AAS Associated Thrombosis

Michael Scally MD

Doctor of Medicine
10+ Year Member
[OA] Anabolic Steroid Abuse: What Shall It Profit a Man to Gain Muscle and Suffer the Loss of His Brain?

The use of anabolic androgenic steroids may be an underestimated cause of cerebral venous thrombosis. The pervasive yet clandestine use of these and other endocrine modulating drugs amongst athletes challenges the epidemiological study of their pro-thrombotic consequences and by extension the astuteness of the clinician in such a circumstance as depicted in this case.

A 30 year-old previously well bodybuilder presented with a 3-day history of increasingly frequent focal motor seizures of his left upper limb and subtle dyscognitive changes ranging from 10 to 30 s duration. Soon after admission, he developed dysarthria and a left sided hemiparesis with greater weakness in the upper limb.

There was no history of headaches or visual changes and his medical, surgical and family history were unremarkable. There was no history of smoking but drug history revealed the consistent use of cycles of anabolic androgenic steroids (AAS) for the preceding 2 years.

The cycles involved parenteral testosterone enanthate 500 mg combined with nandrolone decanoate 400 mg weekly for 3 months. This was alternated with a post-cycle regimen of daily clomiphene citrate 100 mg and tamoxifen citrate 40 mg as well as weekly tapering doses of beta-human chorionic gonadotropin (hCG) 5000 IU for almost 2 months before resuming androgens.

Physical examination exhibited a 90 kg man of athletic build with mild dysarthria and a dense, flaccid left sided hemiparesis including the face. Otherwise, there were no abnormalities.

Laboratory investigations showed a haemoglobin of 18.0 g/dl and a haematocrit of 52.9% with no morphological abnormalities on the blood film. Screening tests for connective tissue and hypercoaguable disorders (including erythrocyte sedimentation rate, anti-neutrophilic antibodies, factor V Leiden, protein C, protein S and lupus anticoagulant) were negative. Renal and liver function tests were also within normal limits but JAK2 mutation testing was not obtained due to financial constraints.

Magnetic resonance imaging with venography of the brain revealed acute superior sagittal sinus thrombosis with an associated cortical based acute infarct in the right parietal lobe. No haemorrhagic conversion was noted at that time.

The patient was treated with sodium valproate to control seizures and low molecular weight heparin was used as a prelude to initiating anticoagulation with warfarin. The pivotal factor in further management was counselling against future use of performance enhancement drugs.

Over the ensuing 6 months of follow-up, with strict compliance to management, there was marked improvement in power and the haematocrit decreased to 45%. Additionally, he has remained seizure free allowing the discontinuation of the anticoagulation and anti-epileptic drugs. Fortunately, there appears to be no residual adverse effects.

Omar M, Abdul R, Panday A, Teelucksingh S. Anabolic steroid abuse: what shall it profit a man to gain muscle and suffer the loss of his brain? QJM. Anabolic steroid abuse: what shall it profit a man to gain muscle and suffer the loss of his brain? | QJM: An International Journal of Medicine | Oxford Academic
 
So, where was he in the cycle? PCT? What were his E2 levels when this event started?

Estrogen and SERMs are known to have thrombosis risks. Androgens are not - but T raises E so they could.

Question for @Michael Scally MD: does this change your observation and statement "As far as we can determine, no testosterone associated thromboembolic events have been reported to date" ? Or was this just about legit TRT? Dr. Michael Scally Talks About TRT and Steroid Side Effects, Part 1

From what I've read, thrombosis events with T are from previously at risk individuals.
 
Nothing is more important in this world than controlling hematocrit. EVERYONE on gear should keep it at 45 or lower.
 
Nothing is more important in this world than controlling hematocrit. EVERYONE on gear should keep it at 45 or lower.
As someone who's had a PE I'm going to agree with you. But I also carry the factor V Leiden and protein s disorder. Which if I knew prior I never would of done gear.
 
Is there any evidence that dosages of test E at or around TRT level, or < 250mg , especially in "over-aromatizers", is capable of increasing the risk of VTE/Thrombosis?

Also, how long would it take having elevated e2 to present these increased risks? I understand that AIs are pro-thrombotic so would not decrease the risk.
 
