Another Blood donation thread

[pahlevan]

So I have hemocrat of 18 and Doc wants it down. I've done the double cell and regular donations but not often enough. They alow blood donations of only once every 8 weeks but i may need to do it more often. Being that we have 2 blood banks in my area I can switch between them.
Question is, how often can I SAFELY DONATE a pint?

 

[thethinker48]

Hemoglobin of 18 right?

You’d be the walking dead with a hct of 18.

What are the other numbers? Hgb? Platelets? Mpv, mcv etc


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[maldorf]

You are best off having it done through a doctor. Get one to perform them or prescribe it for you. I see a hematologist for mine, once every 2 or 3 months I get my CBC done to see where my hemoglobin is. He wants mine to be around 15.

You don't want to worry about driving all over looking for a place to go etc. It is much nicer to have a good doctor take care of it for you.

 

[Rex Feral]

So I have hemocrat of 18 and Doc wants it down. I've done the double cell and regular donations but not often enough. They alow blood donations of only once every 8 weeks but i may need to do it more often. Being that we have 2 blood banks in my area I can switch between them.
Question is, how often can I SAFELY DONATE a pint?

"Furthermore, we trust that the urge to correct any abnormal laboratory data by a therapeutic intervention should be tempered by consideration of the risk-benefit ratio of any such intervention. The routine practice of phlebotomy for elevated hematocrit, with its inevitable iron deficiency (which leads to inhibition of PHD2, increased HIF, and increased erythropoietin) and potential detrimental thrombotic effects, should be re-evaluated."

Victor R. Gordeuk, Nigel S. Key, Josef T. Prchal
Haematologica April 2019 104: 653-658; Doi:10.3324/haematol.2018.210732

Rex.

 

[MyNameIsJeff]

"Furthermore, we trust that the urge to correct any abnormal laboratory data by a therapeutic intervention should be tempered by consideration of the risk-benefit ratio of any such intervention. The routine practice of phlebotomy for elevated hematocrit, with its inevitable iron deficiency (which leads to inhibition of PHD2, increased HIF, and increased erythropoietin) and potential detrimental thrombotic effects, should be re-evaluated."

Victor R. Gordeuk, Nigel S. Key, Josef T. Prchal
Haematologica April 2019 104: 653-658; Doi:10.3324/haematol.2018.210732

Rex.

What HCT level do you consider the threshold above which the benefits of phlebotomization outweigh the costs? 54? 56? 58?

 

[Rex Feral]

What HCT level do you consider the threshold above which the benefits of phlebotomization outweigh the costs? 54? 56? 58?

Phlebotomy is never indicated for secondary polycythemia in the absence of genetic thrombotic factors. So it is not a matter of a number but a cause. So T/AAS, altitude, smoking/COPD, renal cell carcinoma, hepatocellular carcinoma, adrenal adenoma, von Hippel-Lindau disease, Cushing’s syndrome, etc all cause secondary polycythemia. The only people we phlebotomize with secondary polycythemia are people on T/AAS and that's simply because of foolish quack TRT doctors and GPs adopting treatment of polycythemia vera/primary polycythemia in a healthy population because they really don't know any better and no other reason.

Rex.

 

[nothuman]

Phlebotomy is never indicated for secondary polycythemia in the absence of genetic thrombotic factors. So it is not a matter of a number but a cause. So T/AAS, altitude, smoking/COPD, renal cell carcinoma, hepatocellular carcinoma, adrenal adenoma, von Hippel-Lindau disease, Cushing’s syndrome, etc all cause secondary polycythemia. The only people we phlebotomize with secondary polycythemia are people on T/AAS and that's simply because of foolish quack TRT doctors and GPs adopting treatment of polycythemia vera/primary polycythemia in a healthy population because they really don't know any better and no other reason.

Rex.

I was walking around at 60 once and felt totally normal. I still donated because it freaked me out but I was surprised how normal I felt. My endurance was as good as ever too. Normal BP and RHR.

Would I have been ok if I didn't donate?

 

[Rex Feral]

I was walking around at 60 once and felt totally normal. I still donated because it freaked me out but I was surprised how normal I felt. My endurance was as good as ever too. Normal BP and RHR.

Would I have been ok if I didn't donate?

