AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

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 -- Circulation: Heart Failure

Background—Although illicit anabolic-androgenic steroid (AAS) use is widespread, the cardiac effects of long-term AAS use remain inadequately characterized. We compared cardiac parameters in weightlifters reporting long-term AAS use to those in otherwise similar weightlifters without prior AAS exposure.

Methods and Results—We performed 2D tissue-Doppler and speckle-tracking echocardiography to assess left ventricular (LV) ejection fraction, LV systolic strain, and conventional indices of diastolic function in long-term AAS users (n=12) and otherwise similar AAS nonusers (n=7). AAS users (median [quartile 1, quartile 3] cumulative lifetime AAS exposure, 468 [169, 520] weeks) closely resembled nonusers in age, prior duration of weightlifting, and current intensity of weight training. LV structural parameters were similar between the two groups; however, AAS users had significantly lower LV ejection fraction (50.6% [48.4, 53.6] versus 59.1% [58.0%, 61.7%]; P=0.003 by two-tailed Wilcoxon rank sum test), longitudinal strain (16.9% [14.0%, 19.0%] versus 21.0% [20.2%, 22.9%]; P=0.004), and radial strain (38.3% [28.5%, 43.7%] versus 50.1% [44.3%, 61.8%]; P=0.02). Ten of the 12 AAS users showed LV ejection fractions below the accepted limit of normal ( 55%). AAS users also demonstrated decreased diastolic function compared to nonusers as evidenced by a markedly lower early peak tissue velocity (7.4 [6.8, 7.9] cm/s versus 9.9 [8.3, 10.5] cm/s; P=0.005) and early-to-late diastolic filling ratio (0.93 [0.88, 1.39] versus 1.80 [1.48, 2.00]; P=0.003).

Conclusions—Cardiac dysfunction in long-term AAS users appears to be more severe than previously reported and may be sufficient to increase the risk of heart failure.

 

[Michael Scally MD]

Re: AAS Use & Left Ventricular Dysfunction

EDITORIAL: Parker MW, Thompson PD. Anabolic-Androgenic Steroids: Worse for the Heart Than We Knew? Circ Heart Fail 2010;3(4):470-1.

The use of anabolic-androgenic steroids (AAS) among athletes is not new, nor is concern about their potential cardiac effects, but it has been difficult to definitively document deleterious cardiovascular effects from these drugs. There are case reports of unexpected myocardial infarctions1 and even sudden cardiac death2 in AAS users, but such reports are relatively rare given the reported widespread use of AAS. Moreover, their effects on cardiovascular risk factors are confusing. Oral synthetic steroids, such as stanozolol, reduce high-density lipoprotein and increase low-density lipoprotein cholesterol more than parenterally administered testosterone at similar androgenic doses,3suggesting that oral AAS are more atherogenic, but both stanozolol4 and testosterone5 decrease lipoprotein (a), an important atherosclerotic risk factor. There is also concern that AAS increase blood pressure, but even the literature on this topic is equivocal,6 and some of the purported increase in blood pressure with AAS may be due to the use of undersized sphygmomanometer cuffs in subjects with increased arm circumference.7 Consequently, the overall clinical effect of AAS use on atherosclerotic risk and events is not clear.

AAS have more consistently been shown to impair left ventricular (LV) diastolic function,8–10 and these clinical studies are supported by pathological evidence of increased myocardial collagen content after exposure to AAS.11 Evidence of LV systolic dysfunction with AAS use has been evasive,12 but recent studies using measures of myocardial strain8,9 suggest that AAS also subtly impair cardiac systolic performance.

In contrast to these subtle effects of AAS on systolic function, Baggish . . . See Attachment

 

[Millard]

Whereas the media and anti-steroid "educators" tend to focus on overstated, exaggerated, and imaginary steroid side effects, this is one potential side effect that deserves close attention.

 

[Paulo Souza]

Finally, those anti-steroid "educators" you mentioned, who rely on anecdotal evidence or no evidence at all, have at least one study to backup one of their claims.

