AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

Dos Santos MR, Dias RG, Laterza MC, et al. Impaired Post Exercise Heart Rate Recovery in Anabolic Steroid Users. Int J Sports Med. https://www.thieme-connect.de/ejournals/abstract/10.1055/s-0032-1331741

Previous study showed that muscle sympathetic nerve activity (MSNA) was augmented in anabolic steroids users (AASU). In the present study, we tested the hypothesis that the heart rate (HR) responses after maximal exercise testing would be reduced in AASU. 10 male AASU and 10 AAS nonusers (AASNU) were studied. Cardiopulmonary exercise was performed to assess the functional capacity and heart rate recovery. MSNA was recorded directly from the peroneal nerve by microneurography technique. Peak oxygen consumption (VO2) was lower in AASU compared to AASNU (43.66+/-2.24 vs. 52.70+/-1.68 ml/kg/min, P=0.005). HR recovery (HRR) at first and second minute was lower in AASU than AASNU (21+/-2 vs. 27+/-2 bpm, P=0.02 and 37+/-4 vs. 45+/-2 bpm, P=0.05, respectively). MSNA was higher in AASU than AASNU (29+/-3 vs. 20+/-1 bursts/min, P=0.01). Further analysis showed a correlation between HRR and MSNA (r=- 0.64, P=0.02), HRR at first minute and peak VO2 (r=0.70, P=0.01) and HRR at second minute and peak VO2 (r=0.62, P=0.02). The exacerbated sympathetic outflow associated with a lower parasympathetic activation after maximal exercise, which impairs heart rate recovery, strengthens the idea of autonomic imbalance in AASU.

 

[Michael Scally MD]

Highlights
• Testosterone improves hypetrophy and myonuclear accretion in cells (PD) with atrophic phenotypes.
• PD myotubes hypertrophied to same extent as control myotubes with T.
• This suggests a similar intrinsic ability to respond to exogenous T administration.
• The action of T appeared to be mediated by PI3 K/Akt pathway.


Deane CS, Hughes DC, Sculthorpe N, Lewis MP, Stewart CE, Sharples AP. Impaired hypertrophy in myoblasts is improved with testosterone administration. J Steroid Biochem Mol Biol. ScienceDirect.com - The Journal of Steroid Biochemistry and Molecular Biology - Impaired hypertrophy in myoblasts is improved with testosterone administration

We investigated the ability of testosterone (T) to restore differentiation in multiple population doubled (PD) murine myoblasts, previously shown to have a reduced differentiation in monolayer and bioengineered skeletal muscle cultures vs. their parental controls (CON) (Sharples et al., 2011, Sharples et al., 2012). Cells were exposed to low serum conditions in the presence or absence of T (100nM)+/-PI3K inhibitor (LY294002) for 72hrs and 7 days (early and late muscle differentiation respectively).

Morphological analyses were performed to determine myotube number, diameter (mum) and myonuclear accretion as indices of differentiation and myotube hypertrophy. Changes in gene expression for myogenin, mTORC1 and myostatin were also performed.

Myotube diameter in CON and PD cells increased from 17.32+/-2.56mum to 21.02+/-1.89mum and 14.58+/-2.66mum to 18.29+/-3.08mum (P </= 0.05) respectively after 72hrs of T exposure. The increase was comparable in both PD (+25%) and CON cells (+21%) suggesting a similar intrinsic ability to respond to exogenous T administration. T treatment also significantly increased myonuclear accretion (% of myotubes expressing 5+ Nuclei) in both cell types after 7 days exposure (P </= 0.05).

Addition of PI3K inhibitor (LY294002) in the presence of T attenuated these effects in myotube morphology (in both cell types) suggesting a role for the PI3K pathway in T stimulated hypertrophy. Finally, PD myoblasts showed reduced responsiveness to T stimulated mRNA expression of mTORC1 vs. CON cells and T also reduced myostatin expression in PD myoblasts only.

