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Don't worry about high hematocrit/RBC/Hemoglobin?

Would specific blood work/testing be able to show these results?
https://www.summitmedicalgroup.com/library/adult_health/car_hemodynamic_monitoring/

lol i lived in summit for a while and know the ppl at SMG.

I would have to look up to see what new fun test are available for endothelial inflammation but im sure there are a few .

In general I strongly feel its important to not let your HCT creep up too high over your normal levels. Slightly elevated is ok but if you are normally around 45-46 and then your up around 53+... ive seen guys at 60+... cmon now..

Will it cause issues in every guy.. not at all but we are striving for optimal health while doing something that is inherently unhealthy ( at levels greater then trt)
 
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I don’t see it specified that the high hematocrit individuals had no underlying health issues causing elevated hematocrit (poly vera does more than just elevate HCT). Heart disease isn’t more rampant in Denver and average HCT is >50.

Anyone is foolish to think that sporting a 55% plus hematocrit is healthy, especially when you are taking steroid hormones that interfere with the clotting cascade. I once had a hematocrit over 60%. If a person doesn't keep an eye on it, it is possible it will slowly creep up that high. It is especially a risk nowadays when guys don't ever get off the sauce and cruise on 200 mg plus.
 
Anyone is foolish to think that sporting a 55% plus hematocrit is healthy, especially when you are taking steroid hormones that interfere with the clotting cascade. I once had a hematocrit over 60%. If a person doesn't keep an eye on it, it is possible it will slowly creep up that high. It is especially a risk nowadays when guys don't ever get off the sauce and cruise on 200 mg plus.

Exactly.

People will find a study or two or try to quote someone who they think knows what they are talking about ( we know most of these experts even physicans are not) in order to support something they want to be true. We see it all the time.. There was a thread about not aspirating when injecting, not needing AI's, HDL levels arent important, HCT is fine if its elevated, nandrolone is more cardiotoxic then others so avoid that and your ok and the list goes on and on..

Theres the truth and then theres what you may want to be true but probably isnt. We learn more every day and my own opinions change overtime but lets use some common sense people.

Ive spoken to these gurus, to these HRT physicians who you all cite, internet experts... MOST are nothing to be respected, at least not to the level which I see online. Im certainly not all knowing..not be a long shot.. but i dont make up nonsense like some of these people in order to try to sound smart.
 
Exactly.

People will find a study or two or try to quote someone who they think knows what they are talking about ( we know most of these experts even physicans are not) in order to support something they want to be true. We see it all the time.. There was a thread about not aspirating when injecting, not needing AI's, HDL levels arent important, HCT is fine if its elevated, nandrolone is more cardiotoxic then others so avoid that and your ok and the list goes on and on..

Theres the truth and then theres what you may want to be true but probably isnt. We learn more every day and my own opinions change overtime but lets use some common sense people.

Ive spoken to these gurus, to these HRT physicians who you all cite, internet experts... MOST are nothing to be respected, at least not to the level which I see online. Im certainly not all knowing..not be a long shot.. but i dont make up nonsense like some of these people in order to try to sound smart.

I know you and Maldorf are intelligent individuals. And I hope the assumptions you are making are not about me because they are wrong. A healthy person living at sea level elevation not taking any form of AAS should not have an HCT over 50 (there are rare exceptions). So a study pointing towards hematocrit and heart disease without any information on the individuals who have HCT over 50 is worthless. A comparison study should be made between people at sea level elevation and HCT below 50 and elevated living like Denver where average HCT is over 50. I am all for good studies, but this doesn’t look like one. I am in no way saying “blast away, HCT doesn’t matter”, but how much and how high it has to be to matter I don’t know. Hell, my last “blast” was 300/mg test p and 200mg npp a week for 8 weeks and back to 100mg TRT after because staying on long and/or high doses are scary to me:eek:. So I am in no way looking for a way to make myself feel better about my use, but when a study looks bad it should be pointed out.
 
Its seems like alot of guys HCT will jump back to where it was after a few weeks post donation and then even climb higher. I guess i dont see the point in donations if this is what is happening. I dont have evidence that this would happen to me as I have never donated before. Either way it would be nice if someone could explain why high HCT with testosterone is different then high HCT being at a high elevation.
 
