AAS and Cardiovascular/Pulmonary Function

[Michael Scally MD]

[Rats] The Effect of Nandrolone Treatment with and Without Enforced Swimming On Histological and Biochemical Changes in The Heart and Coronary Artery

OBJECTIVE: Chronic anabolic androgenic steroid (AAS) consumption increases incidence of cardiovascular abnormalities in athletes and mechanisms underlying those abnormalities continue to be investigated. This study examines whether nandrolone consumption induced cardiac and coronary artery wall abnormalities via oxidative stress. It was also designed to determine whether enforced swimming augmented possible cardiotoxic effects of nandrolone in rat heart.

METHODS: Twenty-four male Wistar rats were divided into 3 groups: control, nandrolone, and nandrolone with enforced swimming. Nandrolone group received 10 mg/kg body weight nandrolone 3 times a week for 6 weeks. Nandrolone group with enforced swimming received the same amount of nandrolone and was forced to swim with excess weight of 20% body weight.

RESULTS: After 6 weeks of treatment, results indicated proliferation of heart muscle and coronary smooth muscle cells and lipid peroxidation; significant rise in levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), nicotinamide adenine dinucleotide phosphate oxidase, homocysteine (Hcy), apolipoprotein B, low-density lipoprotein, and cholesterol, as well as severe fibrosis in heart tissue and around coronary arteries of nandrolone and nandrolone with enforced swimming groups compared with control group.

CONCLUSION: These findings strongly support idea that nandrolone intake by sedentary rats and exercised rats induced heart abnormality mediated by oxidative stress, which was manifest in increased lipid peroxidation, Hcy, and 8-OHdG in heart tissue.

Tofighi A, Shirpoor M, Ansari MH, Shirpoor A, Zerehpoosh M. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of male rats. Anatol J Cardiol. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of m... - PubMed - NCBI

 

[hurricane]

[Rats] The Effect of Nandrolone Treatment with and Without Enforced Swimming On Histological and Biochemical Changes in The Heart and Coronary Artery

OBJECTIVE: Chronic anabolic androgenic steroid (AAS) consumption increases incidence of cardiovascular abnormalities in athletes and mechanisms underlying those abnormalities continue to be investigated. This study examines whether nandrolone consumption induced cardiac and coronary artery wall abnormalities via oxidative stress. It was also designed to determine whether enforced swimming augmented possible cardiotoxic effects of nandrolone in rat heart.

METHODS: Twenty-four male Wistar rats were divided into 3 groups: control, nandrolone, and nandrolone with enforced swimming. Nandrolone group received 10 mg/kg body weight nandrolone 3 times a week for 6 weeks. Nandrolone group with enforced swimming received the same amount of nandrolone and was forced to swim with excess weight of 20% body weight.

RESULTS: After 6 weeks of treatment, results indicated proliferation of heart muscle and coronary smooth muscle cells and lipid peroxidation; significant rise in levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), nicotinamide adenine dinucleotide phosphate oxidase, homocysteine (Hcy), apolipoprotein B, low-density lipoprotein, and cholesterol, as well as severe fibrosis in heart tissue and around coronary arteries of nandrolone and nandrolone with enforced swimming groups compared with control group. Maybe it was the gear. Who knows??

CONCLUSION: These findings strongly support idea that nandrolone intake by sedentary rats and exercised rats induced heart abnormality mediated by oxidative stress, which was manifest in increased lipid peroxidation, Hcy, and 8-OHdG in heart tissue.

Tofighi A, Shirpoor M, Ansari MH, Shirpoor A, Zerehpoosh M. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of male rats. Anatol J Cardiol. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of m... - PubMed - NCBI

 

[ronin17]

[Rats] The Effect of Nandrolone Treatment with and Without Enforced Swimming On Histological and Biochemical Changes in The Heart and Coronary Artery

OBJECTIVE: Chronic anabolic androgenic steroid (AAS) consumption increases incidence of cardiovascular abnormalities in athletes and mechanisms underlying those abnormalities continue to be investigated. This study examines whether nandrolone consumption induced cardiac and coronary artery wall abnormalities via oxidative stress. It was also designed to determine whether enforced swimming augmented possible cardiotoxic effects of nandrolone in rat heart.

