AAS and Cardiovascular/Pulmonary Function

[Dr JIM]

NRR
That was the reasoning for the question I posed to Dr S.

I mean heck considering all of the past and present BB whom have used AAS the incidence of SYMPTOMATIC LV dysfunction has to be quite LOW.

Since we all know if this association (the recreational use of AAS are associated with an increased incidence of symptomatic Left Ventricular Dysfunction), was based on solid evidence the media and medical establishment would have plastered this "factoid" throughout the lay press!)

Consequently based on my personal experience and those of my patients (where other RF are excluded) I believe the jury is "deadlocked" and the verdict pending until more conclusive studies are performed.

Jim

 

[Michael Scally MD]

Highlights
• Supraphysiological DECA treatment on heart redox metabolism was investigated during I/R in sedentary and exercised rats.
• DECA reduced SOD and GR activities in exercised rats upon reperfusion.
• Reduced antioxidant enzyme activities promote heart thiol oxidation in exercised rats.
• Anabolic androgenic steroid abuse cardiotoxicity involves redox imbalance in exercised animals.

Chaves EA, Fortunato RS, Carvalho DP, Nascimento JH, Oliveira MF. Exercise-induced cardioprotection is impaired by anabolic steroid treatment through a redox-dependent mechanism. J Steroid Biochem Mol Biol. Exercise-induced cardioprotection is impaired by anabolic steroid treatment through a redox-dependent mechanism

High doses of anabolic androgenic steroids (AAS) impair the cardioprotective effects of exercise against ischemia/reperfusion (I/R) insult, possibly through cellular redox imbalance. Here, the effect of nandrolone decanoate (DECA) treatment on heart redox metabolism was investigated during I/R in sedentary and exercised rats. DECA treatment significantly reduced superoxide dismutase and glutathione reductase activities in exercised rats after heart reperfusion. Catalase and glutathione peroxidase activities were not affected by DECA in both sedentary and trained rats, regardless the I/R period. DECA also induced myocardial oxidative stress, as evidenced by the reduced levels of total reduced thiols after heart reperfusion in exercised rats treated with the anabolic steroid. These results indicate that cardiotoxic effects of supraphysiological doses of AAS involve reduced heart antioxidant capacity.

 

[Nemesis RR]

Highlights
• Supraphysiological DECA treatment on heart redox metabolism was investigated during I/R in sedentary and exercised rats.
• DECA reduced SOD and GR activities in exercised rats upon reperfusion.
• Reduced antioxidant enzyme activities promote heart thiol oxidation in exercised rats.
• Anabolic androgenic steroid abuse cardiotoxicity involves redox imbalance in exercised animals.

Chaves EA, Fortunato RS, Carvalho DP, Nascimento JH, Oliveira MF. Exercise-induced cardioprotection is impaired by anabolic steroid treatment through a redox-dependent mechanism. J Steroid Biochem Mol Biol. Exercise-induced cardioprotection is impaired by anabolic steroid treatment through a redox-dependent mechanism

High doses of anabolic androgenic steroids (AAS) impair the cardioprotective effects of exercise against ischemia/reperfusion (I/R) insult, possibly through cellular redox imbalance. Here, the effect of nandrolone decanoate (DECA) treatment on heart redox metabolism was investigated during I/R in sedentary and exercised rats. DECA treatment significantly reduced superoxide dismutase and glutathione reductase activities in exercised rats after heart reperfusion. Catalase and glutathione peroxidase activities were not affected by DECA in both sedentary and trained rats, regardless the I/R period. DECA also induced myocardial oxidative stress, as evidenced by the reduced levels of total reduced thiols after heart reperfusion in exercised rats treated with the anabolic steroid. These results indicate that cardiotoxic effects of supraphysiological doses of AAS involve reduced heart antioxidant capacity.

Using the doses listed in this study would translate to 850 mg per week of DECA for a 185lb man. This is abuse in my opinion so of course the heart may be effected. What we need is more studies at lower levels.

 

[Michael Scally MD]

Testosterone and the Cardiovascular System

An increasing number of elderly men are receiving exogenous testosterone to treat hypogonadism, low libido, and general weakness. The impact of testosterone on the cardiovascular system is controversial.

Elderly men are typically at higher risk for adverse cardiovascular events than age?matched women, and one study suggested that exogenous testosterone was associated with an increase in adverse cardiovascular events in this population.

