Is it true that an elevated hematocrit level on TRT does not require blood donation?

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You obviously post but don't really read anything that you post including the literature. I just sent you a quote from Abraham Morgenthaler that I have actually tape recorded. It is from April of this year he has changed his stance or did you not catch that with my previous explanation. You should probably read and learn something from time to time instead of immediately thinking about what you wanna say without processing what you could have read. Morgentaler adamantly states now that the hematocrit of 54% on testosterone is not harmful even if going above it. It's only harmful because of what other physicians don't know about it. Those are exact quotes from him, so what do you not get that I'm telling you? You're posting an old lecture. Get with the times the updated times. And what is your definition of absurdly high levels? That's your opinion not based on any clinical observations are any actual treatment of men yourself. You have zero clinical experience. It's your opinion. And let me ask you this. Why does anybody have to have a trough? Do you even know why they test at trough? Doctors were taught to do that because they didn't want to see the levels at peak because it would scare them. Depending on the dose whether it be one or 200 mg of testosterone cypionate some mens levels will be anywhere from 2 to 4000.
And the father of testosterone. Well, I know him personally and I talked to him personally regarding the hematocrit issue this year. So get rid of the old information and come on in with the new.
So you don't understand what he's doing with that slide presentation do you? He understands and knows there's no harm with raising the hematocrit above 54% when men are on testosterone as he has stated publicly. I will be glad to send you the recording of him at the androgen society. The reason he makes these recommendations on the slides is to prevent other physicians from getting in trouble by their colleagues that don't know any better. So the point is he knows there's no harm but we all still use that 54% to protect ourselves from our colleagues. He pointed this out very specifically. It doesn't cause harm he said, but others don't know that and that could cause you harm if something happens to the patient because they're going to blame it on you even though we know it doesn't cause harm. Let that sink in a little bit madman because you're just not privy to the inside information.

Again who stated it is harmful?

Get Abe on here.

Better yet let's get Khera and Ramasamy on here!

Throw Mulhall in there too while you are at it.

Yes, I was there! (SMSNA Round Table Webinar)



Dr. Khera (41:47-43:02) and Dr. Mulhall (43:02-43:58)

HCT (34:04-49:36)





post #4


Hematocrit (3:35-6:10) and Secondary Erythrocytosis/Polycythemia/Polycythemia Vera (6:11-7:37)


HCT (32:10-44:58)



So you don't understand what he's doing with that slide presentation do you?

Sure do!

Yet...........

*The clinical significance of a hematocrit >54% is unknown




post #13


Take-home points

*The clinical significance of a hematocrit >54% is unknown


*Although it is not yet clear what upper limit of hematocrit level is clinically desirable, dose adjustments may be necessary to keep hematocrit below 52–54%
 
Defy Medical TRT clinic doctor
This is the only study to date about the risks of high hematocrit in men on TRT (from Dr Ramasamy):



Abstract​

Purpose: An unsafe hematocrit threshold for men receiving testosterone therapy (TT) has never been tested. This study seeks to determine whether secondary polycythemia among men receiving TT confers an increased risk of major adverse cardiovascular events (MACE) and venous thromboembolic events (VTE).
Materials and methods: Using a multi-institutional database of 74 million patients, we identified 2 cohorts of men with low testosterone (total testosterone <350 ng/dl) who received TT and subsequently either developed polycythemia (5,887) or did not (4,2784). Polycythemia was defined as hematocrit ≥52%. As a secondary objective, we identified 2 cohorts of hypogonadal men without polycythemia, who either did (26,880) or did not (27,430) receive TT. Our primary outcome was the incidence of MACE and VTE in the first year after starting TT. We conducted a Kaplan-Meier survival analysis to assess differences in MACE and VTE survival time, and measured associations following propensity score matching.
Results: A total of 5,842 men who received TT and developed polycythemia were matched and compared to 5,842 men who did not develop polycythemia. Men with polycythemia had a higher risk of MACE/VTE (number of outcomes: 301, 5.15%) than men who had normal hematocrit (226, 3.87%) while on TT (OR 1.35, 95% CI 1.13-1.61, p <0.001). In hypogonadal men who received testosterone, no increased risk of MACE and VTE was identified as compared to hypogonadal men naïve to TT.
Conclusions: Developing polycythemia while on TT is an independent risk factor for MACE and VTE in the first year of therapy. Future research on the safety of TT should include hematocrit as an independent variable.
Keywords: adverse effects; hypogonadism; polycythemia; testosterone; thromboembolism.
 