METHODS: Twenty-four male Wistar rats were divided into 3 groups: control, nandrolone, and nandrolone with enforced swimming. Nandrolone group received 10 mg/kg body weight nandrolone 3 times a week for 6 weeks. Nandrolone group with enforced swimming received the same amount of nandrolone and was forced to swim with excess weight of 20% body weight.

RESULTS: After 6 weeks of treatment, results indicated proliferation of heart muscle and coronary smooth muscle cells and lipid peroxidation; significant rise in levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), nicotinamide adenine dinucleotide phosphate oxidase, homocysteine (Hcy), apolipoprotein B, low-density lipoprotein, and cholesterol, as well as severe fibrosis in heart tissue and around coronary arteries of nandrolone and nandrolone with enforced swimming groups compared with control group.

CONCLUSION: These findings strongly support idea that nandrolone intake by sedentary rats and exercised rats induced heart abnormality mediated by oxidative stress, which was manifest in increased lipid peroxidation, Hcy, and 8-OHdG in heart tissue.

Tofighi A, Shirpoor M, Ansari MH, Shirpoor A, Zerehpoosh M. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of male rats. Anatol J Cardiol. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of m... - PubMed - NCBI

Damn it. Thanks for ruining my day. Jk. Thank you for the info.

 

[ronin17]

It's amazing. That is only after six weeks. What makes it so detrimental to the heart ? Is it the increased heart rate?

 

[hurricane]

[Rats] The Effect of Nandrolone Treatment with and Without Enforced Swimming On Histological and Biochemical Changes in The Heart and Coronary Artery

OBJECTIVE: Chronic anabolic androgenic steroid (AAS) consumption increases incidence of cardiovascular abnormalities in athletes and mechanisms underlying those abnormalities continue to be investigated. This study examines whether nandrolone consumption induced cardiac and coronary artery wall abnormalities via oxidative stress. It was also designed to determine whether enforced swimming augmented possible cardiotoxic effects of nandrolone in rat heart.

METHODS: Twenty-four male Wistar rats were divided into 3 groups: control, nandrolone, and nandrolone with enforced swimming. Nandrolone group received 10 mg/kg body weight nandrolone 3 times a week for 6 weeks. Nandrolone group with enforced swimming received the same amount of nandrolone and was forced to swim with excess weight of 20% body weight.

RESULTS: After 6 weeks of treatment, results indicated proliferation of heart muscle and coronary smooth muscle cells and lipid peroxidation; significant rise in levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), nicotinamide adenine dinucleotide phosphate oxidase, homocysteine (Hcy), apolipoprotein B, low-density lipoprotein, and cholesterol, as well as severe fibrosis in heart tissue and around coronary arteries of nandrolone and nandrolone with enforced swimming groups compared with control group.

CONCLUSION: These findings strongly support idea that nandrolone intake by sedentary rats and exercised rats induced heart abnormality mediated by oxidative stress, which was manifest in increased lipid peroxidation, Hcy, and 8-OHdG in heart tissue.

Tofighi A, Shirpoor M, Ansari MH, Shirpoor A, Zerehpoosh M. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of male rats. Anatol J Cardiol. The effect of nandrolone treatment with and without enforced swimming on histological and biochemical changes in the heart and coronary artery of m... - PubMed - NCBI

Like I said, my cardiac specialists couldn't confirm or negate the affects that the AAS use had on determining my heart conditions. There is no doubt in my mind it played some part. And also remember I have dialated cardiomyopathy on top of it. Can only move forward, but hopefully this will be read by others who think twice.

 

[hurricane]

It's amazing. That is only after six weeks. What makes it so detrimental to the heart ? Is it the increased heart rate?

