Raising ferritin FAST (a how-to, not a question)

[Clear]

There is a high probability that your body does not make hepcidin and you are a carrier, or have, C282Y hemochromatosis.
For a basic explanation as to how you would have low ferritin but have or carry hereditary hemochromatosis, see this post on FB:

https://www.********.com/groups/591473358577668/posts/792355721822763/

If on the other hand you are 55 or older, it's not likely but you may have a different HFE genetic mutation. I've run into a few guys who ran the protocol, it didn't work, and came up positive for hereditary hemochromatosis.

I am 35 years old. I finished my protocol, 7 days with doctors best high absorption 100% chelated with ferrochel iron. Ferrous bisglycinate chelate. I did 81 mg three times a day, 9am 3pm 9pm. The iron expires this month, if that matters...

Labs before:
21 ferritin
16.1 hemoglobin

I donated blood at red cross, single red
Ran protocol

Labs after:
18 ferritin
16.1 hemoglobin
Iron total 121
Uibc 260
Tibc 381
% saturation 32

During protocol I took a single PPI on day 2. I ate white bread with no vitamin C or D in it, however I did eat chicken a couple times. I drank black tea on day 2 twice without thinking. I did not eat anything other than toast and a couple servings of chicken.

My hemotologist did test me for any sort of hemochromotosis gene mutations, a bunch of different ones, however I do not specifically see C282Y tested for. Is there any other name for that? I can list all that she tested me for if it would help.

I am at a loss. I ran your protocol before and felt great for about two months, however the Dr screwed up and only ran a normal iron panel that didn't include ferritin and instead referred me to a hemotologist. So I don't know 100% if it actually increased my ferritin last time, though I think it did because the headaches i had for months stopped around day 4 and falling asleep driving also stopped around that time.

Any advice on what to do?

Any idea what might have caused this? She referred me to get my gut checked out. I do have GERD.

 

[Systemlord]

You’re not absorbing the iron. I always drink 9 ounces of orange juice and take vitamin D with my iron supplement.

Both vitamins are responsible for the absorption of iron.

The only thing I can think of is an iron storage disorder.

 

[Clear]

You’re not absorbing the iron. I always drink 9 ounces of orange juice and take vitamin D with my iron supplement.

Both vitamins are responsible for the absorption of iron.

The only thing I can think of is an iron storage disorder.

I thought the point of the protocol was that you DON'T want to absorb the iron because for guys on TRT that will raise hemoglobin. My understanding was we just take iron without vitamin C or D so the body stimulates hepcidin production which blocks intestinal iron absorption and the body recycles 80% of RBC which are stored as ferritin.
I usually run at an 18-20 hemoglobin level and donate to keep it around 16

 

[Systemlord]

I thought the point of the protocol was that you DON'T want to absorb the iron because for guys on TRT that will raise hemoglobin.

I don’t get it, your ferritin is insanely low, and you don’t want to absorb iron?

You want to prevent yourself from absorbing iron so you can keep hemoglobin at 16, donating blood, while keeping ferritin in a deficient state.

I don’t get it!

I usually run at an 18-20 hemoglobin level and donate to keep it around 16

Mines in the high 17 to 18 range. Tons of endless energy!

Why are you trying to keep hemoglobin at 16?

 

[Clear]

I don’t get it, your ferritin is insanely low, and you don’t want to absorb iron?

You want to prevent yourself from absorbing iron so you can keep hemoglobin at 16, donating blood, while keeping ferritin in a deficient state.

I don’t get it!


Mines in the high 17 to 18 range. Tons of endless energy!

Why are you trying to keep hemoglobin at 16?

Well at red cross I've been tested at a 20.5 before and when I reached a 17.9 at doctors labs, my doctor said she wasn't comfortable prescribing trt at a number above 18, especially with my blood pressure, so I've tried to keep it below that so I don't run into any issues with her. My blood pressure constantly runs very high, 150-160 / 105 or so routinely.

 

[Cataceous]

Well at red cross I've been tested at a 20.5 before and when I reached a 17.9 at doctors labs, my doctor said she wasn't comfortable prescribing trt at a number above 18, especially with my blood pressure, so I've tried to keep it below that so I don't run into any issues with her. My blood pressure constantly runs very high, 150-160 / 105 or so routinely.

Information here on why your doctor is right to be concerned about higher levels. Ignore those who would downplay the issue.

What worries me about the recommendations I've listened to is that some poor fellow is going to use this advice and think an Hct level in the mid 50s is perfectly reasonable and nothing should be done to correct this. ... But for the vast majority of folks looking for functional longevity and compression of morbidity, the medical literature is quite clear a corrective action should be taken. In this thread I'll share some literature, resources to help inform TRT users and demonstrate that elevated Hct is not benign.​

What is your TRT protocol? What are total testosterone and SHBG? Free testosterone measured with equilibrium dialysis or ultrafiltration would also be useful.