I guess this shit is no joke. I just had a pulmonary embolism and a few days later my crotch area blew up from a clot lodged there. Some lung damage occurred and im on an inhaler now. Im supposed to be following up with a cardiologist and some other bs. But i really dont want to be off aas. Shit is nerve racking.
 
I guess this shit is no joke. I just had a pulmonary embolism and a few days later my crotch area blew up from a clot lodged there. Some lung damage occurred and im on an inhaler now. Im supposed to be following up with a cardiologist and some other bs. But i really dont want to be off aas. Shit is nerve racking.
Please listen bro. You know I've been through all of that. Come off gear!! It's not worth your life. It's just not. And please follow up with a cardiologist. Probably a good idea to see a hematologist as well. Tell me your on some type of blood thinner. Or at least a baby aspirin. Again bud I urge you to stop. I didn't want to either. But Jess said simply to choose. Either your family or gear. I wasn't going to lose my family or life to AAS. Your family needs you. I'm always around to talk bud. Praying for your health.
 
[OA] Anabolic Steroid Abuse: What Shall It Profit a Man to Gain Muscle and Suffer the Loss of His Brain?

The use of anabolic androgenic steroids may be an underestimated cause of cerebral venous thrombosis. The pervasive yet clandestine use of these and other endocrine modulating drugs amongst athletes challenges the epidemiological study of their pro-thrombotic consequences and by extension the astuteness of the clinician in such a circumstance as depicted in this case.

A 30 year-old previously well bodybuilder presented with a 3-day history of increasingly frequent focal motor seizures of his left upper limb and subtle dyscognitive changes ranging from 10 to 30 s duration. Soon after admission, he developed dysarthria and a left sided hemiparesis with greater weakness in the upper limb.

There was no history of headaches or visual changes and his medical, surgical and family history were unremarkable. There was no history of smoking but drug history revealed the consistent use of cycles of anabolic androgenic steroids (AAS) for the preceding 2 years.

The cycles involved parenteral testosterone enanthate 500 mg combined with nandrolone decanoate 400 mg weekly for 3 months. This was alternated with a post-cycle regimen of daily clomiphene citrate 100 mg and tamoxifen citrate 40 mg as well as weekly tapering doses of beta-human chorionic gonadotropin (hCG) 5000 IU for almost 2 months before resuming androgens.

Physical examination exhibited a 90 kg man of athletic build with mild dysarthria and a dense, flaccid left sided hemiparesis including the face. Otherwise, there were no abnormalities.

Laboratory investigations showed a haemoglobin of 18.0 g/dl and a haematocrit of 52.9% with no morphological abnormalities on the blood film. Screening tests for connective tissue and hypercoaguable disorders (including erythrocyte sedimentation rate, anti-neutrophilic antibodies, factor V Leiden, protein C, protein S and lupus anticoagulant) were negative. Renal and liver function tests were also within normal limits but JAK2 mutation testing was not obtained due to financial constraints.

Magnetic resonance imaging with venography of the brain revealed acute superior sagittal sinus thrombosis with an associated cortical based acute infarct in the right parietal lobe. No haemorrhagic conversion was noted at that time.

The patient was treated with sodium valproate to control seizures and low molecular weight heparin was used as a prelude to initiating anticoagulation with warfarin. The pivotal factor in further management was counselling against future use of performance enhancement drugs.

Over the ensuing 6 months of follow-up, with strict compliance to management, there was marked improvement in power and the haematocrit decreased to 45%. Additionally, he has remained seizure free allowing the discontinuation of the anticoagulation and anti-epileptic drugs. Fortunately, there appears to be no residual adverse effects.

Omar M, Abdul R, Panday A, Teelucksingh S. Anabolic steroid abuse: what shall it profit a man to gain muscle and suffer the loss of his brain? QJM. Anabolic steroid abuse: what shall it profit a man to gain muscle and suffer the loss of his brain? | QJM: An International Journal of Medicine | Oxford Academic

Is there any evidence that blocking conversion to E2 via an AI removes inherited thrombophilia risk such as FVL, in the absence of our risk such as high HCT etc? Are there any studies being done to this effect? Are all AIs thrombogenic in themselves? Is there research happening in the area of vte/pe harm minimisation in relation to AAS/trt?
 
