managing varying levels of volume and consequent pressure. My āPSIā rating may be different than another, and staying under 50 is necessary. Ideally around 45 for me.
Doctors are not infallible, I would even argue many of them are useless in more complicated issues such as this.
I actually did. Just like you actually went on the internet and actually sought advice from strangers regarding a medical condition which may be serious. You did this without reporting even a minimal amount of medical history, for starters, perhaps your age, height and weight?
Yeah, as if. I would think not, because if you did, you would have a satisfactory solution and/or explanation to your problem. Therefore you would not have felt the need to seek out advice on the internet. Part of a normal history would include previous tests, exams, consultations, etc. Since I now know you consulted your doctor, I concede my assumption was incorrect. Sorry.
I assume whatever your doctor did or said was insufficient, leading you to the internet for information and solutions. Good luck, hope you find your answers.
Yet here we are on a forum with thousands and thousands of posts from men who indeed see a doctor regularly and no consensus seems to have been reached on these issues between medical professionals. So I thought, Hey why not see what sort of solutions other people may have found that hasnāt become standard treatment. Among the valuable things I learned here was ferritin loss occurs with frequent phlebotomies. My doctor, the all knowing, wasnāt even testing for ferretin. I had to request it, thanks to āgoing on the internet and seeking advice from strangers.ā
Their posts were constructive. Yours, not so much.
I take a beef liver supplement (not liver king fwiw) and my ferritin stays in line. I donate every three months for context.
Your ferritin was low with those values high?
Your MCV, MCH and MCHC were low following phlebotomy?