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Thread: Anabolic-Androgenic Steroids: worse for the heart than we knew?

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    Anabolic-Androgenic Steroids: worse for the heart than we knew?

    Anabolic-Androgenic Steroids: worse for the heart than we knew?


    Anabolic-Androgenic Steroids
    Worse for the Heart Than We Knew?


    Matthew W. Parker, MD and Paul D. Thompson, MD
    From the Division of Cardiology, Hartford Hospital, Hartford, Conn, and the University of Connecticut School of Medicine, Farmington, Conn.

    Correspondence to Paul D. Thompson, MD, Director of Cardiology, Hartford Hospital, 80 Seymour St, Hartford, CT 06102. E-mail [email protected]



    Key Words: Editorials • anabolic steroids • systolic dysfunction


    An extract of the first 250 words of the full text is provided, because this article has no abstract.




    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,3 suggesting 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.

    Article see p 472

    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.




    Anyone able to access the full paper of this important study without paying the $20.00. If not, I'll pay it.

    I think this could be an excellent insight into AAS and thier effects on the heart.

    This study is also brand spanking new (Jul 2010).

  2. #2
    I wouldn't consider this new news really.anyone who has done their research knows the risk of use.nice find on this study though its a very interesting read.check out pub med or research gate they might have the study for free.

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    Quote Originally Posted by thauncle View Post
    I wouldn't consider this new news really.anyone who has done their research knows the risk of use.nice find on this study though its a very interesting read.check out pub med or research gate they might have the study for free.
    They dont mate. Tried all that.

    If I have to I'll buy it...

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    I get pains in the left side of chest / heart area.

    Have since I first started with Clen (which was my first step into 'this world')

    had so many tests done, and no issues can be found. I still deal with random jolts of pain in the heart sometimes.

    wonder if anyone's heard of that.

    (tests include: CT scans, blood tests, radiology, running on a treadmill covered in wires, etc.)

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    Looking forward to reading more....

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    @ the guy with. Chest pain. Are u still. On clen I seem to get it while on clen and don't use it. It sounds like anxiety, if u had ekgs done and bw and stress tests it should be fine they should have done a echogram to show size and function of. Heart. I had the same issues but it was bad anxiety steroids I think mess us up more phsycologically more than anything or trigger physciatric problems, let me know bud thanks

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    The issues regarding negative changes to the lipid profile (HDL/LDL balance and cholesterol in general) is well founded. It's also well known.

    For years there was a lot of talk about ventricular hypertrophy, which is the enlargement of the ventricles in the heart. Many have claimed that this is due to the same hypertrophy effect that steroids have on skeletal muscle. Personally, I consider this to be bunk. First, skeletal muscle and cardiac muscle are not the same. If steroids had this effect then all males would get this condition with puberty. Second, all athletes that spend a lot of time lifting weights have this condition, whether they have used steroids or not.

    My guess is that this is yet another "medical paper" that contains research done in improper fashion, with consequent "results" from which sound conclusions are impossible. Until proper trials are done on such claimed effects the "facts" presented in such work are at best heresay.

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    Quote Originally Posted by New2Anabolic View Post
    I get pains in the left side of chest / heart area.

    Have since I first started with Clen (which was my first step into 'this world')

    had so many tests done, and no issues can be found. I still deal with random jolts of pain in the heart sometimes.

    wonder if anyone's heard of that.

    (tests include: CT scans, blood tests, radiology, running on a treadmill covered in wires, etc.)
    If you didnt get these pains pre-Clen and Clen is giving these sides, get off it.

    Use Albuterol.

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    Quote Originally Posted by TKO Performance View Post
    The issues regarding negative changes to the lipid profile (HDL/LDL balance and cholesterol in general) is well founded. It's also well known.

    For years there was a lot of talk about ventricular hypertrophy, which is the enlargement of the ventricles in the heart. Many have claimed that this is due to the same hypertrophy effect that steroids have on skeletal muscle. Personally, I consider this to be bunk. First, skeletal muscle and cardiac muscle are not the same. If steroids had this effect then all males would get this condition with puberty. Second, all athletes that spend a lot of time lifting weights have this condition, whether they have used steroids or not.

    My guess is that this is yet another "medical paper" that contains research done in improper fashion, with consequent "results" from which sound conclusions are impossible. Until proper trials are done on such claimed effects the "facts" presented in such work are at best heresay.
    I agree with what your saying, but your final paragraph is "heresay" unless you have read the full paper.

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    Ugh, I avoided reading this thread the moment I saw it was about negative AAS affects. I like using the 'if I dont see it, it isnt there' defense when it comes to different down sides to AAS use, but since Swifto put it up, I finally caved in.

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    Quote Originally Posted by G4R View Post
    Ugh, I avoided reading this thread the moment I saw it was about negative AAS affects. I like using the 'if I dont see it, it isnt there' defense when it comes to different down sides to AAS use, but since Swifto put it up, I finally caved in.
    hahahaha

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    Quote Originally Posted by G4R View Post
    Ugh, I avoided reading this thread the moment I saw it was about negative AAS affects. I like using the 'if I dont see it, it isnt there' defense when it comes to different down sides to AAS use, but since Swifto put it up, I finally caved in.
    haha x2.

