Levels of SHBG are higher in older men, therefore levels of free T decline more steeply than total T as men's age increases.
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shared by Nathan Goodyear on 24 Mar 15
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Testosterone suppresses ventricular remodeling and improves left ventricular function i... - 0 views
www.ncbi.nlm.nih.gov/...PMC4353801
Testosterone therapy heart heart health myocardial infarction heart attack male hormone hormones CVD cardiovascular disease
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shared by Nathan Goodyear on 08 Jun 13
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Evidence for hyperoestrogenaemia as a risk factor for... [Lancet. 1976] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/59076
aromatase aromatase activity testosterone estrogen estradiol estrone MI myocardial infarction low libido gynecomastia low T
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This is just an abstract due to the publication date. However, this study, though small, found that elevated estradiol and estrone levels preceded myocardial infarctions in small study group (15). The surprise was that physical symptoms of slow beard growth, loss of libido, and gynecomastia preceded the events. Also, the testosterone levels were normal. Got that: elevated estrogen levels with normal testosterone levels result in significant symptoms.
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The effect of intravenous vitamin C infusion on periprocedural myocardial injury for pa... - 0 views
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shared by Nathan Goodyear on 15 Jan 14
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Sex steroids and cardiovascular disease Yeap BB - Asian J Androl - 0 views
www.ajandrology.com/article.asp
cardiovascular disease CVD sex estradiol carotid intima-media thickness hormones hormone men Testosterone estrogen
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calculations based on mass action equations may not reflect precisely free T measured using a reference method
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free T declines more steeply with age than total T in both cross-sectional [35] and longitudinal studies, [36] as does free E2 in comparison to total E2
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T may slow development of or progression of atherosclerosis by modulating effects on insulin resistance, inflammation, endothelial function, preclinical atherosclerosis or the vasculature.
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these cross-sectional and longitudinal studies support a relationship between low circulating T with CIMT and higher E2 with its progression
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low levels of total or bioavailable T were associated with aortic atherosclerosis manifested as calcified deposits detected by radiography
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Men with total or free T in the lowest quartile had increased adjusted ORs for PAD defined as ABI <0.90, as did men with free E2 in the highest quartile of values
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The apparent association of SHBG with intermittent claudication reflects the correlation of total T with SHBG, while the contribution of E2 to risk of PAD remains unclear
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men with total T in the lowest quartile of values (<11.7 nmol l−1 ) experienced an increased incidence of stroke or transient ischemic attack
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cohort studies in mostly older men have supported the association of lower androgen levels with higher mortality
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lower total or free T levels were associated with mortality in older men, but with discordant results for cause-specific mortality and for associations of E2
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several large studies identifying lower endogenous levels of total or free T as independent predictors of all-cause or CVD-related deaths in middle-aged and older men
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T exhibits anti-inflammatory effects, enhances flow-mediated brachial artery reactivity, and reduces arterial stiffness
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Short-term T therapy had a beneficial effect on exercise-induced myocardial ischemia in middle-aged men with coronary artery disease or chronic stable angina, [95],[96],[97] and reduced angina frequency in older men with diabetes and coronary artery disease
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there are interventional studies supporting a protective effect of exogenous T against myocardial ischemia in men with coronary artery disease
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Observational studies indicate that lower levels of endogenous T in older men are associated with the presence of carotid atherosclerosis, aortic and peripheral vascular disease, and incidence of CVD events and mortality
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Interventional studies have shown beneficial effects of exogenous T on vascular function and on exercise-induced myocardial ischemia in men with coronary artery disease
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shared by Nathan Goodyear on 30 Jan 14
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PLOS ONE: Increased Risk of Non-Fatal Myocardial Infarction Following Testosterone Ther... - 0 views
www.plosone.org/...10.1371%2Fjournal.pone.0085805
Testosterone therapy cardiovascular disease men male hormones
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In men aged 65 years and older the RR was 2.19 (1.27, 3.77), while in men under age 65 years the RR was 1.17
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For TT prescription, in men under age 65 years, the RR was 2.90 (1.49, 5.62) for those with a history of heart disease and 0.90 (0.61, 1.34) for those without
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In men aged 65 year and older, the RR was 2.16 (0.92, 5.10) for those with a history of heart disease and 2.21 (1.09, 4.45) for those without.