The present study demonstrates testosterone administration improves hypertrophy in myoblasts that basally display impaired differentiation and hypertrophic capacity vs. their parental controls, the action of testosterone in this model was mediated by PI3K/Akt pathway.

 

[solo47]

After many years of bodybuilding and then growing old, with AAS & GH use, my cholesterol is still great. I do, however, have HBP & BPH, and most BB who use or used gear get the same problems. I had cancer, but I believe that to be unrelated to AAS, though probably exacerbated by GH. I'm fine now, and running "sensible" cycling levels (but no Tren, no Deca, and no EQ, just 500 mg/wk of Test e + 450 mg/wk of Mast p). BP & prostate medication keeps things under control. In a while I'll go back 100 mg/wk of Test cypionate, basic HRT. I feel good even on that amount, though 200 mg/wk is better yet.

What these studies posted by Doc Scally seem to reveal is something most of us have known for quite some time — regular cycling – on and then off expecting return to normal HPTA over a long period of time is not very likely. Oh, there may be a rare few who do one 10 week cycle per year and then stay off and keep returning to normal, but in most cases it takes longer and longer to reattain a natural HPTA, until one comes to the realization that it's just not going to happen any more.

Part of this is probably psychological: one just does not feel as alive, as invigorated waiting to return to normal and, when one does reach "normal", it does not feel as invigorated as being on cycle. In short, running AAS over a number of years is pretty well a guarantee that you will require HRT at some point.

This is not so bad in itself if you find a good physician who helps you monitor all aspects of your health. The real problem is that many AAS users who find they are not returning to normal do not seek medical help. Instead they just go permanently on-cycle. This pretty well guarantees heart problems and other organ problems (liver, kidney, prostate) at some point. This permanent "cycle" situation is much more common than most people will admit and this is the meaning of "steroid abuse".

The body needs a regular, long break from steroids to function like a body should. However, even with breaks, you may still have other problems as you age, but they can be dealt with. You should be able, in fact, to keep your health and age as well as (or better than) most other people. The biggest problem is long-term use at high levels w/o medical supervision.

Respects,
Solo

 

[OhNoYo]

Re: AAS Use & Left Ventricular Dysfunction

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.

I haven't had time to read this thread, but I've been saying this from Day 1, that potentially impaired diastolic dysfunction from long-term AAS may possibly lead to HF in ppl who take this issue lightly. That's why I feel long-term AAS users should get periodic echocardiograms to check BOTH systolic & diastolic function. If long-term AAS users just get periodic bloodwork & BP checked and everything is A-Okay, they could slowly be killing themselves by developing HF and not even know it. The bad thing about HF also is that once you have it, prognosis is poor, and the only real "cure" is LVAD & heart transplantation. Who wants to live with a LVAD & have poor-quality of life? In terms of hearts waiting to be transplanted, they are like kidneys, not nearly enough for the demand of ppl who need them.

What I don't understand, MB, is why don't ppl do cardio to try to prevent (or at least daily) developing HF when they take long-term AAS?

 

[Dr JIM]

There are many causes for HF and the prognosis correlates with the underlying etiology an the associated Left Ventricular Ejection Fraction..

With the causations varying from HTN "cardiomyopathy" to IHD, obviously the treatments and prognosis vary considerably.

Nonetheless the outcome still correlates quite nicely with the time honored NYA functional classification of CHF.

Importantly this classification is "functionally" derived based on those ADL which reproduce the patients symptoms from walking two blocks to sleeping on "two pillows" out necessity.

The only difference for athletes is a matter of degree. Since essentially all BB (yes I'm aware those with CVAs or DM may not) with early CHF experience exertional symptoms; such as SOB, chest soreness, weakness, unusual fatigue etc, the development of these or other "unusual" EXERCISE RELATED symptoms mandates prompt medical evaluation.


Jim

 

[OhNoYo]

There are many causes for HF and the prognosis correlates with the underlying etiology an the associated Left Ventricular Ejection Fraction..