 

[Patriotaa]

Hey,
In may my HCT was 55, HGB 17,8 RBC 17,8. From May to August I made 4 donations. I didn't know about ferritin then. My hair started falling out and I felt bad. I learned about ferritin. My blood test results was then:

RBC 5,47
HGB 15,08
HCT 44,7
Iron 35 (norms 59-158)
Ferritin 15,21 (norms 21,81-275,66)

I didn't want to wait and made the protocol. I was taking 81mg ferrous disglycinate for 5 days according to protocol. I was taking it then 500mg/week testosterone cypionate and 400mg/week nandrolone decanoate. I stopped taking all dietary supplements, I spent 5 days at home but i had a problem with my diet. I ate pasta with a very small amount of tomato passata (100g per meal), some potatoes, chicken, protein wpc, oat flakes, nuts and I saved myself with a frozen pizza. I also drank very small amounts of Coke Zero. Could these products have canceled the protocol? My blood results after the protocol:

RBC 5,60
HGB 15,00
HCT 47,1
Iron 138 (norms 70-180)
Ferritin 16,1 (norms 23,9-336)

Was my hemoglobin too low for the protocol to fail? Maybe my diet was wrong? I was desperate and started taking feroplex prescribed by the internist. After a week I did blood tests:

RBC 6,0
HGB 16,1
HCT 51
Iron 100 (norms 70-180)
Ferritin 10,3 (norms 23,9-336)

I will have to make another donation soon. Should I repeat the protocol now? Does anyone have any ideas to help me?

 

[RobRoy]

Information here on why your doctor is right to be concerned about higher levels. Ignore those who would downplay the issue.

What worries me about the recommendations I've listened to is that some poor fellow is going to use this advice and think an Hct level in the mid 50s is perfectly reasonable and nothing should be done to correct this. ... But for the vast majority of folks looking for functional longevity and compression of morbidity, the medical literature is quite clear a corrective action should be taken. In this thread I'll share some literature, resources to help inform TRT users and demonstrate that elevated Hct is not benign.​

What is your TRT protocol? What are total testosterone and SHBG? Free testosterone measured with equilibrium dialysis or ultrafiltration would also be useful.

Terrible information you were recommending and it's not based on men on testosterone or men living at high altitude that also have a secondary erythrocytosis. BASELINE ELEVATIONS IN HCT IS NOT THE SAME AS THE SECONDARY ERYTHROCYTOSIS FROM TESTOSTERONE.

 

[Deleted member 16042]

Terrible information you were recommending and it's not based on men on testosterone or men living at high altitude that also have a secondary erythrocytosis. BASELINE ELEVATIONS IN HCT IS NOT THE SAME AS THE SECONDARY ERYTHROCYTOSIS FROM TESTOSTERONE.

I experience symptoms with HCT at 54, relieved by phlebotomy: Higher BP, reduced physical output with earlier onset of bounding heart, more fatigue and recovery time from exercise and a feeling of fullness in the chest. This has been repeatable many times over.

Are you recommending I ignore these?

EDIT, Also, any links to references, articles, data, studies, etc supporting your view would be appreciated, as well as parsing out what the differences are between the causative circumstances and why these differences are pertinent. The statement "Polycythemia vera is different than testosterone induced erythrocytosis" does not provide any background, supporting data etc. I'd like to make my own assessment based on knowing the reasons, and seeing the literature rather than hearsay from an anonymous forum participant.

This is of specific interest to me because my case of erythrocytosis is complex at this point, but the supposed causes are secondary, not primary. It is quite a challenge to sort out, even with several doctors involved including a renowned hormone specialist and a hematologist.

Thanks

 

[Cataceous]

Terrible information you were recommending and it's not based on men on testosterone or men living at high altitude that also have a secondary erythrocytosis. BASELINE ELEVATIONS IN HCT IS NOT THE SAME AS THE SECONDARY ERYTHROCYTOSIS FROM TESTOSTERONE.

The author of that thread invited you to comment many times, but you demurred. Why? It would surely help your credibility if you made a serious attempt to rebut the stated concerns.

 

[RobRoy]

The author of that thread invited you to comment many times, but you demurred. Why? It would surely help your credibility if you made a serious attempt to rebut the stated concerns.

I have commented on that author's comments multiple times. He can't produce anything at all related to testosterone and raising hematocrit causing harm. Not a single and I mean not a single piece of literature.