In contrast, other clinical studies suggest that testosterone is beneficial to the cardiovascular system and that low levels of testosterone negatively affect the cardiovascular system.

Because of the increase in the number of prescriptions and use of testosterone in adult males for the treatment of hypogonadism, low libido, and weakness, an investigation of the effects of testosterone on the cardiovascular system in basic science studies was carried out.

The benefits of testosterone relating to the cardiovascular system are as follows.

• Testosterone has been shown to exhibit potential antiarrhythmic properties in the form of decreasing action potential duration, early after depolarizations, and shortened QTc interval.

• Testosterone has also been shown to reduce myocardial infarct size compared with that in subjects not treated with testosterone by modulating the myocardial KATP channel, enhancing vasodilation, improving lipid metabolism, and improving Diabetes Mellitus (DM).

These conclusions do not come without controversy. Much of the literature suggests that testosterone attenuates atherosclerosis, but some studies suggest otherwise.

Further deleterious effects of testosterone on the cardiovascular system have been shown in studies on vasoconstriction, inflammation, and death signaling.

These findings suggest that testosterone may simultaneously benefit and harm the cardiovascular system by different pathways. The complexity of this relationship is obvious, and thus additional basic science studies are required for a better understanding of the relationship between testosterone and the cardiovascular system.


Herring MJ, Oskui PM, Hale SL, Kloner RA. Testosterone and the Cardiovascular System: A Comprehensive Review of the Basic Science Literature. J Am Heart Assoc 2013;2(4):e000271. Testosterone and the Cardiovascular System: A Comprehensive Review of the Basic Science Literature

 

[techlogik]

I hear drinking a quart of liquor a day will eventually kill you also...is this really surprising based on this information from the study.

Basically cumulative high dose use from 3-10yrs in total?!?! No kidding, this has a negative effect on your body?

" 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. "

Nooooo...reaaaalllyy?!?! This kind of massive amount of steroids will do harm. Duh.

 

[kobefan]

Dr.Salvatore Trazzera MD says that AAS decreases LDL particle size which can makes the LDL particles more prone to oxidation and plaque build up.

He says all his patients using AAS are on ARB or ACE inhibitors.

 

[Michael Scally MD]

Dr.Salvatore Trazzera MD says that AAS decreases LDL particle size which can makes the LDL particles more prone to oxidation and plaque build up.

He says all his patients using AAS are on ARB or ACE inhibitors.

ARB or ACE for LDL???

 

[kobefan]

ARB or ACE for LDL???

no no sorry. He says that all his patients using AAS are on ARB or ACE inhibitors to protect AAS induced hypertension which is bad for the kidneys / heart

The LDL comment was separate, sorry. He says the smaller the LDL particle the more atherogenic they can be. or something like that

 

[kobefan]

Here is patient that I personally know who is insulin resistant. I convinced him to pay the money for the VAP Cholesterol Test. ( $150 ) . Diet = 70% Carb / 30% protein + fat. Patient is taking Zocor ( Simvastatin ) for high LDL. As you can see LDL = < 130 mg / dL but particle size of LDL = small highly atherogenic.

 

[OhNoYo]

Here is patient that I personally know who is insulin resistant. I convinced him to pay the money for the VAP Cholesterol Test. ( $150 ) . Diet = 70% Carb / 30% protein + fat. Patient is taking Zocor ( Simvastatin ) for high LDL. As you can see LDL = < 130 mg / dL but particle size of LDL = small highly atherogenic.

Tell your buddy to cut out some carbs & focus on good fats, particularly foods high in MUFA & Omega-3.

 

[Dr JIM]

Hey Kob why don't you try posting what "he says" rather than misquoting "him"!

 

[Dr JIM]

Oh and why your at it posting "his" credentials would seem relevant at this juncture.

 

[CensoredBoardsSuck]

Oh and why your at it posting "his" credentials would seem relevant at this juncture.

Apparently, he's a board certified cardiologist with an interest in sports and athletes. He's Dave Palumbo's cardiologist. Here's a link to an interview he did on Palumbo's radio show where he discusses AAS and cardiac function. It starts at 02:04:05.

Heavy Muscle Radio (1/14/13) Cardiologist Dr. Sal Trazzera. What You Should Know About Your Heart!