The increased heart rate would keep you in a prolonged state of sinus tachycardia(heart racing), which could cause an enlarged heart because of the extra stress put on it. It could also damage your hearts pumping function, which could lead to cardiomyopathy. If I'm wrong explaining that Doc correct me please.

 

[Michael Scally MD]

Liao PW, Wu CC, Chen KC, et al. Testosterone Threshold for Increased Cardiovascular Risk in Middle-Aged and Elderly Men: A Locally Weighted Regression Analysis. J Sex Med. http://www.jsm.jsexmed.org/article/S1743-6095(16)30459-3/abstract

INTRODUCTION: Although testosterone deficiency has a well-known association with increased risk of cardiovascular disease (CVD), the threshold remains to be determined.

AIM: To investigate whether there is a discriminatory testosterone level below which the CVD risk increases.

METHODS: The study included 876 men 45 to 74 years old who underwent a general health checkup. The Framingham Risk Score was used to estimate the 10-year CVD risk; a high-sensitivity C-reactive protein (hsCRP) level of at least 1 mg/L was considered an indicator of increased CVD risk. Aging symptoms and sexual function were evaluated with the Aging Males' Symptom Scale.

MAIN OUTCOME MEASURES: Locally weighted regression was performed to determine the testosterone threshold for Framingham CVD risk and increased hsCRP.

RESULTS: The mean age was 56.6 +/- 7.0 years. The mean total testosterone level was 394.3 +/- 115.7 ng/dL. The mean 10-year Framingham CVD risk was 16.6 +/- 10.7%, and 169 (19.3%) had increased hsCRP. The locally weighted regression showed that total testosterone levels of 440 and 480 ng/dL were associated with increased Framingham CVD risk and an increased probability of increased hsCRP, respectively.

Men with sexual dysfunction (poor sexual performance, decreased morning erection, and loss of libido) had significantly greater CVD risk. Their risk appeared to increase at a relatively higher testosterone level, and it reached a plateau at a testosterone level of 300 to 350 ng/dL.

In contrast, the risk in those with no or less sexual dysfunction remained low at a higher testosterone level, and a threshold level of 425 to 475 ng/dL was associated with increased CVD risk. A similar pattern and threshold were identified in the analyses of the relation between testosterone and hsCRP.

CONCLUSION: These data showed that a testosterone threshold of 440 ng/dL was associated with increased Framingham 10-year CVD risk in middle-aged and elderly men. Poor sexual performance, decreased morning erection, and loss of libido had an impact on the testosterone threshold for CVD risk. The threshold level was higher in men with sexual dysfunction. Further study is required to evaluate the validity of these testosterone thresholds for CVD risk.

 

[Dr JIM]

It's amazing. That is only after six weeks. What makes it so detrimental to the heart ? Is it the increased heart rate?

Oh I don't know IF thats the case at all …….. BUT ……..

Maybe the DOSE in these RATS had something to do with it?

Let's see so @ 10mg/kg THREE times a WEEK the "average" 80kg BB would be pinning
TWO THOUSAND FOUR-HUNDRED mg of DECA !! (compare that to the average therapeutic dose in humans of between 50-100 mg/wk AND an "average BB dose" of between 200-800mg/wk)

OR maybe is was THE EXERCISE since "signs of oxidative stress" are a part of aerobic activity itself.

OR maybe it was the RATS whose lifespan of a couple years is thought to be the result their "fast metabolism" and the "oxidative stress" that follows. (Rats have a high neoplastic rate compared to humans)

OR maybe it was the RESEARCH DESIGN ……………. such as how "oxidative stress" was quantified ……. free radical byproduct accumulation ?

THE POINT; the devil or truth, if there is any, usually lies in the details.

JIM

 

[Dr JIM]

GREAT THREAD @Michael Scally MD

 

[hurricane]

Oh I don't know IF thats the case at all …….. BUT ……..

Maybe the DOSE in these RATS had something to do with it?

