AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

Re: Steroids and heart disease

AAS and Cardiovascular/Pulmonary Function

Baggish AL, Weiner RB, Kanayama G, et al. Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction. Circ Heart Fail 2010;3(4):472-6. Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction -- Baggish et al. 3 (4): 472 --...

thinksteroids.com

 

[Michael Scally MD]

Effects Of Anabolic Androgenic Steroids On Chylomicron Metabolism

Highlights

? AAS may increase the serum concentration of LDL-cholesterol.
? The use of AAS diminishes HDL-cholesterol.
? Chylomicron-like emulsion was used to access the kinetic parameters of 31 subjects.
? The AAS users showed delayed removal of chylomicrons remnants.


Morikawa AT, Maranhao RC, Alves MJ, Negrao CE, da Silva JL, Vinagre CG. Effects of anabolic androgenic steroids on chylomicron metabolism. Steroids. ScienceDirect.com - Steroids - Effects of anabolic androgenic steroids on chylomicron metabolism

Objective To evaluate the effects of anabolic androgenic steroids (AAS) on chylomicron metabolism.

Methods An artificial lipid emulsion labeled with radioactive cholesteryl ester (CE) and triglycerides (TG) mimicking chylomicrons was intravenously injected into individuals who regularly weight trained and made regular use of AAS (WT + AAS group), normolipidemic sedentary individuals (SDT group) and individuals who also regularly weight trained but did not use AAS (WT group). Fractional clearance rates (FCR) were determined by compartmental analysis for emulsion plasma decay curves.

Results FCR-CE for the WT + AAS group was reduced (0.0073 ± 0.0079 min?1, 0.0155 ± 0.0100 min?1, 0.0149 ± 0.0160 min?1, respectively; p < 0.05), FCR-TG was similar for both the WT and SDT groups. HDL-C plasma concentrations were lower in the WT + AAS group when compared to the WT and SDT groups (22 ± 13; 41 ± 7; 38 ± 13 mg/dL, respectively; p < 0.001). Hepatic triglyceride lipase activity was greater in the WT + AAS group when compared to the WT and SDT groups (7243 ± 1822; 3898 ± 1232; 2058 ± 749, respectively; p < 0.001). However, no difference was observed for lipoprotein lipase activity.

Conclusions Data strongly suggest that AAS may reduce the removal from the plasma of chylomicron remnants, which are known atherogenic factors.

 

[Effeminate_builder]

Will go through all these abstracts and papers later on,even if it is mostly greek to me.
But what i wanted to know is if the Cardio-toxicity stuff is irreversible?
or things return to normal after couple of months to a year after stopping cycle.

 

[Michael Scally MD]

Angell PJ, Chester N, Sculthorpe N, Whyte G, George K, Somauroo J. Performance enhancing drug abuse and cardiovascular risk in athletes: implications for the clinician. Br J Sports Med 2012;46 Suppl 1:i78-i84. Performance enhancing drug abuse and cardiovascular risk in athletes: implications for the clinician -- Angell et al. 46 (Suppl 1): i78 -- British Journal of Sports Medicine

The use of performance-enhancing and social drugs by athletes raises a number of ethical and health concerns. The World Anti-Doping Agency was constituted to address both of these issues as well as publishing a list of, and testing for, banned substances in athletes. Despite continuing methodological developments to detect drug use and associated punishments for positive dope tests, there are still many athletes who choose to use performance and image enhancing drugs. Of primary concern to this review are the health consequences of drug use by athletes. For such a large topic we must put in place delimitations. Specifically, we will address current knowledge, controversies and emerging evidence in relation to cardiovascular (CV) health of athletes taking drugs. Further, we delimit our discussion to the CV consequences of anabolic steroids and stimulant (including amphetamines and cocaine) use. These drugs are reported in the majority of adverse findings in athlete drug screenings and thus are more likely to be relevant to the healthcare professionals responsible for the well-being of athletes. In detailing CV health issues related to anabolic steroid and stimulant abuse by athletes we critique current research evidence, present exemplar case studies and suggest important avenues for on-going research. Specifically we prompt the need for awareness of clinical staff when assessing the potential CV consequences of drug use in athletes.

 

[Pericles]

I too wonder about Cardio effects. One variable, however, is that my eating is much cleaner and I do a lot more cardio when I am on.

I should also mention that the cycle I am currentyly completing is the first one in over 7 years. Back then I did an excellent pct and was fine for more than 5 years. Then I started having symptoms of low T, was measured at 271 and went on replacement therapy. 3 months ago I decided to do an actual cycle w/ a full pct and then go back on replacement.

I wonder, who is healthier, me, w/ a clean diet and 4 days of weights a week along w/ 6 days of cardio, or the slob who never works out and has a crap diet?

 

[krom808]

The one who dies a happy man? Or, the one who dies last?

