Is letro the best option on high dose cycles?Estrogen acts on the liver and increases production of certain factors within the clotting cascade.
Elevated HCT levels increase viscosity of the blood and makes clot formation more likely
Screwed up BP and lipids coupled with jacked up HCT can cause endothelial damage..again down the road can result in clot formation.
Aspirin is NOT a substitute for lovenox when that is prescribed. Granted the previous posters patella issue probably didnt warrant it if they were being very active.
And please please stop thinking that arimidex will control estrogen on higher doses. Learn about E1 and E2. Arimidex is better suited for lower dose test.
Estrogen acts on the liver and increases production of certain factors within the clotting cascade.
Elevated HCT levels increase viscosity of the blood and makes clot formation more likely
Screwed up BP and lipids coupled with jacked up HCT can cause endothelial damage..again down the road can result in clot formation.
Aspirin is NOT a substitute for lovenox when that is prescribed. Granted the previous posters patella issue probably didnt warrant it if they were being very active.
And please please stop thinking that arimidex will control estrogen on higher doses. Learn about E1 and E2. Arimidex is better suited for lower dose test.
Always very helpful!
Letrozole definitely has been shown to have a superior suppression of E1S over Arimidex, in some clinical settings. From my readings, Aromasin had a lower percentage of suppression on E1 and E1S.
Although, this is subjective to the individuals expression and genetic action of 17β-HSD1 to estrone sulfate (E1S) <> E2.
Thoughts?
As always my time has been very compressed. A few things I'd like to add to your list gg.
Do not overdo it on phlebotomies, tanking your iron stores. It's been observed that iron deficiency (even without anemia) will increase platelets to become more "sticky", increasing the chance of clotting to occur.
Know your genetic background. If any first degree relative has a clotting disorder or any type of autoimmune diseases. Check for Factor V Leiden, Prothrombin mutation, MTHFR and Galectin-3, which has been implicated in the venous thrombogenesis process. Iron deficiency would exacerbate and an elevated level Galectin-3 potentiating the risk of a clot several fold.
One could also check their Fibrinogen levels, hs-CRP, Lp-PLA², Homocysteine and Myeloperoxidase levels.
One last thing, those that push the envelope on running high T3 doses. This can be pro-thrombotic in a hyperthyroid state.
Always very helpful!
Letrozole definitely has been shown to have a superior suppression of E1S over Arimidex, in some clinical settings. From my readings, Aromasin had a lower percentage of suppression on E1 and E1S.
Although, this is subjective to the individuals expression and genetic action of 17β-HSD1 to estrone sulfate (E1S) <> E2.
Thoughts?
As always my time has been very compressed. A few things I'd like to add to your list gg.
Do not overdo it on phlebotomies, tanking your iron stores. It's been observed that iron deficiency (even without anemia) will increase platelets to become more "sticky", increasing the chance of clotting to occur.
Know your genetic background. If any first degree relative has a clotting disorder or any type of autoimmune diseases. Check for Factor V Leiden, Prothrombin mutation, MTHFR and Galectin-3, which has been implicated in the venous thrombogenesis process. Iron deficiency would exacerbate and an elevated level Galectin-3 potentiating the risk of a clot several fold.
One could also check their Fibrinogen levels, hs-CRP, Lp-PLA², Homocysteine and Myeloperoxidase levels.
One last thing, those that push the envelope on running high T3 doses. This can be pro-thrombotic in a hyperthyroid state.
Wouldn't any T3 dose over what the body naturally produces (25-30mcg I believe) put you at hyperthyroid levels? Or are you saying only high doses of say 100+mcg is what you should be careful with?
Typically if your TSH goes below 0.5 mIU/L this would indicate one is in a hyperthyroidism state. Termed factitious hyperthyroidism. FT3 and FT4 could be pulled and used diagnostically, not necessary if factitious hyperthyroidism is the known cause.
Always very helpful!
Letrozole definitely has been shown to have a superior suppression of E1S over Arimidex, in some clinical settings. From my readings, Aromasin had a lower percentage of suppression on E1 and E1S.
Although, this is subjective to the individuals expression and genetic action of 17β-HSD1 to estrone sulfate (E1S) <> E2.
Thoughts?
As always my time has been very compressed. A few things I'd like to add to your list gg.
Do not overdo it on phlebotomies, tanking your iron stores. It's been observed that iron deficiency (even without anemia) will increase platelets to become more "sticky", increasing the chance of clotting to occur.
Know your genetic background. If any first degree relative has a clotting disorder or any type of autoimmune diseases. Check for Factor V Leiden, Prothrombin mutation, MTHFR and Galectin-3, which has been implicated in the venous thrombogenesis process. Iron deficiency would exacerbate and an elevated level Galectin-3 potentiating the risk of a clot several fold.
One could also check their Fibrinogen levels, hs-CRP, Lp-PLA², Homocysteine and Myeloperoxidase levels.
One last thing, those that push the envelope on running high T3 doses. This can be pro-thrombotic in a hyperthyroid state.
Typically if your TSH goes below 0.5 mIU/L this would indicate one is in a hyperthyroidism state. Termed factitious hyperthyroidism. FT3 and FT4 could be pulled and used diagnostically, not necessary if factitious hyperthyroidism is the known cause.
Stewie , you mentioned carnitine. What are your thoughts on that? Just in general I mean. I used to think it had benefit in terms of fat loss but with the recent carntine atherosclerosis studies I'm starting to be on the fence about it and might not recommended it. Haven't completely made up my mind but the small fat loss benefits might not be worth it.Late edit: Everyone doesn't respond to to same dosage. Drug-drug interactions has to be taking into consideration e.g., beta blockers, dopamine agonists, birth control, l- Carnitine, NSAIDs, ect, ect all interact with thyroidal function. Either by thyrotropin levels reduced, inhibited peripheral conversion of T4->T3, or displacement of thyroid binding globulin.