AAS and Cardiovascular/Pulmonary Function

[CensoredBoardsSuck]

Not only that but AAS + resistance training is synergistically bad -- at least in rats

The Troponin level increased more three fold from baseline which is very worrisome if these results were to be reproduced in humans as such changes are consistent with a "heart attack".

How is this evidence of a synergistic effect? At best it shows a slightly additive effect of TE to resistance training with the majority of the trop increase being due to resistance training alone. Looks like a sensationalistic study.

 

[eryximachus]

Many of these “low TT” folk are requesting or are interested in reaching levels two to three times their age related limits and THATS where I suspect the “risk” of TRT, however small it is, encroaches upon “benefit”, esp for those older folk with a lifelong history of csrdiac risk factors.

Jim

It is fairly common knowledge that at all age levels, testosterone levels are upwards of 50% what they were in the 1950s. It is perhaps not medically necessary for survival, but for those social psychologists critical of the world - a world of servile, obsequious bitches - one can't help but speculate that perhaps pervasive low T is the reason.

 

[grey]

a world of servile, obsequious bitches

That is tasty right there...

 

[Dr JIM]

a world of servile, obsequious bitches - one can't help but speculate that perhaps pervasive low T is the reason.

Our maternaistic educational system provides an answer as such servility has infiltrated every aspect of "manhood".

While TT levels have declined over the past few decades, while tempting, its erronius to assert such a 20-40ng/dl decline has resulted in readily definable psychological or physiological ailments.


JIM

 

[Dr JIM]

View attachment 77677

How is this evidence of a synergistic effect? At best it shows a slightly additive effect of TE to resistance training with the majority of the trop increase being due to resistance training alone. Looks like a sensationalistic study.

Because Troponin is such a highly sensitive and specific biochemical marker, even minimal changes are worrisome in HUMANS as it strongly suggests myocardial injury.

Can such an effect be extrapolated to humans, based upon a single RAT study, of course not, but the CV "toxicity" of AAS, especially at HIGH DOSES, remain unexplained and this study is one of the first to provide a PATHOLOGICAL explanation.

One can only wonder if such screening is worthwhile in BB running high doses, especially if those involved have noted a diminished aerobic capacity or a variety of other signs and/or symptoms of Cardio-Pulmonary disease.

JIM

 

[CensoredBoardsSuck]

Because Troponin is such a highly sensitive and specific biochemical marker, even minimal changes are worrisome in HUMANS as it strongly suggests myocardial injury.

Perhaps, but that doesn't address the fact that the study's authors claimed to have found a synergistic effect between resistance training and TE when their own data doesn't support that conclusion.

but the CV "toxicity" of AAS, especially at HIGH DOSES, remain unexplained and this study is one of the first to provide a PATHOLOGICAL explanation.

This study from Iran, the bastion of science and medical excellence that modern day Persia is, didn't even bother to include a pathological explanation for their most alarming finding: the increase in troponin from resistance training alone.

Some might choose to use more diplomatic language to describe the study, but it's sensationalistic trash.

 

[Dr JIM]

View attachment 77677

How is this evidence of a synergistic effect? At best it shows a slightly additive effect of TE to resistance training with the majority of the trop increase being due to resistance training alone. Looks like a sensationalistic study.

Here's a study investigating the utility of serum Troponin changes as a predictor of CHF in patients receiving Anthracycline a known cardiotoxic chemotherapy drug.

Which begs the question ----- are AAS cardiotoxic, especially when used in high dosages.
Of note the changes were similar to those observed in the research posted by @Michael Scally MD

One can only hope the study is repeated.

 

[CensoredBoardsSuck]

Which begs the question ----- are AAS cardiotoxic, especially when used in high dosages.

I think the more pertinent question raised by this study is whether resistance training alone is cardiotoxic. It might be for those with pre-existing heart disease but it certainly isn't for healthy trainees.

 

[Dr JIM]

I think the more pertinent question raised by this study is whether resistance training alone is cardiotoxic. It might be for those with pre-existing heart disease but it certainly isn't for healthy trainees.

In the presence of obstructive arterial disease once the rate of oxygen consumption exceeds supply the net effect is ischemia or myocardial injury.

And what accounts for the relatively high rate of SCD in cyclists with non-obstructive coronary arterial disease?

