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

[sbstrum_MD]

Rosier is talking rubbish, platelets having little to do with it, I have polycythaemia Vera since 13 years and have consulted many of the worlds experts Haematologit’s. It’s the Hct or Hgb or RBC that are the main culprits for clotting, WBC a bit maybe, platelets are not usually treated or a concern unless weLL over 1 million unless symptomatic or other relevant health risks

Sorry, as someone that has been in cancer medicine for 60 years, platelet numbers do matter. High platelets can result in thrombosis or in bleeding. Other factors come into play here as well and relate to what medications & supplements the patient is taking. For example, a patient taking aspirin will increase their chance of a hemorrhagic event due to aspirin's effects on platelet aggregation and adhesion. And in comparing the potential adverse effect of an elevated platelet count vs. WBC, the former is far more important unless the patient's WBC is in the 20,000 or higher range. HCT and HGB essentially reflect the same information. I rely on HCT as the slightly more accurate test but the rule of thumb is Hgb x 3 ≈ HCT. For adults, I know of no hematologist, or oncologist who bothers with the RBC count unless you are dealing with a patient having a hemoglobinopathy like thalassemia.
It is also important to not only examine the patient's context regarding medicines and supplements vs. bleeding or thrombosis, but also the patient's total health picture. Some co-existing diseases can heighten the risk of thrombosis. For example, cancer patients. have an ↑risk of thrombosis. Those with inflammation as a component of their illness (e.g., Crohn's disease, ulcerative colitis, collagen-vascular diseases) will increase their risk of thrombosis.
I do agree with your main statement, however, that it is the HCT that is the major or a major factor in vascular thrombosis.
Stephen B. Strum, MD, FACP

 

[Systemlord]

It's not a KNOWN or PROVEN risk, it is a theoretical risk

This ^^.

 

[Systemlord]

We had to push my T3 levels above the normal range, and then, finally, without hand shaking, no increase in BP, no increase in heart rate, no detectable side effects, then I got relief.

I can’t even handle high normal T3 levels. I’m normal at midrange. We’re all different.

 

[Cataceous]

... I think, it would be smart for everyone to take a step back, and rephrase the question and issue. It's not a KNOWN or PROVEN risk, it is a theoretical risk, but one which could carry SEVERE consequences including death. ...

What you mean is that it's not a well-quantified risk. The increase in blood viscosity with HCT is clearly demonstrated. The risks of higher viscosity are more than abstract, suggested even in the high-altitude data, where individuals with higher inflammation and/or reduced compensatory mechanisms appear to get into trouble.

For the average Joe on TRT there is no good reason to be on supraphysiological amounts of testosterone, risking side effects such as elevated HCT. What is the point if hypogonadism can be resolved with 50-100 mg TC/week? It's down to the misguided more-is-better mentality. If a guy truly needs excessive doses of testosterone to feel better then there's something else going on, and a good doctor would try to find out what it is.

... Having been thru getting adequate treatment for hypothyroidism, and the fact that even many endocrinologists don't want to stray from the therapeutic windows created by lab results of unhealthy people, who simply have not been diagnosed as hypothyroid and therefore called "normal" and still feeling very sluggish, in the middle of that range, I am a little skeptical when the community wants to label a certain number as normal, and a tick or so above, is abnormal. We had to push my T3 levels above the normal range, and then, finally, without hand shaking, no increase in BP, no increase in heart rate, no detectable side effects, then I got relief. ...

I'd argue the same principle applies here. I would be very uneasy if I lacked an understanding of why I needed such high levels to feel better. With respect to elevated T3, the mortality statistics are not reassuring. But then we're back to "it's only observational, and doesn't prove causality". Fine, but the results better be pretty good to bet your life on it.

 

[Systemlord]

If a guy truly needs excessive doses of testosterone to feel better then there's something else going on, and a good doctor would try to find out what it is.

Like testosterone resistance, which can have multiple causes. The why doesn’t always lead to something actionable.

I’m resistant to all type 2 diabetes drugs.

Sometimes, more testosterone is better.

 

[BigTex]

First off, thank you very much for taking the time to reply doctor. With all due respect, I use the same lab every time (Quest) and am certainly not close to being dehydrated. I drink at minimum 1 gal of water/day and have for years. I absolutely have no symptoms including headache, fatigue, blurred vision and/or paresthesias. Not even when I had a HCT of ~59%. I might expect some fatigue since I take metoprolol, telmisartan, rhGH and Mk677.

