Good God are you kidding me!
MESO-Rx
Anabolic Steroids
AAS and Cardiovascular/Pulmonary Function
- Thread starter Michael Scally MD
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Good God are you kidding me!
[Open Access] Testosterone and Cardiovascular Disease
Cardiovascular disease [CVD] is a leading cause of mortality accounting for a global incidence of over 31%.
Atherosclerosis is the primary pathophysiology underpinning most types of CVD.
Historically, modifiable and non-modifiable risk factors were suggested to precipitate CVD.
Recently, epidemiological studies have identified emerging risk factors including [LOW] HYPOtestosteronaemia, which have been associated with CVD.
Previously considered in the realms of reproductive biology, testosterone is now believed to play a critical role in the cardiovascular system in health and disease.
The actions of testosterone as they relate to the cardiac vasculature and its implication in cardiovascular pathology is reviewed.
Tambo A, Roshan MH, Pace NP. Testosterone and Cardiovascular Disease. Open Cardiovasc Med J 2016;10:1-10. Testosterone and Cardiovascular Disease ~ Fulltext
Cardiovascular disease [CVD] is a leading cause of mortality accounting for a global incidence of over 31%.
Atherosclerosis is the primary pathophysiology underpinning most types of CVD.
Historically, modifiable and non-modifiable risk factors were suggested to precipitate CVD.
Recently, epidemiological studies have identified emerging risk factors including [LOW] HYPOtestosteronaemia, which have been associated with CVD.
Previously considered in the realms of reproductive biology, testosterone is now believed to play a critical role in the cardiovascular system in health and disease.
The actions of testosterone as they relate to the cardiac vasculature and its implication in cardiovascular pathology is reviewed.
Tambo A, Roshan MH, Pace NP. Testosterone and Cardiovascular Disease. Open Cardiovasc Med J 2016;10:1-10. Testosterone and Cardiovascular Disease ~ Fulltext
Gosai JN, Charalampidis P, Nikolaidou T, et al. Revascularization with percutaneous coronary intervention does not affect androgen status in males with chronic stable angina pectoris. Andrology. Revascularization with percutaneous coronary intervention does not affect androgen status in males with chronic stable angina pectoris - Gosai - 2016 - Andrology - Wiley Online Library
There is a clear association between low serum testosterone and coronary artery disease (CAD) in men.
Hypotestosteronaemia is associated with accelerated atherosclerosis and a quarter of men with CAD are biochemically hypogonadal. Amongst those with CAD, hypotestosteronaemia is associated with increased mortality.
Testosterone vasodilates coronary arteries, and exogenous testosterone reduces ischaemia. Whether hypotestosteronaemia is a cause or a consequence of CAD remains unanswered.
The aim of this prospective observational study was to investigate whether coronary revascularization affected androgen status in men with stable angina pectoris. Twenty five men (mean age 62.7, SD 9.18) with angiographically significant CAD and symptomatic angina underwent full coronary revascularization by percutaneous coronary intervention.
Androgen status and symptoms of angina, stress, depression and sexual function were assessed before, and at one and 6 months after the coronary revascularization. All patients underwent complete revascularization which was associated with a significant reduction in angina symptoms and ischaemia.
No significant difference was seen in total testosterone (11.33 nmol/L baseline; 12.56, 1 month post; 13.04 at 6 months; p = 0.08). A significant and sustained rise in sex hormone-binding globulin was seen (33.99 nm/L baseline; 36.11 nm/L 1 month post PCI; 37.94 nm/L at 6 months; p = 0.03).
Overall, there was no significant alteration in any other marker of androgen status including free testosterone or bioavailable testosterone. There was no change in symptoms of anxiety, depression or sexual function. Coronary revascularization has no sustained effect on androgen status.
This supports the hypothesis that hypotestosteronaemia is not a consequence of angina pectoris or myocardial ischaemia.
There is a clear association between low serum testosterone and coronary artery disease (CAD) in men.
Hypotestosteronaemia is associated with accelerated atherosclerosis and a quarter of men with CAD are biochemically hypogonadal. Amongst those with CAD, hypotestosteronaemia is associated with increased mortality.
Testosterone vasodilates coronary arteries, and exogenous testosterone reduces ischaemia. Whether hypotestosteronaemia is a cause or a consequence of CAD remains unanswered.
The aim of this prospective observational study was to investigate whether coronary revascularization affected androgen status in men with stable angina pectoris. Twenty five men (mean age 62.7, SD 9.18) with angiographically significant CAD and symptomatic angina underwent full coronary revascularization by percutaneous coronary intervention.
Androgen status and symptoms of angina, stress, depression and sexual function were assessed before, and at one and 6 months after the coronary revascularization. All patients underwent complete revascularization which was associated with a significant reduction in angina symptoms and ischaemia.
No significant difference was seen in total testosterone (11.33 nmol/L baseline; 12.56, 1 month post; 13.04 at 6 months; p = 0.08). A significant and sustained rise in sex hormone-binding globulin was seen (33.99 nm/L baseline; 36.11 nm/L 1 month post PCI; 37.94 nm/L at 6 months; p = 0.03).
Overall, there was no significant alteration in any other marker of androgen status including free testosterone or bioavailable testosterone. There was no change in symptoms of anxiety, depression or sexual function. Coronary revascularization has no sustained effect on androgen status.
This supports the hypothesis that hypotestosteronaemia is not a consequence of angina pectoris or myocardial ischaemia.
Testosterone Deprivation Accelerates Cardiac Dysfunction In Obese Male Rats
Low testosterone level is associated with increased risks of cardiovascular diseases. Since obese-insulin resistant condition could impair cardiac function and that the incidence of obesity is increased in ageing men, a condition of testosterone deprivation could aggravate the cardiac dysfunction in obese-insulin resistant subjects. However, the mechanism underlying this adverse effect is unclear.