And how about the putative higher rate of of cardiomyopathy in AAS runners, is it "the exercise" (apparently not based upon existing data) or are these drugs cardiotoxic?

IDK but trop levels may help to define causation, IMO

 

[Michael Scally MD]

[Mice] Chronic Exercise Reduces CETP and Mesterolone Treatment Counteracts Exercise Benefits on Plasma Lipoproteins Profile

Regular exercise and anabolic androgenic steroids have opposing effects on the plasma lipoprotein profile and risk of cardio-metabolic diseases in humans. Studies in humans and animal models show conflicting results.

Here, we used a mice model genetically modified to mimic human lipoprotein profile and metabolism. They under-express the endogenous LDL receptor gene (R1) and express a human transgene encoding the cholesteryl ester transfer protein (CETP), normally absent in mice.

The present study was designed to evaluate the independent and interactive effects of testosterone supplementation, exercise training and CETP expression on the plasma lipoprotein profile and CETP activity. CETP/R1 and R1 mice were submitted to a 6-week swimming training and mesterolone (MEST) supplementation in the last 3 weeks.

MEST treatment increased markedly LDL levels (40%) in sedentary CETP/R1 mice and reduced HDL levels in exercised R1 mice (18%). A multifactorial ANOVA revealed the independent effects of each factor, as follows. CETP expression reduced HDL (21%) and increased non-HDL (15%) fractions. MEST treatment increased the VLDL concentrations (42%) regardless of other interventions.

Exercise training reduced triacylglycerol (25%) and free fatty acids (20%), increased both LDL and HDL (25-33%), and reduced CETP (19%) plasma levels. Significant factor interactions showed that the increase in HDL induced by exercise is explained by reducing CETP activity and that MEST blunted the exercise-induced elevation of HDL-cholesterol.

These results reinforce the positive metabolic effects of exercise, resolved a controversy about CETP response to exercise and evidenced MEST potency to counteract specific exercise benefits.

Casquero AC, Berti JA, Teixeira LLS, de Oliveira HCF. Chronic Exercise Reduces CETP and Mesterolone Treatment Counteracts Exercise Benefits on Plasma Lipoproteins Profile: Studies in Transgenic Mice. Lipids. Chronic Exercise Reduces CETP and Mesterolone Treatment Counteracts Exercise Benefits on Plasma Lipoproteins Profile: Studies in Transgenic Mice

 

[CensoredBoardsSuck]

The present study was designed to evaluate the independent and interactive effects of testosterone supplementation, exercise training and CETP expression

And yet the authors chose not to use testosterone at all. They used Proviron instead.

R1 mice were submitted to a 6-week swimming training and mesterolone (MEST) supplementation in the last 3 weeks.

 

[Dr JIM]

And yet the authors chose not to use testosterone at all. They used Proviron instead.

So they effectively compared placebo to placebo

And the problem with a LARGE portion of existing rodent research, the design itself.

It’s for this reason clinical trials must be conducted before extrapolating said results to humans, with few exceptions.

Jim

 

[Michael Scally MD]

Li H, Mitchell L, Zhang X, et al. Testosterone Therapy and Risk of Acute Myocardial Infarction in Hypogonadal Men: An Administrative Health Care Claims Study. J Sex Med 2017;14:1307–17. http://www.jsm.jsexmed.org/article/S1743-6095(17)31427-3/abstract

Background - There are some ongoing debates on the potential link between testosterone therapy (TT) and risk of acute myocardial infarction (MI).

Aim - To investigate the association between acute MI and TT use compared with non-use in men having documented hypogonadism (diagnostic International Classification of Diseases, Ninth Revision codes 257.2, 257.8, 257.9, 758.7) in patient claims records.

Methods - This retrospective cohort study used a real-world US-based administrative health care claims database (MarketScan 2004–2013; Truven Health Analytics, Ann Arbor, MI, USA) to compare MI rates between TT-treated men and a cohort of untreated hypogonadal men matched by a calendar time-specific propensity score. Subgroup analyses were performed by route of administration, age, and prior cardiovascular disease (CVD).

Outcomes - Incidence rates of MI (per 1,000 person-years) and hazard ratio.

