AAS and Cardiovascular/Pulmonary Function

[Old]

Health Consequences of Androgenic Anabolic Steroids

Background - The lifetime prevalence of androgenic anabolic steroid abuse is estimated to be around 6% for men, but there is limited knowledge about the side effects of these drugs.

Objective - To investigate mortality and morbidity amongst users of androgenic anabolic steroids (AAS).

Methods - In this retrospective matched cohort study, 545 male subjects tested positive for AAS in Danish fitness centres during the period 3 January 2006 to 1 March 2018. Subjects were matched with 5450 male controls. In addition, 644 men who were sanctioned because they refused to submit to a doping test and 6440 controls were included as a replication cohort.

Results - Mortality was three times higher amongst users of AAS than amongst nonuser controls (hazard ratio 3.0, 95% CI 1.3–7.0). The median annual number of hospital contacts was 0.81 in the cohort of AAS users and 0.36 in the control cohort (P < 0.0001). Acne, gynaecomastia and erectile dysfunction affected more than 10% of the androgenic anabolic steroid users, and the prevalence of these disorders was significantly higher than in the control group (P < 0.0001). The results could be replicated in a similar cohort.

Conclusion - Androgenic anabolic steroid users have an increased risk of dying and significantly more hospital admissions than their nonuser peers. Side effects of AAS and their metabolites were highly prevalent. Given the high rate of androgenic anabolic steroid abuse, these side effects are of public health concern.

Horwitz H, Andersen JT, Dalhoff KP. Health consequences of androgenic anabolic steroids. J Intern Med. 2018. https://onlinelibrary.wiley.com/doi/abs/10.1111/joim.12850

What exactly does "Mortality was three times higher"mean? Does it translate to a certain number of months/years of lifespan? Certainly doesn't mean they die at 27 (1/3 of 80). Perhaps of the hospital admissions, 3 times more likely to not make it? And what were the figures ... 3 AAS user admittees verses 10 control admittees would be 3 times (of study groups) but not a very high number. Also, were these deaths all cardiovascular?

 

[Michael Scally MD]

What exactly does "Mortality was three times higher"mean? Does it translate to a certain number of months/years of lifespan? Certainly doesn't mean they die at 27 (1/3 of 80). Perhaps of the hospital admissions, 3 times more likely to not make it? And what were the figures ... 3 AAS user admittees verses 10 control admittees would be 3 times (of study groups) but not a very high number. Also, were these deaths all cardiovascular?

I have sent for the full-text. I take these studies with a great degree of skepticism.

 

[Old]

I have sent for the full-text. I take these studies with a great degree of skepticism.

It would be nice to have some 'pure' science for a change. Too much agenda on all sides. It a 'sociological' inevitability given pride, greed and fear.
I liked Dr Jim's terminology of: 'medical dogma' vs 'Bro lore'

 

[Michael Scally MD]

Before Starting A Statin, Talk It Over With Your Doctor
Before Starting A Statin, Talk It Over With Your Doctor


The problem for statins for primary prevention of heart disease: they are significantly over-prescribed.

Benefits and Harms of Using Statins to Prevent Cardiovascular Disease
Benefits and Harms of Using Statins to Prevent Cardiovascular Disease | Annals of Internal Medicine | American College of Physicians


What did the researchers find?
The level of risk at which statins should be prescribed is higher than the currently recommended level. Also, the level varies widely according to the person's age and sex and the type of statin.


Yebyo HG, Aschmann HE, Puhan MA. Finding the balance between benefits and harms when using statins for primary prevention of cardiovascular disease: A modeling study. Annals of Internal Medicine 2018. http://dx.doi.org/10.7326/M18-1279

Background: Many guidelines use expected risk for cardiovascular disease (CVD) during the next 10 years as a basis for recommendations on use of statins for primary prevention of CVD. However, how harms were considered and weighed against benefits is often unclear.

Objective: To identify the expected risk above which statins provide net benefit.

Design: Quantitative benefit–harm balance modeling study.

Data Sources: Network meta-analysis of primary prevention trials, a preference survey, and selected observational studies.

Target Population: Persons aged 40 to 75 years with no history of CVD.

Time Horizon: 10 years.

Perspective: Clinicians and guideline developers.

Intervention: Low- or moderate-dose statin versus no statin.