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This is the only study to date about the risks of high hematocrit in men on TRT (from Dr Ramasamy):



Abstract​

Purpose: An unsafe hematocrit threshold for men receiving testosterone therapy (TT) has never been tested. This study seeks to determine whether secondary polycythemia among men receiving TT confers an increased risk of major adverse cardiovascular events (MACE) and venous thromboembolic events (VTE).
Materials and methods: Using a multi-institutional database of 74 million patients, we identified 2 cohorts of men with low testosterone (total testosterone <350 ng/dl) who received TT and subsequently either developed polycythemia (5,887) or did not (4,2784). Polycythemia was defined as hematocrit ≥52%. As a secondary objective, we identified 2 cohorts of hypogonadal men without polycythemia, who either did (26,880) or did not (27,430) receive TT. Our primary outcome was the incidence of MACE and VTE in the first year after starting TT. We conducted a Kaplan-Meier survival analysis to assess differences in MACE and VTE survival time, and measured associations following propensity score matching.
Results: A total of 5,842 men who received TT and developed polycythemia were matched and compared to 5,842 men who did not develop polycythemia. Men with polycythemia had a higher risk of MACE/VTE (number of outcomes: 301, 5.15%) than men who had normal hematocrit (226, 3.87%) while on TT (OR 1.35, 95% CI 1.13-1.61, p <0.001). In hypogonadal men who received testosterone, no increased risk of MACE and VTE was identified as compared to hypogonadal men naïve to TT.
Conclusions: Developing polycythemia while on TT is an independent risk factor for MACE and VTE in the first year of therapy. Future research on the safety of TT should include hematocrit as an independent variable.
Keywords: adverse effects; hypogonadism; polycythemia; testosterone; thromboembolism.

Yes, Khera laid it out here. (41:47-43:02)

Better yet Mulhall put the icing on the cake! (43:02-43:58)


 
But hey brother, you realize the hematocrit is 60% is normal in some labs don’t you? It’s normal on our nuclear aircraft carriers. It’s normal if you live at high altitude in certain areas of the world. Why are they not all dropping dead a heart attack strokes and blood clots? Can you answer me that?
curious how we know Hct of 60 is normal on Nuclear aircraft carriers?
 
But hey brother, you realize the hematocrit is 60% is normal in some labs don’t you? It’s normal on our nuclear aircraft carriers. It’s normal if you live at high altitude in certain areas of the world. Why are they not all dropping dead a heart attack strokes and blood clots? Can you answer me that?
"In order to compensate for the low partial pressure of oxygen at altitude, the human body undergoes a number of physiological changes. A vital component in this process is the increase in the concentration of circulating hemoglobin. The role of HIF-1alpha, erythropoietin and red blood cells in this acclimatization process is described, together with the fall in plasma volume that increases the concentration of hemoglobin in the early stages of hypoxic exposure."

Difference between these people at high altitudes and men on TRT: Men on TRT have increased plasma & blood volume AND increased hemoglobin/hematocrit.

Full paper: Heights and haematology: the story of haemoglobin at altitude

Prevalence, Clinical Profile, Iron Status, and Subject-Specific Traits for Excessive Erythrocytosis in Andean Adults Living Permanently at 3,825 Meters Above Sea Level

"We found a lower prevalence of high red blood cells than in previous reports in the Peruvian Andes. Although the presence of hypoxemia and decreased vital capacity were strongly associated with excessive erythrocytosis, being overweight or having metabolic syndrome were associated with an important fraction of cases in our study population."

Lack of Prominent Compensatory Polycythemia in Traditional Native Andeans Living at 4,200 Meters

Abstract
Red blood cell count (RBC), hemoglobin concentration ([Hb]) and hematocrit (Hct) were measured in 303 male Quechua children and adults, aged 6 to 57 years, living a lifestyle as traditional pastoralists and horticulturalists at a mean altitude of 4,200 m in the Southern Peruvian Andes. Values for RBC, [Hb], and Hct increased with age from middle childhood to young adulthood. However, among adults there was no significant association between age and any of these three parameters. Overall, there was approximately a 10-12% increase in the RBC, [Hb], and Hct above sea-level norms for all age groups. Mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) showed a slight but significant increase with age in children and adolescents, but the mean corpuscular hemoglobin concentration (MCHC) did not. We conclude that the study of highland Quechua Indians, living a traditional lifestyle as pastoralists and horticulturalists, does not support the long-held belief that altitude hypoxia provokes a dramatic compensatory polycythemia in healthy Andeans.
_________________________________________
"
We demonstrated that developing secondary polycythemia while receiving TT, defined as a hematocrit over 52%, was associated with increased risk of developing MACE and VTE during the first year of therapy. TT itself, in the absence of polycythemia, did not appear to increase risk of MACE/VTE in hypogonadal men. To our knowledge, this is the first study to establish secondary polycythemia from TT as an independent risk factor for MACE/VTE using a specific hematocrit-based cutoff."