This study investigated the effects of obesity on metabolic parameters, heart rate variability (HRV), left ventricular (LV) function and cardiac mitochondrial function in testosterone-deprived rats. Orchiectomized or sham operated male Wistar rats (n=36/group) were randomly divided into groups and were given either a normal diet (19.77% fat) or a high-fat diet (57.60% fat) for 12 weeks. Metabolic parameters, HRV, LV function and cardiac mitochondrial function were determined at 4, 8 and 12 weeks after the start of each feeding program.
We found that insulin resistance was seen after 8 weeks of the consumption of a high-fat diet in both sham (HFS) and orchiectomized (HFO) rats. Neither the normal diet sham (NDS) group nor normal diet orchiectomized (NDO) rats developed insulin resistance. The development of depressed HRV, LV contractile dysfunction and increased cardiac mitochondrial reactive oxygen species production was observed earlier in orchiectomized (NDO and HFO) rats at week 4, whereas HFS rats exhibited these impairments later at week 8.
These findings suggest that testosterone deprivation accelerates the impairment of cardiac autonomic regulation and LV function via increased oxidative stress and impaired cardiac mitochondrial function in obese-orchiectomized male rats.
Pongkan W, Pintana H, Sivasinprasan S, Jaiwongkam T, Chattipakorn S, Chattipakorn N. Testosterone deprivation accelerates cardiac dysfunction in obese male rats. Journal of Endocrinology. http://joe.endocrinology-journals.org/content/early/2016/03/21/JOE-16-0002.abstract
Low testosterone level is associated with increased risks of cardiovascular diseases. Since obese-insulin resistant condition could impair cardiac function and that the incidence of obesity is increased in ageing men, a condition of testosterone deprivation could aggravate the cardiac dysfunction in obese-insulin resistant subjects. However, the mechanism underlying this adverse effect is unclear.
This study investigated the effects of obesity on metabolic parameters, heart rate variability (HRV), left ventricular (LV) function and cardiac mitochondrial function in testosterone-deprived rats. Orchiectomized or sham operated male Wistar rats (n=36/group) were randomly divided into groups and were given either a normal diet (19.77% fat) or a high-fat diet (57.60% fat) for 12 weeks. Metabolic parameters, HRV, LV function and cardiac mitochondrial function were determined at 4, 8 and 12 weeks after the start of each feeding program.
We found that insulin resistance was seen after 8 weeks of the consumption of a high-fat diet in both sham (HFS) and orchiectomized (HFO) rats. Neither the normal diet sham (NDS) group nor normal diet orchiectomized (NDO) rats developed insulin resistance. The development of depressed HRV, LV contractile dysfunction and increased cardiac mitochondrial reactive oxygen species production was observed earlier in orchiectomized (NDO and HFO) rats at week 4, whereas HFS rats exhibited these impairments later at week 8.
These findings suggest that testosterone deprivation accelerates the impairment of cardiac autonomic regulation and LV function via increased oxidative stress and impaired cardiac mitochondrial function in obese-orchiectomized male rats.
Pongkan W, Pintana H, Sivasinprasan S, Jaiwongkam T, Chattipakorn S, Chattipakorn N. Testosterone deprivation accelerates cardiac dysfunction in obese male rats. Journal of Endocrinology. http://joe.endocrinology-journals.org/content/early/2016/03/21/JOE-16-0002.abstract
ACCELERATE Puts the Brake on CETP Inhibition [HDL]
http://cardiobrief.org/2016/04/03/accelerate-puts-the-brake-on-cetp-inhibition/
12,000 high risk patients were randomized to evacetrapib or placebo.
Evacetrapib, as anticipated, had a potent effect on lipids levels. HDL was dramatically increased by 130%, from 46 mg/dL in the placebo group to a whopping 104 mg/dL in the evacetrapib group. LDL levels also underwent a big change, from 84 mg/dL in the placebo group to 55 mg/dL in the evacetrapib group. One surprising finding was that the hsCRP increased by 4.6% under evacetrapib but decreased by 8% in the placebo group.
But the lipid results did not translate into clinical benefit. The primary endpoint (CV death, MI, stroke, coronary revascularization or hospitalization for unstable angina) was nearly identical in the two groups: 12.8% in the evacetrapib group versus 12.7% in the placebo group. There were no significant differences in any of the secondary endpoints.
The failure of the CETP trials has led many experts to abandon the idea that simply raising HDL levels would prove to be beneficial. Opinion is now divided whether or not HDL has an important independent mechanistic role. Some believe that HDL still plays an important role but the HDL number is less important than measurements of its function.
http://cardiobrief.org/2016/04/03/accelerate-puts-the-brake-on-cetp-inhibition/
12,000 high risk patients were randomized to evacetrapib or placebo.
Evacetrapib, as anticipated, had a potent effect on lipids levels. HDL was dramatically increased by 130%, from 46 mg/dL in the placebo group to a whopping 104 mg/dL in the evacetrapib group. LDL levels also underwent a big change, from 84 mg/dL in the placebo group to 55 mg/dL in the evacetrapib group. One surprising finding was that the hsCRP increased by 4.6% under evacetrapib but decreased by 8% in the placebo group.
But the lipid results did not translate into clinical benefit. The primary endpoint (CV death, MI, stroke, coronary revascularization or hospitalization for unstable angina) was nearly identical in the two groups: 12.8% in the evacetrapib group versus 12.7% in the placebo group. There were no significant differences in any of the secondary endpoints.
The failure of the CETP trials has led many experts to abandon the idea that simply raising HDL levels would prove to be beneficial. Opinion is now divided whether or not HDL has an important independent mechanistic role. Some believe that HDL still plays an important role but the HDL number is less important than measurements of its function.
Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition With Evacetrapib in Patients at a High Risk for Vascular Outcomes - ACCELERATE
Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition With Evacetrapib in Patients at a High Risk for Vascular Outcomes - American College of Cardiology
Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition With Evacetrapib in Patients at a High Risk for Vascular Outcomes - American College of Cardiology
Clinical Effects of Testosterone Supplementation Among Hypo-Androgenic Men With Preexisting Severe Coronary Artery Disease: The Intermountain Heart Collaborative Study
Program Planner
Introduction: Low serum testosterone (T) is an independent risk factor for CV and total mortality. The impact of T therapy on CV outcomes, especially among older men with pre-existing severe CAD, is unknown.
