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This past week's bloodwork. Thoughts?

OuchThatHurts

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Was time for my bi-monthly blood work-up. Includes Comp Met Panel, CBC w/auto-diff, Reticulocytes, Ferritin, Folate, Iron + TIBC, B12, and Vit D Hydroxy.

This is a new one. My HCT, Hgb, MCV were high (as usual) but my RBCs, were normal (unusual). I don't know how HCT can be 57.6 with a normal RBC count. Iron, Ferritin, Folate were fine but B12 and D were deficient. The midday low blood sugar was odd but I can see because I keep my insulin sensitivity high with metformin and beberine but B12 and D with the amount of meat I eat makes no sense. Maybe Intrinsic Factor (IF) problem? I eat a ton of B12 but I suppose I could do injections but that could increase HCT.

TestC 600mg/wk
150mg TrenA/wk
12.5mg Stanzolol/day
5iu hGH Mon-Fri
w/daily metformin 500mg, berberine 1,200mg, Synthergine 2ml, Synthetine 400mg, telmisartan 40mg

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Met has a tendency to reduce vitamin B12 & rhGH has a tendency to reduce serum vitamin D3. You can increase supplementation to compensate (should).
I suppose I don't have a choice bc Monday I'm going to give up a unit or two to normalize my HCT and Hgb (therapeutic).
 
I suppose I don't have a choice bc Monday I'm going to give up a unit or two to normalize my HCT and Hgb (therapeutic).
It's a good idea here. You don't want to take supplemental iron in my view, it's just too likely to rebound dramatically (and just contributes to further increases in HCT/Hb). Just look forward to your therapeutic phlebotomy, as >57% HCT is just not something you want to be walking around with.
 
>57% HCT is just not something you want to be walking around with.
You're not kidding. Welcome to my world. On a positive note, I had been 51-53% for a while but skipped offloading a few units and boom, popped right back up. Plus I stopped taking my daily aspirin which was nice while it lasted but.....
 
It's a good idea here. You don't want to take supplemental iron in my view, it's just too likely to rebound dramatically (and just contributes to further increases in HCT/Hb). Just look forward to your therapeutic phlebotomy, as >57% HCT is just not something you want to be walking around with.
Agreed. My doc told me to stop the supplemental iron due to increase of H&H.
 
Do you have untreated sleep apnea? That can increase hematocrit. Don't get trapped in the cycle of HCT up, donate, rebound, donate, etc.
With polyscythemia you can't donate blood. Well, I suppose one could, but I do not. When I give blood, it is by prescription only and even then, it is disposed. Which is itself no great tragedy given that my blood type is AB+. This means that my blood, like all AB pos people, has A+B antigens on the cells and immunoglobulins in plasma (along with rh factor) that allows me to be a "universal recipient" of anyone's blood but a donor to about 1 person in 25 (other AB+ people).

In a similar but exactly opposite way, O- is considered a "universal donor" because they can give blood to anyone. O negative blood is very sought after for this very reason. But while they can give to anyone, they require O- blood. (O negs should give as much blood as they can obviously)

The only available methods of treatment for erythrocytosis are therapeutic phlebotomy (blood letting) or some type of myelosuppressive agent which is a last resort in the most severe cases where erythrocytosis is causing scarring of bone marrow tissue. I'm not in that category. At that point, it is a form of leukemia called myelofibrosis. At the point scarring begins to appear, instead of producing too many erythrocytes, the marrow then slowly begins producing too few RBCs.
 
Agreed. My doc told me to stop the supplemental iron due to increase of H&H.
Good observation. My oncologist/hematologist is probably going to recommend Fe supp, D3 supp, and B12 injections to increase my iron sat bc it's sitting at 15% (borderline low) combined with phlebotomy to correct these H/H numbers. But aside from Fe being on the low edge and B12 and D deficiencies my bloodwork is excellent. Liver values, kidneys, BG, electrolytes, ECG, all still excellent.