I know you and Maldorf are intelligent individuals. And I hope the assumptions you are making are not about me because they are wrong. A healthy person living at sea level elevation not taking any form of AAS should not have an HCT over 50 (there are rare exceptions). So a study pointing towards hematocrit and heart disease without any information on the individuals who have HCT over 50 is worthless. A comparison study should be made between people at sea level elevation and HCT below 50 and elevated living like Denver where average HCT is over 50. I am all for good studies, but this doesn’t look like one. I am in no way saying “blast away, HCT doesn’t matter”, but how much and how high it has to be to matter I don’t know. Hell, my last “blast” was 300/mg test p and 200mg npp a week for 8 weeks and back to 100mg TRT after because staying on long and/or high doses are scary to me:eek:. So I am in no way looking for a way to make myself feel better about my use, but when a study looks bad it should be pointed out.

I agree that there is probably some merit to this within reason. Also, the more you donate, the more your HCT wants to keep coming back. HCT of 55 I don't think is the end of the world if all other heart tests are ok. HCT of 60, probably not good, however. Just my educated guess though.
 
Good article here

This article mentions everything that has been mentioned here. It really seems like more research needs to be done in order for it to be fully understood. It is still undeniable that having a high enough hematocrit puts you at risk of blood clot. The only question is, is it because of the direct effect of the high hematocrit, because of another condition that the subject has along with high HCT, or is it a combo of both.

High hematocrit as a risk factor for venous thrombosis. Cause or innocent bystander? | Haematologica

Anabolic steroids though have been shown to increase chances of clotting, so some of this is moot.
 
I agree that there is probably some merit to this within reason. Also, the more you donate, the more your HCT wants to keep coming back. HCT of 55 I don't think is the end of the world if all other heart tests are ok. HCT of 60, probably not good, however. Just my educated guess though.

With doing phlebotomies, I have mine now so that I only need to get it done 3 or 4 times a year. Used to be monthly at first. So for me it became less frequent once we got the iron in my blood down enough. Mine is well under control now thank goodness. I only take 100 mg/wk testosterone in HRT though. Would have to be more frequent if I were still doing what I used to do.
 
I agree that there is probably some merit to this within reason. Also, the more you donate, the more your HCT wants to keep coming back. HCT of 55 I don't think is the end of the world if all other heart tests are ok. HCT of 60, probably not good, however. Just my educated guess though.

I have noticed this as well. It’s almost like a negative rebound. The more frequent you donate the quicker your HCT goes back up especially if you’re on anything higher than TRT. It’s almost as if you need to donate at a time that you’re going to really do a true TRT and go at least three or four months on true TRT to keep HCT at bay. Bloodletting is healthy as it was done centuries ago but I think the amount plays a crucial role. I don’t see how it could be healthy anymore than a couple times a year at most. Definitely not what Red Cross and most associations allow every 54 days that will just deplete ferritin and cause so much mitochondrial damage you have far more to worry about.

I found this interesting as well. Testosterone suppresses hepcidin which is the master controller of iron. I believe It can cause iron to be too high in some situations and anemia in other situations.
https://www.ncbi.nlm.nih.gov/pubmed/20660052/
 
I do not currently take aspirin. I made a thread asking if I should take aspirin and people said it wouldn't be useful but they did not know my platelet count was in the 400's.

Do you think I should start taking it? :(

Absolutely.
 
Hematological response to higher elevations doesn't necessarily mean there's adaptation, moreso, without consequent.

There's plenty of literature that thee good ole Dr. Neil Rouzier fails to communicate with the general audience. He uses the analogy of comparison of those living in higher elevation to those with secondary polycthemia.

Apparently the smooth talking Dr. must of missed the bus on treating either acute or chronic mountain sickness. Not in all cases, although phlebotomy is often performed.



As I mentioned in my first post:

I can see this casting misinterpretation throughout the interweb.
 
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Hematological response to higher elevations doesn't necessarily mean there's adaptation, moreso, without consequent.

There's plenty of literature that thee good ole Dr. Neil Rouzier fails to communicate with the general audience. He uses the analogy of comparison of those living in higher elevation to those with secondary polycthemia.

Apparently the smooth talking Dr. must of missed the bus on treating either acute or chronic mountain sickness. Not in all cases, although phlebotomy is often performed.



As I mentioned in my first post:

Do you think he’s right when he says the association of platelet count and WBC are the underlining factors that separate risk of stroke in those with true polycythemia vs secondary erythrocytosis?