They do all the fuss and unrealistic claims with no evidence, now imagine with this one only evidence. LOL.

Good article, thanks for educating us Dr. Scally.

 

[Millard]

Finally, those anti-steroid "educators" you mentioned, who rely on anecdotal evidence or no evidence at all, have at least one study to backup one of their claims.

They do all the fuss and unrealistic claims with no evidence, now imagine with this one only evidence. LOL.

Good article, thanks for educating us Dr. Scally.

Steroid education should be just that - it shouldn't be anti-steroid or pro-steroid. It should be about the true side effects.

Anti-steroid groups who use scare tactics based on numerous unsupported claims have little credibility among the groups they target even if a few of the things they say are true.

The credible people are the ones who consistently remain objective to the scientific evidence.

 

[Michael Scally MD]

Anabolic Steroids and Cardiovascular Risk

In summary, whilst it has become quite apparent that AS use can have a significantly negative effect on HDL levels, and therefore increase cardiovascular risk, much of the research that has assessed the association of AS use with alterations in CVD risk factors is limited, contradictory and may be multifactorial. It is, therefore, worthwhile reflecting on case study data in table I, where there are no clear patterns of measurable CVD disease risk in cases with ‘hard’ CV-event endpoints. Scope for on-going work reflecting long-term poly-drug users with attention paid to variations with cycle phase is apparent. Further, when available data for CVD risk factors in AS users are combined with case study reports, one could surmise that factors additional to traditional CVD risk factors may be responsible for any association between AS use and CVD occurrence. It is for this reason that other research groups have assessed the link between AS use and cardiac electrical, structural and functional parameters as well as any impact of AS use on vascular health.

Angell P, Chester N, Green D, Somauroo J, Whyte G, George K. Anabolic Steroids and Cardiovascular Risk. Sports Med. Anabolic Steroids and Cardiovascular Risk. [Sports Med. 2012] - PubMed - NCBI

Recent reports from needle exchange programmes and other public health initiatives have suggested growing use of anabolic steroids (AS) in the UK and other countries. Data indicate that AS use is not confined to bodybuilders or high-level sportsmen. Use has spread to professionals working in emergency services, casual fitness enthusiasts and subelite sportsmen and women. Although the precise health consequences of AS use is largely undefined, AS use represents a growing public health concern.

Data regarding the consequences of AS use on cardiovascular health are limited to case studies and a modest number of small cohort studies. Numerous case studies have linked AS use with a variety of cardiovascular disease (CVD) events or endpoints, including myocardial infarction, stroke and death. Large-scale epidemiological studies to support these links are absent. Consequently, the impact of AS use upon known CVD risk factors has been studied in relatively small, case-series studies. Data relating AS use to elevated blood pressure, altered lipid profiles and ECG abnormalities have been reported, but are often limited in scope, and other studies have often produced equivocal outcomes. The use of AS has been linked to the appearance of concentric left ventricular hypertrophy as well as endothelial dysfunction but the data again remains controversial.

The mechanisms responsible for the negative effect of AS on cardiovascular health are poorly understood, especially in humans. Possibilities include direct effects on myocytes and endothelial cells, reduced intracellular Ca2+ levels, increased release of apoptogenic factors, as well as increased collagen crosslinks between myocytes. New data relating AS use to cardiovascular health risks are emerging, as novel technologies are developed (especially in non-invasive imaging) that can assess physiological structure and function. Continued efforts to fully document the cardiovascular health consequences of AS use is important to provide a clear, accurate, public health message to the many groups now using AS for performance and image enhancement.

 

[whitegato777]

Re: Anabolic Steroids and Cardiovascular Risk

do you think AAS use could effect cardiac risk by its effects on thyroid function and could be corrected with thyroid supplementation?

 

[Michael Scally MD]

Adverse Cardiovascular Effects Of Anabolic Steroids: Pathophysiology Imaging

It is notable that therapeutic treatment with AAS in hypogonadic men has recently been shown to be linked with a higher cardiovascular event rate. This important finding underscores that there is a delicate balance between benefits and risks related to AAS use as a treatment option for patients suffering from androgen deficiency. Adding up clinical AAS use and illegal AAS use rates represent a new wave of AAS-associated cardiovascular adverse consequences, in which early diagnosis can reduce health burden.