Bioethics , LOL

 

[sade]

Will go through all these abstracts and papers later on,even if it is mostly greek to me.
But what i wanted to know is if the Cardio-toxicity stuff is irreversible?
or things return to normal after couple of months to a year after stopping cycle.

Well, my cholesterol readings are perfect!!! my HDL is way over range which means that I'm less likely to suffer from cardiovascular disease than most people.

 

[Pericles]

Will go through all these abstracts and papers later on,even if it is mostly greek to me.
But what i wanted to know is if the Cardio-toxicity stuff is irreversible?
or things return to normal after couple of months to a year after stopping cycle.

Just read the coclusion and the abstract (a summary of the article at the beginning).

 

[toolman]

I always suspected there were more cardiac issues with AAS usage than people suspect. Unfortunately most that run large cycles do not do regular bloodwork. The higher hematocrit and increased BP on high test cycles alone have to add to the thickening of the LV wall.

FOr the poster that asked does it normalize, the docs would be better suited to answer but once your heart enlarges it does not just go down. Once the LV wall is thickened, I do not believe their is any way of returning it back to normal, but that is just from a laymans understanding. Docs feel free to correct me if I am wrong.

 

[Dr JIM]

Nice insight TM!
FYI
LVH from AAS use alone absent other CV risk factors, has been observed in a few case studies, implying the hypertropy (cellular cardiac muscle enlargement) is the direct result of AAS use. However a direct correlation has NOT been found in any controlled study. Consequently although the association between anabolics and increased skeletal muscle mass (hypertrophy) is undeniable, a similar effect has NOT observed on cardiac muscle. Otherwise, AAS "abusers" would have a much higher incidence of "cardiomyopathy", which again has not been demonstrated ESPECIALLY when other RF are accounted for.
Nonetheless those whom do use AAS should be ultra vigilant in controlling those RF which increase CV mortality such as HTN and the varied dyslipidemias!
Moreover providing the "erythrocytosis" does NOT exceed a Hgb of 17.5 g/dl or a "crit" of 52%, the CV risk per say is not increased. IME the overwhelnming majority of BB do NOT exceed these limits, providing no other PED's are used which increase RBC production such as erythropoietin.

 

[Michael Scally MD]

Franquni JV, do Nascimento AM, de Lima EM, et al. Nandrolone decanoate determines cardiac remodelling and injury by an imbalance in cardiac inflammatory cytokines and ACE activity, blunting of the Bezold-Jarisch reflex, resulting in the development of hypertension. Steroids. ScienceDirect.com - Steroids - Nandrolone decanoate determines cardiac remodelling and injury by an imbalance in cardiac inflammatory cytokines and ACE activity, blunting of the Bezold-Jarisch reflex, resulting in the development of hypertension

The aims of this study were to evaluate the effects of nandrolone (ND) on cardiac inflammatory cytokines, ACE activity, troponin I, and the sensitivity of the Bezold-Jarisch reflex (BJR).

Male Wistar rats were administered either ND (20 mg/kg; DECA) or vehicle (control animals; CONT) for 4 weeks. BJR was analyzed by measuring the bradycardia and hypotension responses elicited by serotonin administration (2-32 mug/kg). Mean arterial pressure (MAP) was assessed and myocyte hypertrophy was determined by the heart weight/body weight ratio and by morphometric analysis. Matrix collagen deposition was assessed by histological analysis of the picrosirius red-stained samples. Mesenteric vascular reactivity was performed and central venous pressure (CVP) evaluated. Cardiac inflammatory cytokine levels and angiotensin-converting enzyme (ACE) activity were studied as well the biomarker of cardiac lesion, troponin I.

DECA group showed enhancement of matrix type I collagen deposition (p<0.01) and cardiac ACE activity (p<0.01) compared with the CONT. Interleukin (IL)-10 was reduced (p<0.01) and pro-inflammatory cytokines (TNF-alpha and IL-6; p<0.01) were increased in the DECA group compared with CONT. Cardiac injury was observed in the DECA group shown by the reduction in cardiac troponin I (p<0.01) compared with the CONT group. Animals in the DECA group also developed myocyte hypertrophy and reduction of BJR sensitivity. The MAP of animals treated with ND reached hypertensive levels (p<0.01; compared with CONT). No changes in CVP and vascular reactivity were observed in both experimental groups.

We conclude that high doses of ND elicit cardiotoxic effects with cardiac remodelling and injury. Cardiac changes reduce the BJR sensitivity. Together, these abnormalities contributed to the development of hypertension in animals in the DECA group.

 

[Michael Scally MD]

[Re: HDL] Will Cholesteryl Ester Transfer Protein Inhibition Succeed Primarily By Lowering Low-Density Lipoprotein Cholesterol?