With the causations varying from HTN "cardiomyopathy" to IHD, obviously the treatments and prognosis vary considerably.

Nonetheless the outcome still correlates quite nicely with the time honored NYA functional classification of CHF.

Importantly this classification is "functionally" derived based on those ADL which reproduce the patients symptoms from walking two blocks to sleeping on "two pillows" out necessity.

The only difference for athletes is a matter of degree. Since essentially all BB (yes I'm aware those with CVAs or DM may not) with early CHF experience exertional symptoms; such as SOB, chest soreness, weakness, unusual fatigue etc, the development of these or other "unusual" EXERCISE RELATED symptoms mandates prompt medical evaluation.


Jim

LVEF used to be thought of as a good prognostic indicator for HF patients, but this is now being questioned, specifically in ppl who have DHF, HFNEF, heart failure with preserved ejection fraction, moderate/severe diastolic dysfunction... hell, whatever ppl wanna call it:

MMS: Error
MMS: Error

Here is a nice read for ppl who want to know a wealth of information about HF from a very reputable source: Heart Failure

 

[Dr JIM]

Since the final common pathway in EVERYONE who dies is a reduction of LVEF and NO known therapy reduces the mortality of HFNEF the point is?

Moreover because the overwhelming majority of HFNEF patients are older than age 65, have AF, DM, or prolonged HTN, this study is not reflective of those patients whom MAY be at increased risk, BB using AAS, because for them signs and symptoms of a reduced LVEF will predominate their clinical presentation.

Jim

 

[OhNoYo]

Since the final common pathway in EVERYONE who dies is a reduction of LVEF and NO known therapy reduces the mortality of HFNEF the point is?

Moreover because the overwhelming majority of HFNEF patients are older than age 65, have AF, DM, or prolonged HTN, this study is not reflective of those patients whom MAY be at increased risk, BB using AAS, because for them signs and symptoms of a reduced LVEF will predominate their clinical presentation.

Jim

jim, now c'mon & think about this response, as it can also be said that cardiac arrest & asystole is the COD of everyone as well, but when say a female dies of endometrial cancer, the physician, coroner, medical examiner, whatever you want to say here, doesn't state the COD to be either of those things, as the cancer resulted in LVEF to cease to zero along with cardiac arrest & asystole.

I encourage you to "re-read" the NEJM articles I posted so you may learn. I mean, MB, plz correct me if I'm wrong here, but the two primary reasons for MESO is to learn & inform. For some strange reason regarding my posts, you unfortunately have done neither, jim. You failed to do it in this thread when I was correct (https://thinksteroids.com/community/threads/134330540) and you have failed to do it here, so you are instead mis-informing in addition to not learning.

It appears you have a reasonable knowledge base, but you please need to stop getting offended when individuals have different opingions, suggestions, answers, ect. to your posts, especially when the person is correct like I was w/ tren cough & am here in this post. If AAS increase collagen synthesis in the myocardium like scientists & researchers speculate, you can guarantee that will make the left ventricle stiffer and less flexible to expand with blood, possibly resulting in diastolic dysfunction, which may potentially lead to HF.

In the tren cough thread, I asked for you to please keep an open mind, and I strongly suggest you attempt to do that from now on, because if you do not, it will be difficult for you to adapt & increase your current knowledge, Sir,

 

[Dr JIM]

If you took the first sentence as a point of contention your wrong.

The point is HF presents with similar signs and symptoms regardless of "EF" Moreover treatments to improve DHF have proved abysmal.

Lastly because those mates who use AAS are much younger with minimal to no RF for DHF,your screening the wrong patient population for that condition.

Ergo in BB, lifters and athletes in general their EF, or stroke volume to be even nor precise, determines signs, symptoms and prognosis.

Consequently your suggestion AAS users be screened vian expensive test, such as 3-D or bimode echo, is unfounded when clinical features, in addition perhaps to a BNP, are more than adequate, especially in patients with equivocal signs/symptoms.
Jim

 

[Dr JIM]

Your proved me wrong in the Tren cough post, really show me how and where, lol!