Methods: All men >50 yrs of age, with severe CAD (≥70% stenosis), a low (<212 ng/dL) baseline T level, 1 follow-up (f/u) T level and 3 yrs of clinical f/u were evaluated. T was stratified into categories: persistent low (<212), normal (212-742), and high (>742). Cox hazard regression analysis was performed to associate T categories with major adverse cardiovascular events (MACE) including death [D], non-fatal MI, and stroke.
Results: A total of 755 men (age 68.0 ± 9.6 y, diabetes: 50%, hypertension: 83%, hyperlipidemia: 81%, smokers: 33%, prior MI: 23%) were studied. Event rates at 1 and 3-y by achieved T level, and adjusted HRs, are shown in Table. Overall 3-y rates of MACE, D and MI were 24.5%, 17.6% and 8.1% respectively. Pts supplemented to normal/high T had reduced 3-y MACE (HR=0.77 [0.56-1.04]), D (HR=0.67 [0.47-0.97]) and MI (HR 0.52 [0.31, 0.87]) compared to low T subjects. Results were similar for 1-y MACE (HR=0.63 [0.40, 1.00]), D (HR=0.93 [0.51, 1.69]) and MI (HR=0.26 [0.31, 0.87]).
Conclusions: Among elderly men with severe CAD and low T, T therapy was associated with reduced MACE, D and MI over 3-y compared to no or ineffective supplementation. A marked protective effect of T supplementation on MI incidence during first yr of f/u was noted, giving further evidence of CV safety associated with T supplementation.
Program Planner
Introduction: Low serum testosterone (T) is an independent risk factor for CV and total mortality. The impact of T therapy on CV outcomes, especially among older men with pre-existing severe CAD, is unknown.
Methods: All men >50 yrs of age, with severe CAD (≥70% stenosis), a low (<212 ng/dL) baseline T level, 1 follow-up (f/u) T level and 3 yrs of clinical f/u were evaluated. T was stratified into categories: persistent low (<212), normal (212-742), and high (>742). Cox hazard regression analysis was performed to associate T categories with major adverse cardiovascular events (MACE) including death [D], non-fatal MI, and stroke.
Results: A total of 755 men (age 68.0 ± 9.6 y, diabetes: 50%, hypertension: 83%, hyperlipidemia: 81%, smokers: 33%, prior MI: 23%) were studied. Event rates at 1 and 3-y by achieved T level, and adjusted HRs, are shown in Table. Overall 3-y rates of MACE, D and MI were 24.5%, 17.6% and 8.1% respectively. Pts supplemented to normal/high T had reduced 3-y MACE (HR=0.77 [0.56-1.04]), D (HR=0.67 [0.47-0.97]) and MI (HR 0.52 [0.31, 0.87]) compared to low T subjects. Results were similar for 1-y MACE (HR=0.63 [0.40, 1.00]), D (HR=0.93 [0.51, 1.69]) and MI (HR=0.26 [0.31, 0.87]).
Conclusions: Among elderly men with severe CAD and low T, T therapy was associated with reduced MACE, D and MI over 3-y compared to no or ineffective supplementation. A marked protective effect of T supplementation on MI incidence during first yr of f/u was noted, giving further evidence of CV safety associated with T supplementation.
[Open Access] 2016 ACC Expert Consensus Decision Pathway on the Role of Non-Statin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk
http://content.onlinejacc.org/article.aspx?articleID=2510936
The American College of Cardiology and American Heart Association have issued new guidance on initiating non-statin therapy to lower LDL cholesterol in patients who are currently using, or have attempted to use, statins.
The document offers algorithms for adjunctive non-statin therapy in the four distinct patient groups identified in the ACC/AHA 2013 lipid guidelines:
• Patients with clinical atherosclerotic cardiovascular disease
• Those with LDL levels at or above 190 mg/dL not caused by secondary conditions (e.g., hypothyroidism)
• Patients aged 40–75 with diabetes and LDL levels between 70 and 189 mg/dL
• Those aged 40–75 without diabetes but with LDL levels between 70 and 189 mg/dL and with predicted 10-year risk for atherosclerotic cardiovascular disease of 7.5% or higher
For most higher-risk patients, the new guidelines recommend considering ezetimibe (10 mg) as the first non-statin therapy. Recommendations on incorporating the PCSK9 inhibitors evolocumab and alirocumab, approved in 2015, are also offered.
http://content.onlinejacc.org/article.aspx?articleID=2510936
The American College of Cardiology and American Heart Association have issued new guidance on initiating non-statin therapy to lower LDL cholesterol in patients who are currently using, or have attempted to use, statins.
The document offers algorithms for adjunctive non-statin therapy in the four distinct patient groups identified in the ACC/AHA 2013 lipid guidelines:
• Patients with clinical atherosclerotic cardiovascular disease
• Those with LDL levels at or above 190 mg/dL not caused by secondary conditions (e.g., hypothyroidism)
• Patients aged 40–75 with diabetes and LDL levels between 70 and 189 mg/dL
• Those aged 40–75 without diabetes but with LDL levels between 70 and 189 mg/dL and with predicted 10-year risk for atherosclerotic cardiovascular disease of 7.5% or higher
For most higher-risk patients, the new guidelines recommend considering ezetimibe (10 mg) as the first non-statin therapy. Recommendations on incorporating the PCSK9 inhibitors evolocumab and alirocumab, approved in 2015, are also offered.
Chapter 89. Anabolic Androgenic Steroids and Stroke
Depending on the type of injury produced in the brain, stroke is classified as ischemic (80–85%) or hemorrhagic (15–20%), ischemic stroke being the most frequently reported to be associated with anabolic androgenic steroids (AAS) consumption and the focus of this chapter.