Kaplan-Marans, Elie. "Secondary Polycythemia in Men Receiving Testosterone Therapy Increases Risk of Major Adverse Cardiovascular Events and Venous Thromboembolism in the First Year of Therapy. Letter." The Journal of Urology (2022): 10-1097.

 
"We demonstrated that developing secondary polycythemia while receiving TT, defined as a hematocrit over 52%, was associated with increased risk of developing MACE and VTE during the first year of therapy. TT itself, in the absence of polycythemia, did not appear to increase risk of MACE/VTE in hypogonadal men.
I think this is important and speaks to the possibility that high hematocrit is a biomarker for the type of unhealthy man that is at higher risk for MACE and not necessarily the causative factor:

baseline hematocrit was higher in the men who developed polycythemia vs those who did not (47.4% and 42.5%, respectively).
we were not able to match the 2 groups by baseline hematocrit, as the men in the polycythemia group had a higher baseline hematocrit. Therefore, we cannot definitively determine whether the increased risk of MACE/VTE is due to hematocrit reaching 52% or due to men with higher baseline hematocrit starting TT.

From what I've read, most people's hematocrit will increase somewhere around 5% on average when they start TRT. There are some other factors like dosage and protocol but where you end up is largely dictated by where you began. And the type of person that has a high baseline hematocrit is usually suffering one or more of the following associated conditions: obesity, hypertension, smoker, insulin-resistant / pre-diabetic / diabetic, sleep apnea, metabolic syndrome, heart failure, etc.

Boy, if that isn't a group of people that would be at much higher risk for MACE. Now, they tried to control for this in the study with "propensity matching": including equal numbers of people with obesity, hypertension, etc. in both groups. However, all of these conditions exist across a wide spectrum of severity. I think it is likely that the high baseline HCT group had higher severity comorbidities than the low baseline HCT group. That seems like the most plausible explanation for the HCT differences, because HCT correlates closely and positively with the severity of those conditions.

So, if elevated HCT is something to worry about, it may not be because it does anything harmful itself. It may just be an indicator that you are suffering from any number of other conditions that increase your MACE risk.
 
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Didn’t you just babble that the leaders in the field made the cut off at 54% ? I pointed out to you that Morgentaler has changed his stance and Mel knows that a Hct above 54% is not harmful while on testosterone. You also bully and degrade men for having testosterone levels outside of the normal sick range. Yes, madman men need testosterone , and they need their levels to be super physiologic most of the time. The upper cut off is 917 now so 918 is now super physiologic. You have a strong opinion on numbers. Let me give you an example if you were a physician. A patient comes to see you and he needs testosterone so you give it to him at your normal starting dose. His levels come back at 700 let’s say and a free 18 and he says I’m still having a lot of problems with erectile dysfunction and fatigue and depression and I’m continuing to gain weight and lose muscle despite exercising and dieting, etc. So mad man hopefully will increase the dose And then he comes back with a level of 1500 and he says man I feel great. All my symptoms have completely resolved. My lipids have improved, I’ve lost 30 pounds, I no longer have any erectile dysfunction, I don’t have any fatigue, and I feel great. I’m off of my statin and I don’t take blood pressure medicines anymore. My free testosterone is 50 by the way. Mad man then says “no man needs a free testosterone of 50 you need to lower your dose “so he lowers his dose and then he goes back to feeling bad and comes back and says I don’t feel good mad man And mad man will say too bad because you don’t need the level that you had before. Madman treats, a number not a patient. You have repeatedly done this over and over again the men on this forum where you attacked them for their levels yet they’re doing fine with their levels, and every parameter of their health are improving. You need to get your head out of where the sun doesn’t shine.
not getting personal here, everyone has an opinion but when I started TRT via my general doc, he literally told me he doesn't want to treat numbers, but he HAS to treat numbers. and this sums up the entire western medical system in 1 sentence. a cluster fuck beyond repair. now not saying to ignore fasting glucose, but T levels and HTC levels and lipids to some extent are a different story
 
Concerns brought up by @tareload and @Dr Justin Saya MD have not been addressed.