There is no evidence AAS SELECTIVELY increase collagen synthesis, NONE!

The administration of AAS do increase collagen synthesis under two conditions 1) when endogenous TT levels are low, duh 2) when a collagen substrate such as vitamin C or certain Amino Acids, are diminished, double duh!

The reason for DHF is NOT speculation as you suggest, but is due to pathologic LVH.

LVH compromises STROKE VOLUME while maintaining EF by two mechanisms 1) it decreases left ventricular ELASTICITY 2) it decreases left ventricular VOLUME

So YO YO tell me, enlightened one, since their SV is decreased and elasticity increased, by what MECHANISM are these patients able to maintain their EF.
(How are these patients "best" treated and why does that become problematic therapeutically?)

Was the mechanism not a part of that SINGLE NEJM article you read and hurriedly concluded long term AAS users should have annual screening echocardiograms.

(FYI I subscribe to NEJM and that article was reviewed in journal club in Sept 1999, according to the EM/TRAUMA resident journal club ledger)

Perhaps you believe your research and/or reading is so extensive that a justifiably NEW indication should be added to the existing echocardiogram protocols set forth by the AHA and ACA. (FYI the protocols are to be updated at the end of 2014, so submit that letter or evidence ASAP)

Please, learning is more than a suggestion based on supposition, speculation thereafter morphed into fiction or fantasy for the sake of interpersonal recognition or self esteem, it's based on experience and extensive applied reading, neither of which your adept at, especially in the field of medicine, what a joke.

I do wonder why I waste my time!

 

[OhNoYo]

If you took the first sentence as a point of contention your wrong.

The point is HF presents with similar signs and symptoms regardless of "EF" Moreover treatments to improve DHF have proved abysmal.

Lastly because those mates who use AAS are much younger with minimal to no RF for DHF,your screening the wrong patient population for that condition.

Ergo in BB, lifters and athletes in general their EF, or stroke volume to be even nor precise, determines signs, symptoms and prognosis.

Consequently your suggestion AAS users be screened vian expensive test, such as 3-D or bimode echo, is unfounded when clinical features, in addition perhaps to a BNP, are more than adequate, especially in patients with equivocal signs/symptoms.
Jim

True to a point, but left vs right sided HF will actually produce some different signs/symptoms.

If a BB'er who takes megadoses of AAS year round would get periodic echos, I feel it can only benefit them. I mean, sum ppl just constantly take +1g of AAS consistently on an annual basis, and do they really need to take the much AAS? If periodic echos showed that sum1s E/A ratio reversed, to say < 0.8, when before it was > 1.5 with no restrictive filling of course, then that would be a red flag to be where, maybe I shouldn't be megadosing & taking this amount of AAS for so long. I feel a BNP test can actually supplement an echo test, but like I said, periodic echos, based on personal requests & what the cardiologist deems fit, surely cannot hurt.

 

[OhNoYo]

Your proved me wrong in the Tren cough post, really show me how and where, lol!

There is no evidence AAS SELECTIVELY increase collagen synthesis, NONE!

The administration of AAS do increase collagen synthesis under two conditions 1) when endogenous TT levels are low, duh 2) when a collagen substrate such as vitamin C or certain Amino Acids, are diminished, double duh!

The reason for DHF is NOT speculation as you suggest, but is due to pathologic LVH.

LVH compromises STROKE VOLUME while maintaining EF by two mechanisms 1) it decreases left ventricular ELASTICITY 2) it decreases left ventricular VOLUME

So YO YO tell me, enlightened one, since their SV is decreased and elasticity increased, by what MECHANISM are these patients able to maintain their EF.
(How are these patients "best" treated and why does that become problematic therapeutically?)

Was the mechanism not a part of that SINGLE NEJM article you read and hurriedly concluded long term AAS users should have annual screening echocardiograms.

