AAS, Test, Estrogens: Thrombosis is a real and higher risk ?

[Slacker78]

Hello guys. After reading some threads about users ( especially those ones are on TRT ) had blood clots issues; googling about Thrombosis/Thrombophilia and its potential connection with Testosterone and Estrogens, i was seriously thinking about how much could it be safe to cycling, even observing in a maniacal way, all the well-known, safety guidelines, blood count and E2 primarily. It's well-known that an underlying anomalies about antithrombin, 5° Leidein Factor, S protein deficit, C protein deficit, fibrinogen etc, associated with AAS ( and possibly with an AI also ) could raise a thrombotic episode.

All these things, don't give me the serenity while i'm on cycling, even i use moderate dosages of simply molecules ( E.g. Test and Deca ) and i observe with a great scrupulosity, all safety guidelines.

What i think, is that i'm afraid, that's all. I wouldn't give up to Test at least and a moderate dosages, but if I should perform 1-2 annual cycles at max and despite following scrupulously all safety guidelines, highly risking to die, i think it's better avoid at all.

This thread looks for searching by you not a "magic" reassurance, but to try to get useful informations which could me give major clearness about things that possibly i don't know well as you and for this reason, i'm fearing exaggeratedly....

Thank you to all those ones, who will dedicate me their time ( and not just to me but to all guys frequenting this awesome forum ).

[Mr.BB]

Yes, taking AAS will increase risk of thrombosis, or at least puts added stress in the circulatory system.

This is why we try to advice guys on the most safe way of cycling, and this includes regular bloodwork. Unfortunnaly as you know the majority only does bloodwork when they face problems after a poorly planned cycle.

Its scarry how guys stay on test and eq for long periods without taking a basic hemogram to check how thick their blood is.
The risk of polycithemia is very real, although the degree will be very genetic influenced.

Donating blood is the only treatment available.

[almostgone]

I will absolutely second Mr.BB's comments about being proactive in monitoring your hematocrit, hemoglobin, E2, and other relevant components.
I am one of the Factor V Leiden TRT patients and I am extremely fortunate to find a Dr. willing to work with me and I absolutely do not neglect my labs. I actually have a standing order on my file for a CBC.
Preventing problems are always better than try to correct the result of a problem.
Unfortunately you encounter so many guys that neglect their labs and wonder why they feel so tired and beat down and their BP is out of control. Not to say that is the only cause of BP issues and clotting problems, but thick blood puts an increased workload on the heart and generally seems to compound the problem the further it gets from a safe range.
Just my thoughts.

[Slacker78]

Thank you to both, for your provisions. I understand how genetic play a crucial role in Thrombosis risk. But you are mentioned the blood thickness ( hematocrit in this case ) and E2, during cycles, as primary risk factors. Yes, this is in conjunction with genetic and underdiagnosed pre-existing issues, and at this point before using AAS, each of us, should be check its genetic and related predispositions it about. So, looking E2, Hematocrit/Blood count, homocysteine and the well-known stuff, should be just merely partial and relatively guarantor of safe cycling. It would be better to check other stuff before cycling i think, because i think that an hematocrit around 52-53% could be not so critical for someone but very dangerous for another one who unknow having an underlying predisposition to develop a Thrombotic episode... for this matter, i'm going to evaluate the idea to interrupt use of AAS definitively, even i never had in my first previous 3 months-cycle, any issues and in my family/generation there never were cases about cardiovascular disease neither thrombosis/strokes issues.

In another threads i read an interview made to an authoritative doctor, who told about AAS/Test/TRT and thrombosis ( Almostgone, i remember you joined to that thread ); he concluded, before start a cycle and/or TRT, to check always its genetic predisposition to Thrombophilia. In this forum, to evaluate this before starting any AAS cycle, is little mentioned as it seems that just observing primarily blood cells count, E2 and lipids panel provide the safety each needs; nevertheless many users, sometimes reach hematocrit critical level, even over 55%, and a certain predisposition could be fatal in these cases, before they go to draw out their blood. What is the time before a thrombosis could occur, when someone is at 55% hematocrit or higher ??? Nobody can tell... it could be 24 hours as 3 months or never! Or when E2 is high ? Sometimes E2 raise and we adjust AI to lowering it... but that raising, even a little, could be fatal for someone ( or could be fatal raising AI, being it's prothrombotic ! ) ....

These are my thoughts.

[Slacker78]

Testosterone therapy, thrombosis, thrombophilia, cardiovascular events. - PubMed - NCBI

Testosterone, thrombophilia, thrombosis. - PubMed - NCBI

[numbere]

Slacker, if your worried about a blood clot then you should lower your body fat before cycling.

Your amount of bf is almost twice that of what many would consider safe to begin a cycle.

Androgen Receptor Gene CAG Repeat Length and Body Mass Index Modulate the Safety of Long-Term Intramuscular Testosterone Undecanoate Therapy in Hypogonadal Men

Elevated body fat is a risk factor for venous thromboembolism and thrombotic complications

Anthropometry, Body Fat, and Venous Thromboembolism

Location Of Body Fat Affects Risk Of Blood Clots In Men, Women

The effects of obesity on venous thromboembolism

[Slacker78]

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."

Regard me: i'm stopping to cycling regardless of all and what above reported, is *INDIPENDENT* about BF. We are not talking about the increased risk, but the baseline risk existence and its critical issues. The

[Slacker78]

Slacker, if your worried about a blood clot then you should lower your body fat before cycling.

Your amount of bf is almost twice that of what many would consider safe to begin a cycle.

Androgen Receptor Gene CAG Repeat Length and Body Mass Index Modulate the Safety of Long-Term Intramuscular Testosterone Undecanoate Therapy in Hypogonadal Men

Elevated body fat is a risk factor for venous thromboembolism and thrombotic complications

Anthropometry, Body Fat, and Venous Thromboembolism

Location Of Body Fat Affects Risk Of Blood Clots In Men, Women

The effects of obesity on venous thromboembolism

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."

About me: i'm stopping to cycling regardless of all and what above reported, is *INDIPENDENT* about BF. We are not talking about the increased risk, but the baseline risk existence and its critical issues.