Let's see so @ 10mg/kg THREE times a WEEK the "average" 80kg BB would be pinning
TWO THOUSAND FOUR-HUNDRED mg of DECA !! (compare that to the average therapeutic dose in humans of between 50-100 mg/wk AND an "average BB dose" of between 200-800mg/wk)

OR maybe is was THE EXERCISE since "signs of oxidative stress" are a part of aerobic activity itself.

OR maybe it was the RATS whose lifespan of a couple years is thought to be the result their "fast metabolism" and the "oxidative stress" that follows. (Rats have a high neoplastic rate compared to humans)

OR maybe it was the RESEARCH DESIGN ……………. such as how "oxidative stress" was quantified ……. free radical byproduct accumulation ?

THE POINT; the devil or truth, if there is any, usually lies in the details.

JIM

Which in my opinion keeps proper studies of AAS use in humans in the dark. Obviously science isn't about to take human guinea pigs and inject those doses. I wonder if we will ever truly get an unbiased opinion on AAS use that actually uses BB doses? Wishful thinking on my part. To both doctors, I am going up to Harvard University the week after Thanksgiving. They are going to perform some genetic testing on me. I won't have answers right away, but I'll let you know how it goes. Hope all is well Doc.

 

[Michael Scally MD]

[OA] Men, Testosterone, and Arteriosclerosis

Dr Vicky MacRae speaks to Mark Nicholls about research which could help explain why men are more likely to suffer cardiovascular disease than their similarly aged female counterparts 

Nicholls M. Men, testosterone, and arteriosclerosis. Eur Heart J 2016;37(46):3430. Men, testosterone, and arteriosclerosis | European Heart Journal

 

[Michael Scally MD]

[OA] Gururani K, Jose J, George PV. Testosterone as a marker of coronary artery disease severity in middle aged males. Indian Heart J 2016;68 Suppl 3:S16-S20. https://www.sciencedirect.com/science/article/pii/S0019483216302607

Historically, higher levels of serum testosterone were presumed deleterious to the cardiovascular system. In the last two decades, studies have suggested that low testosterone levels are associated with increased prevalence of risk factors for cardiovascular disease (CVD), including dyslipidemia and diabetes.

This is a cross sectional study. The aim of our study was to determine the relationship between serum testosterone levels and angiographic severity of coronary artery disease (CAD). Serum testosterone levels were also correlated with flow mediated dilation of brachial artery (BAFMD) - an indicator of endothelial function.

Consecutive male patients, aged 40-60 years, admitted for coronary angiography (CAG) with symptoms suggestive of CAD, were included in the study. Out of the 92 patients included in the study, 32 patients had normal coronaries and 60 had CAD on coronary angiography. Severity of CAD was determined by Gensini coronary score.

The group with CAD had significantly lower levels of total serum testosterone (363+/-147.1 vs 532.09+/-150.5ng/dl, p<0.001), free testosterone (7.1215+/-3.012 vs 10.4419+/-2.75ng/dl, p<0.001) and bioavailable testosterone (166.17+/-64.810 vs 247.94+/-62.504ng/dl, p<0.001) when compared to controls.

Adjusting for the traditional risk factors for CAD, a multiple linear regression analysis showed that low testosterone was an independent predictor of severity of CAD (beta=-0.007, p<0.001). This study also showed that levels of total, free and bioavailable testosterone correlated positively with BAFMD %.

 

[heady muscle]

D‐Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study

 

[Dr JIM]

D‐Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study

A study on CHF patients with a control duration of only three weeks sorely lacks validity especially when a subjective questionare is integrated to enhance outcome.

Also what is NOT mentioned is whether the changes in "atrial diameter" improved the subjects afterload, preload or more importantly EJECTION
FRACTION.

Compare the studies data to traditional therapy, such as the use of an ACE inhibitor, and the results would appear PALTRY.

 

[heady muscle]

A study on CHF patients with a control duration of only three weeks sorely lacks validity especially when a subjective questionare is integrated to enhance outcome.