(FYI I subscribe to NEJM and that article was reviewed in journal club in Sept 1999, according to the EM/TRAUMA resident journal club ledger)

Perhaps you believe your research and/or reading is so extensive that a justifiably NEW indication should be added to the existing echocardiogram protocols set forth by the AHA and ACA. (FYI the protocols are to be updated at the end of 2014, so submit that letter or evidence ASAP)

Please, learning is more than a suggestion based on supposition, speculation thereafter morphed into fiction or fantasy for the sake of interpersonal recognition or self esteem, it's based on experience and extensive applied reading, neither of which your adept at, especially in the field of medicine, what a joke.

I do wonder why I waste my time!

Go back to the Tren Cough thread to read the nice post by MR10X, that sound much more reasonable than your opinions on what causes cough in trenbolone. I'm sure most others on this forum would agree with me on this, too.

AAS have also been shown to increase collagen synthesis w/o the two condition present that you propose. Just do a simple pubmed or google scholar search regarding this, you will find plenty, trust me.

What you state about pathological LVH is pretty spot-on, but not universal, as LVH is only a RF for HF, as there is no causality associated with pathological LVH & HF. Also, there r ppl who developed HF w/o having LVH, yes it doesn't occur often, but it does happen. Also, if you are going to discuss this matter about what you stated about pathological LVH, compensated vs decompensated HF needs to be addressed. In terms of how should patients be best treated, global recommendations, etc., I'm not a physician (or a cardiologist for that matter), so have no business attempting to answer this, so have no comment on this. If BB'ers are worried about their hearts, then like I said before, requested periodic echos cannot hurt.

What all this comes down to regarding this thread, is that you stated prognosis of HF ultimately depends on LVEF, I simply corrected you & showed evidence that this is now being questioned. Instead of just admitting your error, you now bring up things that make you sound like you were correct by using clinical terms & big words w/ the attempt to try & get ppl on this forum 2 assume you were correct & weasel your way out of it. I do know what you're talking about & trying to do though, so its not fooling me. I mean, is what ppl think on an anonymous forum that important to you? You claim to be a physician, so shouldn't the truth override this personal gratification? For a physician, you certainly have alota free time on your hands to practically live on MESO. As for me, unfortunately I just don't have as much time as I used to, to logon to MESO, and I don't want to spend this time correcting you.

So please, just answer this w/ a simple yes or no answer on the latter of this ?, (b/c the former is pretty spot-on but the latter is incorrect) so we may both move on & contribute to the forum: Does HF prognosis correlate w/ the underlying etiology an the associated LVEF?

Just a simple yes or no will suffice, and as sum1 who claims to be a physician, I hope you tell the truth this time.

 

[Michael Scally MD]

Hajimoradi B, Kazerani H. Echocardiographic findings in power athletes abusing anabolic androgenic steroids. Asian J Sports Med 2013;4(1):10-4. http://asjsm.tums.ac.ir/files/journals/1/articles/233/public/233-933-5-PB.pdf

PURPOSE: Anabolic androgenic steroids (AAS) abuse for improving physical appearance and performance in body builders is common and has been considered responsible for serious cardiovascular effects. Due to disagreement about cardiovascular side effects of these drugs in published articles, this case control study was designed to evaluate the echocardiographic findings in body builder athletes who are current and chronic abusers of these drugs.

METHODS: Body builder athletes with continuous practice for the preceding two years and were training at least twice weekly were selected and divided into AAS abuser and non user and compared with age and BMI matched non athletic healthy volunteers (15 cases in each group).

RESULTS: There was no significant difference in left ventricular size or function either systolic or diastolic in comparison to cases and control groups. The only difference was in diastolic size of septum and free wall but observed differences were only significant (P = 0.05) between first (athletic with AAS abuser) and third group (non athletic and nonuser). The difference between the above-mentioned indexes were not significant between two groups of athletes.