Outcome Measures: The 10-year risk for CVD at which statins provide at least a 60% probability of net benefit, with baseline risk, frequencies of and preferences for statin benefits and harms, and competing risk for non-CVD death taken into account.

Results of Base-Case Analysis: Younger men had net benefit at a lower 10-year risk for CVD than older men (14% for ages 40 to 44 years vs. 21% for ages 70 to 75 years). In women, the risk required for net benefit was higher (17% for ages 40 to 44 years vs. 22% for ages 70 to 75 years). Atorvastatin and rosuvastatin provided net benefit at lower 10-year risks than simvastatin and pravastatin.

Results of Sensitivity Analysis: Most alternative assumptions led to similar findings.

Limitation: Age-specific data for some harms were not available.

Conclusion: Statins provide net benefits at higher 10-year risks for CVD than are reflected in most current guidelines. In addition, the level of risk at which net benefit occurs varies considerably by age, sex, and statin type.

 

[hurricane]

Before Starting A Statin, Talk It Over With Your Doctor
Before Starting A Statin, Talk It Over With Your Doctor


The problem for statins for primary prevention of heart disease: they are significantly over-prescribed.

Benefits and Harms of Using Statins to Prevent Cardiovascular Disease
Benefits and Harms of Using Statins to Prevent Cardiovascular Disease | Annals of Internal Medicine | American College of Physicians


What did the researchers find?
The level of risk at which statins should be prescribed is higher than the currently recommended level. Also, the level varies widely according to the person's age and sex and the type of statin.


Yebyo HG, Aschmann HE, Puhan MA. Finding the balance between benefits and harms when using statins for primary prevention of cardiovascular disease: A modeling study. Annals of Internal Medicine 2018. http://dx.doi.org/10.7326/M18-1279

Background: Many guidelines use expected risk for cardiovascular disease (CVD) during the next 10 years as a basis for recommendations on use of statins for primary prevention of CVD. However, how harms were considered and weighed against benefits is often unclear.

Objective: To identify the expected risk above which statins provide net benefit.

Design: Quantitative benefit–harm balance modeling study.

Data Sources: Network meta-analysis of primary prevention trials, a preference survey, and selected observational studies.

Target Population: Persons aged 40 to 75 years with no history of CVD.

Time Horizon: 10 years.

Perspective: Clinicians and guideline developers.

Intervention: Low- or moderate-dose statin versus no statin.

Outcome Measures: The 10-year risk for CVD at which statins provide at least a 60% probability of net benefit, with baseline risk, frequencies of and preferences for statin benefits and harms, and competing risk for non-CVD death taken into account.

Results of Base-Case Analysis: Younger men had net benefit at a lower 10-year risk for CVD than older men (14% for ages 40 to 44 years vs. 21% for ages 70 to 75 years). In women, the risk required for net benefit was higher (17% for ages 40 to 44 years vs. 22% for ages 70 to 75 years). Atorvastatin and rosuvastatin provided net benefit at lower 10-year risks than simvastatin and pravastatin.

Results of Sensitivity Analysis: Most alternative assumptions led to similar findings.

Limitation: Age-specific data for some harms were not available.

Conclusion: Statins provide net benefits at higher 10-year risks for CVD than are reflected in most current guidelines. In addition, the level of risk at which net benefit occurs varies considerably by age, sex, and statin type.

I'm completely in agreement with these new findings. Why prescribe a 40 yo with a statin medication on a "what if" basis.
I agree I may have just simplified the issue but I do have issues with some of these so called "preventative" medications. Statins being one of them.
How about discussing with patients ways to lower their cvd risk. Quit smoking, lose weight, exercise.
Of course there will always be patients who need statins regardless of lifestyle changes. But why put those at a low risk of cvd on a medication which may have little to no benefit to them?

 

[heady muscle]

@Michael Scally MD

Not sure you posted this on here or not. It's a great read:
Homocysteine induced cardiovascular events: a consequence of long term anabolic‐androgenic steroid (AAS) abuse

 

[heady muscle]

@Michael Scally MD

Not sure you posted this on here or not. It's a great read:
Homocysteine induced cardiovascular events: a consequence of long term anabolic‐androgenic steroid (AAS) abuse

Homocysteine Reduction | Life Extension

 

[Michael Scally MD]

Riaz H, Khan SU, Rahman H, et al. Effects of high-density lipoprotein targeting treatments on cardiovascular outcomes: A systematic review and meta-analysis. European journal of preventive cardiology 2018:2047487318816495. SAGE Journals: Your gateway to world-class journal research

Background - The effects of increasing high-density lipoprotein cholesterol on cardiovascular outcomes remain uncertain.