Neil says phlebotomies are not given for other secondary erythrocytosis conditions such as sleep apnea, COPD and smokers due to platelet count. Seems like secondary Erythrocytosis from AAS does not cause an increase in platelets but in sleep apnea and COPD patients it does so he may have contradicted himself there.
https://www.ncbi.nlm.nih.gov/m/pubmed/12713015/

https://www.researchgate.net/publication/228515555_Platelets_Indicator_of_inflammation_in_COPD


In smokers it’s a little diff as:
platelet “adhesion” was altered in smokers causing Arterial thrombosis. Not necessarily platelet count.
https://www.ncbi.nlm.nih.gov/m/pubmed/17357291/
 
Hematological response to higher elevations doesn't necessarily mean there's adaptation, moreso, without consequent.

There's plenty of literature that thee good ole Dr. Neil Rouzier fails to communicate with the general audience. He uses the analogy of comparison of those living in higher elevation to those with secondary polycthemia.

Apparently the smooth talking Dr. must of missed the bus on treating either acute or chronic mountain sickness. Not in all cases, although phlebotomy is often performed.



As I mentioned in my first post:

Do you think he’s right when he says the association of platelet count and WBC are the underlining factors that separate risk of stroke in those with true polycythemia vs secondary erythrocytosis?


Neil says phlebotomies are not given for other secondary erythrocytosis conditions such as sleep apnea, COPD and smokers due to platelet count. Seems like secondary Erythrocytosis from AAS does not cause an increase in platelets but in sleep apnea and COPD patients it does so he may have contradicted himself there.
https://www.ncbi.nlm.nih.gov/m/pubmed/12713015/

https://www.researchgate.net/publication/228515555_Platelets_Indicator_of_inflammation_in_COPD


In smokers it’s a little diff as:
platelet “adhesion” was altered in smokers causing Arterial thrombosis. Not necessarily platelet count.
https://www.ncbi.nlm.nih.gov/m/pubmed/17357291/

Altitude is also interesting
https://www.ncbi.nlm.nih.gov/pubmed/19658003/

Looks like platelet “count” isn’t as important as checking platelet adhesions. Dammit I thought I was done with blood tests. Now time to test for adhesions.


“Although platelet counts are normal in anabolic steroid abusers, platelet aggregation is increased. This is possibly caused by an increased production of thromboxane in platelets, and a decreased prostacyclin production in vessel walls [44–46]. Indirect mechanisms, such as increased low-density lipoprotein cholesterol concentrations that are associated with anabolic steroid abuse, may increase platelet sensitivity [44]. Androgens increase the produc- tion of procoagulant factors such as factors VII and IX [47]. Increased vascular reactivity associated with the anabolic steroids is mediated by impaired nitric oxide activity [48].”

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2044.2005.04218.x
 
Last edited:
This is a post I made yesterday on a Facebook group I'm a member of. I wanted to mention genotypes, tho it was getting late and I had a couple glasses of wine going on :)

Yes I do believe he's fooling himself and the layperson on several accounts.

Secondary erythrocytosis is used synonymously, or interchangeably used with secondary polycthemia. It's not synonymous with the diseased state of "vera". They're two different distinctive etiologies.

Mistakenly there's a perception that high elevations dwellers are associated with no possible pathophysiological fallout. Sadly, there is with some of these individuals (as with those on testosterone replacement) in which some of these unfortunate individuals develop pulmonary arterial hypertension from hypoxic hypoxia-secondary polycthemia, as well they develop hyperuricemia and high altitude renal syndrome. The literature is out there. It's very easy to find. As a side note: if pulmonary arterial hypertension develops, this can lead to right-sided heart failure, or cor pulmonale.

Given that. The issue I see with the message that Dr. Rouzier is conveying to a subset of the population that will take his word as gospel. Although, what he's failing to comprehend is that he's spreading this through YouTube videos to thousands of sheeple unknowingly what each and everyone of their health parameters are, individually.

Finally, similarities between those with uncontrolled OSA and those living in higher elevation in which are chronically exposed to hypoxic hypoxia environments, in conjunction with the stimuli of erythropoiesis from testosterone is a recipe for bad things to occur, as aforementioned.

I'm personally not one that jumps on the bandwagon of once an individuals HH hits a certain percentage---g/dL it's time to phelbot. I've hovered around 59% (this was before I was diagnosed with severe OSA) for a few months before I dumped, without issue.

Although, I knew what my homocysteine, Fibrinogen, Nt-proBNP and Galectin-3 levels where and that I have no inherent coagulation traits--- Factor V Leiden, Prothrombin and MTHFR.

Again the issue I have with these statements put fourth by Dr. Rouzier and the likes. They have no clue of any underlying condition(s) or morbidity you may have.