CONCLUSION: Observed differences in diastolic size of septum and free wall is in favor of that long term abuse of anabolic steroid results in accentuation of physiologic hypertrophy due to long term sport most probably due to higher rate pressure product. Furthermore long term abuse and supra pharmacologic doses do not have significant effect in size and left ventricular function.

 

[Michael Scally MD]

He J, Bhasin S, Binder EF, et al. Cardiometabolic risks during anabolic hormone supplementation in older men. Obesity (Silver Spring) 2013;21(5):968-75. Cardiometabolic risks during anabolic hormone supplementation in older men - He - 2013 - Obesity - Wiley Online Library

OBJECTIVE: To determine the cardiometabolic risks of testosterone and growth hormone (GH) replacement therapy to youthful levels during aging.

DESIGN AND METHODS: A double-masked, partially placebo controlled study in 112 men 65-90 years-old was conducted. Transdermal testosterone (5 g vs. 10 g/day) using a Leydig Cell Clamp and subcutaneous recombinant GH (rhGH) (0 vs. 3 vs. 5 mug/kg/day) were administered for 16-weeks. Measurements included testosterone and IGF-1 levels, body composition by DEXA, and cardiometabolic risk factors (upper body fat, blood pressure, insulin sensitivity, fasting triglycerides, HDL-cholesterol, and serum adiponectin) at baseline and after 16 weeks of treatment.

RESULTS: Some cardiometabolic factors improved (total and trunk fat, triglycerides, HDL-cholesterol) and others worsened (systolic blood pressure, insulin sensitivity index [QUICKI], adiponectin). Cardiometabolic risk composite scores (CRCSs) improved (-0.69 +/- 1.55, P < 0.001). In multivariate analyses, QUICKI, triglycerides, and HDL-cholesterol contributed 33%, 16%, and 14% of the variance in CRCS, respectively. Pathway analyses indicated that changes in fat and lean mass were related to individual cardiometabolic variables and CRCS in a complex manner. Changes in BMI, reflecting composite effects of changes in fat and lean mass, were more robustly associated with cardiometabolic risks than changes in fat mass or LBM individually.

CONCLUSIONS: Testosterone and rhGH administration was associated with diverse changes in individual cardiometabolic risk factors, but in aggregate appeared not to worsen cardiometabolic risk in healthy older men after 4-months. The long-term effects of these and similar anabolic therapies on cardiovascular events should be investigated in populations with greater functional limitations along with important health disabilities including upper body obesity and other cardiometabolic risks.

 

[Dr JIM]

Dr S I've been noticing a few more articles on AAS and CV function over the past few years, yet I'm not aware of ANY which have made the correlation to SYMPTOMATIC reductions of LV function EXCLUSIVE of other risk factors.

Have you uncovered any evidence to that effect?

Thx
Jim

 

[Michael Scally MD]

Dr S I've been noticing a few more articles on AAS and CV function over the past few years, yet I'm not aware of ANY which have made the correlation to SYMPTOMATIC reductions of LV function EXCLUSIVE of other risk factors.

Have you uncovered any evidence to that effect?

Thx
Jim

My overall and general sense of the literature is an adverse effect for AAS other than testosterone. This is countered by testosterone's positive effect, although even this is confusing.

 

[Michael Scally MD]

Aparicio VA, Sanchez C, Ortega FB, et al. Effects of the Dietary Amount and Source of Protein, Resistance Training and Anabolic-Androgenic Steroids on Body Weight and Lipid Profile of Rats. Nutr Hosp 2013;28(1):127-36. http://www.nutricionhospitalaria.com/pdf/6055.pdf

Introduction: Dietary protein amount and source, hypertrophy resistance training (RT) and anabolic androgenic steroids (AAS) may affect body weight and plasma and hepatic lipid profile.

Material and Methods: 157 adult male Wistar rats were randomly distributed in 16 experimental groups resulting in: normal-protein (NP) or high-protein (HP) diets, whey or soy-protein diets, with or without RT and with or without AAS, for 3 months.