Testosterone Therapy as a cause of Secondary Erythrocytosis

The most common side effect of testosterone therapy, and the one that causes the most concern for the patient and their family physician, is a secondary erythrocytosis which is an increase in red blood cells. It is often described by the patient and their physician as “thick blood” requiring a blood donation because they fear it could possibly lead to a heart attack, stroke, or blood clot.
Where does this fear originate? When the family physician or internist sees an increase in red blood cells along with hemoglobin and hematocrit, it is frequently misinterpreted as the patient having Polycythemia Vera which is a myeloproliferative neoplasm of the bone marrow (bone marrow cancer). Thrombosis (blood clots) are a leading cause of morbidity and mortality in this disorder. Polycythemia vera is known as a primary erythrocytosis where there is an unregulated proliferation of hematopoietic clonal stem cells which leads to over production of red blood cells, white blood cells, and platelets. In Polycythemia Vera, in contrast to the secondary erythrocytosis from testosterone therapy, not only is there a quantitative change in the number of circulating blood cells, but there is also a qualitative change that leads to the expression of procoagulant characteristics. In addition there are abnormalities involving the vascular endothelial cells which become procoagulant in response to inflammatory stimuli. These abnormalities result in a hypercoagulable state leading to an increase in arterial thrombosis and venous thrombosis. Therefore part of the recommended treatment is blood donation to reduce the risk of thrombosis. The risk of elevated hematocrit seen in patients with polycythemia vera cannot be extrapolated to hematocrit elevation seen during testosterone therapy. They are not the same and should not be treated as such.
The secondary erythrocytosis from testosterone therapy is an increase in red blood cells only leading to an increase in hemoglobin and hematocrit. Themechanisms behind testosterone stimulating red blood cell production is not completely understood but is thought to occur through stimulation of erythropoietin, stimulation of hematopoietic progenitor cells, and reduced hepcidin. A secondary erythrocytosis is also seen in other conditions such as smoking, obstructive sleep apnea, chronic obstructive pulmonary disease, and living at high altitude. While a primary erythrocytosis has been well established as a risk factor for thromboembolic events the secondary erythrocytosis from testosterone therapy has not been shown to cause an increase in thromboembolic events in any randomized control trial or prospective study to date. Most guidelines recommend following hematocrit after initiating testosterone therapy and if the Hct exceeds 54% clinicians should either adjust testosterone dosage, stop therapy, order phlebotomy, or recommend a combination of these. These recommendations are based on assumptions and the Hct cut off of 54% was arbitrarily chosen and not based on any study showing harm when this value is exceeded with testosterone therapy. In fact, when Dr. Glenn Cunningham one of the authors of the Endocrine Society's guidelines for testosterone therapy was asked by Dr. Abraham Morgentaler where the upper limit of 54% came from he replied that “the number was not based on any actual medical data ,but we had to pick a number and it seemed like a reasonable number”. The upper limit of normal for hematocrit in most laboratory reference ranges for healthy adult males is 54% which is where this value is likely derived. Also creating confusion is the fact that different labs have different upper limits of normal for hematocrit. Some may use an upper limit of normal of 50% and others 54%. If you are a midshipmen on the USS Eisenhower, one of our nuclear aircraft carriers, the upper limit of normal for hematocrit in their lab is 60% (image 1)
These normal ranges of hematocrit are for men without a secondary erythrocytosis and not for men on testosterone or living at high altitude for instance. There are over 80 million people that live higher than 2,500 meters and they develop a secondary erythrocytosis. Men in parts of Bolivia for instance have a normal range of Hct from 45-61%. These men are not at an increased risk of thrombotic events nor do they have to undergo phlebotomies to manage their hematocrit. One also cannot ignore the observation that literally tens of thousands of men presently use and abuse testosterone in this country and have done so for decades. A large percentage of these men are not under the supervision of a physician or getting lab work and yet we have not seen an epidemic of heart attacks, strokes, or blood clots in these men. Almost all previously reported cases of testosterone therapy related venous thromboembolism were seen in patients with a previously undiagnosed thrombophilia like factor five Leiden deficiency.
The other concern with increasing hematocrit is that it will increase viscosity and decrease blood flow resulting in thrombotic events. In experimental studies using rigid glass viscometers or cone-plate viscometers there is a logarithmic increase in viscosity with increasing hematocrit. It is inappropriate to correlate these in vitro viscosity readings to what occurs to flowing blood through tiny distensible vessels in vivo. In other words, viscometer measures in these experiments do not translate to human blood vessels. Firstly, the flow through these narrow blood vessels is rapid (high shear rate), which in a non-Newtonian fluid such as blood causes a marked decrease in viscosity. Second, blood flowing through these narrow channels is axial with a central core of packed red blood cells sliding over a peripheral layer of lubricating low viscosity plasma. With a secondary erythrocytosis there is an increase in blood volume which enlarges the vascular bed, decreases peripheral resistance and increases cardiac output. Therefore, in a secondary erythrocytosis optimal oxygen transport with increased blood volume occurs at a higher hematocrit value than with a normal blood volume. A moderate increase in hematocrit may be beneficial despite the increased viscosity.
Testosterone also exerts multiple beneficial effects on the vasculature and its components which may protect against thrombosis. In other words testosterone has positive effects on vascular reactivity.
Testosterone is a vasodilator and increases nitric oxide
T decreases plasma concentrations of pro coagulatory substances T improves erythrocyte membrane lipid composition and fluidity
T increases red blood cell deformability
T reduces levels of lipoprotein a
Donating blood to reduce hematocrit may also provide men with a false sense of security.
In a study done over a two-year period of time they looked at men who donated blood that were on testosterone therapy at least 25% of them had a hematocrit above 54% and when they came back for repeat donations 44% of them had a
persistent elevation of hematocrit above 54%. So it essentially showed that repeat donations were insufficient to maintain a hematocrit below 54%.
Testosterone therapy was first used clinically 1937 and it has been used in thousands of randomized control trials. There is not a single randomized control trial to date that shows an increased risk of major adverse cardiac events with testosterone therapy.