Lowering HCT while maintaining Fe, B12, folate, transferrin, D, etc while offloading whole blood is the challenge here. Because although by RBCs are normal in number, my MCV (mean corpuscular volume) is high meaning instead of having nice little donut-like erythrocytes, my cells look more like little rafts and are large in size. This is bad.

But post-phlebotomy with those supps, my bloodwork by this time next week should be greatly improved. My physical performance is still very good. Many here have questioned my use of almost excessive aerobic exercise (if there is such a thing) but this is good for everyone. Anyone reading this, please believe me on this. Please get your cardio in. It doesn't have to be painful. Increased heart rate and respiration is all you need. If you're feeling the burn, that's anaerobic. That's not aerobic. You'll get enough anaerobic from your training.

Nobody wants polyscythemia but please use my bloodwork (full workup every two months) as a visible example of how what we do effects our most important health factor: the blood. Consider blood as almost an organ in itself and keep it healthy. I have a blood disorder but because of how closely monitored I am, I will likely outlive many of my friends who I constantly preach to, including this board, on the importance of getting your butts to the lab to monitor and watch your numbers like a hawk.

With the recent string of deaths we see that many people used large quantities of anabolics which wrecked their numbers WHILE KNOWING they had comorbidities! It's madness. In fact, deadly as we have unfortunately witnessed.
 
Lipids?
 
Yup. Lipids are this week with another CBC w/diff and CMP post-phlebotomy. My last two lipid panels were fine. I have mine from 2 months ago but I didn't add those old numbers. They are in my thread in the log section though if you want to see those factors. HDL was understandably elevated. My triglycerides I was not happy with at all but the metformin cut those by a third. My HDL is good. I'll post those up after next Friday.

Edit: I failed to mention that this is bloodwork ordered by my hematologist/oncologist. My GP orders my standard panels (CBC, Lipids, Met, PSA score, etc). Those are a separate set from my cardiologist over at the campus hospital.
 
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I have erythrocytosis too and I'm also have AB+ blood type. I was doing bloodwork every 10-12 weeks to keep an eye on things.
My hematologist told my not to draw blood that often because every small vial is about 10ml and it takes 3 days to replenish your RBC after drawing blood.
He doesn't seem overly concerned and he knows why my blood is thick. He wants me to do follow-up blood work 6 months from last draw.
He said if my hemoglobin hits 17 I need to see him. It usually runs about 14.5-15.0. If my numbers are high he'll probably prescribe a therapeutic phlebotomy.
 
Have you been checked for sleep apnea at all? I didn't show up on any of the surveys but mine was mega severe (low iron too so similar to yours maybe). I have always been top of range for hgb and crit so polyc was my diagnosis as well. Now that I've been on a CPAP for a while I still sit at top of range but not nearly as bad elevation from anabolics. I am never below 48 and even on longer big cycles I maybe hit 51 now versus 54-57 before.

Huge difference plus quality of life improvement. Had no idea I even had sleep apnea.
 
It's a good idea here. You don't want to take supplemental iron in my view, it's just too likely to rebound dramatically (and just contributes to further increases in HCT/Hb). Just look forward to your therapeutic phlebotomy, as >57% HCT is just not something you want to be walking around with.
How is donating blood a good idea with an iron and iron sat% as low as his? There is virtually no risk of cardiovascular problems from a high hematocrit/hemoglobin without high platelets. Donating blood would be a terrible idea for him. That hematocrit will just jump right back up in a few weeks and his iron will be even lower.

The LAST thing I would do in donate blood in this case. I would eat high iron foods with vitamin C as much as possible. And of course, take methylated B12 and Vitamin D/K.

The rest looks fine.
 