Design - We conducted a meta-analysis to investigate the effects of high-density lipoprotein cholesterol modifiers (niacin, fibrates and cholesteryl ester transfer protein inhibitors) on cardiovascular outcomes.

Methods - Thirty-one randomized controlled trials (154,601 patients) with a follow-up of 6 months or more and a sample size of 100 or more patients were selected using MEDLINE, EMBASE and CENTRAL database (inception January 2018).

Results - High-density lipoprotein cholesterol modifiers had no statistically significant effect on cardiovascular mortality in terms of relative risk (RR) (RR 0.94, 95% confidence interval (CI) 0.89–1.00, P = 0.05, I2 = 13%) or absolute risk (risk difference −0.0001, 95% CI −0.0014, 0.0011, P = 0.84, I2 = 28%).

High-density lipoprotein cholesterol modifiers reduced the RR of myocardial infarction (RR 0.87, 95% CI 0.82–0.93, P < 0.001, I2 = 37%). This significant effect was derived by the use of fibrates (RR 0.80, 95% CI 0.73–0.87, P < 0.001, I2 = 22%) and meta-regression analysis showed that this benefit was consistent with an absolute reduction in low-density lipoprotein cholesterol.

High-density lipoprotein cholesterol modifiers had no effect on stroke (RR 1.00, 95% CI 0.93–1.09, P = 0.94, I2 = 25%) or all-cause mortality (RR 1.02, 95% CI 0.97–1.08, P = 0.48, I2 = 49%). Meta-regression analyses failed to demonstrate a significant association of pharmacologically increased high-density lipoprotein cholesterol with key endpoints.

In studies with background statin therapy, high-density lipoprotein cholesterol modifiers had no statistically significant impact on cardiovascular mortality, myocardial infarction, stroke or all-cause mortality (P > 0.05).

Conclusion - The use of high-density lipoprotein cholesterol modifying treatments had no significant effect on cardiovascular mortality, stroke or all-cause mortality. The beneficial effect on myocardial infarction was lost when drugs were used with statin therapy.

 

[Michael Scally MD]

Chasland LC, Knuiman MW, Divitini ML, et al. Higher circulating androgens and higher physical activity levels are associated with less central adiposity and lower risk of cardiovascular death in older men. Clin Endocrinol (Oxf). 2018;00:1–9. https://doi.org/10.1111/cen.13905

Objective - Low endogenous sex hormones and low physical activity (PA) levels have been associated with CVD risk. Whether these interact to influence CVD outcomes remains unclear. We assessed whether sex hormone concentrations and PA were additively associated with lower central adiposity and CVD risk.

Patients - 3351 community‐dwelling men, mean age 77 years.

Measurements - Baseline testosterone (T), dihydrotestosterone (DHT) and oestradiol (E2) were assayed. Levels of PA were ascertained by questionnaire. Men were stratified using median splits into high hormone + high PA (H/H), high hormone + low PA (H/L); low hormone + high PA (L/H) and low hormone + low PA (L/L) groups.

Results - A total of 865 CVD events and 499 CVD deaths occurred during 10‐year mean follow‐up. Men with higher T, DHT or SHBG and higher PA had the lowest BMI, waist circumference and risk of metabolic syndrome. Men with higher T had the lowest risk of incident CVD events, irrespective of PA level. Men with higher T or DHT and higher PA had the lowest risk of dying from CVD (eg, hazard ratios for T/PA H/H 0.76 P = 0.031; H/L 0.85 P = 0.222; L/H 0.80 P = 0.075; L/L 1.00).

Conclusion - Higher circulating androgens and higher PA were associated with less central adiposity at baseline and fewer CVD deaths during follow‐up. These findings are consistent with a potential additive effect of androgens and PA on cardiometabolic outcomes in older men.