 

[RobRoy]

 

[Deleted member 16042]

I have commented on that author's comments multiple times. He can't produce anything at all related to testosterone and raising hematocrit causing harm. Not a single and I mean not a single piece of literature.

Testosterone Therapy as a cause of Secondary Erythrocytosis

The most common side effect of testosterone therapy, and the one that causes the most concern for the patient and their family physician, is a secondary erythrocytosis which is an increase in red blood cells. It is often described by the patient and their physician as “thick blood” requiring a blood donation because they fear it could possibly lead to a heart attack, stroke, or blood clot.
Where does this fear originate? When the family physician or internist sees an increase in red blood cells along with hemoglobin and hematocrit, it is frequently misinterpreted as the patient having Polycythemia Vera which is a myeloproliferative neoplasm of the bone marrow (bone marrow cancer). Thrombosis (blood clots) are a leading cause of morbidity and mortality in this disorder. Polycythemia vera is known as a primary erythrocytosis where there is an unregulated proliferation of hematopoietic clonal stem cells which leads to over production of red blood cells, white blood cells, and platelets. In Polycythemia Vera, in contrast to the secondary erythrocytosis from testosterone therapy, not only is there a quantitative change in the number of circulating blood cells, but there is also a qualitative change that leads to the expression of procoagulant characteristics. In addition there are abnormalities involving the vascular endothelial cells which become procoagulant in response to inflammatory stimuli. These abnormalities result in a hypercoagulable state leading to an increase in arterial thrombosis and venous thrombosis. Therefore part of the recommended treatment is blood donation to reduce the risk of thrombosis. The risk of elevated hematocrit seen in patients with polycythemia vera cannot be extrapolated to hematocrit elevation seen during testosterone therapy. They are not the same and should not be treated as such.
The secondary erythrocytosis from testosterone therapy is an increase in red blood cells only leading to an increase in hemoglobin and hematocrit. Themechanisms behind testosterone stimulating red blood cell production is not completely understood but is thought to occur through stimulation of erythropoietin, stimulation of hematopoietic progenitor cells, and reduced hepcidin. A secondary erythrocytosis is also seen in other conditions such as smoking, obstructive sleep apnea, chronic obstructive pulmonary disease, and living at high altitude. While a primary erythrocytosis has been well established as a risk factor for thromboembolic events the secondary erythrocytosis from testosterone therapy has not been shown to cause an increase in thromboembolic events in any randomized control trial or prospective study to date. Most guidelines recommend following hematocrit after initiating testosterone therapy and if the Hct exceeds 54% clinicians should either adjust testosterone dosage, stop therapy, order phlebotomy, or recommend a combination of these. These recommendations are based on assumptions and the Hct cut off of 54% was arbitrarily chosen and not based on any study showing harm when this value is exceeded with testosterone therapy. In fact, when Dr. Glenn Cunningham one of the authors of the Endocrine Society's guidelines for testosterone therapy was asked by Dr. Abraham Morgentaler where the upper limit of 54% came from he replied that “the number was not based on any actual medical data ,but we had to pick a number and it seemed like a reasonable number”. The upper limit of normal for hematocrit in most laboratory reference ranges for healthy adult males is 54% which is where this value is likely derived. Also creating confusion is the fact that different labs have different upper limits of normal for hematocrit. Some may use an upper limit of normal of 50% and others 54%. If you are a midshipmen on the USS Eisenhower, one of our nuclear aircraft carriers, the upper limit of normal for hematocrit in their lab is 60% (image 1)
These normal ranges of hematocrit are for men without a secondary erythrocytosis and not for men on testosterone or living at high altitude for instance. There are over 80 million people that live higher than 2,500 meters and they develop a secondary erythrocytosis. Men in parts of Bolivia for instance have a normal range of Hct from 45-61%. These men are not at an increased risk of thrombotic events nor do they have to undergo phlebotomies to manage their hematocrit. One also cannot ignore the observation that literally tens of thousands of men presently use and abuse testosterone in this country and have done so for decades. A large percentage of these men are not under the supervision of a physician or getting lab work and yet we have not seen an epidemic of heart attacks, strokes, or blood clots in these men. Almost all previously reported cases of testosterone therapy related venous thromboembolism were seen in patients with a previously undiagnosed thrombophilia like factor five Leiden deficiency.
The other concern with increasing hematocrit is that it will increase viscosity and decrease blood flow resulting in thrombotic events. In experimental studies using rigid glass viscometers or cone-plate viscometers there is a logarithmic increase in viscosity with increasing hematocrit. It is inappropriate to correlate these in vitro viscosity readings to what occurs to flowing blood through tiny distensible vessels in vivo. In other words, viscometer measures in these experiments do not translate to human blood vessels. Firstly, the flow through these narrow blood vessels is rapid (high shear rate), which in a non-Newtonian fluid such as blood causes a marked decrease in viscosity. Second, blood flowing through these narrow channels is axial with a central core of packed red blood cells sliding over a peripheral layer of lubricating low viscosity plasma. With a secondary erythrocytosis there is an increase in blood volume which enlarges the vascular bed, decreases peripheral resistance and increases cardiac output. Therefore, in a secondary erythrocytosis optimal oxygen transport with increased blood volume occurs at a higher hematocrit value than with a normal blood volume. A moderate increase in hematocrit may be beneficial despite the increased viscosity.
Testosterone also exerts multiple beneficial effects on the vasculature and its components which may protect against thrombosis. In other words testosterone has positive effects on vascular reactivity.
Testosterone is a vasodilator and increases nitric oxide
T decreases plasma concentrations of pro coagulatory substances T improves erythrocyte membrane lipid composition and fluidity
T increases red blood cell deformability
T reduces levels of lipoprotein a
Donating blood to reduce hematocrit may also provide men with a false sense of security.
In a study done over a two-year period of time they looked at men who donated blood that were on testosterone therapy at least 25% of them had a hematocrit above 54% and when they came back for repeat donations 44% of them had a
persistent elevation of hematocrit above 54%. So it essentially showed that repeat donations were insufficient to maintain a hematocrit below 54%.
Testosterone therapy was first used clinically 1937 and it has been used in thousands of randomized control trials. There is not a single randomized control trial to date that shows an increased risk of major adverse cardiac events with testosterone therapy.