Here is my September testing. I am doing 55mg of test undeconoate every 5 days, sub-q.
PLATELET COUNT 281 Reference Range: 140-400 Thousand/uL
RED BLOOD CELL COUNT 5.66 Reference Range: 4.20-5.80 Million/uL
HEMOGLOBIN 16.8 Reference Range: 13.2-17.1 g/dL
HEMATOCRIT 50.4 H Reference Range: 38.5-50.0 %

By the way, I also hold the cypionate for my E2 levels going crazy. When I started in Jan or 2022 it jumped from 38 to 66 and once I stopped the TC and switched to TU it dropped to 24. My doctor told me to take anastrozole 2 days a week, but I refused to use it because I know it will crash my E2 levels badly.

Everything is in the normal high range except HCT which is 0.4 points high. Most experts in the medical society, as we have already seen posted here, agree that >54% is a problem. So as long as I see it continually going down, I am not going to get excited and do a bunch of blood dumps and risk crashing my iron levels. I have learned a long time ago that patients is a virtue in TRT as well as using anabolic steroids. Figure out what esters work for you and find a sweet spot and stay with it. Drastic changes cause problems which take a while to fix. I honestly think most doctors over prescribe blood dumps and many don't bother testing iron levels. Luckily mine are fine

Here is another test from 2010 when I was on a full blown cycle 250mg of test enanthate/wk, 100mg of primabolin enanthate/wk and 100mg of trenbolone enanthate/wk. I was still competing in powerlifting

PLATELET COUNT 183 140-400 Thousand/uL
WHITE BLOOD CELL COUNT 11.5 H 3.8-10.8 Thousand/uL
RED BLOOD CELL COUNT 5.54 4.20-5.80 Million/uL
HEMOGLOBIN 17.9 H 13.2-17.1 g/dL
HEMATOCRIT 52.9 H 38.5-50.0 %

HEMOGLOBIN- 0.8 point high
HEMATOCRIT- 2.9 points over 50% and well below the >54% mark

Not so bad considering what all I was taking (450mg/wk total).

Yet another in 2017 using 1000mg of test undeconoate/month plus either 20mg of oxandrolone or 25mg of stanozolol/d This is definitely not a TRT dose either

PLATELET COUNT 311 140-400 Thousand/uL
WHITE BLOOD CELL COUNT 9.0 3.8-10.8 Thousand/uL
RED BLOOD CELL COUNT 5.65 4.20-5.80 Million/uL
HEMOGLOBIN 16,8 13.2-17.1 g/dL
HEMATOCRIT 52.9 H 50.9 -50.0 %
TESTOSTERONE - 772

Again, 0.9 points high on the HCT and everything else is well within the normal range. Again, these are not TRT doses.

I have done high doses for many years and have always paid close attention to how much water I consume because of my job. I weighed every day before practice and for every pound I lost in sweat after practice I replaced it in water before i went home. I was a football coach at the time, now retired. I have never had any symptoms of high HCT and would not expect to being <54%. Now, my doctor did send an order for me to do a blood dump, but I am not going to go. I go for more testing next week and expect to be at or less than 50%. Especially eating a grapefruit every day for a year.

Here are my ranges since 2010 - present
PLATELET COUNT 311- 280 140-400 Thousand/uL
WHITE BLOOD CELL COUNT 7. -,14.6, 3.8-10.8 Thousand/uL
RED BLOOD CELL COUNT 5.3 - 6.42 4.20-5.80 Million/uL
HEMOGLOBIN 16,8 - 20.2 13.2-17.1 g/dL
HEMATOCRIT 50.4 - 58.5

ALL of the TRT high ranges were when my doctor put me on test cypionate.

Jan - March(2022) - 2103 Test cyp 150mg every 10 days he started me with 150mg every 10 days. The free testosterone shot up to 2130. HCT shot up as well.

I dropped it to 100mcg every 10 days in March and still the HCT was high. In the time I was doing blood dumps every month with HCT dropping a little bit.. The T levels were still high but dropping..

In April, I dropped the dose to 80bg, every 10 days and still was around 56 HCT. As you can also see my free test also dropped to 549 which for me is totally unacceptable.

In October of 2022 I dropped the test cyp completely and started on 55mg of test undecanoate every 5 days. My hct started dropping from 57 - 53 in 90 days and my test levels gradually started to increase from 549 to the 750-800 level. I stopped the blood dumps and have not done one dump in 2023, yet my HCT continued to drop from 53 to 50.4. Changes in HCT levels are very slow and I know you are aware that it can take 90 days minimum to see changes. Unlike my doctor, I prefer to be very patient in this and know much better what doses I need and what esters work best in my body. I have never reacted good with test cyp since I first used it in 1982. If my patients doesn't do the trick I can always resort to dumps.