 

[Michael Scally MD]

Morden NE, Woloshin S, Brooks CG, Schwartz LM. Trends in testosterone prescribing for age-related hypogonadism in men with and without heart disease. JAMA Internal Medicine 2018. Testosterone Prescribing for Age-related Hypogonadism in Men With and Without Heart Disease

Signals of cardiovascular risk from off-label prescription testosterone use began with the early termination of a placebo-controlled trial in frail, older men. Basaria et al revealed more cardiovascular events among men randomized to receive testosterone than among men randomized to receive placebo. Some observational studies reinforced these concerns for cardiovascular risk. In 2014, the US Food and Drug Administration (FDA) issued a safety communication about testosterone drugs, and the Endocrine Society expressed particular concern about testosterone use by men with heart disease. In 2015, the FDA revised testosterone labels, highlighting the lack of efficacy evidence for age-related hypogonadism and adding a warning about possible increased cardiovascular risk.

 

[Michael Scally MD]

Low Serum Free Testosterone Association With Cardiovascular Mortality in Men With Stable CAD

Our results demonstrated for the first time that FT levels are inversely associated with 5-year CV mortality in men with stable CAD, independently of CV risk factors, hsCRP, and ejection fraction. The exact mechanism by which low T levels increase CV mortality is largely unknown.

It has been suggested that endogenous T affects atherosclerosis by modifying CV risk factors. Consistent with this, we found that FT was inversely correlated with waist circumference, DM, hsCRP, and IL-6.

Most previous studies measured mainly total T or a few of them FT, and found inconsistent results regarding its prognostic value on CV endpoints. This is the first study to our knowledge to examine the prognostic impact of FT in patients with stable CAD. It is plausible to speculate that FT, the most biologically active form of T, is more likely to identify the impact of T on future CV events.

In addition, we measured FT by competitive radioimmunoassay, which shows a good correlation with equilibrium dialysis, considered the gold standard for FT measurements. A limitation of this study, considering the high diurnal and seasonal variation of T, was its measurement from a single blood sample.

In conclusion, low FT levels are associated with high 5-year CV mortality in men with stable CAD. Large prospective studies are needed to confirm our results and support the hypothesis that FT is the most active and predictive fraction of T.

Rallidis LS, Kotakos C, Tsalavoutas S, et al. Low Serum Free Testosterone Association With Cardiovascular Mortality in Men With Stable CAD. Journal of the American College of Cardiology 2018;72:2674-5. https://www.sciencedirect.com/science/article/pii/S0735109718386364

 

[Bigboy727]

Low Serum Free Testosterone Association With Cardiovascular Mortality in Men With Stable CAD

Our results demonstrated for the first time that FT levels are inversely associated with 5-year CV mortality in men with stable CAD, independently of CV risk factors, hsCRP, and ejection fraction. The exact mechanism by which low T levels increase CV mortality is largely unknown.

It has been suggested that endogenous T affects atherosclerosis by modifying CV risk factors. Consistent with this, we found that FT was inversely correlated with waist circumference, DM, hsCRP, and IL-6.

Most previous studies measured mainly total T or a few of them FT, and found inconsistent results regarding its prognostic value on CV endpoints. This is the first study to our knowledge to examine the prognostic impact of FT in patients with stable CAD. It is plausible to speculate that FT, the most biologically active form of T, is more likely to identify the impact of T on future CV events.

In addition, we measured FT by competitive radioimmunoassay, which shows a good correlation with equilibrium dialysis, considered the gold standard for FT measurements. A limitation of this study, considering the high diurnal and seasonal variation of T, was its measurement from a single blood sample.

In conclusion, low FT levels are associated with high 5-year CV mortality in men with stable CAD. Large prospective studies are needed to confirm our results and support the hypothesis that FT is the most active and predictive fraction of T.

Rallidis LS, Kotakos C, Tsalavoutas S, et al. Low Serum Free Testosterone Association With Cardiovascular Mortality in Men With Stable CAD. Journal of the American College of Cardiology 2018;72:2674-5. https://www.sciencedirect.com/science/article/pii/S0735109718386364

At what point do the benefits outweigh the risks? Does an. Does an Alcoholic do more damage than a AAS to their heart? Is smoking worse? How could one administer testosterone and increase their life expectancy? Is it possible?

 

[Michael Scally MD]

The Association of Genetically-Predicted Testosterone with Thromboembolism, Heart Failure and Myocardial Infarction

Objective: To determine whether endogenous testosterone has a causal role in thromboembolism, heart failure, and myocardial infarction.