· Stroke
· Anabolic Androgenic Steroids
· Stroke and AAS
· Stroke Associated With Other Drug Addictions
· Conclusions
· Definition of Terms
· Key Facts of Stroke
· Summary Points
Carlos García Esperón, Elena López-Cancio M., Pablo García Bermejo, Antonio Dávalos E.. Anabolic Androgenic Steroids and Stroke. 2016:981-990. Neuropathology of Drug Addictions and Substance Misuse Volume 2, 1st Edition | Victor Preedy | ISBN 9780128002124
Depending on the type of injury produced in the brain, stroke is classified as ischemic (80–85%) or hemorrhagic (15–20%), ischemic stroke being the most frequently reported to be associated with anabolic androgenic steroids (AAS) consumption and the focus of this chapter.
· Stroke
· Anabolic Androgenic Steroids
· Stroke and AAS
· Stroke Associated With Other Drug Addictions
· Conclusions
· Definition of Terms
· Key Facts of Stroke
· Summary Points
Carlos García Esperón, Elena López-Cancio M., Pablo García Bermejo, Antonio Dávalos E.. Anabolic Androgenic Steroids and Stroke. 2016:981-990. Neuropathology of Drug Addictions and Substance Misuse Volume 2, 1st Edition | Victor Preedy | ISBN 9780128002124
Low MS, Vilcassim S, Fedele P, Grigoriadis G. Anabolic androgenic steroids, an easily forgotten cause of polycythaemia and cerebral infarction. Intern Med J 2016;46(4):497-9. Anabolic androgenic steroids, an easily forgotten cause of polycythaemia and cerebral infarction - Low - 2016 - Internal Medicine Journal - Wiley Online Library
Excessive anabolic androgenic steroids (both exogenous and endogenous) are known causes of polycythaemia and ischaemic cardiovascular events. Despite this, they are commonly forgotten in the workup of patients. We report a case of exogenous anabolic androgenic steroid-induced polycythaemia and stroke and explore possible pitfalls for clinicians.
Excessive anabolic androgenic steroids (both exogenous and endogenous) are known causes of polycythaemia and ischaemic cardiovascular events. Despite this, they are commonly forgotten in the workup of patients. We report a case of exogenous anabolic androgenic steroid-induced polycythaemia and stroke and explore possible pitfalls for clinicians.
FDA Pulls Approval of Niacin, Fibrate in Combo with Statins
Medscape: Medscape Access
SILVER SPRING, MD — Citing a lack of cardiovascular benefit, the FDA is taking the unusual step of withdrawing approvals it had previously given for their combined use with statins to treat high cholesterol. https://s3.amazonaws.com/public-inspection.federalregister.gov/2016-08894.pdf ; https://s3.amazonaws.com/public-inspection.federalregister.gov/2016-08887.pdf
The decision affects niacin extended-release (Niaspan, AbbVie) and fenofibric acid (Trilipix, AbbVie), as well as AbbVie's Advicorand Simcor, both of which combine niacin with a statin.
Medscape: Medscape Access
SILVER SPRING, MD — Citing a lack of cardiovascular benefit, the FDA is taking the unusual step of withdrawing approvals it had previously given for their combined use with statins to treat high cholesterol. https://s3.amazonaws.com/public-inspection.federalregister.gov/2016-08894.pdf ; https://s3.amazonaws.com/public-inspection.federalregister.gov/2016-08887.pdf
The decision affects niacin extended-release (Niaspan, AbbVie) and fenofibric acid (Trilipix, AbbVie), as well as AbbVie's Advicorand Simcor, both of which combine niacin with a statin.
Statement Issued on Cardiovascular Care of College Athletes
A multidisciplinary task force has issued a joint consensus statement on the cardiovascular care of college athletes. The statement examines cardiovascular risk in student athletes, preparticipation screening (including electrocardiogram to predict risk for sudden death), and recognition and management of cardiac arrest, among other areas.
The task force included representatives from the National Collegiate Athletic Association, American Heart Association, American College of Cardiology, and National Athletic Trainers' Association. The document is available free of charge in the Journal of the American College of Cardiology.
Hainline B, Drezner JA, Baggish A, et al. Interassociation Consensus Statement on Cardiovascular Care of College Student-Athletes. J Am Coll Cardiol. 2016. http://content.onlinejacc.org/article.aspx?articleID=2513587#tab1
Cardiovascular evaluation and care of college student-athletes is gaining increasing attention from both the public and medical communities. Emerging strategies include screening of the general athlete population, recommendations of permissible levels of participation by athletes with identified cardiovascular conditions, and preparation for responding to unanticipated cardiac events in athletic venues. The primary focus has been sudden cardiac death and the utility of screening with or without advanced cardiac screening. The National Collegiate Athletic Association convened a multidisciplinary task force to address cardiovascular concerns in collegiate student-athletes and to develop consensus for an interassociation statement. This document summarizes the task force deliberations and follow-up discussions, and includes available evidence on cardiovascular risk, pre-participation evaluation, and the recognition of and response to cardiac arrest. Future recommendations for cardiac research initiatives, education, and collaboration are also provided.
A multidisciplinary task force has issued a joint consensus statement on the cardiovascular care of college athletes. The statement examines cardiovascular risk in student athletes, preparticipation screening (including electrocardiogram to predict risk for sudden death), and recognition and management of cardiac arrest, among other areas.
The task force included representatives from the National Collegiate Athletic Association, American Heart Association, American College of Cardiology, and National Athletic Trainers' Association. The document is available free of charge in the Journal of the American College of Cardiology.