Please listen bro. You know I've been through all of that. Come off gear!! It's not worth your life. It's just not. And please follow up with a cardiologist. Probably a good idea to see a hematologist as well. Tell me your on some type of blood thinner. Or at least a baby aspirin. Again bud I urge you to stop. I didn't want to either. But Jess said simply to choose. Either your family or gear. I wasn't going to lose my family or life to AAS. Your family needs you. I'm always around to talk bud. Praying for your health.
Do you guys know what your hematocrit was prior to the PE? Sorry to hear about that by the way to both of you and best wishes in your recovery, kind of a reality check this shits no joke
 
Do you guys know what your hematocrit was prior to the PE? Sorry to hear about that by the way to both of you and best wishes in your recovery, kind of a reality check this shits no joke
No I don't. I was rushed to the hospital by ambulance and wasn't on a cycle at the time so didn't have blood work till in the hospital. I can try and dig that info up for you. Definitely a reality check.
 
Don't go out of your way but if you come across it I would be interested in seeing it. Haven't looked into this topic too much but hematocrit definitely seems to be the biggest or one of the biggest risk factors with this whole thing. Did the doctors tell you aas and/or hematocrit was a direct cause? Did you have a history of Cycles with known offenders like nandrolone and EQ?
 
Don't go out of your way but if you come across it I would be interested in seeing it. Haven't looked into this topic too much but hematocrit definitely seems to be the biggest or one of the biggest risk factors with this whole thing. Did the doctors tell you aas and/or hematocrit was a direct cause? Did you have a history of Cycles with known offenders like nandrolone and EQ?
You got lucky. I stumbled upon alot of my old medical records. My hematocrit was 59. Which is high. In my humble opinion hematocrit is the most dangerous side to AAS use. Heart disease may take years to develop(if at all), while a blood clot can kill you on the spot. Again in my opinion EQ is hands down the most dangerous AAS. I would NEVER touch it! While all AAS(no matter how mild), will raise your RBC. EQ raises it even further. Unless your an elite athlete being monitored closely by a doctor I think using EQ is like Russian roulette. I don't think any one not competing should have EQ in their arsenal. I had done 3 previous cycles before my PE. Only test and Masteron were used. While all my doctor's think AAS use didn't help my situation, none have said they caused it. While it's easy to say the high hematocrit was the cause of my PE I've had tons of genetic testing done since then. And it's been found that I have genetic mutations that put me at a greater risk of clots. Such as factor V Leiden. Hope this helped a little. I'm always around to help out the best I can. Any questions just ask. I'm hardly a medical professional but going through my health issues I've acquired a decent amount of knowledge on blood and cardiovascular issues. Stay safe man.
 
You got lucky. I stumbled upon alot of my old medical records. My hematocrit was 59. Which is high. In my humble opinion hematocrit is the most dangerous side to AAS use. Heart disease may take years to develop(if at all), while a blood clot can kill you on the spot. Again in my opinion EQ is hands down the most dangerous AAS. I would NEVER touch it! While all AAS(no matter how mild), will raise your RBC. EQ raises it even further. Unless your an elite athlete being monitored closely by a doctor I think using EQ is like Russian roulette. I don't think any one not competing should have EQ in their arsenal. I had done 3 previous cycles before my PE. Only test and Masteron were used. While all my doctor's think AAS use didn't help my situation, none have said they caused it. While it's easy to say the high hematocrit was the cause of my PE I've had tons of genetic testing done since then. And it's been found that I have genetic mutations that put me at a greater risk of clots. Such as factor V Leiden. Hope this helped a little. I'm always around to help out the best I can. Any questions just ask. I'm hardly a medical professional but going through my health issues I've acquired a decent amount of knowledge on blood and cardiovascular issues. Stay safe man.

This is very interesting, and of course unfortunate - however it seems like despite everything you were a lucky man. I've personally been grateful to meet others who have similar issues around the place who love gear and fitness, but are predisposed to negative clotting outcomes.

From the reading I've done recently, Factor V leiden related thrombophilia, in absence of other risk factors such as obesity, smoking etc. is most likely to be related to the aromatization process in AAS users, as a direct consequence of estrogen and its ability to promote vte/pe related thrombophilia (such as from SERMs etc). Currently I'm trying to ascertain whether controlling e2 via a suicidal AI conveys the same risks, however it seems that all serms are thrombogenic - there appear to be very few studies and little information about this.

Regardless, to not have DVt as a consequence of AAS use with hereditary thrombophilia and instead have a PE possibly as a result of a High HCT indicates your body was likely resilient.