Molecular imaging is a promising method to target and image certain biomarkers in the process of cardiovascular pathology that can be used for early detection of AAS-associated adverse effects. A number of modalities and tracers are currently being developed that may become useful to delineate functional abnormalities in several pathways involved in AAS induced cardiovascular injury at the preclinical and clinical level.

In this study, researchers review previous literature on cardiovascular side effects associated with AAS use and misuse and promising molecular imaging techniques that are currently available to reveal the pathological abnormalities at the tissue level.


Golestani R, Slart RH, Dullaart RP, et al. Adverse cardiovascular effects of anabolic steroids: pathophysiology imaging. Eur J Clin Invest. Adverse cardiovascular effects of anabolic steroids: pathophysiology imaging - Golestani - 2012 - European Journal of Clinical Investigation - Wiley Online Library

Background Anabolic-androgenic steroids (AAS) are widely abused for enhancing muscle mass, strength, growth and improving athletic performance. Materials and methods In recent years, many observational and interventional studies have shown important adverse cardiovascular effects of AAS abuse. Conclusions This review discusses established and future perspectives of novel molecular imaging techniques that may serve as potential tools for early detection of AAS-associated cardiovascular disorders.

 

[Millard]

Are any of these "molecular imaging techniques" something that long-term steroid users on MESO-Rx could request from their doctor?

 

[Michael Scally MD]

Are any of these "molecular imaging techniques" something that long-term steroid users on MESO-Rx could request from their doctor?

 

[Michael Scally MD]

Single Dose Testosterone Increases Cholesterol Levels

Single Dose Testosterone Increases Total Cholesterol Levels And Induces The Expression Of HMG CoA Reductase

There is a comprehensive body of evidence documenting that AAS induce various deleterious alterations of the lipoprotein profile. The most prominent changes include elevations of low density lipoprotein (LDL) and decreases of high density lipoprotein (HDL). The long-term consequences of these alterations are still unknown but it is possible that the perturbation of the lipid profile may be associated with an increase in risk of coronary artery disease.

Cholesterol is mainly synthesized in the liver and the rate-limiting step is the reduction of 3- hydroxy-3methylglutaryl coenzyme A (HMG-CoA) to mevalonate, a reaction catalyzed by HMG-CoA reductase (HMGCR). Normally in mammalian cells the transcription of HMGCR is suppressed by cholesterol derived from the internalization and degradation of LDL via the LDL receptor. Competitive inhibitors of the HMGCR by statins lead to induction of the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the concentration of cholesterol in plasma. It is conceived that statins have a preventive effect on cardiovascular disease to a great extent by these mechanisms in several populations.

In this study, researchers investigated whether a single dose of testosterone enanthate affects the cholesterol profile and the expression of HMGCR in healthy volunteers. The lipoprotein profile was analyzed prior to, and two and fifteen days after administration of 500 mg testosterone enanthate. The protein expression of HMGCR in whole blood was determined by Western blotting. Moreover, human liver cells (HepG2) were exposed to supra-physiological concentrations of testosterone enathate and the mRNA HMGCR level was quantified by real time analysis.

Even though accumulating evidence indicates that testosterone may have adverse effect on the lipoprotein profile and cardiovascular health, this is, to the best of their knowledge, the first time an increase in total cholesterol level has been observed after only one single dose of testosterone. 15 days after the testosterone administration the cholesterol levels in the volunteers was back to baseline levels.