    If its put up by another member, i wont read it because im sick of childish people posting propaganda about AAS. When i saw it was swifto i read it because i trust his sources.


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    Clen was day 1 - waaay back when I got into all this.

    I was given a pump full of gel (literally used for horses - acting as the bronchodilator that it is) - I do believe that I missused it.

    Taking it until I felt it.

    Then if i I wasn't feeling much of it anymore, I would take another pump of it..

    I recall vague aspects of it - but again, that was a long time ago.

    I've used clen/eca since then, but I'm saying that I get random jolts of pain in the 'heart area' periodically.
    It's usually after I eat, or if I'm hungry. I'm not sure what it could be though; what with all of thoses tests I've gone through.

    The coolest test was when they put those wires/sticky pads on me and I wsa able to SEE my heart. Maybe that was teh echocardiogram?

    Anywho...

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    we have to be joking are selves if we all seriously think steroids aren't bad for us...

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    clen made my heart act a little iffy. besides the stronger faster beat, sometimes I'd get a strange feeling..almost like a spasm, that felt like it was on the left side...

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    clen only heats me up and makes me shake. My heart is fine... from what i can tell, have no idea what's happening within.

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    Quote Originally Posted by TKO Performance View Post
    The issues regarding negative changes to the lipid profile (HDL/LDL balance and cholesterol in general) is well founded. It's also well known.

    For years there was a lot of talk about ventricular hypertrophy, which is the enlargement of the ventricles in the heart. Many have claimed that this is due to the same hypertrophy effect that steroids have on skeletal muscle. Personally, I consider this to be bunk. First, skeletal muscle and cardiac muscle are not the same. If steroids had this effect then all males would get this condition with puberty. Second, all athletes that spend a lot of time lifting weights have this condition, whether they have used steroids or not.
    My guess is that this is yet another "medical paper" that contains research done in improper fashion, with consequent "results" from which sound conclusions are impossible. Until proper trials are done on such claimed effects the "facts" presented in such work are at best heresay.


    Well, here is a study stating AAS can make the problem worse (to put it simply).


    Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction.

    Original Articles

    Circulation: Heart Failure. 3(4):472-476, July 2010.
    Baggish, Aaron L. MD; Weiner, Rory B. MD; Kanayama, Gen MD, PhD; Hudson, James I. MD, ScD; Picard, Michael H. MD; Hutter, Adolph M. Jr MD; Pope, Harrison G. Jr MD
    Abstract:
    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.

    (C) 2010 American Heart Association, Inc.


    Again, brand spanking new (Jul 2010).

    I dont like what I'm reading either to the other members who know AAS cause health concerns... Maybe I should stop now trying to research AAS and the heart...

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    Dangit Swifto...... you are screwing my 'blind eye' up here.

    Next thing I know, there will be a report that all AAS users kick little puppies into ponds and steal from homeless shelters.... all while having a heart attack.

    Ugh, its not looking good....

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    no swifto keep going we need to see this...

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    Quote Originally Posted by G4R View Post
    Dangit Swifto...... you are screwing my 'blind eye' up here.

    Next thing I know, there will be a report that all AAS users kick little puppies into ponds and steal from homeless shelters.... all while having a heart attack.

    Ugh, its not looking good....
    Ha ha... Sorry mate.

    I've been looking into AAS effects on mood, agression and the heart recently and my findings wernt what I was expecting at all (not good).

    I dont think this causes great need for concern cocern though. There are a fair few members who have lost their lives because of heart problems (T-Mos, Big Bapper, SwoleCat to name a few) but it remains to be seen if AAS made their problems worse of were infact the causitive factor.

    There are a few members over at PM.com who have had minor heart attacks and blame it on AAS. They now dont cycle at all.

    AAS can negatively effect the heart IMO, but I'd like to see if the problems then caused can be reveresed post AAS use. That would be intresting.

    Eat healthy, use moderate doses, train hard, do cardio, get BW done and stay safe IMO.

    There are Pro's walking around right this very second on massive doses. Look at it like that if you want to make yourseld feel better!

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    I may have missed it, but did the articles say if any of the test subjects had family history of heart issues? I assume if they did their chances were increased, but what of those who dont have a history of it? I mean, obviously the chances increase regardless while using AAS, but how much more of an increase is it compared to the person who has the heart issues in their family?

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    Quote Originally Posted by G4R View Post
    I may have missed it, but did the articles say if any of the test subjects had family history of heart issues? I assume if they did their chances were increased, but what of those who dont have a history of it? I mean, obviously the chances increase regardless while using AAS, but how much more of an increase is it compared to the person who has the heart issues in their family?
    I dont have the full papers yet mate. When I do, it will say in both of them I hope about hereditory conditions.

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    Quote Originally Posted by Swifto View Post
    Ha ha... Sorry mate.

    I've been looking into AAS effects on mood, agression and the heart recently and my findings wernt what I was expecting at all (not good).

    I dont think this causes great need for concern cocern though. There are a fair few members who have lost their lives because of heart problems (T-Mos, Big Bapper, SwoleCat to name a few) but it remains to be seen if AAS made their problems worse of were infact the causitive factor.