Design: Two sample Mendelian randomization study to test for causal effects of endogenous testosterone on thromboembolism, heart failure, and myocardial infarction. Mendelian randomization exploits genetic variants as instrumental variables, randomly allocated at conception, to infer causality as additional randomized evidence.

Settings: Reduction by DUtasteride of Prostate Cancer Events randomized controlled trial (REDUCE), UK Biobank and CARDIoGRAMplusC4D 1000 Genomes-based GWAS.

Participants: 3,225 men of European ancestry aged 50 to 75 years in REDUCE, 392,038 men and women of White British ethnicity, aged 40 to 69 years, from the UK Biobank, and 171,875 participants, 77% of European descent, from CARDIoGRAMplusC4D 1000 Genomes-based GWAS in the validation study.

Main outcome measures: Thromboembolism, heart failure and myocardial infarction based on self-reports, hospital episodes and death

Results: In the UK Biobank among 392,038 genetically verified White British participants were 13,691 cases of thromboembolism (6,208 men, 7,483 women), 1,688 of heart failure (1186 men, 502 women) and 12,882 of myocardial infarction (10,136 men and 2,746 women).

In men endogenous testosterone genetically predicted by variants in the JMJD1C gene region was positively associated with thromboembolism (odds ratio (OR) 2.09 per unit increase in log-transformed nmol/L testosterone, 95% confidence intervals (CI) 1.27 to 3.46) and heart failure (OR 7.81, 95% CIs 2.56 to 23.8) but not MI (OR 1.17, 95% CIs 0.78 to 1.75); associations were less obvious in women.

In the validation study, genetically-predicted testosterone in JMJD1C gene region was positively associated with MI (OR 1.37, 95% CIs 1.03 to 1.82). No excess heterogeneity was observed between genetic variants in their associations with the outcomes. However, testosterone genetically predicted by potentially pleiotropic variants in the SHBG gene region had no association with the outcomes.

Conclusions: Endogenous testosterone was positively associated with thromboembolism, heart failure and MI in men, rates of these conditions are higher in men than women. Whether existing treatments that modulate endogenous testosterone could be relevant in thromboembolism and heart failure might be worth considering.

Burgess S. The association of genetically-predicted testosterone with thromboembolism, heart failure and myocardial infarction: a Mendelian randomization study using UK Biobank. BMJ. The association of genetically-predicted testosterone with thromboembolism, heart failure and myocardial infarction: a Mendelian randomization study using UK Biobank

 

[Bigboy727]

The Association of Genetically-Predicted Testosterone with Thromboembolism, Heart Failure and Myocardial Infarction

Objective: To determine whether endogenous testosterone has a causal role in thromboembolism, heart failure, and myocardial infarction.

Design: Two sample Mendelian randomization study to test for causal effects of endogenous testosterone on thromboembolism, heart failure, and myocardial infarction. Mendelian randomization exploits genetic variants as instrumental variables, randomly allocated at conception, to infer causality as additional randomized evidence.

Settings: Reduction by DUtasteride of Prostate Cancer Events randomized controlled trial (REDUCE), UK Biobank and CARDIoGRAMplusC4D 1000 Genomes-based GWAS.

Participants: 3,225 men of European ancestry aged 50 to 75 years in REDUCE, 392,038 men and women of White British ethnicity, aged 40 to 69 years, from the UK Biobank, and 171,875 participants, 77% of European descent, from CARDIoGRAMplusC4D 1000 Genomes-based GWAS in the validation study.

Main outcome measures: Thromboembolism, heart failure and myocardial infarction based on self-reports, hospital episodes and death

Results: In the UK Biobank among 392,038 genetically verified White British participants were 13,691 cases of thromboembolism (6,208 men, 7,483 women), 1,688 of heart failure (1186 men, 502 women) and 12,882 of myocardial infarction (10,136 men and 2,746 women).

In men endogenous testosterone genetically predicted by variants in the JMJD1C gene region was positively associated with thromboembolism (odds ratio (OR) 2.09 per unit increase in log-transformed nmol/L testosterone, 95% confidence intervals (CI) 1.27 to 3.46) and heart failure (OR 7.81, 95% CIs 2.56 to 23.8) but not MI (OR 1.17, 95% CIs 0.78 to 1.75); associations were less obvious in women.

