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03-23-2017, 04:16 AM #1
AAS and blood coagulation.
Hi guys. As you know, AAS could affect blood coagulation, either through RBC count or an high estrogens level and this could be dangerous. If one is not susceptible to hypercoagulation, keeping under control these 2 factors, could it possible to keep a safety profile related to coagulation ?
Further doing a good cardio, taking a baby aspirin and OMEGA-3 fatty acids while on cycle, it's well known to be a good support about coagulation.
Regardless genetic factors ( Leiden V factor, fibrinogen issues etc. ), is it possible to cycling safety observing with careful the parameters told above ?
Thank you for your time
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03-23-2017, 09:11 AM #2
I dont think the coagulation is a major issue. In fact I will need to check, but I believe androgens themselves decrease coagulation of the blood. Unless you are undergoing surgery soon the effect is too small to worry about. If you are concerned with it from a estrogen derivation, take an AI (I recommend aromasin ). Most AAS will led to heightened hematocrit levels, which is essentially a measure of blood thickness with RBCs. The main concern is developing what is known as polycythemia (too many red blood cells) as this can increase risk for DVT and PE blood clots. Aspirin as you mentioned is indicated as a stroke preventative and I see no harm in taking this low dose. Some cardio and omega fats of course good for overall health.
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03-23-2017, 10:53 AM #3
Yes, but i've read as following:
From "Anabolics" book ( and other reliable sources ):
"Anabolic /androgenic steroids can cause a number of
changes in the hematological system that affect blood
clotting. This effect can be very variable, however. The
therapeutic use of these drugs is known to increase
plasmin, antithrombin III, and protein S levels, stimulate
fibrinolysis (clot breakdown), and suppress clotting
factors II, V, VII, and X.114 115 These changes all work to
reduce clotting ability. Prescribing guidelines for
anabolic/androgenic steroids warn of potential increases
in prothrombin time, a measure of how long it takes for a
blood clot to form.116 If prothrombin time increases too
greatly, healing may be impaired. The effects of
anabolic/androgenic steroids on prothrombin time are
generally of no clinical significance to healthy individuals
using these drugs in therapeutic dosages. Patients taking
anticoagulants (blood thinners), however, could be
adversely affected by their use.
Conversely, anabolic/androgenic steroid abuse has been
linked to increases in blood clotting ability. These drugs
can elevate levels of thrombin 117 and C-reactive
protein,1 1S as well as thromboxane A2 receptor density,1 19
which can support platelet aggregation and the
formation of blood clots. Studies of steroid users have
demonstrated statistically significant increases in platelet
aggregation values in some subjects.120 There are also a
growing number of case reports where (sometimes fatal)
blood clots, embolisms, and stokes have occurred in
steroid abusers.121 122 123 124 125 Although it has been
difficult to conclusively link these events directly to
steroid abuse, the adverse effects of anabolic steroids on
components of the blood coagulation system are well
understood. These serious adverse effects are now
regarded as recognized risks of steroid abuse among
many that study these drugs.
In therapeutic levels, the anti-thrombic effects of
anabolic/androgenic steroids seem to dominate
physiology, and decreases in blood clotting ability may be
noted. At a certain supratherapeutic dosage point,
however, the pro-thrombic changes appear to overtake
the anti-thrombic changes, and physiology begins to
favor fast and abnormally thick clot formation
(hypercoagulability). The exact dosage threshold or
conditions required to increase blood clotting has not
been determined, and some studies with steroid users
taking supraphysiological doses fail to demonstrate
increased coagulability.126 Individuals remain warned of
the potential increases in thrombic risk with
anabolic/androgenic steroid abuse. Blood clotting
tendency should return to the pretreated state after the
discontinuance of anabolic/androgenic steroids."
This does not seem to be related to HCT and/or estrogens... but about androgens activity in itself... what do you think it about .. ? ( Yes i always do blood work and i take Arimidex to control estrogens and i observe HDL, Hct and E2 levels constantly ).
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03-23-2017, 01:26 PM #4
As I thought and originally posted, androgens decrease clotting factors and these are of "no clinical significance in healthy individuals". Again bleeding and clotting risk should be assessed prior to a surgery in my opinion to be careful. It would be wise to at least mention to the anesthesiologist. It seems you are worried about very high dosages of AAS causing the exact opposite effect and increasing clotting? I am not sure, or if anyone is even sure, of how that mechanism would directly work--but we do know estrogens increase blood clotting. This is why birth control pills (synthetic progesterones, etc) increase one's risk for DVT/PE clots. It could be that supraphysiological dosages of aromatizing AAS simply distort the clotting factors, as we know higher dosages lead to diminishing returns as higher % is converted to other metabolites, notably estradiol. Hence more gear=more sides. You could do a clinical clotting test (once any aspirin/ASA you take has cleared the body) to see where you stand. I guess the important questions would be: do you have a family history of clots?; and what type of dosages are you running in your cycles and for how long?
Personally I am a believer in the less drugs the better, contrary to the polypharmacy so many on this board seem to practice. E.g. if one is not cutting for a contest or unusually sensitive to aromatase activity then skip the AIs and SERMs during the cycle. Using drugs to mitigate sides of other drugs is a slippery slope. Almost all drugs have some hepatic and renal toxicity, so the less the better unless you really need them. The point being if your answers to the above questions about family history and high dosages are 'no', then putting in an AI for the sole purpose of clot reduction is probably ill-advised since these same estrogens improve blood lipid levels, immune function, and bone health.