    There are a few members over at PM.com who have had minor heart attacks and blame it on AAS. They now dont cycle at all.

    AAS can negatively effect the heart IMO, but I'd like to see if the problems then caused can be reveresed post AAS use. That would be intresting.

    Eat healthy, use moderate doses, train hard, do cardio, get BW done and stay safe IMO.

    There are Pro's walking around right this very second on massive doses. Look at it like that if you want to make yourseld feel better!
    So true...

    It would be interesting to know what these doctors consider worse, doing short mild cycles or going out binge drinking on weekends...
    Do not ask me for a source check.






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    Quote Originally Posted by New2Anabolic View Post
    I get pains in the left side of chest / heart area.

    Have since I first started with Clen (which was my first step into 'this world')

    had so many tests done, and no issues can be found. I still deal with random jolts of pain in the heart sometimes.

    wonder if anyone's heard of that.

    (tests include: CT scans, blood tests, radiology, running on a treadmill covered in wires, etc.)
    I've had the samr probs but mine were probably caused by other things. I wanted to know the answer before I cycled. I'm getting a second oipion soon.

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    Quote Originally Posted by 007 View Post
    So true...

    It would be interesting to know what these doctors consider worse, doing short mild cycles or going out binge drinking on weekends...
    Binge drinking for me. Far worse.

    I know far more people bing drink than use AAS. But alot of people die from alchool or alcohol related side effects every year compared to deaths associated with AAS use.

    I know of not a single case where someone has dropped stone cold dead from an injeciton of AAS.

    I've actually had BW done after a binge weekend. Well, liver values (and I was on cycle). My liver values were around 115, but returned to normal (still on AAS) after 5 days.

    The truth is, quite a few people mix alcohol with AAS. AAS are used by bodybuilders, yeah, but alot of peolple use AAS purely for vanity. Thats then best displayed going out drinking etc...

    There is another full paper I'm after, mixing both AAS and certain white powder and its toxicology effects when combined with exercise.

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    I take steroids am i going to die now?

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    Quote Originally Posted by warchild View Post
    I take steroids am i going to die now?
    Yes, of course.

    Infact, by the time I have sent this post, you would have died.

    RIP.

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    oh crap im dead

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    I tend to feel a bit of a "flutter" in my chest while on steroids and dehydrated. If I stay super-hydrated I dont feel the flutter. I also have a problem with my elbows hurting badly after being dehydrated and lifting. Point; stay hydrated!

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    Quote Originally Posted by Swifto View Post
    I agree with what your saying, but your final paragraph is "heresay" unless you have read the full paper.
    I'll give you that, but from previous experience with medical papers I have to say that there is a definite shortage of good science in a lot of these things. If all variables are not accounted for and held constant with only one variable being tested the results cannot be considered conclusive, yet I see time and again where that it the case.

    Heredity, diet, lifestyle, other drug use, ect. all play into heart issues. Without holding these things constant the results of any such study cannot be considered concrete facts.

    Also, consider the effects of environment and even FDA approved medications. Many people had heart attacks while taking FDA approved medications for the condition they were trying to treat. So much so that several class action lawsuits were filed against the manufacturer (I believe that federal law prohibits suing the FDA directly).

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    Quote Originally Posted by Swifto View Post
    Well, here is a study stating AAS can make the problem worse (to put it simply).


    Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction.

    Original Articles

    Circulation: Heart Failure. 3(4):472-476, July 2010.
    Baggish, Aaron L. MD; Weiner, Rory B. MD; Kanayama, Gen MD, PhD; Hudson, James I. MD, ScD; Picard, Michael H. MD; Hutter, Adolph M. Jr MD; Pope, Harrison G. Jr MD
    Abstract:
    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.

    (C) 2010 American Heart Association, Inc.


    Again, brand spanking new (Jul 2010).

    I dont like what I'm reading either to the other members who know AAS cause health concerns... Maybe I should stop now trying to research AAS and the heart...
    Case in point. If there's more to this I'd like to see/read it. There's no discussion of sample size, distribution, outliers, etc. This alone is not statistically viable research. There also needs to be discussion of individual members of the study and how things like heredity, diet, lifestyle, etc. were accounted for and held constant. Without those pieces this proves less than nothing.

    Any first year premed student would be required to provide this information, but when someone slaps MD after their name all the sudden good scientific method goes out the window. Couple that with the fact that often the papers are done for the furthering of careers and we have an environment rife with misinformation and manipulation. Remember that the reason steroids are illegal in the first place in the US has nothing to do with real danger and everything to do with the furthering of political careers. The medical establishment is a lot like the government; neither like having to admit that they are wrong and both will do whatever is necessary to ensure that they remain "right".

  32. #32
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    To all those commenting on the clen:

    Stay far away from it. Seriously. Clen is far worse on the heart (and your cardiovascular system as a whole) than any steroid is. I never had any problems with clen, and used it a few times with no issues, but once I read into clen's effects on the heart (and seeing other testimonies from people who have bad issues with it), i'm never using it ever again. Haven't used it in a couple of years now. Honestly, while laying in bed, I FELT the vibrations through the bed of my heart beating. That was reason enough to terminate the clen and never use it again.