TRT dosing since 2022
March - April - 839 T 100mg every 10 days
April - October - 549T 80mg every 10 days
Nov - present (2023) - 55mg of testosterone undecanoate every 5 days

 

[BigTex]

For the average Joe on TRT there is no good reason to be on supraphysiological amounts of testosterone, risking side effects such as elevated HCT. What is the point

I certainly agree but I know plenty who claim they are on TRT but doing supraphysiological doses as part of blast and cruise method. Especially guys over 50. Correcting these side effects can take a while. I cant disagree at all that starting very low and gradually increasing until you and a sweet spot is best. So may TRT doctors don't agree and use cookie cutter prescriptons..

 

[sbstrum_MD]

Like testosterone resistance, which can have multiple causes. The why doesn’t always lead to something actionable.

I’m resistant to all type 2 diabetes drugs.

Sometimes, more testosterone is better.

Stephen B. Strum, MD, FACP: I hate to invoke something as basic as education and experience, but that is foundational to any discussion. When one is involved in another human life, the integrity of that life is the Prime Directive. This means observing what you are doing and that also goes beyond simply ordering a lab or imaging study. Today's medicine is McMedicine (i.e., fast-food medicine like In n' Out Burger). It misses the mark about "Above all do no harm" and "listen to the biology" and "talking to patients."

When you are dealing with the ramifications of a lab test you MUST take the patient context into account . How is that patient doing, what is the trend, what objectively have you accomplished, and have you put the patient into harm's way? Labs vary from one to another in quality control. I had my own in-office lab but i was trained in pathology and lab science and worked in a lab during med school. The equipment and the controls and the handling of specimens means something. If you obtain a worrisome level on any lab repeat it, and consider a different lab. I have seen major glitches in major commercial labs.

An elevated HCT is about the degree of elevation, the patient context of other risk factors that might end up with the patient dying from pulmonary thrombosis, or an MI, or having deep vein thrombosis (DVT) requiring hospitalization and anti-coagulation. A significantly elevated platelet count can lead to either hemorrhage or thrombosis and such events can be life-ending. And when we give medications, we can measure their effect (often) on the various body thermostats to see if too little, too much or just right. That is one of the beauties of thyroid function tests (TFTs) and looking at levels of TSH, free T3 and free T4 and T3:T4 ratios. This is what I have followed over more than half a century involving many thousands of patients. During those many decades the patient mortality and morbidity resulting from MD initiated medications & supplements has been negligible.

 

[Cataceous]

Like testosterone resistance, which can have multiple causes. The why doesn’t always lead to something actionable.
...
Sometimes, more testosterone is better.

Sure, if you're very unlucky. With such rarity it has little relevance here, and serves as another feeble attempt to rationalize excess dosing.

It affects 1 in 20,000 to 64,000 XY (karyotypically male) births. The condition results in the partial or complete inability of cells to respond to androgens.[2] This unresponsiveness can impair or prevent the development of male genitals, as well as impairing or preventing the development of male secondary sexual characteristics at puberty. It does not significantly impair female genital or sexual development.[3][4] The insensitivity to androgens is therefore clinically significant only when it occurs in genetic males, (i.e. individuals with a Y-chromosome, or more specifically, an SRY gene).[5] Clinical phenotypes in these individuals range from a typical male habitus with mild spermatogenic defect or reduced secondary terminal hair, to a full female habitus, despite the presence of a Y-chromosome.[6]​

[R]

 

[Systemlord]

Sure, if you're very unlucky. With such rarity it has little relevance here, and serves as another feeble attempt to rationalize excess dosing.

It affects 1 in 20,000 to 64,000 XY (karyotypically male) births. The condition results in the partial or complete inability of cells to respond to androgens.[2] This unresponsiveness can impair or prevent the development of male genitals, as well as impairing or preventing the development of male secondary sexual characteristics at puberty. It does not significantly impair female genital or sexual development.[3][4] The insensitivity to androgens is therefore clinically significant only when it occurs in genetic males, (i.e. individuals with a Y-chromosome, or more specifically, an SRY gene).[5] Clinical phenotypes in these individuals range from a typical male habitus with mild spermatogenic defect or reduced secondary terminal hair, to a full female habitus, despite the presence of a Y-chromosome.[6]​

[R]

I think there are environmental factors that we’re not considering, independent of insensitive androgen receptors. Dr Rob Kominiarek mentioned by-lipid membrane inflammation and prevent testosterone from working.

Whatever is lowering testosterone across generations of men is also lowering fertility. Doctors and scientists believe that whatever is lowering, the testosterone and fertility is one and the same Doctors and scientists believe whatever is lowering testosterone and fertility is one and the same cause.