In the validation study, genetically-predicted testosterone in JMJD1C gene region was positively associated with MI (OR 1.37, 95% CIs 1.03 to 1.82). No excess heterogeneity was observed between genetic variants in their associations with the outcomes. However, testosterone genetically predicted by potentially pleiotropic variants in the SHBG gene region had no association with the outcomes.

Conclusions: Endogenous testosterone was positively associated with thromboembolism, heart failure and MI in men, rates of these conditions are higher in men than women. Whether existing treatments that modulate endogenous testosterone could be relevant in thromboembolism and heart failure might be worth considering.

Burgess S. The association of genetically-predicted testosterone with thromboembolism, heart failure and myocardial infarction: a Mendelian randomization study using UK Biobank. BMJ. The association of genetically-predicted testosterone with thromboembolism, heart failure and myocardial infarction: a Mendelian randomization study using UK Biobank

So you increase your odds greatly.

 

[Delt123]

Riaz H, Khan SU, Rahman H, et al. Effects of high-density lipoprotein targeting treatments on cardiovascular outcomes: A systematic review and meta-analysis. European journal of preventive cardiology 2018:2047487318816495. SAGE Journals: Your gateway to world-class journal research

Background - The effects of increasing high-density lipoprotein cholesterol on cardiovascular outcomes remain uncertain.

Design - We conducted a meta-analysis to investigate the effects of high-density lipoprotein cholesterol modifiers (niacin, fibrates and cholesteryl ester transfer protein inhibitors) on cardiovascular outcomes.

Methods - Thirty-one randomized controlled trials (154,601 patients) with a follow-up of 6 months or more and a sample size of 100 or more patients were selected using MEDLINE, EMBASE and CENTRAL database (inception January 2018).

Results - High-density lipoprotein cholesterol modifiers had no statistically significant effect on cardiovascular mortality in terms of relative risk (RR) (RR 0.94, 95% confidence interval (CI) 0.89–1.00, P = 0.05, I2 = 13%) or absolute risk (risk difference −0.0001, 95% CI −0.0014, 0.0011, P = 0.84, I2 = 28%).

High-density lipoprotein cholesterol modifiers reduced the RR of myocardial infarction (RR 0.87, 95% CI 0.82–0.93, P < 0.001, I2 = 37%). This significant effect was derived by the use of fibrates (RR 0.80, 95% CI 0.73–0.87, P < 0.001, I2 = 22%) and meta-regression analysis showed that this benefit was consistent with an absolute reduction in low-density lipoprotein cholesterol.

High-density lipoprotein cholesterol modifiers had no effect on stroke (RR 1.00, 95% CI 0.93–1.09, P = 0.94, I2 = 25%) or all-cause mortality (RR 1.02, 95% CI 0.97–1.08, P = 0.48, I2 = 49%). Meta-regression analyses failed to demonstrate a significant association of pharmacologically increased high-density lipoprotein cholesterol with key endpoints.

In studies with background statin therapy, high-density lipoprotein cholesterol modifiers had no statistically significant impact on cardiovascular mortality, myocardial infarction, stroke or all-cause mortality (P > 0.05).

Conclusion - The use of high-density lipoprotein cholesterol modifying treatments had no significant effect on cardiovascular mortality, stroke or all-cause mortality. The beneficial effect on myocardial infarction was lost when drugs were used with statin therapy.

Any explanation in how/Why?

Niacin for instance is one of those HDL modifiers, it has shown to increase HDL with Some impressive numbers.

Not sure why it couldn't potentially increase life span Than?

 

[Michael Scally MD]

[French] Androgens and Cardiovascular Risk: A Series of Case Report in The French and Canadian Pharmacovigilance Databases

INTRODUCTION: Age-related androgenic deficiency (DALA) is a pathology that is increasingly cited in recent publications. The cardiovascular risk of testosterone is debated: present for the FDA, absent for the European Medicines Agency in 2015. Our objective was to analyze the association between androgens and vascular pathologies in adverse reactions reported in pharmacovigilance databases.

MATERIAL AND METHOD: We conducted a retrospective case series study of the French and Canadian pharmacovigilance databases for the period 2005-2015. Cases were defined as the association of the occurrence of a cardiovascular event (myocardial infarction or stroke) and the presence of testosterone in the treatment of patients.

