Has anyone successfully kept Hematocrit/Hemoglobin low without donating?
- Thread starter Arcane
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Vince
Super Moderator
I haven't donated for almost 8 years now. When I switched to daily injections my HCT stabilized. I don't know if it was because of longevity or daily injections. I do love not having to donate blood.
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Vince's Labs from 4/15/24
My protocol, 16 mg of testosterone cypionate daily, 500 iu of hcg every third day and no AI. Pregnenolone 10 mg and 10 mg of DHEA. My last injection before labs, about 27 1/2 hrs. Labs are from LabCorp. I lowered my dhea from 25 mg to 10 mg daily, it may have lowered my E2. Used black cumin...
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Mr_Fusion
Member
Due to being in remission from Hodgkin’s Lymphoma, I am unable to donate blood. I recently started taking 10,800 FU of nattokinase (NK) daily which has been proven to lower Hemocrit according to research studies: Nattokinase: A Promising Alternative in Prevention and Treatment of Cardiovascular Diseases - PMC
Last edited:
FunkOdyssey
Seeker of Wisdom
ARBs and ACEs are a good option if you are also trying to optimize your blood pressure (ARBs would be my preference for less sides and greater benefits):
Hematocrit-lowering effect following inactivation of renin-angiotensin system with angiotensin converting enzyme inhibitors and angiotensin receptor blockers - PubMed
Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary...
pubmed.ncbi.nlm.nih.gov
Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary disease, and congestive heart failure. Accordingly, RAS inactivation may confer susceptibility to the hematocrit-lowering effects of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Indeed, a dose-dependent decrease in hematocrit is observed within the first month of such therapy. In the majority of patients with hypertension decreases in hematocrit values after RAS inactivation are small and not clinically important. In extreme conditions, however, such as erythrocytosis after successful renal transplantation, secondary polycythemia of chronically hypoxemic COPD patients, erythrocytosis associated with renovascular hypertension, severe cardiac or renal failure, the hematocrit-lowering effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blocker may be profound and even lead to or worsen anemia. Hematocrit reaches its nadir value within three months, and then it remains stable during long-term observations. After discontinuation of RAS blockade, hematocrit values rise gradually over the next three to four months towards the pretreatment levels. The mechanism(s) related to this phenomenon is not yet fully understood, but angiotensin II seems to be responsible for inappropriately sustaining secretion of erythropoietin despite hematocrit elevation and capable to directly stimulate the erythroid progenitors in bone marrow to produce erythrocytes.
mooseman109
Active Member
I was on losartan for years after my heart attack for a couple years. Unfortunately, it did not lower my hct at all! I was really hoping, but we are all differentARBs and ACEs are a good option if you are also trying to optimize your blood pressure (ARBs would be my preference for less sides and greater benefits):
Hematocrit-lowering effect following inactivation of renin-angiotensin system with angiotensin converting enzyme inhibitors and angiotensin receptor blockers - PubMed
Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary...
Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary disease, and congestive heart failure. Accordingly, RAS inactivation may confer susceptibility to the hematocrit-lowering effects of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Indeed, a dose-dependent decrease in hematocrit is observed within the first month of such therapy. In the majority of patients with hypertension decreases in hematocrit values after RAS inactivation are small and not clinically important. In extreme conditions, however, such as erythrocytosis after successful renal transplantation, secondary polycythemia of chronically hypoxemic COPD patients, erythrocytosis associated with renovascular hypertension, severe cardiac or renal failure, the hematocrit-lowering effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blocker may be profound and even lead to or worsen anemia. Hematocrit reaches its nadir value within three months, and then it remains stable during long-term observations. After discontinuation of RAS blockade, hematocrit values rise gradually over the next three to four months towards the pretreatment levels. The mechanism(s) related to this phenomenon is not yet fully understood, but angiotensin II seems to be responsible for inappropriately sustaining secretion of erythropoietin despite hematocrit elevation and capable to directly stimulate the erythroid progenitors in bone marrow to produce erythrocytes.
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