    And I don't think Albuterol is any better, folks. I haven't used it but it's basically a sister compound to clen. No Thanks. The only sympathomimetic I would even think of considering use would be ephedrine, but even I think that is a little risky.

    As for this study, i'd like to see more of it and how the AAS was used, the dosages and duration, etc. before we can make a good judgement on the study.

    I make sure now to use lots of fish oils, vitamin E, and cardiovascular enhancing supplements (such as Lipid Stabil) while on and off cycle to help my heart out. Think about this: bodybuilders and people using AAS back in the 70s, 80s, and even 90s never did that... but we can do it today. Just stay safe with what you do and take all the precautions NO MATTER THE COST IN DOLLARS so that you don't have to pay dearly later... with your health.

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    Anabolic-Androgenic Steroids: worse for the heart than we knew? + full papers (x2)

    Quote Originally Posted by Swifto View Post
    Well, here is a study stating AAS can make the problem worse (to put it simply).


    Long-Term Anabolic-Androgenic Steroid Use Is Associated With Left Ventricular Dysfunction.

    Original Articles

    Circulation: Heart Failure. 3(4):472-476, July 2010.
    Baggish, Aaron L. MD; Weiner, Rory B. MD; Kanayama, Gen MD, PhD; Hudson, James I. MD, ScD; Picard, Michael H. MD; Hutter, Adolph M. Jr MD; Pope, Harrison G. Jr MD
    Abstract:
    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.

    (C) 2010 American Heart Association, Inc.


    Again, brand spanking new (Jul 2010).

    I dont like what I'm reading either to the other members who know AAS cause health concerns... Maybe I should stop now trying to research AAS and the heart...
    Right I have both full papers now.

    To sum up...

    It doesnt make comfortable reading at all. But dont bury your head in the sand and think AAS do NOT effect the heart, they do.

    The study size is small (17 AAS user's, 9 non).

    Mean age is 40 years old.

    To quote:

    ...none of the participants had a history of hypertension,
    atherosclerotic vascular disease, heart failure, or exercise
    intolerance.
    AAS users reported taking median (quartile 1,
    quartile 3) weekly doses of 675 (513, 950) mg of testosterone
    equivalent for 468 (169, 520) lifetime weeks. The groups were
    similar in age, prior duration of weightlifting, current number of
    hours per week of weight training and other intense athletic
    activity, body mass index, and body surface area, but as
    expected, AAS users were significantly more muscular than
    nonusers as measured by fat-free mass index (Table 1). In other
    words, the AAS users had a similar body mass index to nonusers
    because the former group had more muscle but less body fat.
    Four of the 12 AAS users were currently taking supraphysiologic
    doses of AAS at the time of evaluation; 3 were currently
    taking only physiological doses of testosterone at 50 to 100
    mg/week; 1 had discontinued a course of supraphysiologic AAS
    3 weeks prior to evaluation; and the remaining 4 had not used
    AAS for at least 6 months prior to the evaluation.



    Six (50%) of the AAS users but none of the nonusers
    reported a past history of opioid, cocaine, or alcohol dependence.
    None of the participants reported amphetamine dependence.
    Two (17%) AAS users but none of the nonusers
    reported cannabis dependence, 1 past and 1 current. None of
    the participants reported a history of cigarette use. Nine
    (75%) AAS users but none of the nonusers reported at least
    some use of human growth hormone, and 6 of these reported
    human growth hormone use for 3 months



    Discussion

    Results from this study are consistent with previous findings
    showing LV diastolic dysfunction10–12 and subclinical LV systolic
    impairment10 in AAS users. However, our results suggest
    that the cardiac impairment in long-term AAS users may be
    more severe than previously reported. Specifically, long-term
    AAS users were found to have significant LV systolic dysfunction
    both by relative standards (compared to the AAS nonuser
    cohort) and by absolute standards (as defined by current clinical
    practice). To our knowledge, this study is the first to demonstrate
    an association between long-term AAS use and a clinically
    relevant reduction in LV ejection fraction.


    There is a well-established relationship between LV dysfunction
    and exposure both to certain medications29 and to
    some drugs of abuse.30–32 Further, the prognostic importance
    of toxin-induced cardiac dysfunction has been well documented.
    33–36 Data from this study suggest that AAS, particularly
    when used over long durations, may be another
    important cause of toxin-mediated myocardial impairment.
    Although confirmatory data are required, results from this
    study suggest that AAS exposure should be a diagnostic
    consideration among persons with asymptomatic LV dysfunction
    or incident heart failure.

    Although several previous studies have reported mild cardiac
    dysfunction, LV dysfunction among our AAS users was more severe than previously reported. Several hypotheses might explain
    this discrepancy. First, our AAS users were several years
    older, on average, than those in 2 of the 3 most recent
    studies.10,12 Second, these previous studies selected top-level
    competitive bodybuilders,10 squad athletes,12 or individuals from
    bodybuilding studios,12 thus possibly favoring healthier individuals
    with better cardiac function than the largely noncompetitive
    individuals21 in our study.