Garevik N, Skogastierna C, Rane A, Ekstrom L. Single dose testosterone increases total cholesterol levels and induces the expression of HMG CoA Reductase. Subst Abuse Treat Prev Policy 2012;7(1):12. SATPP | Abstract | Single dose testosterone increases total cholesterol levels and induces the expression of HMG CoA Reductase

BACKGROUND: Cholesterol is mainly synthesised in liver and the rate-limiting step is the reduction of 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) to mevalonate, a reaction catalysed by HMG-CoA reductase (HMGCR). There is a comprehensive body of evidence documenting that anabolic-androgenic steroids are associated with deleterious alterations of lipid profile. In this study we investigated whether a single dose of testosterone enanthate affects the cholesterol biosynthesis and the expression of HMGCR.

METHODS: 39 healthy male volunteers were given 500 mg testosterone enanthate as single intramuscular dose of Testoviron Depot. The total cholesterol levels prior to and two days after testosterone administration were analysed. Protein expression of HMGCR in whole blood was investigated by Western blotting. In order to study whether testosterone regulates the mRNA expression of HMGCR, in vitro studies were performed in a human liver cell-line (HepG2).

RESULTS: The total cholesterol level was significantly increased 15% two days after the testosterone injection (p = 0.007). This is the first time a perturbation in the lipoprotein profile is observed after only a single dose of testosterone. Moreover, the HMGCR mRNA and protein expression was induced by testosterone in vitro and in vivo, respectively.

CONCLUSION: Here we provide a molecular explanation how anabolic androgenic steroids may impact on the cholesterol homeostasis, i.e. via an increase of the HMGCR expression. Increasing knowledge and understanding of AAS induced side-effects is important in order to find measures for treatment and care of these abusers.

 

[whitegato777]

Re: Single Dose Testosterone Increases Cholesterol Levels

Ive been on hrt since 2007 and my has been off for a while. but since I've been on thyroid meds my cholesterol is completely normalized.

 

[Nemesis RR]

Re: Single Dose Testosterone Increases Cholesterol Levels

I think they should have addressed levels more common with HRT as well.

 

[Realgains]

I did a study's on myself years ago with the following...and on separate occasions. Blood work done on 8th day of the cycle at 9am.

Testosterone only at 500mg/week, Primo only 500mg/week, Deca only 500mg/week, tren only 300mg/week and dbol only at 50mg per day.

Lipid profiles done after one week as mentioned ...then I'd stack the cycle for the remainder of each cycle of course. No AI's used prior to the blood work.
Results....BIG drop in hdl. moderate increase in ldl and total cholesterol.
My hdl went super low guys... Dr Scally that was scarry.
This is the main reason I only did 2 week cycle after this. I would not want to have a next to zero hdl for 6 months out of every year, if doing two 10-12 weekers per year.

Funny, you'd think it would be worse on a 17aa roids like dbol....nope...worst was tren, second was testosterone! However, there was not much difference with any of them.

I find that taking 3 grams of regular niacin a day in two divided doses helped reduced the hdl drop to some degree but not to an acceptable level.

NOTE: It is not advised to take 3 grams of niacin a day AND a 17aa roid re: more liver stress.

RG

 

[Michael Scally MD]

Anabolic Androgenic Steroid Use Is Associated With Ventricular Dysfunction

Controversy remains over the cardiac adaptations of strength athletes to resistance training. The influence of androgenic anabolic steroids (AAS) use on structural cardiac adaptation is similarly unclear, but likely to be clinically relevant, as AAS-use has been reported to have adverse effects on ventricular function and the cardiovascular system in general. The prevalence of AAS use is probably underestimated by most physicians, and is reckoned to be over 3%. As different sports disciplines impose different patterns of hemodynamic strain upon the heart, they are likely to result in different patterns and degrees of cardiac adaptation. A useful and well established framework for classifying sports disciplines, based upon the degree of dynamic (endurance/isotonic) and static (resistance/ isometric) strain they exert, would classify typical strength training as low dynamic–high static (LD–HS).

LD–HS sports cause an increased afterload due to an elevation of arterial blood pressure of up to 480/350 mm Hg, while cardiac output remains virtually the same. Under these conditions, an adaptive pattern of concentric hypertrophy with selective ventricular wall thickening and without substantial changes in ventricular volume has been postulated and is known as the ‘Morganroth hypothesis’. Additionally, they assume that the upper limits of cardiac adaptation in strength athletes will fall within those of high dynamic–high static (HD–HS) athletes.