While I appreciate the assessment and logic, what I am hearing here is that the idea of no harm from Testosterone therapy (secondary erythrocytosis) comes from the reasoning that no evidence of harm equates as evidence of no harm. These are not the same.

I look forward theoretically to the day for clinical documentation of no harm. As with other medical mythbusting, debunking occurs at a glacial pace. I hope you are actually correct, and this becomes clinically proven.

And I still would like citations for the statistics and studies referred to in your diatribe. You have not provided a single reference in this regard.

I will continue to have phlebotomies when I become symptomatic. I am personally not OK trying to exercise/work out when I experience the symptoms listed above... oh, and some abnormal SOB also occurs with exertions when my HCT is high... And for the record. I have isolated erythrocytosis, I do not have other cythemias. So in my N=1 case, while your logic mostly rings true, and I understand the mechanisms you refer to in terms of physiology accommodating the viscosity, my symptoms indicate to me that the viscosity is actually problematic.

Anyway, thanks.

 

[RobRoy]

While I appreciate the assessment and logic, what I am hearing here is that the idea of no harm from Testosterone therapy (secondary erythrocytosis) comes from the reasoning that no evidence of harm equates as evidence of no harm. These are not the same.

I look forward theoretically to the day for clinical documentation of no harm. As with other medical mythbusting, debunking occurs at a glacial pace. I hope you are actually correct, and this becomes clinically proven.

And I still would like citations for the statistics and studies referred to in your diatribe. You have not provided a single reference in this regard.

I will continue to have phlebotomies when I become symptomatic. I am personally not OK trying to exercise/work out when I experience the symptoms listed above... oh, and some abnormal SOB also occurs with exertions when my HCT is high... And for the record. I have isolated erythrocytosis, I do not have other cythemias. So in my N=1 case, while your logic mostly rings true, and I understand the mechanisms you refer to in terms of physiology accommodating the viscosity, my symptoms indicate to me that the viscosity is actually problematic.

Anyway, thanks.

While I appreciate the assessment and logic, what I am hearing here is that the idea of no harm from Testosterone therapy (secondary erythrocytosis) comes from the reasoning that no evidence of harm equates as evidence of no harm. These are not the same.

I look forward theoretically to the day for clinical documentation of no harm. As with other medical mythbusting, debunking occurs at a glacial pace. I hope you are actually correct, and this becomes clinically proven.

And I still would like citations for the statistics and studies referred to in your diatribe. You have not provided a single reference in this regard.

I will continue to have phlebotomies when I become symptomatic. I am personally not OK trying to exercise/work out when I experience the symptoms listed above... oh, and some abnormal SOB also occurs with exertions when my HCT is high... And for the record. I have isolated erythrocytosis, I do not have other cythemias. So in my N=1 case, while your logic mostly rings true, and I understand the mechanisms you refer to in terms of physiology accommodating the viscosity, my symptoms indicate to me that the viscosity is actually problematic.

Anyway, thanks.