    Finally, the specific AAS compounds
    and dosages typically used by our American participants may
    have differed from those of participants in previous studies,
    which were largely conducted in Europe.
    It is noteworthy that our analysis revealed no significant
    relationship between cumulative AAS use and cardiac dysfunction.
    This observation suggests that AAS-associated
    cardiotoxicity might be only partially and unpredictably
    related to lifetime dose in a manner similar to the cardiac
    toxicity of alcohol.37 Further work is required to determine
    whether cardiac function is influenced by factors such as the
    recency of AAS use (eg, current versus long past), specific
    AAS used (eg, possibly more toxic oral agents5,38 versus
    injectable agents), duration of exposure to very high doses
    (eg, 2000 mg/wk), or concomitant use of other drugs (eg,
    human growth hormone39,40).

    There are several important limitations to this study. First,
    our sample might not be representative of the overall source
    population of long-term AAS users or comparison weightlifters.
    Although we used recruitment procedures designed to
    generate a sample that is maximally representative,20,21 it is
    possible that the group of AAS users in the present study is
    not entirely representative of the overall population. Second,
    our sample sizes were small and unequal. However, this
    limitation would likely produce false-negative findings (ie,
    type II errors) rather than false-positive results due to the
    reduced statistical power afforded by small sample sizes.
    Therefore, the highly statistically significant findings in the
    present study, despite the small sample size, suggest that the
    association between AAS use and cardiac pathology may be
    particularly strong (ie, a very large effect size). Conversely,
    the possibility of a type II error must be considered in
    instances where group comparisons were not significant. For
    example, the lack of association between AAS exposure and
    cardiac dysfunction must be interpreted with caution. Future
    study with adequate statistical power is warranted to examine
    this issue. A third limitation is our reliance on participants’
    self-reporting of AAS use. We recognize that errors based on
    self-report could have arisen if actual AAS users denied use
    and were misclassified as nonusers; individuals classified as
    nonusers had unknowingly ingested supplements contaminated contaminated
    with actual AAS; or individuals classified as users had
    ingested only counterfeit black market AAS and, hence, had
    not used genuine drugs.

    However, each form of misclassification
    would only narrow the differences between groups,
    causing us to underestimate the true association of AAS use
    with cardiac pathology. A fourth limitation is our use of
    retrospective exercise exposure assessment and the possibility
    that AAS-users differed from nonusers with respect to
    exercise intensity. However, it is unlikely that this factor
    contributed to our observations because no prior studies have
    demonstrated LV dysfunction secondary to intense, sustained
    exercise training. Finally, the cross-sectional nature of this
    exploratory study does not permit definitive conclusions
    about the long-term clinical implications of our findings and
    represents an important area of future work.


    In summary, data from the present study suggest that
    AAS-induced LV dysfunction may be greater than previously
    reported. The reductions in LV systolic function observed in
    this group of AAS users are of a magnitude shown to increase
    the risk of heart failure and sudden cardiac death in other
    populations.41,42 Further work is needed to confirm our
    findings and to determine the extent to which AAS-associated
    cardiac dysfunction leads to adverse clinical outcomes.




    Ouch!
    Last edited by Swifto; 08-05-2010 at 04:03 PM.

  34. #34
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    Quote Originally Posted by Swifto View Post
    Anabolic-Androgenic Steroids: worse for the heart than we knew?


    Anabolic-Androgenic Steroids
    Worse for the Heart Than We Knew?


    Matthew W. Parker, MD and Paul D. Thompson, MD
    From the Division of Cardiology, Hartford Hospital, Hartford, Conn, and the University of Connecticut School of Medicine, Farmington, Conn.

    Correspondence to Paul D. Thompson, MD, Director of Cardiology, Hartford Hospital, 80 Seymour St, Hartford, CT 06102. E-mail [email protected]



    Key Words: Editorials • anabolic steroids • systolic dysfunction


    An extract of the first 250 words of the full text is provided, because this article has no abstract.




    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,3 suggesting 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.

    Article see p 472

    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.




    Anyone able to access the full paper of this important study without paying the $20.00. If not, I'll pay it.

    I think this could be an excellent insight into AAS and thier effects on the heart.

    This study is also brand spanking new (Jul 2010).
    I'll copy/paste all of this study as its only 3 pages long.




    Anabolic-Androgenic Steroids: Worse for the Heart Than We Knew?

    Copyright © 2010 American Heart Association. All rights reserved. Print ISSN: 1941-3289. Online
    Dallas, TX 72514
    Circulation: Heart Failure is published by the American Heart Association. 7272 Greenville Avenue,
    DOI: 10.1161/CIRCHEARTFAILURE.110.957720
    Circ Heart Fail 2010;3;470-471


    Anabolic-Androgenic Steroids
    Worse for the Heart Than We Knew?
    Matthew W. Parker, MD; Paul D. Thompson, MD

    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,3 suggesting 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.
    Article see p 472

    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 et al13 in this issue of Circulation: Heart
    Failure present evidence that chronic, high-dose AAS use
    produces a dramatic impairment of LV systolic function.
    These authors recruited 19 male weightlifters, including 12
    with prolonged AAS use. Recruitment was designed to
    minimize selection biases. Standardized questionnaires were
    used to determine participants’ lifetime AAS exposure as well as their use of illicit drugs and other ergogenic drugs
    including growth hormone.