Well, there is nothing to suggest that you wouldn't have been. Look at it this way, if you were natural, moved to Peru and lived in the Andes for 6 months and came home with a HCT of 60 no one would be talking about phlebotomy. If you were a normal person who never used T/AAS you'd literally think nothing of it. Why wouldn't you be sent for phlebotomy in that instance if a HCT of 60 is so dangerous? What if you smoked a pack a day for 30 years and developed COPD and had a HCT of 62? They still wouldn't phlebotomize you. So who adopted this practice of using primary polycythemia treatments/phlebotomy to treat secondary polycythemia and based upon what evidence? And why is it only applied to secondary polycythemia caused by T/AAS? So then what makes you think that you wouldn't have been "ok?" To me this is sort of like renal failure in T/AAS in that as long as BP is controlled it trumps other factors. I say this because I've never seen a person in renal failure that wasn't hypertensive except for genetic causes. In the same way if you have a BP of 110/70 explain to me how your blood is thick and viscous and that it's sludge and somehow damaging the vessels or causing clots. I don't buy it. A UK study showed increased stroke risk in HCT > 51 in hypertensive patients but not in normotensive patients. So just as a hgh HCT may exacerbate clotting in those with genetic factors it increases risk in those with hypertension. But I'd still say the hypertension and the genetic clotting factors were the cause not HCT. The bigger question is if there is increased risk associated with T/AAS induced secondary poiycythemia, where is the evidence that phlebotomy ameliorates these risks? There is on the other clear evidence of increased thrombosis with phlebotomy. How do you know or why do you think that you decreased your risk of clots by having phlebotomy and not increased it? Remember Big Bapper, the phlebotomy champion until he dropped dead of a stroke. I'm sure he thought he was decreasing his risk as well and he probably got his stupid HCT # down. A lot of good it did him. I'd listen to the study authors and exercise caution in simply treating lab numbers with unproven interventions. It really sounds stupid when you put it like that doesn't it.

Rex.

Rex.

 

[Reload]

Well, there is nothing to suggest that you wouldn't have been. Look at it this way, if you were natural, moved to Peru and lived in the Andes for 6 months and came home with a HCT of 60 no one would be talking about phlebotomy. If you were a normal person who never used T/AAS you'd literally think nothing of it. Why wouldn't you be sent for phlebotomy in that instance if a HCT of 60 is so dangerous? What if you smoked a pack a day for 30 years and developed COPD and had a HCT of 62? They still wouldn't phlebotomize you. So who adopted this practice of using primary polycythemia treatments/phlebotomy to treat secondary polycythemia and based upon what evidence? And why is it only applied to secondary polycythemia caused by T/AAS? So then what makes you think that you wouldn't have been "ok?" To me this is sort of like renal failure in T/AAS in that as long as BP is controlled it trumps other factors. I say this because I've never seen a person in renal failure that wasn't hypertensive except for genetic causes. In the same way if you have a BP of 110/70 explain to me how your blood is thick and viscous and that it's sludge and somehow damaging the vessels or causing clots. I don't buy it. A UK study showed increased stroke risk in HCT > 51 in hypertensive patients but not in normotensive patients. So just as a hgh HCT may exacerbate clotting in those with genetic factors it increases risk in those with hypertension. But I'd still say the hypertension and the genetic clotting factors were the cause not HCT. The bigger question is if there is increased risk associated with T/AAS induced secondary poiycythemia, where is the evidence that phlebotomy ameliorates these risks? There is on the other clear evidence of increased thrombosis with phlebotomy. How do you know or why do you think that you decreased your risk of clots by having phlebotomy and not increased it? Remember Big Bapper, the phlebotomy champion until he dropped dead of a stroke. I'm sure he thought he was decreasing his risk as well and he probably got his stupid HCT # down. A lot of good it did him. I'd listen to the study authors and exercise caution in simply treating lab numbers with unproven interventions. It really sounds stupid when you put it like that doesn't it.

Rex.

Rex.

So what if you have hypertension and on meds? Would that be an exception?

 

[Rex Feral]

So what if you have hypertension and on meds? Would that be an exception?

Well, if you are controlled then you are normotensive and based on a study of 7400 men in the UK then you are not at increased risk for stroke. If like many people on BP meds you are still poorly controlled then the evidence would suggest that you are at increased risk for stroke at a HCT > 51.