If utilizing testosterone for 85 years and the most common side effect is a secondary erythrocytosis which hasn't caused an epidemic of heart attacks, strokes, clots , or any disorder, then I don't know what more you need to be convinced. Would 100 years be adequate? Wasn't that long ago we thought testosterone cause prostate cancer or worse than that but now we used to treat prostate cancer and we know that actually protects against it. The exact opposite of what was thought for over 70 years. No harm does equate to no harm. What do you not get about this? Tell me, why do we not Phlebotomize everyone that lives about 2500 m? Why don't we treat those 80 million people with blood donations? You didn't read what was written, very closely or you would maybe understand it. The fact that testosterone has been used for 85 years and abused for over half of that time as well and yeah, it has caused no harm. How can I provide you evidence when there is none. But why don't you do this? Why don't you provide evidence that it has caused harm. Can you do that? because no one else can. You can also continue to believe that testosterone causes prostate cancer or worsens it, and you can continue to believe that estrogen is the devil. What you cannot understand is that the secondary erythrocytosis from testosterone just like living at altitude doesn't cause harm and has never caused harm. Therefore, no one can provide you with evidence that it caused harm. You believe it causes harm but you can't provide evidence that it has caused harm.

 

[Deleted member 16042]

If utilizing testosterone for 85 years and the most common side effect is a secondary erythrocytosis which hasn't caused an epidemic of heart attacks, strokes, clots , or any disorder, then I don't know what more you need to be convinced. Would 100 years be adequate? Wasn't that long ago we thought testosterone cause prostate cancer or worse than that but now we used to treat prostate cancer and we know that actually protects against it. The exact opposite of what was thought for over 70 years. No harm does equate to no harm. What do you not get about this? Tell me, why do we not Phlebotomize everyone that lives about 2500 m? Why don't we treat those 80 million people with blood donations? You didn't read what was written, very closely or you would maybe understand it. The fact that testosterone has been used for 85 years and abused for over half of that time as well and yeah, it has caused no harm. How can I provide you evidence when there is none. But why don't you do this? Why don't you provide evidence that it has caused harm. Can you do that? because no one else can. You can also continue to believe that testosterone causes prostate cancer or worsens it, and you can continue to believe that estrogen is the devil. What you cannot understand is that the secondary erythrocytosis from testosterone just like living at altitude doesn't cause harm and has never caused harm. Therefore, no one can provide you with evidence that it caused harm. You believe it causes harm but you can't provide evidence that it has caused harm.

I do "get it". I fully understand your arguments. But "getting it" does not mean wholesale acceptance of your conclusions. I remain unconvinced for the reasons I have already stated. I am not going to argue with you further on that basis.

I am surprised you apparently did not notice my last comment about the glacial pace of debunking medical myth. I agree, from what I can tell now, the testosterone and prostate issue exemplifies this, and it is glacially entering the mainstream now. But that is not the issue at hand, and has no bearing on the physiology of hematocrit.

Why have I not provided evidence that it is harmful?

Because I am not a clinical researcher. I only seek answers, and you have not convinced me based on my own N-1 experience which is contrary to your entire hypothesis. No amount of double negative circular logic will change that. My own symptoms remain the benchmark for my treatment decisions.

Good luck to you! I do appreciate your perspective.

EDIT: You know, actually I do have a side question for you: I used to be a high altitude mountaineer, in part educated by Dr Peter Hackett, an altitude researcher, and I taught high altitude physiology to mountaineers. At that time one of the purported limiting factors to altitude adaptation was the stacking phenomenon of RBCs passing through capillaries. The RBCs need to be able to present their flat/concave surface to the membrane for gas transfer to occur, but with erythrocytosis, there comes a point that they stack like stacks of poker chips which prevents gas exchange. Has there been follow up or updates to this info?

 

[RobRoy]

I do "get it". I fully understand your arguments. But "getting it" does not mean wholesale acceptance of your conclusions. I remain unconvinced for the reasons I have already stated. I am not going to argue with you further on that basis.

I am surprised you apparently did not notice my last comment about the glacial pace of debunking medical myth. I agree, from what I can tell now, the testosterone and prostate issue exemplifies this, and it is glacially entering the mainstream now. But that is not the issue at hand, and has no bearing on the physiology of hematocrit.

Why have I not provided evidence that it is harmful?

Because I am not a clinical researcher. I only seek answers, and you have not convinced me based on my own N-1 experience which is contrary to your entire hypothesis. No amount of double negative circular logic will change that. My own symptoms remain the benchmark for my treatment decisions.

Good luck to you! I do appreciate your perspective.

EDIT: You know, actually I do have a side question for you: I used to be a high altitude mountaineer, in part educated by Dr Peter Hackett, an altitude researcher, and I taught high altitude physiology to mountaineers. At that time one of the purported limiting factors to altitude adaptation was the stacking phenomenon of RBCs passing through capillaries. The RBCs need to be able to present their flat/concave surface to the membrane for gas transfer to occur, but with erythrocytosis, there comes a point that they stack like stacks of poker chips which prevents gas exchange. Has there been follow up or updates to this info?