Results - After 1:1 calendar time-specific propensity score matching, 207,176 TT-treated men and 207,176 untreated hypogonadal men were included in the analysis (mean age = 51.8 years). Incidence rates of MI were 4.20 (95% CI = 3.87–4.52) in the TT-treated cohort and 4.67 (95% CI = 4.43–4.90) in the untreated hypogonadal cohort.

Cox regression model showed no significant association between TT use and MI when comparing TT-treated with untreated hypogonadal men overall (hazard ratio = 0.99, 95% CI = 0.89–1.09), by age, or by prior CVD.

A significant association was observed when comparing a subgroup of injectable (short- and long-acting combined) TT users with untreated hypogonadal men (hazard ratio = 1.55, 95% CI = 1.24–1.93).

Clinical Implication - In this study, there was no association between TT (overall) and risk of acute MI.

Strengths and Limitations - Strengths included the use of a comprehensive real-world database, sophisticated matching based on calendar blocks of 6 months to decrease potential bias in this observational study, carefully chosen index dates for the untreated cohort to avoid immortal time bias, and implemented sensitivity analysis to further investigate the findings (stratification by administration route, age, and prior CVD).

Key limitations included no information about adherence, hypogonadism condition based solely on diagnosis (no information on clinical symptoms or testosterone levels), lack of information on disease severity, inability to capture diagnoses, medical procedures, and medicine dispensing if corresponding billing codes were not generated and findings could contain biases or fail to generalize well to other populations.

Conclusion - This large, retrospective, real-world observational study showed no significant association between TT use and acute MI when comparing TT-treated with untreated hypogonadal men overall, by age, or by prior CVD; the suggested association between injectable TT and acute MI deserves further investigation.

 

[Michael Scally MD]

A 3-Year Observation of Testosterone Deficiency in Chinese Patients with Chronic Heart Failure

Testosterone deficiency is present in a certain proportion men with chronic heart failure (CHF). Low testosterone levels in American and European patients with CHF lead to the high mortality and readmission rates. Interestingly, this relationship has not been studied in Chinese patients.

To this end, 167 Chinese men with CHF underwent clinical and laboratory evaluations associated with determinations of testosterone levels. Total testosterone (TT) levels and sex hormone-binding globulin were measured by chemiluminescence or immunoassays assays and free testosterone (FT) levels were calculated.

Based upon results from these assays, patients were divided into either a low testosterone (LT; n = 93) or normal testosterone (NT; n = 74) group. Subsequently, records from each patient were reviewed over a follow-up duration of at least 3 years.

Patients in the LT group experienced worse cardiac function and a higher prevalence of etiology (ischemic vs. no ischemic) and comorbidity (both P < 0.05). In addition, readmission rates of patients in the LT group were higher than that of patients in the NT group (3.32 +/- 1.66 VS 1.57 +/- 0.89). Overall, deficiencies in FT levels were accompanied with increased mortalities (HR = 6.301, 95% CI 3.187-12.459, P < .0001).

Han Y, Sun W, Sun G, et al. A 3-year observation of testosterone deficiency in Chinese patients with chronic heart failure. Oncotarget 2017;8(45):79835-42. http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path[]=19816&path[]=63270

 

[Michael Scally MD]

Labos C, Brophy JM, Smith GD, Sniderman AD, Thanassoulis G. Evaluation of the Pleiotropic Effects of Statins. Arteriosclerosis, Thrombosis, and Vascular Biology. Evaluation of the Pleiotropic Effects of Statins

Objective—To reanalyze data from recent randomized trials of statins to assess whether the benefits and risks of statins are mediated primarily via their LDL-C (low-density lipoprotein cholesterol) lowering effects or via other mechanisms.

Approach and Results—We adapted Egger regression, a technique frequently used in Mendelian randomization studies to detect genetic pleiotropy, to reanalyze the available randomized control trial data of statin therapy. For cardiovascular end points, each 1 mmol/L change in LDL-C with statin therapy was associated with a hazard ratio of 0.77 (95% confidence interval, 0.71–0.84) with an intercept that was indistinguishable from zero (intercept, −0.0032; [95% confidence interval, −0.090 to 0.084]; P=0.94), indicating no pleiotropy. For incident diabetes mellitus, a 1 mmol/L change in LDL-C with statin therapy was associated with a hazard ratio of 1.07 (95% confidence interval, 0.99–1.16) and an intercept nondistinguishable from zero (intercept, −0.015; [95% confidence interval, −0.30 to 0.27]; P=0.91), again indicating no pleiotropy.