 

[Dr JIM]

Oh a "cardiologist"? Aren't they the doctors that keep Post AMI "stented" patients on Plavix "for life" in spite of NO evidence the benefit exceeds SIX MONTHS
(and even that is questionable) compared to ASA and or Cumadin.

Wasn't a "cardiologist" at MJs bedside before his demise?

The point most know nothing more about the PRACTICE OF MEDICINE than a three vessel angiogram and the newest cardiovascular drug that will take them to Tahiti.

Jim

 

[CensoredBoardsSuck]

The point most know nothing more about the PRACTICE OF MEDICINE than a three vessel angiogram and the newest cardiovascular drug that will take them to Tahiti.

Jim

I've always wanted to go to Tahiti. Bora Bora to be exact. If Bristol-Myers are offering all-expense-paid trips, I'll put "Plavix" in my sig line. Put me down for next January. I'd like a floating villa with a glass floor, please.

 

[Dr JIM]

Visited Bora Bora for "8hrs" on an Australian cruise and although it was indeed georgeous it's become an tourist trap.

I stayed one month in Indonesia on a diving sabbatical and LOVED IT.

I don't believe there is any better diving in the world in part because commercial fishing has been severely restricted.

They allow personal spear fishing by TOURISTs only and ya have to show a passport to prove your GTG.

We stayed on several of the small islands called "lesser Jandu".

My colleagues used a two man diving ROV capable of reaching 1K.

Me, I studied several indigenous and visiting beach species and many were "molting" before my very eyes, lol.

Jimmy

 

[kobefan]

Hey Kob why don't you try posting what "he says" rather than misquoting "him"!

It was kind of hard because Dave Palumbo kept interrupting him.

I thought the interview was interesting.

 

[solo47]

Back to the topic of this thread, AAS & cardiovascular function.

I'm on a great cycle (Test-Mast), but I began it in late May but never really got to the gym until mid-July. Now I'm growing like a youth (old muscle memory I guess) while hurting like an old ox; I am very fatigued and often short of breath — not when I'm doing stairmaster or sets, but between sets I gasp for air so people stare. Last BW showed higher RBC, so I assume that's the culprit. (No sign of returning cancer and high BP is under control.)

Now I can't donate blood because of the brush with cancer I had (though I could mark it "do not use" which is an option once you've been bled), so the only other choice I have is to go off all AAS for a while (and it's about time). But I also want to keep hitting the gym. Taking my young lady to a Mexican beach for Xmas again, so I expect to return to the same cycle probably in October.

Will a month and a half off all AAS allow the RBC to recede somewhat? (I will use no nandrolone, EQ, or Tren after reading Dr Scally's posts in this thread!)

Respects,
Solo

 

[Michael Scally MD]

Back to the topic of this thread, AAS & cardiovascular function.

I'm on a great cycle (Test-Mast), but I began it in late May but never really got to the gym until mid-July. Now I'm growing like a youth (old muscle memory I guess) while hurting like an old ox; I am very fatigued and often short of breath — not when I'm doing stairmaster or sets, but between sets I gasp for air so people stare. Last BW showed higher RBC, so I assume that's the culprit. (No sign of returning cancer and high BP is under control.)

Now I can't donate blood because of the brush with cancer I had (though I could mark it "do not use" which is an option once you've been bled), so the only other choice I have is to go off all AAS for a while (and it's about time). But I also want to keep hitting the gym. Taking my young lady to a Mexican beach for Xmas again, so I expect to return to the same cycle probably in October.

Will a month and a half off all AAS allow the RBC to recede somewhat? (I will use no nandrolone, EQ, or Tren after reading Dr Scally's posts in this thread!)

Respects,
Solo

Minimal to none.

Do you have a CBC?

Once you develop polycythemia, the problem can quickly escalate. When I mean escalate, I mean within weeks or shorter. Herein lies the problem. Red blood cells (RBC) have a half-life of about 120 days. If you were to stop all AAS, it would take a long time for the RBC to decrease where the H/H is normal.

 

[Dr JIM]

Solo have you noticed a correlation between the SOB and it's temporal relationship to your last TT injection?

If so weigh yourself before the Pinning and roughly 36-48 hours later. Any weight gained during that interval is WATER and if significant a diuretic may be helpful