RESULTS: Of the 10 years analyzed, 12 French cases and 6 Canadian cases (representing 13 MIs and 5 strokes) were recorded in men aged 55 years on average. All were doubtful: differential diagnoses were possible (2.4 confounding conditions on average per patient) and overall cardiovascular risk was high for the majority of cases.

CONCLUSION: Our study shows a very low report of cardiovascular effects under testosterone, all doubtful. Pending further studies, it seems reasonable to consider the cardiovascular risk of patients who are candidates for hormone therapy for age-related androgen deficiency.

Rochoy M, Thomas R, Béné J, et al. Androgènes et risque cardiovasculaire : série de cas dans les bases de pharmacovigilance française et canadienne. Progrès en Urologie 2018;28:315-21. https://www.sciencedirect.com/science/article/pii/S1166708718300794

 

[Michael Scally MD]

Vieira TM, Junior WCR, Da Re Guerra F, Damiao B, Marques PP, Esteves A. Effect of testosterone cypionate and stanozolol on the heart of young trained mice: a morphometric study. Steroids 2019. https://www.sciencedirect.com/science/article/pii/S0039128X19300364?via=ihub

Highlights
· AAS which are synthetic substances that possess functions similar to testosterone.
· AAS changed significantly the heart morphology.
· Testosterone cypionate led to an increase in the ventricular lumen.
· Stanozolol increased left ventricle myocardium thickness.

Testosterone cypionate and Stanozolol are Anabolic-Androgenic Steroids (AAS) which are synthetic substances that possess functions similar to testosterone. The use of these substances has increased considerably among youngsters and sports practitioners aiming better performance of with aesthetic purposes. The major concern is the effects caused by the inappropriate use of the substances, such as hypertension, myocardial ischemia, and left ventricle hypertrophy.

The objective of the present research was to measure the diameter of the left ventricle lumen and the thickness of the left ventricle myocardium in mice submitted to supraphysiological doses of AAS. A total of 30 female Swiss mice were used in the experiments. The animals received supraphysiological doses of the AAS for 30 days, and during the treatment period, they were put to swim in intercalated days. After treatment animals were euthanized and slides were made from the hearts for measurements.

Results demonstrated that both AAS changed significantly the heart morphology: Testosterone cypionate led to an increase in the ventricular lumen and stanozolol increased left ventricle myocardium thickness. In conclusion, the use of AAS in supraphysiological doses can change the heart morphology and can lead to serious health consequences.

 

[Old]

Vieira TM, Junior WCR, Da Re Guerra F, Damiao B, Marques PP, Esteves A. Effect of testosterone cypionate and stanozolol on the heart of young trained mice: a morphometric study. Steroids 2019. https://www.sciencedirect.com/science/article/pii/S0039128X19300364?via=ihub

Highlights
· AAS which are synthetic substances that possess functions similar to testosterone.
· AAS changed significantly the heart morphology.
· Testosterone cypionate led to an increase in the ventricular lumen.
· Stanozolol increased left ventricle myocardium thickness.

Testosterone cypionate and Stanozolol are Anabolic-Androgenic Steroids (AAS) which are synthetic substances that possess functions similar to testosterone. The use of these substances has increased considerably among youngsters and sports practitioners aiming better performance of with aesthetic purposes. The major concern is the effects caused by the inappropriate use of the substances, such as hypertension, myocardial ischemia, and left ventricle hypertrophy.

The objective of the present research was to measure the diameter of the left ventricle lumen and the thickness of the left ventricle myocardium in mice submitted to supraphysiological doses of AAS. A total of 30 female Swiss mice were used in the experiments. The animals received supraphysiological doses of the AAS for 30 days, and during the treatment period, they were put to swim in intercalated days. After treatment animals were euthanized and slides were made from the hearts for measurements.

Results demonstrated that both AAS changed significantly the heart morphology: Testosterone cypionate led to an increase in the ventricular lumen and stanozolol increased left ventricle myocardium thickness. In conclusion, the use of AAS in supraphysiological doses can change the heart morphology and can lead to serious health consequences.

While I don't disagree with the study, another Of-Mice-And-Men is tedious. There would be plenty of human volunteers for AAS (though they wouldn't want their heart cut out ... but neither did the mice).