Hainline B, Drezner JA, Baggish A, et al. Interassociation Consensus Statement on Cardiovascular Care of College Student-Athletes. J Am Coll Cardiol. 2016. http://content.onlinejacc.org/article.aspx?articleID=2513587#tab1
Cardiovascular evaluation and care of college student-athletes is gaining increasing attention from both the public and medical communities. Emerging strategies include screening of the general athlete population, recommendations of permissible levels of participation by athletes with identified cardiovascular conditions, and preparation for responding to unanticipated cardiac events in athletic venues. The primary focus has been sudden cardiac death and the utility of screening with or without advanced cardiac screening. The National Collegiate Athletic Association convened a multidisciplinary task force to address cardiovascular concerns in collegiate student-athletes and to develop consensus for an interassociation statement. This document summarizes the task force deliberations and follow-up discussions, and includes available evidence on cardiovascular risk, pre-participation evaluation, and the recognition of and response to cardiac arrest. Future recommendations for cardiac research initiatives, education, and collaboration are also provided.
Prevalence and Prognosis of a Low Serum Testosterone in Men with Type 2 Diabetes
Background: Since published studies have involved imprecise assays and selected patients with limited additional data and follow-up, the consequences of a low serum testosterone in diabetes are unclear. The present study assessed the prevalence, associates and prognosis of a low testosterone in community-dwelling men with type 2 diabetes.
Design: Longitudinal observational study.
Patients: 788 (mean±SD age 65.8±11.3 years) followed for 4.0±1.1 years.
Measurements: Serum testosterone, SHBG, erectile dysfunction (ED; Sexual Health Inventory for Men score <22), anaemia (haemoglobin <130 g/L), all-cause mortality.
Results: The mean±SD total serum testosterone by liquid chromatography/mass spectrometry was 13.1±5.9 nmol/L (30.6% <10 nmol/L). Most men with a total testosterone <10 nmol/L (67.0%) had a normal/low serum LH.
Serum testosterone was independently associated with anaemia (P<0.001) but not ED (P=0.80) in logistic regression models. The optimal cut-point (Youden Index) for anaemia was 9.8 nmol/L (sensitivity 53.6%, specificity 75.4%).
During follow-up, 102 men (12.9%) died. There was a U-shaped relationship between total serum testosterone quintiles and death (P=0.003, log rank test). The middle quintile (>11.1 to ≤13.7 nmol/L) had the lowest risk and there was a 78% increased risk for highest (>16.9 nmol/L) vs lowest (≤8.6 nmol/L) quintile in Cox proportional hazards modelling (P=0.036). Free serum testosterone and SHBG quintiles were not associated with death.
Conclusions: These data provide some support for the general conventional serum testosterone <10 nmol/L cut-point in identifying an increased risk of anaemia and subsequent death in men with type 2 diabetes but indicate that high-normal levels are also an adverse prognostic indicator. This article is protected by copyright. All rights reserved.
Hamilton EJ, Davis WA, Makepeace A, et al. Prevalence and prognosis of a low serum testosterone in men with type 2 diabetes: The Fremantle Diabetes Study Phase II. Clinical Endocrinology. Prevalence and prognosis of a low serum testosterone in men with type 2 diabetes: The Fremantle Diabetes Study Phase II - Hamilton - 2016 - Clinical Endocrinology - Wiley Online Library
Background: Since published studies have involved imprecise assays and selected patients with limited additional data and follow-up, the consequences of a low serum testosterone in diabetes are unclear. The present study assessed the prevalence, associates and prognosis of a low testosterone in community-dwelling men with type 2 diabetes.
Design: Longitudinal observational study.
Patients: 788 (mean±SD age 65.8±11.3 years) followed for 4.0±1.1 years.
Measurements: Serum testosterone, SHBG, erectile dysfunction (ED; Sexual Health Inventory for Men score <22), anaemia (haemoglobin <130 g/L), all-cause mortality.
Results: The mean±SD total serum testosterone by liquid chromatography/mass spectrometry was 13.1±5.9 nmol/L (30.6% <10 nmol/L). Most men with a total testosterone <10 nmol/L (67.0%) had a normal/low serum LH.
Serum testosterone was independently associated with anaemia (P<0.001) but not ED (P=0.80) in logistic regression models. The optimal cut-point (Youden Index) for anaemia was 9.8 nmol/L (sensitivity 53.6%, specificity 75.4%).
During follow-up, 102 men (12.9%) died. There was a U-shaped relationship between total serum testosterone quintiles and death (P=0.003, log rank test). The middle quintile (>11.1 to ≤13.7 nmol/L) had the lowest risk and there was a 78% increased risk for highest (>16.9 nmol/L) vs lowest (≤8.6 nmol/L) quintile in Cox proportional hazards modelling (P=0.036). Free serum testosterone and SHBG quintiles were not associated with death.
Conclusions: These data provide some support for the general conventional serum testosterone <10 nmol/L cut-point in identifying an increased risk of anaemia and subsequent death in men with type 2 diabetes but indicate that high-normal levels are also an adverse prognostic indicator. This article is protected by copyright. All rights reserved.
Hamilton EJ, Davis WA, Makepeace A, et al. Prevalence and prognosis of a low serum testosterone in men with type 2 diabetes: The Fremantle Diabetes Study Phase II. Clinical Endocrinology. Prevalence and prognosis of a low serum testosterone in men with type 2 diabetes: The Fremantle Diabetes Study Phase II - Hamilton - 2016 - Clinical Endocrinology - Wiley Online Library
Chan YX, Knuiman MW, Hung J, et al. Neutral associations of testosterone, dihydrotestosterone and estradiol with fatal and non-fatal cardiovascular events, and mortality in men aged 17-97 years. Clinical Endocrinology. Neutral associations of testosterone, dihydrotestosterone and estradiol with fatal and non-fatal cardiovascular events, and mortality in men aged 17-97 years - Chan - 2016 - Clinical Endocrinology - Wiley Online Library
Context: Lower testosterone (T) is associated with poorer health outcomes in older men, however, the relationship between T, dihydrotestosterone (DHT) and estradiol (E2) with cardiovascular disease (CVD) in younger to middle-aged men remains unclear.
Objectives: We assessed associations between endogenous sex hormones with mortality (all-cause and CVD) and CVD events, in a cohort of men aged 17-97 years.
Participants and methods: Sex hormones were assayed using mass spectrometry in 2,143 men from the 1994/5 Busselton Health Survey. Outcomes to December 2010 were analysed.