Existing studies on LD–HS athletes have come to contradictory conclusions, varying between reports of absence of ventricular changes, moderate changes and greater adaptations that are similar to those observed in HD–HS athletes. A complicating factor in the assessment of physiologic cardiac adaptation in strength athletes is the frequent use of AAS, as AAS-use results in generalized muscular hypertrophy.

In conclusion, low dynamic–high static (strength) sports yield very little cardiac adaptation, not exceeding ventricular volume and wall mass measures of non-athletic controls, unless accompanied by AAS-use. AAS-use is associated with larger ventricular volume and wall mass, not exceeding that of HD–HS athletes, together with systolic dysfunction and impaired ventricular inflow. The observed ventricular changes in AAS-using athletes are of great clinical importance, given the widespread and often illicit use of AAS.


Luijkx T, Velthuis BK, Backx FJ, et al. Anabolic androgenic steroid use is associated with ventricular dysfunction on cardiac MRI in strength trained athletes. Int J Cardiol. ScienceDirect.com - International Journal of Cardiology - Anabolic androgenic steroid use is associated with ventricular dysfunction on cardiac MRI in strength trained athletes

BACKGROUND: Uncertainty remains about possible cardiac adaptation to resistance training. Androgenic anabolic steroids (AAS) use plays a potential role and may have adverse cardiovascular effects.

OBJECTIVE: To elucidate the effect of resistance training and of AAS-use on cardiac dimensions and function.

PARTICIPANTS: Cardiac magnetic resonance (CMR) were performed in 156 male subjects aged 18-40years: 52 non-athletes (maximum of 3exercise hours/week), 52 strength-endurance (high dynamic-high static, HD-HS) athletes and 52 strength (low dynamic-high static, LD-HS) trained athletes (athletes >/=6exercise hours/week). 28 LD-HS athletes denied and 24 admitted to AAS use for an average duration of 5years (range 3months-20years).

RESULTS: No significant differences were found between non-athletes and non-AAS-using LD-HS athletes. AAS-using LD-HS athletes had significantly larger LV and RV volumes and LV wall mass than non-AAS-using LD-HS athletes, but lower than HD-HS athletes. In comparison to all other groups AAS-using LD-HS athletes showed lower ejection fractions of both ventricles (LV/RV EF 51/48% versus 55-57/51-52%) and lower E/A ratios (LV/RV 1.5/1.2 versus 1.9-2.0/1.4-1.5) as an indirect measure of diastolic function. Linear regression models demonstrated a significant effect of AAS-use on LV EDV, LV EDM, systolic function and mitral valve E/A ratio (all ANOVA-tests p<0.05).

CONCLUSIONS: Strength athletes who use AAS show significantly different cardiac dimensions and biventricular systolic dysfunction and impaired ventricular inflow as compared to non-athletes and non-AAS-using strength athletes. Increased ventricular volume and mass did not exceed that of strength-endurance athletes. These findings may help raise awareness of the consequences of AAS use.

 

[Michael Scally MD]

Toma M, McAlister FA, Coglianese EE, et al. Testosterone Supplementation in Heart Failure: A Meta-Analysis. Circulation: Heart Failure. Testosterone Supplementation in Heart Failure: A Meta-Analysis

Background—Low testosterone is an independent predictor of reduced exercise capacity and poor clinical outcomes in patients with heart failure (HF). We sought to determine if testosterone therapy improves exercise capacity in patients with stable chronic HF.