Ahhh, once again, a baseline observation that has nothing to do with men on testosterone and what testosterone does. What are you reporting has absolutely zero to do with middle testosterone, and how it affects vascular activity. Let's stick to testosterone and the secondary erythrocytosis. The secondary erythrocytosis that people get from living at high altitude also doesn't cause harm. Altitude sickness is a completely other issue. This is what read a lot always did is get sidetracked on a non-related issue. Let's stick to the 85 years that testosterone has been used and abused and the fact that it has never caused harm. Remember literally millions of me on right now are using it, and are not under the supervision of the physician and the most common side effect is a secondary erythrocytosis. There is not an epidemic of heart attacks, strokes, or blood clots in these men. Just like we didn't see an epidemic of prostate cancer in men that were on testosterone when it was first being used, even though the party line for 70 years was that it would cause a worsening prostate cancer or cause prostate cancer. Testosterone increases red blood cell deformability. Look at the diameter of a red blood cell and some of the capillaries it has to go through and their diameter. They go through single file. So the question still remains. Are the over 80 million people that live above 2500 m at risk because they have a secondary erythrocytosis? When has the secondary erythrocytosis from testosterone been shown to cause harm? There wasn't even an adequate test for testosterone until the 1970s. Prior to that men were given testosterone without being able to measure testosterone, precisely or even at all. Yet, no harm. We were all taught to fear a baseline secondary erythrocytosis because of polycythemia vera. We were taught to fear hematocrit because of studies done in laboratories, using rigid glass viscometer's. A primary erythrocytosis causes harm, but not a secondary erythrocytosis. Let me ask you another question. Why do we not have our patients with COPD get phlebotomies? They also develop a secondary erythrocytosis. Why do we not have our patients with sleep apnea and a secondary erythrocytosis donate blood? These are all also a secondary erythrocytosis. The difference between these other conditions and testosterone is that testosterone has so many positive affects on vascular reactivity. None of them have been shown to cause harm but we have been taught to fear testosterone.
But the question still remains when has testosterone and the secondary erythrocytosis that causes ever been shown to cause harm in any study or even when it's been abused? In 85 years of use and abuse I believe we would've seen it by now don't you?

 

[Deleted member 16042]

Ahhh, once again, a baseline observation that has nothing to do with men on testosterone and what testosterone does. What are you reporting has absolutely zero to do with middle testosterone, and how it affects vascular activity. Let's stick to testosterone and the secondary erythrocytosis. The secondary erythrocytosis that people get from living at high altitude also doesn't cause harm. Altitude sickness is a completely other issue. This is what read a lot always did is get sidetracked on a non-related issue. Let's stick to the 85 years that testosterone has been used and abused and the fact that it has never caused harm. Remember literally millions of me on right now are using it, and are not under the supervision of the physician and the most common side effect is a secondary erythrocytosis. There is not an epidemic of heart attacks, strokes, or blood clots in these men. Just like we didn't see an epidemic of prostate cancer in men that were on testosterone when it was first being used, even though the party line for 70 years was that it would cause a worsening prostate cancer or cause prostate cancer. Testosterone increases red blood cell deformability. Look at the diameter of a red blood cell and some of the capillaries it has to go through and their diameter. They go through single file. So the question still remains. Are the over 80 million people that live above 2500 m at risk because they have a secondary erythrocytosis? When has the secondary erythrocytosis from testosterone been shown to cause harm? There wasn't even an adequate test for testosterone until the 1970s. Prior to that men were given testosterone without being able to measure testosterone, precisely or even at all. Yet, no harm. We were all taught to fear a baseline secondary erythrocytosis because of polycythemia vera. We were taught to fear hematocrit because of studies done in laboratories, using rigid glass viscometer's. A primary erythrocytosis causes harm, but not a secondary erythrocytosis. Let me ask you another question. Why do we not have our patients with COPD get phlebotomies? They also develop a secondary erythrocytosis. Why do we not have our patients with sleep apnea and a secondary erythrocytosis donate blood? These are all also a secondary erythrocytosis. The difference between these other conditions and testosterone is that testosterone has so many positive affects on vascular reactivity. None of them have been shown to cause harm but we have been taught to fear testosterone.
But the question still remains when has testosterone and the secondary erythrocytosis that causes ever been shown to cause harm in any study or even when it's been abused? In 85 years of use and abuse I believe we would've seen it by now don't you?

Thanks, I'll ponder this.

I was not conflating this stacking effect with high hematocrit with testosterone use, it was a side question. It is interesting to me how you took that. Thanks for the detailed reply.

I do live at altitude, and suck on an oxygen concentrator at night to counteract sleep hypoxia. It works extraordinarily well, I pulse ox consistently in the high 90s with O2. No obstructive apnea.

OK, so we are going in circles now.