When combined, the clinical trial results and the human genetic findings cast doubt on the notion that raising HDL cholesterol in isolation will reduce risk for Atherosclerotic CardioVascular Disease (ASCVD). For several decades, the biomedical research community has assumed that if an intervention raises HDL cholesterol, then that intervention will reduce risk for ASCVD. Now, it seems prudent to rethink this assumption and re-evaluate the use of HDL cholesterol as a biomarker predictive of ASCVD in intervention studies.

In contrast with the HDL cholesterol biomarker, human genetic studies strongly suggest that both LDL cholesterol and plasma lipoprotein(a) cause ASCVD. Rare mutations that lead to extremely high LDL cholesterol consistently increase risk for ASCVD. About 3% of individuals carry an LDL cholesterol– lowering variant in the proprotein convertase subtilisin/ kexin type 9 gene, and these individuals are at lower risk for myocardial infarction. A genotype score crafted from 13 variants that affected LDL cholesterol in isolation was strongly associated with myocardial infarction risk. In addition, polymorphisms that increase plasma lipoprotein(a) consistently confer increased risk for ASCVD.

What are the implications of these data for the 2 CETP inhibitors — anacetrapib and evacetrapib — that remain in clinical development? These CETP inhibitors do not seem to have off-target effects on blood pressure or aldosterone. The pattern of lipid effects for anacetrapib and evacetrapib (higher HDL cholesterol, lower LDL cholesterol, lower triglycerides, and lower lipoprotein(a)) mirrors that seen by Johannsen et al. for the 2 CETP variants that are associated with lower CETP activity and lower risk for ASCVD. As such, the work of Johannsen et al. increases confidence that anacetrapib and evacetrapib will successfully reduce risk for ASCVD.

By providing direct evidence in humans prior to a clinical trial, studies of genetic variation represent powerful approaches to validate gene targets and pinpoint causal biomarkers. CETP inhibition by anacetrapib and evacetrapib is likely to succeed. However, we have learned that any potential benefit clearly cannot be ascribed to the HDL biomarker per se. Insights from human genetics and the completed dalcetrapib trial suggest that the success of CETP inhibitors may be more related to their effect on LDL cholesterol and lipoprotein(a) rather than through HDL elevation.


Kathiresan S. Will cholesteryl ester transfer protein inhibition succeed primarily by lowering low-density lipoprotein cholesterol? Insights from human genetics and clinical trials. J Am Coll Cardiol 2012;60(20):2049-52. ScienceDirect.com - Journal of the American College of Cardiology - Will Cholesteryl Ester Transfer Protein Inhibition Succeed Primarily by Lowering Low-Density Lipoprotein Cholesterol?: Insights From Human Genetics and Clinical Trials? ?Editorials p

 

[Pericles]

Am currently finishing the highest dosage cycle (went up to about 900 mgs total a week) in nearly 18 years. Have been tapering down, but very slowly. My body is more than transformed, something that was necessary for business related purposes. At this point I really have no reason to stay on high dosages.

These studies have convinced me to accelerate my return to trt dosages (200 mg a week).

 

[Michael Scally MD]

Skogastierna C, Hotzen M, Rane A, Ekstrom L. A supraphysiological dose of testosterone induces nitric oxide production and oxidative stress. Eur J Prev Cardiol. A supraphysiological dose of testosterone induces nitric oxide production and oxidative stress

Background - Accumulating evidence indicates that abuse of anabolic androgenic steroids may cause cardiovascular adverse side-effects, including endothelial dysfunction. The aim of the present study was to investigate the effects of supra-physiological doses of testosterone on the endothelial production of nitric oxide (NO) and oxidative stress in vitro and in vivo.

Methods - Testosterone enanthate was administrated as of a single 500 mg dose to healthy volunteers (N = 27). Gene expression was studied in human vascular endothelial cells exposed to testosterone.

Results - The in vivo results show that the urinary NO level and the antioxidative capacity were significantly decreased two days after testosterone administration. In agreement, our in vitro studies show that testosterone inhibits the gene expression of endothelial NO synthase (eNOS) after 48 hours. When the antioxidant seleno-L-methionine was added, the down-regulation of mRNA specific eNOS was partly abrogated. The mRNA expression of antioxidizing enzyme genes was significantly inhibited after eight hours and recovered 48 hours after testosterone treatment of endothelial cells.

Conclusion - These results show that a supraphysiological dose of testosterone decreases the expression of eNOS and consequently the formation of NO, which could partly be explained by oxidative stress. These results indicate that supraphysiological doses of testosterone may induce endothelial dysfunction, which is of interest in relation to the cardiovascular adverse side-effects observed in anabolic androgenic steroid abusers.

 

[beezil]

Thanks Doc for posting these journals. They should be a must read for anybody contemplating the use of AAS.... as well as, old timers like myself.