Have you tested positive for any other risk factors? ApC, Lupus anticoagulant, Prothrombin, Protein C/S? Do you know if you were heterozygous or homozygous for the gene allele? Do you have information about your e2 levels, or Factor VIII levels at the time of any of your thrombosis events? You mentioned you had cardiovascular issues as well - I'm not sure if you mentioned them in the other thread.
 
This is very interesting, and of course unfortunate - however it seems like despite everything you were a lucky man. I've personally been grateful to meet others who have similar issues around the place who love gear and fitness, but are predisposed to negative clotting outcomes.

From the reading I've done recently, Factor V leiden related thrombophilia, in absence of other risk factors such as obesity, smoking etc. is most likely to be related to the aromatization process in AAS users, as a direct consequence of estrogen and its ability to promote vte/pe related thrombophilia (such as from SERMs etc). Currently I'm trying to ascertain whether controlling e2 via a suicidal AI conveys the same risks, however it seems that all serms are thrombogenic - there appear to be very few studies and little information about this.

Regardless, to not have DVt as a consequence of AAS use with hereditary thrombophilia and instead have a PE possibly as a result of a High HCT indicates your body was likely resilient.

Have you tested positive for any other risk factors? ApC, Lupus anticoagulant, Prothrombin, Protein C/S? Do you know if you were heterozygous or homozygous for the gene allele? Do you have information about your e2 levels, or Factor VIII levels at the time of any of your thrombosis events? You mentioned you had cardiovascular issues as well - I'm not sure if you mentioned them in the other thread.
I also have protein s. Yes I have 4 heart conditions. Dialated cardiomyopathy. Inappropriate sinus tachycardia. Atrial flutter. Atrial fibrillation. My e2 was fine. All my blood work was picture perfect except for hematocrit. Those other tests I'll have to ask my doctor. I don't have those results at home. And being 12 years ago my old ass doesn't remember.
 
You got lucky. I stumbled upon alot of my old medical records. My hematocrit was 59. Which is high. In my humble opinion hematocrit is the most dangerous side to AAS use. Heart disease may take years to develop(if at all), while a blood clot can kill you on the spot. Again in my opinion EQ is hands down the most dangerous AAS. I would NEVER touch it! While all AAS(no matter how mild), will raise your RBC. EQ raises it even further. Unless your an elite athlete being monitored closely by a doctor I think using EQ is like Russian roulette. I don't think any one not competing should have EQ in their arsenal. I had done 3 previous cycles before my PE. Only test and Masteron were used. While all my doctor's think AAS use didn't help my situation, none have said they caused it. While it's easy to say the high hematocrit was the cause of my PE I've had tons of genetic testing done since then. And it's been found that I have genetic mutations that put me at a greater risk of clots. Such as factor V Leiden. Hope this helped a little. I'm always around to help out the best I can. Any questions just ask. I'm hardly a medical professional but going through my health issues I've acquired a decent amount of knowledge on blood and cardiovascular issues. Stay safe man.
Wow 59 is high. Thanks. Glad youre on the right path bro, I applaud you knowing your priorities. At the end of the day health is priceless and we all should be monitoring our health closely and be ready to drop this shit at a moment's notice if necessary.
 
Reading guys like Dr. Chrisler and Rouzier saying hct isn't the cause of thrombosis but rather high platelets. Anyone have any insight on this?
 
Reading guys like Dr. Chrisler and Rouzier saying hct isn't the cause of thrombosis but rather high platelets. Anyone have any insight on this?

Dr. Charles Glueck would disagree, and suggest aromatization to e2 being the main cause, combined with pre-existing thrombophilia.

Personally, I'd be inclined to believe there can be any number of factors combining to create the ideal conditions.

"Different strokes for different folks" if you'll pardon the pun.
 
Please listen bro. You know I've been through all of that. Come off gear!! It's not worth your life. It's just not. And please follow up with a cardiologist. Probably a good idea to see a hematologist as well. Tell me your on some type of blood thinner. Or at least a baby aspirin. Again bud I urge you to stop. I didn't want to either. But Jess said simply to choose. Either your family or gear. I wasn't going to lose my family or life to AAS. Your family needs you. I'm always around to talk bud. Praying for your health.
Do you have a thread of what happened to you?
 
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