...
Blood viscosity is non-linear function of Hct. I cringe when I see videos/posts stating that you actually are just fine in the mid to upper 50s. That’s why those truly informed start talking about protective measures when you start using TRT/AAS to counteract these issues. Some that bear discussion include losartan (ARB), taurine, alpha-lipoic acid, etc. Then there's the even simpler discussion of reducing your T dosage vs phlebotomy.

Do you really want your heart working 20% harder all the time when it’s avoidable. Integrate that work over a significant time span and you start to see potential for early (earlier than it needs to be) heart failure.

Enjoy the reading:
Effect of hematocrit on blood pressure via hyperviscosity
...
The non-linear relationship of hematocrit to blood viscosity is lost in the weeds to many (think 10% increase in hematocrit = 20% increase in blood viscosity). An astute researcher will also note that the slope of the blood viscosity curve starts increasing right around the low-mid 50s for hematocrit.
I've seen a number of comments (even interviews with Experts) trying to rationalize running Hct high because there's plenty of people at high altitude that do just fine with high Hct. Truth is there are a fraction of these folks that suffer significant symptoms and they are a great group to study and see how excess blood viscosity manifests in increased cardiovascular risk:

High Blood Viscosity and Hemoglobin Concentration Contribute to Reduced Flow-Mediated Dilation in High-Altitude Excessive Erythrocytosis
...
 
I have a degree in biochemistry... Thick blood can be dangerous ...It puts pressure on the rest of the body..U see this with BP raises .Heart pups harder with thick blood.....Too many other things to list...

Heres the deal that they refuse to address...When people have high chronic hct/hgb who live in high altitude the body has a compensatory reaction... I have not researched this area, but this is how the body works.. Overtime the body will compensate for something being out of range called [homeostasis]. So if we were to take a deeper dive into this I'm sure we will find a compensatory Factor in high elevation patients..

My opinion is try to keep the hemoglobin in normal range with phlebotomy or naringin pills and take really good iron supplements if ferritin is low ... ... Unless you have hemachromatosis then I would not take Iron unless u get a monthly ferritin check...

Also long-term studies have not come out with artificially raising our hgb/hct in short term ...... Being overcautious never killed anyone...

Most important thing I want to address here.. Listen to your body!! If you don't feel well/right when your hgb gets high then it's your body telling you something..
 
TBH after all of this a feel a bit at square 1. I personally have no symptoms whatsoever with a HTC which is high (it varies 54-57). I was told to reduce my dose, but my HTC was exactly the same 120mg <> 210mg. going lower is not an option i might as well stop. donating - all it does it keeps a clean paper-trail for the clinic. i don't mind helping people with donation ofc, and even just for that I will do it.
my BP is slightly elevated, but it was that way since I was 20y old. taking meds currently and making adjustments in that regard, but it is not TRT ot hematocrit related for sure.
stopping TRT will send me back to my depressed fat state, and TBH even if this level is bad, i rather die a bit younger then continue in a low T vegetable state like. i fully understand that you might get strokes and so on as well ,but where is the data that people on TRT with elevated hematocrit get those at a significantly more percentage - pls send me the link i must have lost it.
 
where is the data that people on TRT with elevated hematocrit get those at a significantly more percentage - pls send me the link i must have lost it.
For argument's sake, lets say people on TRT with elevated hematocrit ARE at higher risk of stroke. How should that affect your personal decision-making?

If what you stated is true, the risk comparison to make is not the stroke risk of a lean healthy person with low HCT versus the same person with high HCT. The comparison is lean healthy person with high HCT versus fat depressed person with low HCT.

Both obesity and depression are cold-blooded killers that increase the risk of all major causes of death, including heart disease, cancer, and dementia. If I were concerned with longevity, I'd take an elevated HCT over obesity or depression any day of the week and let the TRT rip.
 
Interesting conversations going on. Thank you guys for keeping this civil. No we can all learn something.

I am still wondering if the ester of the testosterone can make a different in HCT. I have been on this stuff for almost 43 years now. My HCT has never gone any higher that 50%. So I get on prescription cypionate (which I never used before) and all of the sudden it was 59% at much lower doses than I have ever used. I did a few dumps and got it to 54% but the dramatic change occurred when I stopped the cypionate and went back on undeconoate. Last I checked I was at 50.4%
 
I am still wondering if the ester of the testosterone can make a different in HCT. I have been on this stuff for almost 43 years now. My HCT has never gone any higher that 50%. So I get on prescription cypionate (which I never used before) and all of the sudden it was 59% at much lower doses than I have ever used. I did a few dumps and got it to 54% but the dramatic change occurred when I stopped the cypionate and went back on undeconoate. Last I checked I was at 50.4%
Theoretically it shouldn't make much difference, but having experienced some unique harms at the hands of cypionate myself, I know better than to say it's impossible.