You should check to see if you have undiagnosed sleep apnea. That's where I'd suggest starting.

Good luck.
 
Stewie - really glad to have an educated resource like you on this board.
 
This is a post I made yesterday on a Facebook group I'm a member of. I wanted to mention genotypes, tho it was getting late and I had a couple glasses of wine going on :)

Yes I do believe he's fooling himself and the layperson on several accounts.

Secondary erythrocytosis is used synonymously, or interchangeably used with secondary polycthemia. It's not synonymous with the diseased state of "vera". They're two different distinctive etiologies.

Mistakenly there's a perception that high elevations dwellers are associated with no possible pathophysiological fallout. Sadly, there is with some of these individuals (as with those on testosterone replacement) in which some of these unfortunate individuals develop pulmonary arterial hypertension from hypoxic hypoxia-secondary polycthemia, as well they develop hyperuricemia and high altitude renal syndrome. The literature is out there. It's very easy to find. As a side note: if pulmonary arterial hypertension develops, this can lead to right-sided heart failure, or cor pulmonale.

Given that. The issue I see with the message that Dr. Rouzier is conveying to a subset of the population that will take his word as gospel. Although, what he's failing to comprehend is that he's spreading this through YouTube videos to thousands of sheeple unknowingly what each and everyone of their health parameters are, individually.

Finally, similarities between those with uncontrolled OSA and those living in higher elevation in which are chronically exposed to hypoxic hypoxia environments, in conjunction with the stimuli of erythropoiesis from testosterone is a recipe for bad things to occur, as aforementioned.

I'm personally not one that jumps on the bandwagon of once an individuals HH hits a certain percentage---g/dL it's time to phelbot. I've hovered around 59% (this was before I was diagnosed with severe OSA) for a few months before I dumped, without issue.

Although, I knew what my homocysteine, Fibrinogen, Nt-proBNP and Galectin-3 levels where and that I have no inherent coagulation traits--- Factor V Leiden, Prothrombin and MTHFR.

Again the issue I have with these statements put fourth by Dr. Rouzier and the likes. They have no clue of any underlying condition(s) or morbidity you may have.

You should check to see if you have undiagnosed sleep apnea. That's where I'd suggest starting.

Good luck.
Such a wealth of information in one post. Thanks man:)
 
This is a post I made yesterday on a Facebook group I'm a member of. I wanted to mention genotypes, tho it was getting late and I had a couple glasses of wine going on :)

Yes I do believe he's fooling himself and the layperson on several accounts.

Secondary erythrocytosis is used synonymously, or interchangeably used with secondary polycthemia. It's not synonymous with the diseased state of "vera". They're two different distinctive etiologies.

Mistakenly there's a perception that high elevations dwellers are associated with no possible pathophysiological fallout. Sadly, there is with some of these individuals (as with those on testosterone replacement) in which some of these unfortunate individuals develop pulmonary arterial hypertension from hypoxic hypoxia-secondary polycthemia, as well they develop hyperuricemia and high altitude renal syndrome. The literature is out there. It's very easy to find. As a side note: if pulmonary arterial hypertension develops, this can lead to right-sided heart failure, or cor pulmonale.

Given that. The issue I see with the message that Dr. Rouzier is conveying to a subset of the population that will take his word as gospel. Although, what he's failing to comprehend is that he's spreading this through YouTube videos to thousands of sheeple unknowingly what each and everyone of their health parameters are, individually.

Finally, similarities between those with uncontrolled OSA and those living in higher elevation in which are chronically exposed to hypoxic hypoxia environments, in conjunction with the stimuli of erythropoiesis from testosterone is a recipe for bad things to occur, as aforementioned.

I'm personally not one that jumps on the bandwagon of once an individuals HH hits a certain percentage---g/dL it's time to phelbot. I've hovered around 59% (this was before I was diagnosed with severe OSA) for a few months before I dumped, without issue.

Although, I knew what my homocysteine, Fibrinogen, Nt-proBNP and Galectin-3 levels where and that I have no inherent coagulation traits--- Factor V Leiden, Prothrombin and MTHFR.

Again the issue I have with these statements put fourth by Dr. Rouzier and the likes. They have no clue of any underlying condition(s) or morbidity you may have.

You should check to see if you have undiagnosed sleep apnea. That's where I'd suggest starting.

Good luck.

In other words, if these are all normal/optimal and the person doesn't have any genetic coagulation traits, the likelihood of a cardiovascular event resulting from high H/H isn't as high?
 

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