Results: Of the 1,804 men included in the analysis, mean age was 50.3±16.8 years and 68.9% of men were aged <60. Mean follow-up period was 14.9 years. There were 319 deaths, 141 CVD deaths, and 399 CVD events. Compared to the full cohort, men who died had lower baseline T (12.0±4.4 vs 13.6±4.9 nmol/L), free T (181.9±52.9 vs 218.3±63.8 pmol/L) and DHT (1.65±0.64 vs 1.70±0.72 nmol/L), but higher E2 (64.0±32 vs 60.1±30.2 pmol/L). After adjustment for risk factors, T was not associated with mortality (adjusted HR=0.90, 95% CI 0.79-1.04; p=0.164 for every increase in 1 SD of T), CVD deaths (adjusted HR=1.04, 95% CI 0.84-1.29; p=0.708) or CVD events (adjusted HR=1.03, 95% CI 0.92-1.15, p=0.661). No associations were found for free T, DHT or E2. Results were similar for men older and younger than 60 years.
Conclusions: In predominantly middle-aged men, T, DHT and E2 do not influence mortality or CVD outcomes. This neutral association of hormones with CVD contrasts with prior studies of older men.
Context: Lower testosterone (T) is associated with poorer health outcomes in older men, however, the relationship between T, dihydrotestosterone (DHT) and estradiol (E2) with cardiovascular disease (CVD) in younger to middle-aged men remains unclear.
Objectives: We assessed associations between endogenous sex hormones with mortality (all-cause and CVD) and CVD events, in a cohort of men aged 17-97 years.
Participants and methods: Sex hormones were assayed using mass spectrometry in 2,143 men from the 1994/5 Busselton Health Survey. Outcomes to December 2010 were analysed.
Results: Of the 1,804 men included in the analysis, mean age was 50.3±16.8 years and 68.9% of men were aged <60. Mean follow-up period was 14.9 years. There were 319 deaths, 141 CVD deaths, and 399 CVD events. Compared to the full cohort, men who died had lower baseline T (12.0±4.4 vs 13.6±4.9 nmol/L), free T (181.9±52.9 vs 218.3±63.8 pmol/L) and DHT (1.65±0.64 vs 1.70±0.72 nmol/L), but higher E2 (64.0±32 vs 60.1±30.2 pmol/L). After adjustment for risk factors, T was not associated with mortality (adjusted HR=0.90, 95% CI 0.79-1.04; p=0.164 for every increase in 1 SD of T), CVD deaths (adjusted HR=1.04, 95% CI 0.84-1.29; p=0.708) or CVD events (adjusted HR=1.03, 95% CI 0.92-1.15, p=0.661). No associations were found for free T, DHT or E2. Results were similar for men older and younger than 60 years.
Conclusions: In predominantly middle-aged men, T, DHT and E2 do not influence mortality or CVD outcomes. This neutral association of hormones with CVD contrasts with prior studies of older men.
[Open Access] Testosterone Replacement Therapy: New Data on Efficacy and Cardiovascular Safety
One of the most controversial questions in cardiovascular pharmacology is whether testosterone replacement therapy is safe for the cardiovascular system, especially in elderly men. There is little debate that as men age, their testosterone levels fall and low testosterone levels have an association with more atherosclerosis, coronary artery disease, and heart failure.
A key debated question is whether the administration of exogenous testosterone to increase testosterone levels back to normal alters the incidence of adverse cardiovascular events. In recent papers in the Journal of the American Heart Association,1,2 Journal of the American College of Cardiology,3 and Sexual Medicine Reviews,4 my colleagues and I have reviewed the numerous studies on this subject.
This literature presents some of the most controversial group of papers that I have reviewed, with some studies suggesting that testosterone use is associated with an increase in adverse cardiac events including major adverse cardiac events (cardiovascular death, myocardial infarction, stroke), whereas others suggest just the opposite.
The problem is that many of these studies are observational, the testosterone preparations vary, not all studies have followed up the testosterone levels once therapy is started, some studies included soft end points to describe the adverse cardiac events, the cardiac events were not prespecified as the primary outcome, the duration of follow-up was short, the baseline characteristics of the patients were very heterogeneous with varying degrees of underlying risk factors, and other issues that we have described.
The only way this issue will ever truly be resolved is for a large prospective, randomized, blinded, long-term study to be carried out with major adverse cardiac events as the primary end point. It is my understanding that an industry consortium is developing such a protocol. However, it will be many years before data are available. In the meantime, the Food and Drug Administration has released new restrictions on the labeling for testosterone replacement therapy, as recently described.3
Although testosterone is known to be effective in patients with primary hypogonadism, the significance of the low testosterone associated with aging has been debated. There are mixed data suggesting that in these types of patients, testosterone replacement may improve sexual functioning (improved libido and erectile function), improve muscle mass, decrease fat mass, improve muscle strength, and perhaps improve mood and energy level.
The Testosterone Trials, sponsored by the National Institutes of Health, were conducted to help clarify the confusing literature on testosterone replacement therapy, and the data from these clinical trials are now emerging.5 These studies may answer some of the unresolved issues surrounding testosterone replacement therapy.
…
Importantly and in contrast to some of the recent reports that have caused concern about the use of testosterone,6⇓–8 there was no signal for an increase in adverse cardiovascular events in the testosterone group.
…
Although the authors conclude that the number of patients in the study was too low to draw conclusions about the risk of testosterone replacement therapy, it is at least reassuring that no signal for an increase in adverse cardiovascular events was detected. However, larger studies will be needed to definitively rule out any adverse effects of testosterone on the cardiovascular system. It is likely that additional safety data will emerge from the Testosterone Trials Investigators studies.
These investigators are to be congratulated on a study that uses a well-designed systematic approach to assess and show the effectiveness of testosterone replacement therapy on multiple domains in a well-defined patient population. Hopefully, this will be one of several reports from this important group of studies, which helps to clarify the therapeutic role of testosterone replacement therapy.