Rex.

 

[thethinker48]

Well, there is nothing to suggest that you wouldn't have been. Look at it this way, if you were natural, moved to Peru and lived in the Andes for 6 months and came home with a HCT of 60 no one would be talking about phlebotomy. If you were a normal person who never used T/AAS you'd literally think nothing of it. Why wouldn't you be sent for phlebotomy in that instance if a HCT of 60 is so dangerous? What if you smoked a pack a day for 30 years and developed COPD and had a HCT of 62? They still wouldn't phlebotomize you. So who adopted this practice of using primary polycythemia treatments/phlebotomy to treat secondary polycythemia and based upon what evidence? And why is it only applied to secondary polycythemia caused by T/AAS? So then what makes you think that you wouldn't have been "ok?" To me this is sort of like renal failure in T/AAS in that as long as BP is controlled it trumps other factors. I say this because I've never seen a person in renal failure that wasn't hypertensive except for genetic causes. In the same way if you have a BP of 110/70 explain to me how your blood is thick and viscous and that it's sludge and somehow damaging the vessels or causing clots. I don't buy it. A UK study showed increased stroke risk in HCT > 51 in hypertensive patients but not in normotensive patients. So just as a hgh HCT may exacerbate clotting in those with genetic factors it increases risk in those with hypertension. But I'd still say the hypertension and the genetic clotting factors were the cause not HCT. The bigger question is if there is increased risk associated with T/AAS induced secondary poiycythemia, where is the evidence that phlebotomy ameliorates these risks? There is on the other clear evidence of increased thrombosis with phlebotomy. How do you know or why do you think that you decreased your risk of clots by having phlebotomy and not increased it? Remember Big Bapper, the phlebotomy champion until he dropped dead of a stroke. I'm sure he thought he was decreasing his risk as well and he probably got his stupid HCT # down. A lot of good it did him. I'd listen to the study authors and exercise caution in simply treating lab numbers with unproven interventions. It really sounds stupid when you put it like that doesn't it.



Rex.



Rex.

So a person using AAS would be better served running coagulation tests (factor assays and other coag components) before ever considering donating blood? While of course keeping BP in range.

Another question is that do we see instances of people with crazy high H/H elevations like with AAS use through altitude or hypoxia? A HC of 60+ has been many times with prolonged steroid use; but is it ever seen with someone living in the Himalayas?

This is some real insightful conversation that will change the way we do a lot of things in bodybuilding pharmacology in the upcoming years. Thank you for elucidating on this.


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[Rex Feral]

So what if you have hypertension and on meds? Would that be an exception?

But there is no evidence that phlebotomy will reduce this risk if you have uncontrolled HTN. It may cause problems you don't have and it may actually increase your risk even further. So control your HTN #1 priority.

Rex.

 

[Reload]

But there is no evidence that phlebotomy will reduce this risk if you have uncontrolled HTN. It may cause problems you don't have and it may actually increase your risk even further. So control your HTN #1 priority.

Rex.

Got it!

 

[Rex Feral]

So a person using AAS would be better served running coagulation tests (factor assays and other coag components) before ever considering donating blood? While of course keeping BP in range.

Another question is that do we see instances of people with crazy high H/H elevations like with AAS use through altitude or hypoxia? A HC of 60+ has been many times with prolonged steroid use; but is it ever seen with someone living in the Himalayas?

This is some real insightful conversation that will change the way we do a lot of things in bodybuilding pharmacology in the upcoming years. Thank you for elucidating on this.


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Well, clotting disorders are pretty rare and hopefully they would manifest themselves in some way in the first 18-21 years of life before most would engage in drug use. There is also the cost of screening to identify a very small percentage that wouldn't be seen as justifiable. But if you have the time and money it certainly wouldn't hurt you. Factor V Leiden, prothrombin gene mutation, etc.

Yes, 61% is still normal at altitude. A study of 2k people living at 4000m (about 2.5 miles) in Bolivia found the normal range for men to be 45-61% for HCT and 13-21 g/dl for Hgb.

Rex.

 

[j2048b]

@Rex Feral so whats in ur opinion the best way to lower these values or prevent them?

Hydration at a cellular levels, glycerol? Other supps?