Also what is NOT mentioned is whether the changes in "atrial diameter" improved the subjects afterload, preload or more importantly EJECTION
FRACTION.

Compare the studies data to traditional therapy, such as the use of an ACE inhibitor, and the results would appear PALTRY.

Yeah, I know it's not perfect by any means, but interesting. It would be nice to see a deeper dive into this.

 

[hurricane]

Just wanted to let the Doctors know I received more info from Harvard medical. I have the genetic mutation that can cause long QT syndrome. Don't even know what that is. Doctor said it is chaotic heartbeats. They haven't detected it with my linq recorder, their just telling me what they found. Another visit back down to Yale tomorrow to discuss this with Dr Marieb. I'm assuming nothing will be done since I've shown no signs of it. For Dr Scally and Dr Jim. My total testosterone was 587. Cholesterol was right at the upper limits of normal. Creatinine was above normal but not by much. BP was 132/80. Resting heart rate during my stay was 58-62, rising up to 134 when I had a few bouts of IST. They turned off my pacemaker during the stay at Harvard and my HR at night would drop down to 22-24. All in all nothing much has changed. I feel better since the surgeries but still have times of extreme chest pain. Will keep you updated.

 

[Michael Scally MD]

A paper from 26 years ago on why observational evidence on protective role of HDL (aka good) cholesterol misleading.


Phillips AN, Smith GD. How independent are "independent" effects? Relative risk estimation when correlated exposures are measured imprecisely. J Clin Epidemiol 1991;44(11):1223-31. https://linkinghub.elsevier.com/retrieve/pii/0895-4356(91)90155-3

A relative risk estimate which relates an exposure to risk of disease will tend to be estimated too close to unity if that exposure is subject to random measurement error or intra-subject variability.

"Independent" relative risk estimates, for the effect of one exposure after adjusting for confounding exposures, may be biased in either direction, depending on the amount of measurement imprecision in the exposure of interest and in the confounders.

We describe two methods which estimate the bias in multivariate relative risk estimates due to the effect of measurement imprecision in one or more of the exposure variables in the model.

Results from the two methods are compared in an example involving HDL cholesterol, triglycerides and coronary heart disease.

In this example, the degree of bias in relative risk estimates is shown to be highly dependent on the amount of measurement imprecision ascribed to the exposures.

It is concluded that when two exposures are substantially correlated, and one or both is subject to sizeable measurement imprecision, a study in which exposures are measured only once will be inadequate for investigating the independent effect of the exposures.

Where feasible, epidemiologists should seek study populations where the correlation between the exposures is smaller.

 

[hurricane]

Just got back from seeing Dr Marieb at Yale. The mutation they found was SCN5A. It does increase your risk of ventrical fibrillation according to Dr Marieb. But since I had my cardiac ablation and pacemaker put in they have never seen any issues with VF. When my procedures were done a link recorder was also implanted. Dr Marieb does that with all his patients that have an ablation. His reasoning is so he can have 24 hour monitoring of any abnormal heart activity. I have never shown any signs of VF. Since I'm on coreg, ivabradine, and xarelto he sees no need to change or add anything since I have zero symptoms. He said sodium channel blockers do help some who show symptoms. Obviously they will continue to monitor my linq recorder but I shouldn't worry about this. Easier said then done. Will obviously keep DrJim and Dr Scally updated. Thank you for your time.

 

[Moab]

This thread is freaking me out. I think I'm getting some psychosomatic chest pain.
If I'm keeping every cycle under a gram per week, typically in the 600-700 mg per week range in cycles lasting no more than 16 weeks, and I stick to my TRT dose the rest of the time, how concerned should I be?

Sent from my SM-G900V using Tapatalk

 

[CensoredBoardsSuck]

This thread is freaking me out. I think I'm getting some psychosomatic chest pain.
If I'm keeping every cycle under a gram per week, typically in the 600-700 mg per week range in cycles lasting no more than 16 weeks, and I stick to my TRT dose the rest of the time, how concerned should I be?

Hard to say but I wouldn't buy any green bananas.