Results and Discussion: Final body weight was lower in the RT and AAS groups compared to sedentary and non- AAS groups, respectively (all, p<0.001). Plasma total cholesterol (TC) was lower for the HP compared to the NP diets, for the whey compared to the soy-protein diets and for the AAS compared to the non-AAS groups (all, p<0.001). Plasma HDL-cholesterol was higher in the RT groups (p<0.05) but lower for the AAS groups (p<0.001), the HP and the soy-protein diets (p<0.05). Plasma triglycerides (TAG) were lower for the HP diet (p<0.001), for the RT (p=0.002) and the non-AAS groups (p=0.001). Liver TC was lower for the NP (p<0.01), for the soyprotein (p<0.05) and for the AAS groups (p<0.001). Liver TAG were lower for the whey-protein diet (p<0.001), RT and non-AAS groups (both, p<0.05). Some interactions were found, such as the greater effect of AAS on reducing body weight of rats that performed RT or ingested a HP diet (all, p<0.05). HDL-cholesterol was higher when RT was combined with HP diets (p=0.010) or non-AAS and when HP diets were combined with non-AAS (both,p<0.001). Groups that combined RT with non-AAS administration obtained the lowest hepatic TAG (p<0.05).

Conclusion: Among all the interventions tested, AAS was the factor that most negatively affected plasma and hepatic lipid profile, whereas HP diets and RT could benefit lipid profile, especially when combined.

 

[Michael Scally MD]

IMO, this deserves some serious thought when considering long-term AAS use. This is way too young to die. One of the factors I hoped to impart when being aware of the HPTA is the broader aspect of overall health. Be careful out there. I know of very very few doctors that know diddly about AAS and even less that care.

Former IFBB Pro, Ed Van Amsterdam Dead.

Former Dutch IFBB Pro Bodybuilder, Ed Van Amsterdam reportedly died of a Heart Attack! He was 40 years old. Breaking News- Former IFBB Pro, Ed Van Amsterdam Dead.

thinksteroids.com

 

[CensoredBoardsSuck]

IMO, this deserves some serious thought when considering long-term AAS use. This is way too young to die. One of the factors I hoped to impart when being aware of the HPTA is the broader aspect of overall health. Be careful out there. I know of very very few doctors that know diddly about AAS and even less that care. https://thinksteroids.com/community/threads/134340536

I agree wholeheartedly. Reports of bodybuilders dying suddenly at a young age are becoming too frequent to ignore any longer. We reassure ourselves by ignoring the mounting anecdotal evidence because the "real" evidence is inconclusive but we do so at our own peril.

Anybody that was around bodybuilding in the early 90's when mega dosing became common and cycle durations lengthened from a few weeks to months or longer, quietly wondered what the long term implications on health might be. It's my fear that we are now finding out.

Studies on the long term effects of AAS on cardiovascular function are desperately needed. Until those studies are done, I think we should start paying more attention to the anecdotal reports. Anybody planning to use - or continue to use - AAS should seriously consider the potential risks. For hobbyists in particular, a higher priority should be placed on health and proper medical supervision is mandatory. Cycle durations should be kept short and infrequent with doses as low as possible. IMO, it's time to go back to the more "sane" cycles of the 70's. I.e., 6-8 week, low-dose cycles that were only used a couple times a year.

MHOO.
CBS

 

[Nemesis RR]

IMO, this deserves some serious thought when considering long-term AAS use. This is way too young to die. One of the factors I hoped to impart when being aware of the HPTA is the broader aspect of overall health. Be careful out there. I know of very very few doctors that know diddly about AAS and even less that care. https://thinksteroids.com/community/threads/134340536

Doc do you think the levels used is the more important consideration? I understand long term AAS "abuse", as with any drug, will lead to a detrimental effect. Then I think of Frank Zane. Lets say he only cycled since his first Olympia in 1977. That is 35 years of use. Yet at 71 he looks great and got into insane shape at 64.