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[Rex Feral]

So a person using AAS would be better served running coagulation tests (factor assays and other coag components) before ever considering donating blood? While of course keeping BP in range.

Another question is that do we see instances of people with crazy high H/H elevations like with AAS use through altitude or hypoxia? A HC of 60+ has been many times with prolonged steroid use; but is it ever seen with someone living in the Himalayas?

This is some real insightful conversation that will change the way we do a lot of things in bodybuilding pharmacology in the upcoming years. Thank you for elucidating on this.


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Also, I think I should mention that there should be a distinction between donating blood as you call it and therapeutic phlebotomy. Therapeutic phlebotomy is performed quite frequently. As often as every other day for polycythemia vera with once per week being common until the target HCT is hit. Whereas you would typically wait at least 8-16 weeks between blood donations. So if you like to donate blood for a drive a whatever a few times a year that is not therapeutic phlebotomy.

Rex.

 

[Rex Feral]

@Rex Feral so whats in ur opinion the best way to lower these values or prevent them?

Hydration at a cellular levels, glycerol? Other supps?

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Well, you'd first have to ask yourself is there a need to decrease HCT. If you lived at 4000m with a HCT of 60 you would be considered normal and no one would be discussing treatment. Should there be a different normal for people on exogenous androgens? Again, we are talking about the same condition here, secondary polycythemia. In every other instance of secondary polycythemia increased HCT is seen as normal. I've heard people like Nelson Vergel equate EPO use and stroke to androgens based on HCT numbers and this is just pure horseshit. One is a natural adaptation, one is not.

That being said, there is really nothing you can do but remove the cause. Dante has a great post on his Instagram I would refer you to if you haven't read it. It has a picture of an IP-6 bottle from Swanson. There are two applications that were quite brilliant in their inception. I haven't seen them work personally but I trust Dante and there really is nothing else. Hydrate as you said, low dose aspirin, BP control, the obvious countermeasures. But it's the same as at altitude, the only way to really change it is move to sea level or quit androgens.

The Canadians have guidelines that call for cessation of T at HCT of 54. Doctors, instead of losing patients, have started therapeutic phlebotomy instead despite zero evidence that it does anything positive. "Our findings raise concerns about the persistent risk of vascular events in these donors, particularly when coupled with the misperception by patients and health care providers that donation has reduced or eliminated the risks of TRT-induced polycythemia."
Transfusion. 2017 Mar;57(3):578-581. doi: 10.1111/trf.13970. Epub 2017 Feb 1.
Blood donation and testosterone replacement therapy

Again, if there is risk, phlebotomy won't help. If increased HCT bothers you, quit androgens or get over it.

Personally I take IP-6 at 2 gms qd, low dose ASA, ARB & PDE5 inhibitor.

Rex.

 

[MyNameIsJeff]

Very thought-provoking Rex. Could I get your thoughts on animal models showing very clearly that supra-physiological levels of HCT lead to endothelial dysfunction, thrombogenicity, and cardiovascular risk.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3225673/

I get that the phlebotomy as a 'treatment' for excessive erythrocytosis has severe drawbacks and is overused in current practice. But there is very solid evidence from animal studies that supra-physiological levels of HCT itself is also detrimental (and I have not seen any good arguments for why we can't extrapolate to humans in this context). So in severe cases (HCT 56+), I believe that phlebotomies do have a place, though more care needs to be taken in terms of watching iron status, platelet reaction, coagulation status, etc.

 

[nothuman]

So a person using AAS would be better served running coagulation tests (factor assays and other coag components) before ever considering donating blood? While of course keeping BP in range.

Another question is that do we see instances of people with crazy high H/H elevations like with AAS use through altitude or hypoxia? A HC of 60+ has been many times with prolonged steroid use; but is it ever seen with someone living in the Himalayas?

This is some real insightful conversation that will change the way we do a lot of things in bodybuilding pharmacology in the upcoming years. Thank you for elucidating on this.


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Would sleep apnea be considered an additional risk factor for thrombotic events?

 

[Bio]

Over and over the message on PM is control your BP! It's cheap and easy. If you're still one of the irresponsible people walking around with elevated/high BP you're asking for renal and cardiac issues. Why not put out the extra money for the tests to see if you have any of the genetic clotting factors? Nothing like having peace of mind!