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This past week's bloodwork. Thoughts?

Let me be clear that I'm in no way advocating that an otherwise healthy person donate blood as a form of self-medicating erythrocytosis due to the use of erythropoietic compounds such as Anadrol, Equipoise, EPO, etc (although all AAS have some erythropoietic effect). It requires an entire array of tests to assure that I stay within parameters and quite frankly, healthy. More often than not, a therapeutic phlebotomy is not even warranted or prescribed. But to repeatedly donate blood to lower BP or HCT/Hgb without the corresponding tests for vitamin deficiencies is as hapless as the use/overuse of AAS that caused the condition in the first place.

I do not fall into that category. After my second DVT many years ago, I had a solid bone marrow biopsy taken from the back of my hip indicating enough of a degree of fibrosis to warrant the therapeutic phlebotomy in the prevention or progression of fibrosis into full-blown myelofibrosis which occurs in about 1 in 5 people with polyscythemia (if left untreated). Myelofibrosis is obviously very dangerous. I was certainly not on any AAS at that time. And I have not had any clotting since I began treatment.

Although I am far from a progression into that more severe form, therapeutic phlebotomy under the supervision of a hematologist/oncologist is the only treatment available other than a more dangerous treatment with a myelosuppressive drug with its associated toxicity to prevent the recurrence of blood clots (DVT, for example) by inhibiting primarily red blood cell formation. This is not normally done unless the condition is more progressed.

Since my spleen showed no signs of enlargement, the less radical phlebotomy was prescribed. I learned many years ago that I was simply unable to Vitamin Shoppe my way out of it (on or off the sauce). But I posted this as an oddity that my RBC, WBC, and platelet counts were normal yet my HCT is very high. That was a new one. Those components are usually high also.

Yes @nothuman that's why my doctor is as reluctant as possible to prescribe phlebotomy so you are correct. But let me say that Rex feral (?) is way off. Erythrocytosis secondary to acclimatization to high altitudes is a temporary condition and returns to normal extremely rapidly upon return to sea level. Temporary though it may be, it briefly extremely increases risk of high altitude cardiopulmonary edema, cerebral edema, clotting, stroke. It absolutely poses very real health risks. This is why hydration in acclimatization is so very vital.

@danieltx : An overnight sleep study is scheduled in June. Although I rarely snore, the things I hear from people I know seems like it's definitely worth the test so I'm doing it.
 
Unless you are in the sun often, or supplementing D(2) or (3), it doesn't surprise me that they are low.
 
@danieltx : An overnight sleep study is scheduled in June. Although I rarely snore, the things I hear from people I know seems like it's definitely worth the test so I'm doing it.
Great call here. I did mine on a suggested lark and I proved to be 2.5x the severe threshold with O2 dropping to concerning if not serious levels at night. I went from 55 events an hour to averaging less than 2 with my CPAP. It took some getting used to as my pressures nearly max out most machines (17-23 range I think in a variable machine). Basically I need a full face mask and bolt the fucker on. Worth it though.

I'd recommend not sleeping or minimal sleep the night before. Lots of people have trouble sleeping and getting a good read. You don't need a full night or even great sleep but these appointments are a hassle to get and redo so I'd make it count.
 
I was misdiagnosed with Polycythemia myself. My RBC numbers were always high and my doctor at the time didn't know about my AAS use. Once I'm off everything for awhile my numbers always return to normal. The first time my family doctor seen my numbers he freaked and sent me to a cancer specialist. Like someone else mentioned, sleep apnea will elevate these numbers as well.
 
Note that Ouch has indicated he VERY infrequently phlebotomizes. While I can appreciate concerns for anemia with frequent blood-letting, I don't think Rx'd therapeutic phlebotomy once a year (perhaps even less here) is cause for hysteria.
I agree as once a year phlebotomies have shown profound health benefits but I'd personally feel more comfortable with my ferritin, iron, and sat % being higher if I'm going to do it.
 
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?
I don't see where it mentions their platelet numbers in the study you shared here. That's kind of important to know. If they increased along with the HCT, then that would support my position. If they remained at a normal level, it would support yours.
 
Creatinine is the first thing I look at having past kidney scares, yours is great for your size. I will be getting a physical soon myself.
 
I don't see where it mentions their platelet numbers in the study you shared here. That's kind of important to know. If they increased along with the HCT, then that would support my position. If they remained at a normal level, it would support yours.
Heh, do you actually think the onus is on me to disprove your claim? I proved mine: that HCT is an independent risk factor (i.e., it increases blood viscosity) for thrombotic events. Do note, absolute risk is still very much in one's favor, but I very strongly believe there is a confluence of factors (a "conflagration" perhaps) that androgens present (lipid derangement, endothelial dysfunction, atherosclerosis, hypertension, etc.) that result in greater morbidity versus... Sherpas adapted to living at altitude.
 

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