Too often the most asked questions are...
"what type of cycle should I use for my first run...???"

Instead there should be more questions like...

"What are the effects of AAS on physiology besides hypertrophy of skeletal muscles?" or, "what are the long term effects of AAS??"

Personally, I just had a complete physical and stress test, required by my life insurance company.

During the ECG the nurse responded... we have been seeing this more and more. I questioned her...about what she was referencing. She said that my left ventricle is enlarged. Called it an Athletes Heart...

While i have been an athlete all my life... and no stranger to strenuous cardiac output both aerobic and anaerobic... Your articles have made me reevaluate things. Maybe a little to late.

 

[Pericles]

Doc S: When I use gear, I do 6 days a week cardio, 3 days are very intense (20 minutes bag work...I go so hard that I pretty much collapse at end). I also do 3 days of fairly typical cardio, 30 minutes on a N. Mobia. Even so, I keep my heart rate at 80% of max. This cardio is on top of 4.5 hours per week of high intensity weight training.

When off gear, or replacement levels I cut the very intense bagwork down to once a week. If not I will over-train and lose strength.

Thus, my question is, will the extra cardio done on cycle compensate for the cardiovascular risks of the gear?

 

[beezil]

Doc S: When I use gear, I do 6 days a week cardio, 3 days are very intense (20 minutes bag work...I go so hard that I pretty much collapse at end). I also do 3 days of fairly typical cardio, 30 minutes on a N. Mobia. Even so, I keep my heart rate at 80% of max. This cardio is on top of 4.5 hours per week of high intensity weight training.

When off gear, or replacement levels I cut the very intense bagwork down to once a week. If not I will over-train and lose strength.

Thus, my question is, will the extra cardio done on cycle compensate for the cardiovascular risks of the gear?

P,
I would love to hear the Doc's opinion on your question. I have been contemplating that for the last few months as well.

My opinion is... the high BP range that you and I seem to be frequenting may be the cause of the "Athletes Heart". as well as the stress level that is applied during those high rates.

Maybe reversing your thought process... and training cardio at a higher level when not at Supraphysiological hormone levels. Thoughts???

In my case training with large loads for long distances at high speeds... in various conditions. Desert and jungle.

Also, Doc...could this condition possibly be caused by deep underwater dives with no breathing apparatus? Over the years i have conditioned myself to be able to descend quite deep with prebreathing exercises and a single breath.

 

[Pericles]

Beezil,

I believe that high intensity cardio, which I am doing, needs to be for more than 5 hours per week in order to produce Athletes' Heart. I do half that amount (3-30s, and 3 20s per week).

 

[beezil]

Beezil,

I believe that high intensity cardio, which I am doing, needs to be for more than 5 hours per week in order to produce Athletes' Heart. I do half that amount (3-30s, and 3 20s per week).

P,

Honestly, if it wasn't for the ECG... And Doc Scally's journals I would have never known about Athletes Heart... Or the possible causes.

The nurse indicated triathletes experience this...
Prior, to immersing myself in the body builder world; ultras and tris were my drug of choice. When I was in high school the weekends would come... And i would start running first thing in the morning... When the sun would start setting I would look for a payphone and an address. Call my folks and they would drive out and get me.

 

[idmd]

Skogastierna C, Hotzen M, Rane A, Ekstrom L. A supraphysiological dose of testosterone induces nitric oxide production and oxidative stress. Eur J Prev Cardiol. A supraphysiological dose of testosterone induces nitric oxide production and oxidative stress

Background - Accumulating evidence indicates that abuse of anabolic androgenic steroids may cause cardiovascular adverse side-effects, including endothelial dysfunction. The aim of the present study was to investigate the effects of supra-physiological doses of testosterone on the endothelial production of nitric oxide (NO) and oxidative stress in vitro and in vivo.

Methods - Testosterone enanthate was administrated as of a single 500 mg dose to healthy volunteers (N = 27). Gene expression was studied in human vascular endothelial cells exposed to testosterone.

Results - The in vivo results show that the urinary NO level and the antioxidative capacity were significantly decreased two days after testosterone administration. In agreement, our in vitro studies show that testosterone inhibits the gene expression of endothelial NO synthase (eNOS) after 48 hours. When the antioxidant seleno-L-methionine was added, the down-regulation of mRNA specific eNOS was partly abrogated. The mRNA expression of antioxidizing enzyme genes was significantly inhibited after eight hours and recovered 48 hours after testosterone treatment of endothelial cells.

Conclusion - These results show that a supraphysiological dose of testosterone decreases the expression of eNOS and consequently the formation of NO, which could partly be explained by oxidative stress. These results indicate that supraphysiological doses of testosterone may induce endothelial dysfunction, which is of interest in relation to the cardiovascular adverse side-effects observed in anabolic androgenic steroid abusers.

And potentially ED problems too?