Conclusions—Our reanalysis of the randomized control trial data using Egger regression adds to the existing evidence that the cardiovascular benefits of statins and their association with incident diabetes mellitus are mediated primarily, if not entirely, via their LDL-C lowering properties rather than by any pleiotropic effects.

 

[hurricane]

@Dr JIM @Michael Scally MD . Hope you both are well. Since my stroke I've been having horrible chest pain. I was put on 60mg ER nitro tabs Ed. Since I couldn't stand the massive headaches they took me off it. Horrible chest pain resumed and an echo was done. EF went slightly down to 40-45 and they diagnosed carotid artery spasms. I just recently started 5mg daily of Amlodipine for that. What's your take on that medication. It seems to be helping. Still on Ivabradine, Coreg, and Xarelto. Hope all is well Doctor's.

 

[hurricane]

Meant coronary artery spasms. Not carotid.

 

[Michael Scally MD]

Is it time to retire cholesterol tests?

The next time you go in for a medical checkup, your doctor will probably make a mistake that could endanger your life, contends cardiologist Allan Sniderman of McGill University in Montreal, Canada. Most physicians order what he considers the wrong test to gauge heart disease risk: a standard cholesterol readout, which may indicate levels of low-density lipoprotein (LDL) or non-high density lipoprotein (non-HDL) cholesterol. What they should request instead, Sniderman argues, is an inexpensive assay for a blood protein known as apolipoprotein B (apoB).

ApoB indicates the number of cholesterol-laden particles circulating in the blood—a truer indicator of the threat to our arteries than absolute cholesterol levels, some researchers believe. Sniderman asserts that routine apoB tests, which he says cost as little as $20, would identify millions more patients who could benefit from cholesterol-cutting therapies and would spare many others from unnecessary treatment. "If I can diagnose [heart disease] more accurately using apoB, and if I can treat more effectively using apoB, it's worth 20 bucks," he says.

Sniderman and a cadre of other scientists have been stumping for apoB for years, but recent reanalyses of clinical data, together with genetic studies, have boosted their confidence. At last month's American Heart Association (AHA) meeting in Anaheim, California, for example, Sniderman presented a new take on the National Health and Nutrition Examination Survey (NHANES), a famous census of the U.S. population's health.

The reexamination, which compared people with different apoB levels but the same non-HDL cholesterol readings, crystallizes the importance of measuring the protein, he says. Across the United States, patients who have the highest apoB readings will suffer nearly 3 million more heart attacks, strokes, and other cardiovascular events in the next 15 years than will people with the lowest levels, Sniderman reported. As lipidologist Daniel Rader of the University of Pennsylvania Perelman School of Medicine puts it, the question of whether LDL cholesterol is the best measure of cardiovascular risk now has a clear answer: "No."

But plenty of scientists disagree.

 

[Dr JIM]

@Dr JIM @Michael Scally MD . Hope you both are well. Since my stroke I've been having horrible chest pain. I was put on 60mg ER nitro tabs Ed. Since I couldn't stand the massive headaches they took me off it. Horrible chest pain resumed and an echo was done. EF went slightly down to 40-45 and they diagnosed carotid artery spasms. I just recently started 5mg daily of Amlodipine for that. What's your take on that medication. It seems to be helping. Still on Ivabradine, Coreg, and Xarelto. Hope all is well Doctor's.

Exclusive of CV ailments, the studies I'm familiar with involve the use of Amiodipine as vascular headache, or "migraine", prophylaxis

In this context bc the benefits of Ca blocker therapy are generally favorable and the frequency of adverse effects low, such therapy is worth trying in appropriately selected patients, IMO.

 

[hurricane]

Exclusive of CV ailments, the studies I'm familiar with involve the use of Amiodipine as vascular headache, or "migraine", prophylaxis

In this context bc the benefits of Ca blocker therapy are generally favorable and the frequency of adverse effects low, such therapy is worth trying in appropriately selected patients, IMO.

Thanks Doc. It seems to be working. Chest pain has been much better. Reading patient reviews on the drug are scary. Bad palpitations, racing heartbeat. Dr. Marieb said I should be fine. The only thing he mentioned was possible ankle swelling.