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03-23-2017, 02:10 PM #5
Thank you for your reply Mike. No, nobody in my family history never had clotting disorders, stroke, heart diseases, for the sake of god. My gear dosages are not so high: Test E 250mg/week and Deca 500mg/week, in total 750mg at week. Arimidex is .50 EOD and my E2 is perfectly in control ( around 38pg/ml ). My lipids are good i think:
Total Cholesterol: 168,4
LDL: 103
HDL: 38,8
Triglycerides: 48.7
( Total Cholesterol/HDL ratio is less than 5 and this is pretty good, as i'm very careful with diet.. )
Hct is around 46.8 but i'm at 4th cycle week ( i've planned 10-12 cycle weeks ). I'm investigating about blood clotting just to understand the underlying mechanism, if just actually the androgens activity in itself could alter the hemostasis, over the HCT and E2 level.
These drugs
can elevate levels of thrombin 117 and C-reactive
protein,1 1S as well as thromboxane A2 receptor density,1 19
which can support platelet aggregation and the
formation of blood clots
The snippet above seems to confirm an inverted physiology, although the dosage where this could happen, it's not detectable because i think it's pretty individual. But seems to exists additional factors over HCT and E2 high levels....
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03-23-2017, 02:59 PM #6New Member
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Look into nattokinase. For a natty ingredient its nigh on a miracle; most guys report they can decrease donation frequency by using it. YMMV of course, and will be AAS-dependant (ie nattokinase wont negate the tendency of something like EQ).
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03-23-2017, 06:25 PM #7
Yeah, AAS and coagulation is a tricky issue.
But as you see, thromboxane A2 is one of the clotting factors unregulated.
It is precisely thromboxane A2 that ASA will inactive at 100mg ED.
I always use ASA as a precaution, it's also prevents migraines from developing for some reason. (100mg is way below pain killer/analgesic activity, so we don't know why it helps reduce frequency of migraines)
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03-23-2017, 10:39 PM #8New Member
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Slack Should I be using an AI while on Test and Anavar ? I have a Las and I take Eloquis.
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03-23-2017, 11:15 PM #9New Member
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I have been diagnosed with LAS in 2014 had a PE. I currently take Eloquis. Should I be Using an AI while taking Test Cyp and Anavar ??
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03-23-2017, 11:28 PM #10New Member
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I'm not sure of what you deem as high dosage, but I dose 500 mg of Test Cyp per week and 50mg of Anavar . I do have a family history of blood clots and I had a massive PE in 2014.
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03-23-2017, 11:46 PM #11New Member
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Im running a 10wk to 12wk of Test Cyp 4-5 weeks of Anavar (ed)
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03-24-2017, 12:40 AM #12
Under roids, using an AI is *A MUST*. Is a must too, doing frequent blood work and check where you are. I spend around 200$ at month for my blood work... nothing can tell you what happening other than blood work.
Yes, 100mg ASA ED, deactive the Thromboxane A2 activity, so it's a good support about hypercoagulation issue as OMEGA-3 fatty acids; but ASA could hurt your stomac and being i suffer of gastritis, it could be dangerous. I'm taking omeprazole and i've discovered that it lowering INR ( prothrombin time ) too. I don't know why on forum is often telling about HCT and E2 as clotting factors issues, when in blood work could be also important checking INR and clotting factors related....
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03-24-2017, 01:24 AM #13
antrb1: given your family history about clotting, as a general rule, you should avoid steroids at all. If you want to use them, you should constantly check your clotting factors and find the right balance as dosages, molecules and auxiliary drugs to use them with a low risk profile. Clotting it's not a joke !
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03-24-2017, 02:34 AM #14
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03-24-2017, 03:03 AM #15
LAS ( i think ): LymphAdenopathy Syndrome
PE: Pulmonary Embolism.
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03-24-2017, 05:27 AM #16
Although it is great to discuss this subjects, I have to say that you are somewhat paranoid about deep vein thrombosis (DVT). Its what? The 3rd or 4th thread you start about it?
DVT, and its deadly possible complications, its not the main problem steroid users have to worry about! If you dont have a genetically inherited blood clotting condition the risk of developing DVT cause of steroid usage is very very low.
Of course it you have a irresponsible steroid usage, for example: not controlling E2; not controlling your blood pressure; smoking and drinking; letting your HCT climb above 52%; no cardio; etc, you will be at higher risk of DVT, and other possible complications!
But I will chip in the main discussion, cause I'm surprised you guys still haven't mentioned IMO the main factor for blood clots (in ppl with no genetic clotting disorders): protein factor VIII.
Elevated factor VIII levels and risk of venous thrombosis
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03-24-2017, 06:01 AM #17
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03-24-2017, 07:57 AM #18
IMO you can monitor the prothrombin time, its pretty cheap. Only if result was off I would test fibrinogen, etc
It can be an interesting experiment to test PT on and off cycle. I think it would not change much but I can be wrong.
Reactive C protein is an interesting test to do, but it will only tell if something is wrong, doesnt pin point origin.
Ferritin and iron should also be measured, as low iron will increase blood factor VIII.
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03-24-2017, 09:11 AM #19
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03-24-2017, 09:28 AM #20
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03-24-2017, 10:23 AM #21
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03-24-2017, 03:30 PM #22New Member
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03-25-2017, 07:00 PM #23New Member
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