    The AAS users were remarkable for both their steroid dose
    and duration of use. For comparison, subjects in prior studies
    generally reported weekly AAS doses equivalent to 200 to
    250 mg of testosterone,3,7 whereas subjects in the present
    study reported a median weekly dose equivalent to 675 mg of
    testosterone. The present subjects also reported a median of
    almost 9 years of steroid use.

    These investigators confirmed the decreased early, and
    increased late, diastolic filling in the AAS users noted
    previously. LV hypertrophy did not differ between AAS users
    and control subjects. Both radial and longitudinal strain,
    measures of myocardial systolic function, were decreased in
    the AAS users, but more impressive was the decrease in LV
    ejection fraction (LVEF). Median LVEF was 51% in AAS
    users versus 59% in control subjects, and half of the AAS
    users had LVEF values below 50%.

    This decreased in LVEF has not been observed in prior
    studies of AAS. There was no statistical association between
    dose and duration of AAS use and LVEF, but the small
    sample size precludes eliminating this possibility. We suspect
    that both the dose and duration of use are part of the
    explanation for the novelty of these findings, but this hypothesis
    awaits confirmation. It is difficult to separate duration of
    use from age, however, and the age (median, 40 years) of
    AAS users in the present study is older than in most prior
    reports.

    There are limitations to the present report. The number of
    participants is small. The authors correctly note that this is
    more likely to cause a type II error, or false-negative finding,
    but this assumes that the effect is entirely due to the exposure
    being studied. Other causes of reduced LV systolic function,
    such as other drug use, could be clustered in the AAS
    subjects, confounding the results. Indeed, 9 of the AAS users
    reported prior growth hormone (GH) use and 6 had used GH
    for at least 3 months. Supraphysiologic levels of GH have
    been associated with diastolic14 and systolic dysfunction,
    although the later requires chronic exposure. Consequently,
    GH use may be a significant confounder.

    The authors tried to
    reduce selection bias, but the possibility remains that participants
    enrolled for a medical evaluation because of mild
    symptoms. Blood pressure, ECGs, and an assessment of
    overall atherosclerotic risk were not provided, so occult
    atherosclerotic disease cannot be excluded as a mechanism
    for the effect; however, none of the participants reported
    hypertension, atherosclerotic disease, or heart failure.
    Despite such limitations, the present report by Baggish et al
    is the first to suggest that chronic AAS use can reduce LVEF.
    These results, if confirmed, require that AAS use be consid-ered in the differential diagnosis of LV systolic dysfunction
    and suggest that the prevalence of this problem may increase
    as long-term AAS users reach middle age. These results also
    raise the haunting possibility that long-term AAS use can
    produce a clinically symptomatic cardiomyopathy. This report
    might spur the detection of such cases and the confirmation
    of this possibility.


    Disclosures
    None.

    References

    1. McNutt RA, Ferenchick GS, Kirlin PC, Hamlin NJ. Acute myocardial
    infarction in a 22-year-old world class weight lifter using anabolic
    steroids. Am J Cardiol. 1988;62:164.
    2. Dickerman RD, Schaller F, Prather I, McConathy WJ. Sudden cardiac
    death in a 20-year-old bodybuilder using anabolic steroids. Cardiology.
    1995;86:172–173.
    3. Thompson PD, Cullinane E, Sady SP, Chenevert C, Saritelli AL, Sady
    MA, Herbert PN. Contrasting effects of testosterone and stanozolol on
    serum lipoprotein levels. JAMA. 1989;261:1165–1168.
    4. Albers JJ, Taggart HM, Applebaum-Bowden D, Haffner S, Chesnut CH,
    Hazzard WR. Reduction of lecithin-cholesterol acyltransferase, apolipoprotein
    D and the Lp(a) lipoprotein with the anabolic steroid
    stanozolol. Biochim Biophys Acta. 1984;795:293–296.
    5. Zmuda JM, Thompson PD, Dickenson R, Bausserman LL. Testosterone
    decreases lipoprotein(a) in men. Am J Cardiol. 1996;77:1244 –1247.
    6. Grace F, Sculthorpe N, Baker J, Davies B. Blood pressure and rate
    pressure product response in males using high-dose anabolic androgenic
    steroids (AAS). J Sci Med Sport. 2003;6:307–312.
    7. Riebe D, Fernhall B, Thompson PD. The blood pressure response to
    exercise in anabolic steroid users. Med Sci Sports Exerc. 1992;24:
    633–637.
    8. D’Andrea A, Caso P, Salerno G, Scarafile R, De Corato G, Mita C, Di
    Salvo G, Severino S, Cuomo S, Liccardo B, Esposito N, Calabro` R. Left
    ventricular early myocardial dysfunction after chronic misuse of anabolic
    androgenic steroids: a Doppler myocardial and strain imaging analysis.
    Br J Sports Med. 2007;41:149 –155.
    9. Hassan NA, Salem MF, Sayed MAEL. Doping and effects of anabolic
    androgenic steroids on the heart: histological, ultrastructural, and echocardiographic
    assessment in strength athletes. Hum Exp Toxicol. 2009;
    28:273–283.
    10. Nottin S, Nguyen L-D, Terbah M, Obert P. Cardiovascular effects of
    androgenic anabolic steroids in male bodybuilders determined by tissue
    Doppler imaging. Am J Cardiol. 2006;97:912–915.
    11. Fanton L, Belhani D, Vaillant F, Tabib A, Gomez L, Descotes J, Dehina
    L, Bui-Xuan B, Malicier D, Timour Q. Heart lesions associated with
    anabolic steroid abuse: comparison of post-mortem findings in athletes
    and norethandrolone-induced lesions in rabbits. Exp Toxicol Pathol.
    2009;61:317–323.
    12. Thompson PD, Sadaniantz A, Cullinane E, Bodziony K, Catlin D,
    Torek-Both G, Douglas PS. Left ventricular function is not impaired in
    weight-lifters who use anabolic steroids. J Am Coll Cardiol. 1992;19:
    278–282.
    13. Baggish AL, Weiner RB, Kanayama G, Hudson JI, Picard MH, Hutter
    AM, Pope HG. Long term anabolic-androgenic steroid use is associated
    with left ventricular dysfunction. Circulation Heart Failure. 2010;3:
    472–476.
    14. Sacca` L, Napoli R, Cittadini A. Growth hormone, acromegaly, and heart
    failure: an intricate triangulation. Clin Endocrinol (Oxf). 2003;59:660–671.
    KEY WORDS: Editorials  anabolic steroids  systolic dysfunction
    Parker and Thompson Anabolic-Androgenic Steroids and Heart Failure 471
    Downloaded