Then there’s EDC’s that seems to be completely ignored when assessing someone’s testosterone levels.

The Endocrine Society, mainstream medicine is decades behind the science. That means doctors following medical guidelines are decades behind. By the time new guidelines are written, those guidelines will be outdated by the time they spread around mainstream medicine.

 

[Ribeye]

It seems to me men on TRT are dying of cardiovascular events all the time. They would have to be -- there are probably millions of men on TRT, including old men, and old men die of heart disease. The studies that have been done are reassuring in that the mortality rates of men on TRT are not significantly different than men not on TRT, and the men studied would include a large number of men with elevated HCT because that's what TRT often does.

What do you think happens when a guy on TRT with an elevated HCT dies of a heart attack? You think the alarms would be raised and papers would be published in journals in response? I don't think anything happens at all. I'm not sure why you think we would find out about it. It must happen multiple times a day, every single day.

What you mention is part of my point. Men die of cardiovascular disease all the time. If you are predisposed to it, I can see elevated HCT and HGB could play a role. You would think the physicians who cared for him, along the way would ask a few questions. Especially if he was on the young side, the pathologist would definitely ask questions. With all the men likely on HRT now, it just seems there would be more events seen, that would be identified as at risk due to the elevation of HCT and HGB. As I said, I don't want to take the risk, so I am working on lower mine, hopefully, without having to lower the dose too much or stop TRT. I doubt I would stop unless I had no choice. Quality of life is important too. At 65 I am young enough to have hopefully many more good years, but I don't want to live them the way I lived from 54 to 63. I was a hormonal mess.

 

[BJE]

I am heterozygous for both hereditary hemochromatosis and factor five leiden mutation. Before TRT I was already giving blood to keep my ferritin level at the recommended level which is around 30-50 for someone with hereditary hemochromatosis. Then I started TRT and had the need to donate blood due to elevated hematocrit. The situation I’ve gotten myself into is that despite my genetic propensity to absorb excess iron, I have driven my ferritin levels too low. I really need to donate less blood in order to raise my ferritin to the desired level. Allowing my hematocrit to go a few points higher would allow my ferritin level to increase.

I will add that although my ferritin is low, last test it was 7, my blood iron level is always high.

My regular doctor recommended I take daily aspirin to help prevent clotting due to the factor five leiden but my endocrinologist said that aspirin decreases clotting due to platelets but has no effect on clotting sure to factor five leiden.

 

[Old_Lifter_65]

So to reference the OP's question, it's an interesting video.
I donate blood a few times a year because our blood service agency needs blood. I accept the crashed ferritin and take steps to raise it after donation.

One interesting stat from the 15K altitude paper was median BP, something like 70/100 which was surprising and encouraging with average 60 HCT.

 

[Pnw0031]

Funny you say that..Cyp seems to wreak havoc on me in many ways compared to other esters...I get PVCs ,Thyroid issues (swelling and low Bp drops/Body temp drops )All thyroid related .. Might be the Cotton seed oil inflammatory response ..Ive used MCT oil with not as many issues ..

Funny you mention thyroid here... I switched to cream from cypionate and the thyroid issues I had are reducing among other side effect alleviation. Mine was also in cotton seed oil. Now on 20% cream from empower, three clicks a day. Doing better!

 

[sbstrum_MD]

Is this true? What do you guys think?

I am a hematologist/oncologist that jsut retired after 60 years of medicine, with 40 of those years focused on prostate cancer and other diseases of men. This is a good video and I especially like seeing the peer-reviewed literature referred to. I would ask the physician to add to this the citations of the papers he referred to. For example, he showed the title page of a paper by Gordeuk. The citation should look like this or very similar:

Gordeuk VR, Key NS, Prchal JT: Re-evaluation of hematocrit as a determinant of thrombotic risk in erythrocytosis. Haematologica 104:653-658, 2019

I have attached the PDF of this paper.

What must be emphasized (and it was) in the Gordeuk et al. paper relates to the uniqueness of each person's context. Here is a quote from the Gordeuk paper that speaks to this issue:

"The pressing issue in these disorders is to define factors other than elevated hematocrit that determine thrombotic risk. Defining these predisposing factors in polycythemia and erythrocytosis should then lead to rational therapies and facilitate development of targeted interventions."
The predisposing factors or as I call it "the patient's status" is what leads to, or should lead to, the physician's strategy in how the patient is managed.
Examples: patients with diabetes have ↑ platelet stickiness. Platelets are a key cellular element involved in forming a clot--both normally in response to trauma and abnormally. Dehydration due to high ambient temperatures and inadequate fluid intake, a high hematocrit (HCT), platelet function abnormalities, vascular disease, lipid abnormalities, elevations in estradiol, are but some of the "factors" that need looking at. A patient with CKD (chronic kidney disease) is going to have a lower HCT pending the degree of kidney disease due to diminished erythropoietin (EPO) production by the kidneys. Such a patient, if they happen to be an older gent with hypogonadism or other causes of low testosterone production may be fine on TRT (testosterone replacement therapy) and not have a risk for thrombosis (venous or arterial). But toss in obesity with associated diabetes + hyperlipidemia + elevated estradiol secondary to T ⇢ E2 (estradiol) due to aromatization, and you might see the proverbial perfect storm. High estradiol leads to Antithrombin III deficiency and that leads to a risk of thrombosis. We saw this some decades ago when the Chinese herbal product PC-SPES was being used for treating prostate cancer. We stopped that risk by using the anti-coagulant warfarin (Coumadin®).
It's all about the details- the facts.
"What are the facts? Again and again and again - - what are the facts? Shun wishful thinking, ignore divine revelation, forget "what the stars foretell", avoid opinion, care not what the neighbors think, never mind the unguessable `verdict of history` --what are the facts, and to how many decimal places? You pilot always into an unknown future; facts are your single clue. Get the facts!" --Lazarus Long
So, great video that should lead to further discussion and investigation and a focus on understanding the patient's status.

Stephen B. Strum, MD, FACP

 

[RobRoy]

I am a hematologist/oncologist that jsut retired after 60 years of medicine, with 40 of those years focused on prostate cancer and other diseases of men. This is a good video and I especially like seeing the peer-reviewed literature referred to. I would ask the physician to add to this the citations of the papers he referred to. For example, he showed the title page of a paper by Gordeuk. The citation should look like this or very similar:

Gordeuk VR, Key NS, Prchal JT: Re-evaluation of hematocrit as a determinant of thrombotic risk in erythrocytosis. Haematologica 104:653-658, 2019

I have attached the PDF of this paper.

What must be emphasized (and it was) in the Gordeuk et al. paper relates to the uniqueness of each person's context. Here is a quote from the Gordeuk paper that speaks to this issue:

"The pressing issue in these disorders is to define factors other than elevated hematocrit that determine thrombotic risk. Defining these predisposing factors in polycythemia and erythrocytosis should then lead to rational therapies and facilitate development of targeted interventions."
The predisposing factors or as I call it "the patient's status" is what leads to, or should lead to, the physician's strategy in how the patient is managed.
Examples: patients with diabetes have ↑ platelet stickiness. Platelets are a key cellular element involved in forming a clot--both normally in response to trauma and abnormally. Dehydration due to high ambient temperatures and inadequate fluid intake, a high hematocrit (HCT), platelet function abnormalities, vascular disease, lipid abnormalities, elevations in estradiol, are but some of the "factors" that need looking at. A patient with CKD (chronic kidney disease) is going to have a lower HCT pending the degree of kidney disease due to diminished erythropoietin (EPO) production by the kidneys. Such a patient, if they happen to be an older gent with hypogonadism or other causes of low testosterone production may be fine on TRT (testosterone replacement therapy) and not have a risk for thrombosis (venous or arterial). But toss in obesity with associated diabetes + hyperlipidemia + elevated estradiol secondary to T ⇢ E2 (estradiol) due to aromatization, and you might see the proverbial perfect storm. High estradiol leads to Antithrombin III deficiency and that leads to a risk out f thrombosis. We saw this some decades ago when the Chinese herbal product PC-SPES was being used for treating prostate cancer. We stopped that risk by using the anti-coagulant warfarin (Coumadin®).
It's all about the details- the facts.
"What are the facts? Again and again and again - - what are the facts? Shun wishful thinking, ignore divine revelation, forget "what the stars foretell", avoid opinion, care not what the neighbors think, never mind the unguessable `verdict of history` --what are the facts, and to how many decimal places? You pilot always into an unknown future; facts are your single clue. Get the facts!" --Lazarus Long
So, great video that should lead to further discussion and investigation and a focus on understanding the patient's status.

Stephen B. Strum, MD, FACP

Baseline elevations of estradiol have been "associated" with thrombosis. Association is not causation. Estrogen gets blamed but it is simply an innocent bystander. It is what is causing the elevated estradiol that causes the harm (obesity, dysipidemia, increased visceral fat and insulin resistance etc..). Raising estradiol by giving men testosterone has NEVER caused MACE or thrombosis in over 85 years of use. In fact it is the estradiol from testosterone that provides the protective effects. Giving women estradiol has also never caused any MACE or thrombosis in any RCT to date. DES and CEE are not estradiol.