Kloner RA. Testosterone Replacement Therapy: New Data on Efficacy and Cardiovascular Safety. J Cardiovasc Pharmacol Ther. Testosterone Replacement Therapy
One of the most controversial questions in cardiovascular pharmacology is whether testosterone replacement therapy is safe for the cardiovascular system, especially in elderly men. There is little debate that as men age, their testosterone levels fall and low testosterone levels have an association with more atherosclerosis, coronary artery disease, and heart failure.
A key debated question is whether the administration of exogenous testosterone to increase testosterone levels back to normal alters the incidence of adverse cardiovascular events. In recent papers in the Journal of the American Heart Association,1,2 Journal of the American College of Cardiology,3 and Sexual Medicine Reviews,4 my colleagues and I have reviewed the numerous studies on this subject.
This literature presents some of the most controversial group of papers that I have reviewed, with some studies suggesting that testosterone use is associated with an increase in adverse cardiac events including major adverse cardiac events (cardiovascular death, myocardial infarction, stroke), whereas others suggest just the opposite.
The problem is that many of these studies are observational, the testosterone preparations vary, not all studies have followed up the testosterone levels once therapy is started, some studies included soft end points to describe the adverse cardiac events, the cardiac events were not prespecified as the primary outcome, the duration of follow-up was short, the baseline characteristics of the patients were very heterogeneous with varying degrees of underlying risk factors, and other issues that we have described.
The only way this issue will ever truly be resolved is for a large prospective, randomized, blinded, long-term study to be carried out with major adverse cardiac events as the primary end point. It is my understanding that an industry consortium is developing such a protocol. However, it will be many years before data are available. In the meantime, the Food and Drug Administration has released new restrictions on the labeling for testosterone replacement therapy, as recently described.3
Although testosterone is known to be effective in patients with primary hypogonadism, the significance of the low testosterone associated with aging has been debated. There are mixed data suggesting that in these types of patients, testosterone replacement may improve sexual functioning (improved libido and erectile function), improve muscle mass, decrease fat mass, improve muscle strength, and perhaps improve mood and energy level.
The Testosterone Trials, sponsored by the National Institutes of Health, were conducted to help clarify the confusing literature on testosterone replacement therapy, and the data from these clinical trials are now emerging.5 These studies may answer some of the unresolved issues surrounding testosterone replacement therapy.
…
Importantly and in contrast to some of the recent reports that have caused concern about the use of testosterone,6⇓–8 there was no signal for an increase in adverse cardiovascular events in the testosterone group.
…
Although the authors conclude that the number of patients in the study was too low to draw conclusions about the risk of testosterone replacement therapy, it is at least reassuring that no signal for an increase in adverse cardiovascular events was detected. However, larger studies will be needed to definitively rule out any adverse effects of testosterone on the cardiovascular system. It is likely that additional safety data will emerge from the Testosterone Trials Investigators studies.
These investigators are to be congratulated on a study that uses a well-designed systematic approach to assess and show the effectiveness of testosterone replacement therapy on multiple domains in a well-defined patient population. Hopefully, this will be one of several reports from this important group of studies, which helps to clarify the therapeutic role of testosterone replacement therapy.
Kloner RA. Testosterone Replacement Therapy: New Data on Efficacy and Cardiovascular Safety. J Cardiovasc Pharmacol Ther. Testosterone Replacement Therapy
[For Full-Text Email mike.scally@asih.net (Include Title)]
De Smet MAJ, Lapauw B, De Backer T. Sex steroids in relation to cardiac structure and function in men. Andrologia. Sex steroids in relation to cardiac structure and function in men - De Smet - 2016 - Andrologia - Wiley Online Library
The prevalence of testosterone substitution as well as of androgen deprivation therapy in men is increasing. This review aims to summarise available knowledge of the effects of sex steroids on cardiac structure and function in men.
MEDLINE was searched through PubMed. Original studies, systematic reviews and meta-analyses, and relevant citations were screened. A short-term hormonal intervention study in healthy young men with respect to echocardiographic parameters of structure and function was performed. Preclinical research provides sufficient evidence for the heart as a substrate for sex hormones.
In animals, administration of oestradiol appears to have beneficial effects on cardiac structure and function, whereas administration of testosterone to noncastrated animals adversely affects cardiac function. However, the effects of sex steroids on cardiac function and structure appear more heterogeneous in human observational studies while comparative, prospective studies in humans are lacking.
It is concluded that although effects of testosterone substitution as well as of androgen deprivation on cardiac structure and function can be expected based on pre-clinical research, there exists an important knowledge gap of the effects of hormonal intervention in men. As such, there is a need to address this question in future prospective intervention trials.
De Smet MAJ, Lapauw B, De Backer T. Sex steroids in relation to cardiac structure and function in men. Andrologia. Sex steroids in relation to cardiac structure and function in men - De Smet - 2016 - Andrologia - Wiley Online Library
The prevalence of testosterone substitution as well as of androgen deprivation therapy in men is increasing. This review aims to summarise available knowledge of the effects of sex steroids on cardiac structure and function in men.
MEDLINE was searched through PubMed. Original studies, systematic reviews and meta-analyses, and relevant citations were screened. A short-term hormonal intervention study in healthy young men with respect to echocardiographic parameters of structure and function was performed. Preclinical research provides sufficient evidence for the heart as a substrate for sex hormones.
In animals, administration of oestradiol appears to have beneficial effects on cardiac structure and function, whereas administration of testosterone to noncastrated animals adversely affects cardiac function. However, the effects of sex steroids on cardiac function and structure appear more heterogeneous in human observational studies while comparative, prospective studies in humans are lacking.