Agreed. My doc told me to stop the supplemental iron due to increase of H&H.
I have gotten myself out of iron deficiency while simultaneously having a high H/H by using high doses of iron bisglycinate + vitamin C. Paranoia over an elevated H/H is how we hurt ourselves (assuming we don't have high platelets or any of the clotting mutations we all should check for)
 
I have erythrocytosis too and I'm also have AB+ blood type. I was doing bloodwork every 10-12 weeks to keep an eye on things.
My hematologist told my not to draw blood that often because every small vial is about 10ml and it takes 3 days to replenish your RBC after drawing blood.
He doesn't seem overly concerned and he knows why my blood is thick. He wants me to do follow-up blood work 6 months from last draw.
He said if my hemoglobin hits 17 I need to see him. It usually runs about 14.5-15.0. If my numbers are high he'll probably prescribe a therapeutic phlebotomy.
My hemoglobin is always in the 18-19's. The only way I can bring it down is to remove TRT and become testosterone deficient. Donating blood over and over is a recipe for disaster. I used to do that and I learned a hard lesson from it. Donating once a year is good for overall health but repeatedly doing it is NOT going to bring the H/H down long term if you don't remove the cause of it. Keep the blood pressure healthy, the platelets normal, the fibrinogen normal, and don't have any of the Factor V/prothrombin mutations and then don't worry about it.



And from a third study,
"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
 
How is donating blood a good idea with an iron and iron sat% as low as his? There is virtually no risk of cardiovascular problems from a high hematocrit/hemoglobin without high platelets. Donating blood would be a terrible idea for him. That hematocrit will just jump right back up in a few weeks and his iron will be even lower.

The LAST thing I would do in donate blood in this case. I would eat high iron foods with vitamin C as much as possible. And of course, take methylated B12 and Vitamin D/K.

The rest looks fine.
Therapeutic phlebotomy is a good idea because of elevated HCT/Hb, increased risk of thrombosis, etc.

With the use of AAS, we see decreased Hepcidin & therefore decreased Fe bioavailability (and increased HCT/Hb)... Note that his values are within range and thus normal. Ouch is exhibiting all the markers of supra-physiologic androgen use... This effect on iron metabolism will normalize with dose reduction.

Again, increased iron intake (OK, some dietary increase is fine) is inadvisable in my view here, for the reasons already mentioned.
 
Therapeutic phlebotomy is a good idea because of elevated HCT/Hb, increased risk of thrombosis, etc.

With the use of AAS, we see decreased Hepcidin & therefore decreased Fe bioavailability (and increased HCT/Hb)... Note that his values are within range and thus normal. Ouch is exhibiting all the markers of supra-physiologic androgen use... This effect on iron metabolism will normalize with dose reduction.

Again, increased iron intake (OK, some dietary increase is fine) is inadvisable in my view here, for the reasons already mentioned.
There is no evidence in people with secondary polycythemia that an increased H/H in isolation in the absence of high platelets, clotting mutations, and hypertension increases the risk of clots/strokes/MI, etc. Certainly not at a HCT below 58 or a HG below 19.

From Rex Feral
"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?"

Dr. Neal Rouzier is the one who first spoke out against this misguided practice.

 
There is no evidence in people with secondary polycythemia that an increased H/H in isolation in the absence of high platelets, clotting mutations, and hypertension increases the risk of clots/strokes/MI, etc. Certainly not at a HCT below 58 or a HG below 19.

From Rex Feral
"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?"

Dr. Neal Rouzier is the one who first spoke out against this misguided practice.

Well there's the Tromso study: Braekkan SK, Mathiesen EB, Njølstad I, Wilsgaard T, Hansen JB. Hematocrit and risk of venous thromboembolism in a general population. The Tromso study. Haematologica. 2010 Feb;95(2):270-5. doi: 10.3324/haematol.2009.008417. Epub 2009 Oct 14. PMID: 19833630; PMCID: PMC2817030.

Showing HCT and Hb are independent risk factors for thromboembolism (each 5% increase in HCT beyond 43 - 46% increases risk by ~33%).

Can you suggest a mechanism or some physiological justification for the claim that HCT poses no risk without high thrombocytes?

Tangentially, my understanding is that RBC can contribute to thrombus formation by other mechanisms (besides the increased viscosity by HCT), such as by stimulating platelet aggregation via ADP release or possibly through the exposure of phosphatidylserine.

Can you support a position where AAS abuse/polypharmacy poses less risk for thrombotic events than this analysis of the general population?
 

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