Methods and Results—We searched MEDLINE, EMBASE, Web of Science and Cochrane CENTRAL (1980 to 2010). Eligible studies included randomized trials reporting the effects of testosterone on exercise capacity in HF patients. Reviewers determined the methodological quality of studies and collected descriptive, quality, and outcome data. Four trials (n=198 patients, 84% male, mean age 67 years) were identified reporting the 6-minute walk test (6MWT, 2 RCT), incremental shuttle walk test (ISWT, 2 RCT) or peak VO2 (2 RCT) to assess exercise capacity after up to 52 weeks of treatment. Testosterone therapy was associated with a significant improvement in exercise capacity compared to placebo. The mean increase in the 6MWT, ISWT, and peak VO2 between the testosterone and placebo groups were 54.0 m (95% CI 43.0-65.0m), 46.7m (95% CI 12.6-80.9m), and 2.70 ml/kg/min (95% CI 2.68-2.72 ml/kg/min), respectively. Testosterone therapy was associated with a significant increase in exercise capacity as measured by units of pooled standard deviations (net effect 0.52 SD, 95% CI 0.10-0.94). No significant adverse cardiovascular events were noted.

Conclusions—Given the unmet clinical needs, testosterone appears to be a promising therapy to improve functional capacity in HF patients. Adequately powered RCT are required to assess the benefits of testosterone in this high-risk population assessing quality of life, clinical events and safety.

 

[skywalk]

Steroids and heart disease

have you noticed that many famous bodybuilders get heart problems, some even as young as 40+ years of age?

eg arnold, Mike Matarazzo, Mike mentzer, to name a few....

So this leads me to wonder how we can avoid the same path to (heart) failure.....

did they do too much for too long? how can we do gear, and be as safe as possible? Is there a way to monitor things to prevent future complications?

thanks

 

[Michael Scally MD]

Re: Steroids and heart disease

Montisci M, El Mazloum R, Cecchetto G, et al. Anabolic androgenic steroids abuse and cardiac death in athletes: morphological and toxicological findings in four fatal cases. Forensic Sci Int 2012;217(1-3):e13-8. Elsevier

Anabolic androgenic steroids (AAS) are the main class of doping agents and their consumption produces adverse effects involving several organs and systems. Three cases of sudden cardiac death (SCD) and one of death due to congestive heart failure of previously healthy athletes who were AAS users are herein reported. Concentric cardiac hypertrophy with focal fibrosis (one case), dilated cardiomyopathy with patchy myocyte death (two cases) and eosinophilic myocarditis (one case) were observed and most probably relate to the final event. Molecular investigation for viral genomes was positive in one case (Ebstein virus). Our data confirm previous findings, showing that the most typical cardiac abnormality in AAS abusers is left ventricular hypertrophy, associated with fibrosis and myocytolysis. An exceptional cardiovascular substrate was represented by the case with drug induced eosinophilic myocarditis. These features are at risk of ventricular arrhythmias as well as congestive heart failure. The cause-effect relationship between AAS abuse and cardiac death can be established only by a rigorous methodology with the use of standardized protocols, including precise morphological studies of all target organs to search for chronic toxic effects. Laboratory investigations should focus on AAS searching on a wide range of biological matrices to demonstrate type, magnitude and time of exposure.


Also, see: Dead bodybuilder's heart weighed a kilo

 

[MANWHORE]

Re: Steroids and heart disease

What about all the other people who
have/had heart problems but never used gear?

The pro bodybuilding lifestyle is not healthy, period

Eating huge amounts of food, cutting carbs to zero,
building more muscle than I am sure the human body
was ever built to carry, insulin use, PGF use, HGH use..

That's all I have right now

Not saying gear is healthy, but gear was probably
a good thing compared to what else these guys did.

Mike used speed and smoked cigarettes ..

Did I just mention cigarettes? O NO!

Yeah, cigarettes seem to be taking a beating up here
with all these commercials. ...
Your toe falls off .. Must have been the
cigarettes not the diabetes ..
Heart attack? Must be the smokes, not the 5 big macs you eat every day for 20yrs ..
House went on fire?
Do you smoke? Yes .. It was the cigarettes, for sure.
Aren't you going to investigate? Nope, don't need to.
It was the smoking.

 

[MANWHORE]

Re: Steroids and heart disease

Reminds me of the police focusing all attention
on one person, because they were arrested in the past
for J-Walking, while the real killer is already on a plane
to Jamaca LOL