    The opinions expressed in this article are not necessarily those of the
    editors or of the American Heart Association.

  35. #35
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    Quote Originally Posted by Swifto View Post
    Right I have both full papers now.

    To sum up...

    It doesnt make comfortable reading at all. But dont bury your head in the sand and think AAS do NOT effect the heart, they do.

    The study size is small (17 AAS user's, 9 non).

    Mean age is 40 years old.

    To quote:

    ...none of the participants had a history of hypertension,
    atherosclerotic vascular disease, heart failure, or exercise
    intolerance. AAS users reported taking median (quartile 1,
    quartile 3) weekly doses of 675 (513, 950) mg of testosterone
    equivalent for 468 (169, 520) lifetime weeks. The groups were
    similar in age, prior duration of weightlifting, current number of
    hours per week of weight training and other intense athletic
    activity, body mass index, and body surface area, but as
    expected, AAS users were significantly more muscular than
    nonusers as measured by fat-free mass index (Table 1). In other
    words, the AAS users had a similar body mass index to nonusers
    because the former group had more muscle but less body fat.
    Four of the 12 AAS users were currently taking supraphysiologic
    doses of AAS at the time of evaluation; 3 were currently
    taking only physiological doses of testosterone at 50 to 100
    mg/week; 1 had discontinued a course of supraphysiologic AAS
    3 weeks prior to evaluation; and the remaining 4 had not used
    AAS for at least 6 months prior to the evaluation.


    Six (50%) of the AAS users but none of the nonusers
    reported a past history of opioid, cocaine, or alcohol dependence.
    None of the participants reported amphetamine dependence.
    Two (17%) AAS users but none of the nonusers
    reported cannabis dependence, 1 past and 1 current. None of
    the participants reported a history of cigarette use. Nine
    (75%) AAS users but none of the nonusers reported at least
    some use of human growth hormone, and 6 of these reported
    human growth hormone use for 3 months


    Discussion

    Results from this study are consistent with previous findings
    showing LV diastolic dysfunction10–12 and subclinical LV systolic
    impairment10 in AAS users. However, our results suggest
    that the cardiac impairment in long-term AAS users may be
    more severe than previously reported. Specifically, long-term
    AAS users were found to have significant LV systolic dysfunction
    both by relative standards (compared to the AAS nonuser
    cohort) and by absolute standards (as defined by current clinical
    practice). To our knowledge, this study is the first to demonstrate
    an association between long-term AAS use and a clinically
    relevant reduction in LV ejection fraction.


    There is a well-established relationship between LV dysfunction
    and exposure both to certain medications29 and to
    some drugs of abuse.30–32 Further, the prognostic importance
    of toxin-induced cardiac dysfunction has been well documented.
    33–36 Data from this study suggest that AAS, particularly
    when used over long durations, may be another
    important cause of toxin-mediated myocardial impairment.
    Although confirmatory data are required, results from this
    study suggest that AAS exposure should be a diagnostic
    consideration among persons with asymptomatic LV dysfunction
    or incident heart failure.

    Although several previous studies have reported mild cardiac
    dysfunction, LV dysfunction among our AAS users was more severe than previously reported. Several hypotheses might explain
    this discrepancy. First, our AAS users were several years
    older, on average, than those in 2 of the 3 most recent
    studies.10,12 Second, these previous studies selected top-level
    competitive bodybuilders,10 squad athletes,12 or individuals from
    bodybuilding studios,12 thus possibly favoring healthier individuals
    with better cardiac function than the largely noncompetitive
    individuals21 in our study.