 

[Michael Scally MD]

Long-Term Treatment with Testosterone Undecanoate Injections in Men with Hypogonadism Alleviates Erectile Dysfunction and Reduces Risk of Major Adverse Cardiovascular Events, Prostate Cancer, and Mortality

OBJECTIVE: The association between erectile dysfunction (ED), hypogonadism, cardiovascular disease, and type 2 diabetes is well documented, but long-term data are limited. The aim of this study is to investigate effects of long-term testosterone therapy (TTh) with testosterone undecanoate in men with hypogonadism and ED.

PATIENTS AND METHODS: Observational, prospective registry of 805 hypogonadal men with different degrees of ED, evaluated by the International Index of Erectile Function - Erectile Function Domain. Four hundred and twelve patients underwent TTh, 393 patients served as controls, with an observation period up to 12 years.

RESULTS: TTh led to substantial and sustained reduction of ED; improvement in erectile function was significant for each successive year until year 9. This was accompanied by improvements in cardiometabolic risk factors and urinary function throughout the 12-year follow-up period.

Benefits of TTh were stronger for patients with moderate/severe ED than for patients with no/minor ED. Incidence of prostate cancer, major adverse cardiovascular events, and mortality were significantly lower in men on TTh compared with untreated men.

CONCLUSION: Long-term TTh for up to 12 years alleviates ED, improves cardiometabolic risk factors, and reduces prostate cancer. Patients must stay on TTh consistently for a long time to achieve maximum benefits of TTh.

Saad F, Caliber M, Doros G, Haider KS, Haider A. Long-term treatment with testosterone undecanoate injections in men with hypogonadism alleviates erectile dysfunction and reduces risk of major adverse cardiovascular events, prostate cancer, and mortality. The aging male: the official journal of the International Society for the Study of the Aging Male 2019:1-12. https://www.tandfonline.com/doi/abs/10.1080/13685538.2019.1575354?journalCode=itam20

 

[Michael Scally MD]

Diminished Cholesterol Efflux Mediated by HDL and Coronary Artery Disease in Anabolic Androgenic Steroid Users

Highlights
· Anabolic androgenic steroids (AAS) abuse impairs the cholesterol efflux mediated by HDL.
· AAS abuse seems to be correlated with lower cholesterol efflux and subclinical coronary artery disease (CAD).
· We found at least 2 coronary arteries with plaques in 25% of AAS users.

BACKGROUND AND AIMS: Anabolic androgenic steroids (AAS) have been associated with coronary artery disease (CAD). AAS abuse leads to a remarkable decrease in high-density lipoprotein (HDL) plasma concentration, which could be a key factor in the atherosclerotic process.

Moreover, not only the concentration of HDL, but also its functionality, plays a pivotal role in CAD. We tested the functionality of HDL by cholesterol efflux and antioxidant capacity. We also evaluated the prevalence of CAD in AAS users.

METHODS: Twenty strength-trained AAS users (AASU) age 29+/-5yr, 20 age-matched strength-trained AAS nonusers (AASNU), and 10 sedentary controls (SC) were enrolled in this cross-sectional study.

Functionality of HDL was evaluated by (14)C-cholesterol efflux and the ability of HDL in inhibiting LDL oxidation. Coronary artery was evaluated with coronary computed tomography angiography.

RESULTS: Cholesterol efflux was lower in AASU compared with AASNU and SC (20 vs. 23 vs. 24%, respectively, p<0.001). However, the lag time for LDL oxidation was higher in AASU compared with AASNU and SC (41 vs 13 vs 11min, respectively, p<0.001).

We found at least 2 coronary arteries with plaques in 25% of AASU. None of the AASNU and SC had plaques. The time of AAS use was negatively associated with cholesterol efflux.

CONCLUSIONS: This study indicates that AAS abuse impairs the cholesterol efflux mediated by HDL. Long-term AAS use seems to be correlated with lower cholesterol efflux and early subclinical CAD in this population.

Souza FR, Dos Santos MR, Porello RA, et al. Diminished cholesterol efflux mediated by HDL and coronary artery disease in young male anabolic androgenic steroid users. Atherosclerosis 2019;283:100-5. https://www.atherosclerosis-journal.com/article/S0021-9150(19)30084-X/abstract