Based on the reduction in HCT seen in studies with more frequent dosing, and reduction in HCT by moving from IM to SC injection, we can say that HCT is driven higher by higher peak T values. That means any ester or protocol which keeps levels more stable (like your undecanoate) would minimize impact on HCT.
 
Interesting conversations going on. Thank you guys for keeping this civil. No we can all learn something.

I am still wondering if the ester of the testosterone can make a different in HCT. I have been on this stuff for almost 43 years now. My HCT has never gone any higher that 50%. So I get on prescription cypionate (which I never used before) and all of the sudden it was 59% at much lower doses than I have ever used. I did a few dumps and got it to 54% but the dramatic change occurred when I stopped the cypionate and went back on undeconoate. Last I checked I was at 50.4%
For some reason older people have a way bigger problem with hematocrit than younger people... I was the same way never had a problem with hemoglobin what's so ever ,then when I had 40 all of a sudden huge problems with hemoglobin... This is not uncommon with each factor also other factors sleep apnea etc. etc.... You can develop sleep apnea age and that's a huge contributor..Plus trt exacerbates sleep apnea..
 
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I am still wondering if the ester of the testosterone can make a different in HCT.
@madman created a thread about a urologist using Kyzatrex (oral T) on his patient's and has never seen one case of erythrocytosis.

It could have been Dr. Abraham Morgentaler who said this about oral T. I believe he made this statement on YT that it was due to the rapid decline in hormones over a 12 hour period rather than 3-4 days on injections.

Kyzatrex is cash only and about $150 per month, not as cheap as injections, but if you can run higher T levels without having to worry about HCT, this could be a gamechanger for you!

 
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@madman created a thread about a urologist using Kyzatrex (oral T) on his patient's and has never seen one case of erythrocytosis.

It could have been Dr. Abraham Morgentaler who said this about oral T. I believe he made this statement on YT that it was due to the rapid decline in hormones over a 12 hour period rather than 3-4 days on injections.

Kyzatrex is cash only and about $150 per month, not as cheap as injections, but if you can run higher T levels without having to worry about HCT, this could be a gamechanger for you!

I know the original oral T was terrible ..Was called andriol...Like test creams and gels they just dont work as good...Hence probably why the HCT dont go up ...Anyone who has been on both like me will tell u its a world of difference from cream to injection...Especially anyone who uses it for bodybuilding...The results are a joke..
 
Theoretically it shouldn't make much difference, but having experienced some unique harms at the hands of cypionate myself, I know better than to say it's impossible.

Based on the reduction in HCT seen in studies with more frequent dosing, and reduction in HCT by moving from IM to SC injection, we can say that HCT is driven higher by higher peak T values. That means any ester or protocol which keeps levels more stable (like your undecanoate) would minimize impact on HCT.

TBH my HTC went down slightly when going to daily Tprop injections. my clinic confirmed that some people see this. maybe its not the peaks but lows somehow
 
TBH my HTC went down slightly when going to daily Tprop injections. my clinic confirmed that some people see this. maybe its not the peaks but lows somehow
I think there is another component, which is time spent at the peak. The propionate peak might be too short lived to drive HCT up compared to reaching the same peak with cypionate or enanthate. I think this is why you don't see erythrocytosis with oral T.
 
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For some reason older people have a way bigger problem with hematocrit than younger people... I was the same way never had a problem with hemoglobin what's so ever ,then when I had 40 all of a sudden huge problems with hemoglobin... This is not uncommon with each factor also other factors sleep apnea etc. etc.... You can develop sleep apnea age and that's a huge contributor..Plus trt exacerbates sleep apnea..
In my case I was already doing TU for years at much higher doses (750-1000mg/mo) that I am doing now (55mg every 5 days). My HCT never went over 50%. Before that it was 250mg/wk of enanthate. Never a problem. As soon as my doctor put me on Test cyp (2 years ago), it suddenly shot up to 59%. I am 68 years old. I have been using a CPAP for maybe 15 years. So the only thing I can tie this too is the cypionate.
 
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