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blood clots and AAS

nfernoo

Banned
Joined
Aug 25, 2014
Messages
1,392
My buddy (around 26 27) had a blood clot in his leg.
he's been put on blood thinners for now.

He has a good history of aas as he competes.
He's been on a small amount of test cyp. And arimidex.


What info can I give him.
 
I had surgery on both patellar tendons and to prevent blood clots I took baby aspirin 81mg once per day. The same regimen for heart health. They wanted me to take subcutanenous Enoxaparin injections though, but that was spendy and I moved my feet and legs a lot anyway so I figured low dose aspirin would be effective enough.
 
I was going to do some research on your question though, because FDA does warn that AAS can increase the risk of blood clots and mini-strokes...
 
Just for "safety" reasons I had my GP refer me to a hematologist so I could get tested for any clotting disorders. I did this after a friends co worker (non gear user) died from a clot- he had a genetic clotting disorder that he didn't know about. He was mid 30's.

Also for me, using a CPAP and donating blood as needed to keep my H&H where it needs to be is what I do for "prevention".
 
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.
Is letro the best option on high dose cycles?
 
I had a blood clot in the leg. These come from long plane trips I took. I do a certain regime of vitamins now. He also better not take the AAS like before, they can cause it too. The person who taught me a great regime was Emeric. I learn a lot from him. This is a warning call for this young guy. Time to wake up or not wake up at all.
 
Too many guys on this forum don't get blood work done until it's too late. Your buddy needs to get labs done frequently to make sure his rbc is in range. Let's face it, all aas thickens the blood, not just eq. Blood thinners have some really bad side effects. Your buddy may need to lay off everything for awhile until numbers return to normal.
 
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.

:yeahthat: Very important!
 
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?
 
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.
 
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.

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.
 
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.

Stewie, do you like to check e1s over e2 for any particular reason? I normally prefer aromasin and letro over Arimidex because the latter is fairly poor at blocking the conversion of test to e2. I'm guessing your talking about E1 and e1s because of the small ability of test to back to adione and then to estrone or after the conversion to go from e2 to estrone

Do you know of any lab work from someone on test who had normAL E2 levels but very elevated estrone? That would be interesting.

While I don't directly care about e1s because it's bit bilogically active I still wouldn't want it to be abnormally elevated for other reasons.

People also need to understand you do want estrogen. It is important so don't just try to crush it.
 
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.

Thank you. My latest labs have my TSH3 at 3.03. I'm currently running 40, soon to be 50mcg T3 to aide in some fat loss, no AAS. Any issues here with my levels you think?
 
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.
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.
 

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