You state that taking testosterone alleviates the negative effects of erythrocytosis. But I experience unwanted symptoms from erythrocytosis while taking testosterone. We don't know all details of causation for my case. Testosterone use, altitude sleep hypoxia (Now resolved), are in consideration.

I do have cognitive dissonance here with your perspective. It is extraordinarily simple:

I get unwanted symptoms from erythrocytosis. I am not comfortable living with them as such, they limit my physical/exercise capacity negatively, and are just uncomfortable. This is repeatable. I experience the symptoms prior to confirmation by blood tests. The symptoms are relieved by phlebotomy, The symptoms are:

HTN
Earlier onset of pounding heart prior to normal with exertion
Earlier onset of SOB with exertion
Fatigue and delayed recovery from exercise
An uncomfortable feeling of fullness in the chest

These symptoms do not occur with HCT below 50%, become vague in onset around 52% and definite at 54% and are relieved by phlebotomy.

OK, thanks again, I like your theories, but I find something misaligned about them in my own N=1 case. This is my uncertainty. I am not going to argue my points further. Best to you.

 

[RobRoy]

Thanks, I'll ponder this.

I was not conflating this stacking effect with high hematocrit with testosterone use, it was a side question. It is interesting to me how you took that. Thanks for the detailed reply.

I do live at altitude, and suck on an oxygen concentrator at night to counteract sleep hypoxia. It works extraordinarily well, I pulse ox consistently in the high 90s with O2. No obstructive apnea.

OK, so we are going in circles now.

You state that taking testosterone alleviates the negative effects of erythrocytosis. But I experience unwanted symptoms from erythrocytosis while taking testosterone. We don't know all details of causation for my case. Testosterone use, altitude sleep hypoxia (Now resolved), are in consideration.

I do have cognitive dissonance here with your perspective. It is extraordinarily simple:

I get unwanted symptoms from erythrocytosis. I am not comfortable living with them as such, they limit my physical/exercise capacity negatively, and are just uncomfortable. This is repeatable. I experience the symptoms prior to confirmation by blood tests. The symptoms are relieved by phlebotomy, The symptoms are:

HTN
Earlier onset of pounding heart prior to normal with exertion
Earlier onset of SOB with exertion
Fatigue and delayed recovery from exercise
An uncomfortable feeling of fullness in the chest

These symptoms do not occur with HCT below 50%, become vague in onset around 52% and definite at 54% and are relieved by phlebotomy.

OK, thanks again, I like your theories, but I find something misaligned about them in my own N=1 case. This is my uncertainty. I am not going to argue my points further. Best to you.

Can't help but take the bait, but how does hematocrit affect your ability to recover from exercise? What is the mechanism or physiology behind that? When did an increase in hematocrit cause fatigue? Why do we have our olympic athletes train at high altitude to cause a secondary erythrocytosis if it's going to cause them shortness of breath with exertion or fatigue? This is just another example of someone with underlying medical problems, and then wanting to apply those issues to men on testosterone.
Point is is that you obviously have an underlying medical condition that causes these issues but it doesn't apply to 99.99% of men on testosterone.

 

[Deleted member 16042]

Can't help but take the bait, but how does hematocrit affect your ability to recover from exercise? What is the mechanism or physiology behind that? When did an increase in hematocrit cause fatigue? Why do we have our olympic athletes train at high altitude to cause a secondary erythrocytosis if it's going to cause them shortness of breath with exertion or fatigue? This is just another example of someone with underlying medical problems, and then wanting to apply those issues to men on testosterone.
Point is is that you obviously have an underlying medical condition that causes these issues but it doesn't apply to 99.99% of men on testosterone.

Don't know, but these symptoms happen when hematocrit is high and do not when in normal range based on the same amount of exercise. I exercise and lift regularly. I have a standard routine. This is what I experience. I am sorry it does not fit your perception.

And BTW, perhaps you are right about something else contributing, and I do have co-morbidities, but the phenomenon is isolated to the cycle of high HCT. It seems other non HCT related causes would move independently from the HCT level.

 

[FunkOdyssey]

Ah weird. I've always gotten heart rhythm issues when taking iron supplements. From what I read, it could stimulate the vagus nerve and cause them in certain ppl, especially with those who have GERD, which I do. And my brother has vasovagul response, where sometimes he will pass out when he gets bad stomach cramps. So I'm assuming maybe it's connected. I've read people have good luck with PPI during iron supplementation, but if it increases absorption or messes with hepcidin or something else, I'll just have to deal with it. They are quite uncomfortable feeling tho

GERD causes heart palpitations in susceptible people, including myself, and this is theorized to occur by irritating the vagus nerve. Iron is a harsh substance that causes oxidative stress and damage to any part of the GI tract that it touches, and that would include the esophagus if you are suffering from reflux. In my opinion, if you already know you are someone that suffers palpitations from reflux and then you have palpitations after taking iron, it is probably related to reflux.