It is concluded that although effects of testosterone substitution as well as of androgen deprivation on cardiac structure and function can be expected based on pre-clinical research, there exists an important knowledge gap of the effects of hormonal intervention in men. As such, there is a need to address this question in future prospective intervention trials.
new to the game
New Member
I feel like I need to go to med school to be able to grasp most of these articles. But, and tell me if I'm wrong, it seems that what I have gleaned is that too much Testosterone or too Little can be the cause of heart disease. Is that accurate? Additionally, I have a question. If someone was told by their doctor that they have an irregular heart beat would suggest that they not use AAS? If no, which I assume to be the answer, then is there something that you do suggest they do? (besides quitting their high stress job, and stop using alcohol, tobacco, and caffeine)
Alizade E, Avci A, Tabakci MM, et al. Comparison of Right Ventricle Systolic Function between Long-Term Anabolic-Androgenic Steroid User and Nonuser Bodybuilder Athletes: A Study of Two-Dimensional Speckle Tracking Echocardiography. Echocardiography. Comparison of Right Ventricle Systolic Function between Long-Term Anabolic–Androgenic Steroid User and Nonuser Bodybuilder Athletes: A Study of Two-Dimensional Speckle Tracking Echocardiography - Alizade - 2016 - Echocardiography - Wiley Online Library
BACKGROUND: Right ventricular (RV) effects of long-term use of anabolic-androgenic steroids (AAS) are not clearly known. The aim of this study was to assess RV systolic functions by two-dimensional speckle tracking echocardiography (2DSTE) in AAS user and nonuser bodybuilders.
METHODS: A total of 33 competitive male bodybuilders (15 AAS users, 18 AAS nonusers) were assessed. To assess RV systolic functions, all participants underwent standard two-dimensional and Doppler echocardiography, and 2DSTE.
RESULTS: Interventricular septal thickness, left ventricle posterior wall thickness, relative wall thickness, and left ventricle mass index were significantly higher in AAS users than nonusers. While standard diastolic parameters were not statistically different between the groups, tissue Doppler parameters including RV E' and E'/A' were lower in AAS users than nonusers (10.1 +/- 2.0 vs. 12.7 +/- 2.1; P = 0.001, 1.1 +/- 0.1 vs. 1.5 +/- 0.4; P = 0.009, respectively). Tricuspid annular plane systolic excursion, RV fractional area change, and RV S' were in normal ranges. However, RV S' was found to be lower in users than nonusers (12.2 +/- 2.2 vs. 14.6 +/- 2.8, P = 0.011). RV free wall longitudinal strain and strain rate were decreased in AAS users in comparison with nonusers (-20.2 +/- 3.1 vs. -23.3 +/- 3.5; P = 0.012, -3.2 +/- 0.1 vs. -3.4 +/- 0.1; P = 0.022, respectively). In addition, there were good correlations between 2DSTE parameters and RV S', E', and E'/A'.
CONCLUSION: Despite normal standard systolic echo parameters, peak systolic RV free wall strain and strain rate were reduced in AAS user bodybuilders in comparison with nonusers. Strain and strain rate by 2DSTE may be useful for early determination of subclinical RV dysfunction in AAS user bodybuilders.
BACKGROUND: Right ventricular (RV) effects of long-term use of anabolic-androgenic steroids (AAS) are not clearly known. The aim of this study was to assess RV systolic functions by two-dimensional speckle tracking echocardiography (2DSTE) in AAS user and nonuser bodybuilders.
METHODS: A total of 33 competitive male bodybuilders (15 AAS users, 18 AAS nonusers) were assessed. To assess RV systolic functions, all participants underwent standard two-dimensional and Doppler echocardiography, and 2DSTE.
RESULTS: Interventricular septal thickness, left ventricle posterior wall thickness, relative wall thickness, and left ventricle mass index were significantly higher in AAS users than nonusers. While standard diastolic parameters were not statistically different between the groups, tissue Doppler parameters including RV E' and E'/A' were lower in AAS users than nonusers (10.1 +/- 2.0 vs. 12.7 +/- 2.1; P = 0.001, 1.1 +/- 0.1 vs. 1.5 +/- 0.4; P = 0.009, respectively). Tricuspid annular plane systolic excursion, RV fractional area change, and RV S' were in normal ranges. However, RV S' was found to be lower in users than nonusers (12.2 +/- 2.2 vs. 14.6 +/- 2.8, P = 0.011). RV free wall longitudinal strain and strain rate were decreased in AAS users in comparison with nonusers (-20.2 +/- 3.1 vs. -23.3 +/- 3.5; P = 0.012, -3.2 +/- 0.1 vs. -3.4 +/- 0.1; P = 0.022, respectively). In addition, there were good correlations between 2DSTE parameters and RV S', E', and E'/A'.
CONCLUSION: Despite normal standard systolic echo parameters, peak systolic RV free wall strain and strain rate were reduced in AAS user bodybuilders in comparison with nonusers. Strain and strain rate by 2DSTE may be useful for early determination of subclinical RV dysfunction in AAS user bodybuilders.
^^^^^
Another reason why this is my favorite and most informative Meso thread!
Kudo's to you @Michael Scally MD
Very interesting study, which if confirmed, may prove useful as a means of preventing AAS associated LV dysfunction.
Or are such comments wishful thinking on my behalf?
I mean how often have I informed those who drink ETOH, they are drinking excessively based on the studies before me!
NO, I DO NOT believe AAS are addictive in the same light as ETOH, but for some denial (of adverse effects) supersedes and/or belies reason IMO.
Another reason why this is my favorite and most informative Meso thread!
Kudo's to you @Michael Scally MD
Very interesting study, which if confirmed, may prove useful as a means of preventing AAS associated LV dysfunction.
Or are such comments wishful thinking on my behalf?
I mean how often have I informed those who drink ETOH, they are drinking excessively based on the studies before me!
NO, I DO NOT believe AAS are addictive in the same light as ETOH, but for some denial (of adverse effects) supersedes and/or belies reason IMO.
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1)
CORRECT to little or to much TT may be associated with heart disease, for a variety of reasons
2)
An "irregular heart beat", and how is that defined on a objective basis, as in a specific EKG diagnosis?
3) So is that the reason for your post? You want to run a cycle and your Doc said nope bc you have an "irregular heart beat"?
4) if you're really 32 then you should be familiar with the ANSWER
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