    Finally, the specific AAS compounds
    and dosages typically used by our American participants may
    have differed from those of participants in previous studies,
    which were largely conducted in Europe.
    It is noteworthy that our analysis revealed no significant
    relationship between cumulative AAS use and cardiac dysfunction.
    This observation suggests that AAS-associated
    cardiotoxicity might be only partially and unpredictably
    related to lifetime dose in a manner similar to the cardiac
    toxicity of alcohol.37 Further work is required to determine
    whether cardiac function is influenced by factors such as the
    recency of AAS use (eg, current versus long past), specific
    AAS used (eg, possibly more toxic oral agents5,38 versus
    injectable agents), duration of exposure to very high doses
    (eg, 2000 mg/wk), or concomitant use of other drugs (eg,
    human growth hormone39,40).

    There are several important limitations to this study. First,
    our sample might not be representative of the overall source
    population of long-term AAS users or comparison weightlifters.
    Although we used recruitment procedures designed to
    generate a sample that is maximally representative,20,21 it is
    possible that the group of AAS users in the present study is
    not entirely representative of the overall population. Second,
    our sample sizes were small and unequal. However, this
    limitation would likely produce false-negative findings (ie,
    type II errors) rather than false-positive results due to the
    reduced statistical power afforded by small sample sizes.
    Therefore, the highly statistically significant findings in the
    present study, despite the small sample size, suggest that the
    association between AAS use and cardiac pathology may be
    particularly strong (ie, a very large effect size). Conversely,
    the possibility of a type II error must be considered in
    instances where group comparisons were not significant. For
    example, the lack of association between AAS exposure and
    cardiac dysfunction must be interpreted with caution. Future
    study with adequate statistical power is warranted to examine
    this issue. A third limitation is our reliance on participants’
    self-reporting of AAS use. We recognize that errors based on
    self-report could have arisen if actual AAS users denied use
    and were misclassified as nonusers; individuals classified as
    nonusers had unknowingly ingested supplements contaminated contaminated
    with actual AAS; or individuals classified as users had
    ingested only counterfeit black market AAS and, hence, had
    not used genuine drugs.

    However, each form of misclassification
    would only narrow the differences between groups,
    causing us to underestimate the true association of AAS use
    with cardiac pathology. A fourth limitation is our use of
    retrospective exercise exposure assessment and the possibility
    that AAS-users differed from nonusers with respect to
    exercise intensity. However, it is unlikely that this factor
    contributed to our observations because no prior studies have
    demonstrated LV dysfunction secondary to intense, sustained
    exercise training. Finally, the cross-sectional nature of this
    exploratory study does not permit definitive conclusions
    about the long-term clinical implications of our findings and
    represents an important area of future work.


    In summary, data from the present study suggest that
    AAS-induced LV dysfunction may be greater than previously
    reported. The reductions in LV systolic function observed in
    this group of AAS users are of a magnitude shown to increase
    the risk of heart failure and sudden cardiac death in other
    populations.41,42 Further work is needed to confirm our
    findings and to determine the extent to which AAS-associated
    cardiac dysfunction leads to adverse clinical outcomes.



    Ouch!
    Just highlighted so important points that i thought were interesting...

    I will comment on those tomorrow mate as im being called to bed
    Do not ask me for a source check.






  36. #36
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    Quote Originally Posted by 007 View Post
    Just highlighted so important points that i thought were interesting...

    I will comment on those tomorrow mate as im being called to bed
    I agree, there are limitations.

    F*ck I wish I was called to bed nowadays!!!!

  37. #37
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    I think this is good and you should continue to post these type of studies up for people to read.

    Good reality check for some.

  38. #38
    dec11's Avatar
    dec11 is offline 'everything louder than everything else'
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    oh dear, ah well gota kick the bucket sometime i spose lol

    wondering how safe trt is?

  39. #39
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    stevey_6t9 is offline RIP Aziz "Zyzz" Sergeyevich Shavershian - Veni Vidi Vici
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    AAS users reported taking median (quartile 1,
    quartile 3) weekly doses of 675 (513, 950) mg of testosterone
    equivalent for 468 (169, 520) lifetime weeks.


    486 weeks on 675mg of test.... well there you go....why arent i suprised?

    Second, these previous studies selected top-level
    competitive bodybuilders,10 squad athletes,12 or individuals from
    bodybuilding studios,12 thus possibly favoring healthier individuals
    with better cardiac function than the largely noncompetitive
    individuals21 in our study.


    Top level bodybuilders.... well there you go again. Ofcourse there going to have cardiac impairements at that top level. Who knows there past AAS use history. They could have been all dosed up on 1000mg of tren at the time, id wouldnt b e surprised their cardiac function is below par.

    good article though but it doesnt differentiate between use and abuse.

  40. #40
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    Quote Originally Posted by Reed;5297***
    I think this is good and you should continue to post these type of studies up for people to read.

    Good reality check for some.
    I will.

    I think the opoid or alcohol dependance is important though (50%).
    Last edited by Swifto; 08-09-2010 at 05:10 AM.

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