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Among men aged 65 years and older, we observed a two-fold increase in the risk of MI in the 90 days after filling an initial TT prescription
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Among younger men with a history of heart disease, we observed a two to three-fold increased risk of MI in the 90 days following an initial TT prescription and no excess risk in younger men without such a history
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Among older men, the two-fold increased risk was associated with TT prescription regardless of cardiovascular disease history
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our own findings appear consistent with a higher frequency of thrombotic events following TT prescription among men with more extensive coronary vascular disease.
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Our findings are consistent with a recent meta-analysis of placebo-controlled randomized trials of testosterone therapy lasting 12 or more weeks among mainly older men, which reported that testosterone therapy increased the risk of adverse cardiovascular-related events (OR = 1.54, 95%CI:1.09, 2.18), as well as serious adverse cardiovascular-related events (OR = 1.61, 95%CI:1.01, 2.56) which included myocardial infarction along with other conditions
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This association appeared unrelated to average baseline testosterone level (p = 0.70) but varied by source of funding (p = 0.03), with a stronger summary effect in a meta-analysis of studies not funded by the pharmaceutical industry (OR = 2.06, 95%CI:1.34, 3.17) compared with studies funded by the pharmaceutical industry
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the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men
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there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events
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effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women
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Recently TT has been increasing extraordinarily rapidly, including among younger men and among those without hormone measurement
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Testosterone and the Cardiovascular System: A Comprehensive Review of the Clinical Lite... - 0 views
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Low endogenous bioavailable testosterone levels have been shown to be associated with higher rates of all‐cause and cardiovascular‐related mortality.39,41,46–47 Patients suffering from CAD,13–18 CHF,137 T2DM,25–26 and obesity27–28
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have all been shown to have lower levels of endogenous testosterone compared with those in healthy controls. In addition, the severity of CAD15,17,29–30 and CHF137 correlates with the degree of testosterone deficiency
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In patients with CHF, testosterone replacement therapy has been shown to significantly improve exercise tolerance while having no effect on LVEF
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testosterone therapy causes a shift in the skeletal muscle of CHF patients toward a higher concentration of type I muscle fibers
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Testosterone replacement therapy has also been shown to improve the homeostatic model of insulin resistance and hemoglobin A1c in diabetics26,68–69 and to lower the BMI in obese patients.
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Lower levels of endogenous testosterone have been associated with longer duration of the QTc interval
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negative correlation has been demonstrated between endogenous testosterone levels and IMT of the carotid arteries, abdominal aorta, and thoracic aorta
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These findings suggest that men with lower levels of endogenous testosterone may be at a higher risk of developing atherosclerosis.
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Current guidelines from the Endocrine Society make no recommendations on whether patients with heart disease should be screened for hypogonadism and do not recommend supplementing patients with heart disease to improve survival.
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The Massachusetts Male Aging Study also projects ≈481 000 new cases of hypogonadism annually in US men within the same age group
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since 1993 prescriptions for testosterone, regardless of the formulation, have increased nearly 500%
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Testosterone levels are lower in patients with chronic illnesses such as end‐stage renal disease, human immunodeficiency virus, chronic obstructive pulmonary disease, type 2 diabetes mellitus (T2DM), obesity, and several genetic conditions such as Klinefelter syndrome
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A growing body of evidence suggests that men with lower levels of endogenous testosterone are more prone to develop CAD during their lifetimes
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There are 2 major potential confounding factors that the older studies generally failed to account for. These factors are the subfraction of testosterone used to perform the analysis and the method used to account for subclinical CAD.
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The biologically inactive form of testosterone is tightly bound to SHBG and is therefore unable to bind to androgen receptors
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The biologically inactive fraction of testosterone comprises nearly 68% of the total testosterone in human serum
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The biologically active subfraction of testosterone, also referred to as bioavailable testosterone, is either loosely bound to albumin or circulates freely in the blood, the latter referred to as free testosterone
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It is estimated that ≈30% of total serum testosterone is bound to albumin, whereas the remaining 1% to 3% circulates as free testosterone
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it can be argued that using the biologically active form of testosterone to evaluate the association with CAD will produce the most reliable results
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English et al14 found statistically significant lower levels of bioavailable testosterone, free testosterone, and free androgen index in patients with catheterization‐proven CAD compared with controls with normal coronary arteries
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patients with catheterization‐proven CAD had statistically significant lower levels of bioavailable testosterone
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In conclusion, existing evidence suggests that men with CAD have lower levels of endogenous testosterone,13–18 and more specifically lower levels of bioavailable testosterone
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In a meta‐analysis of these 7 population‐based studies, Araujo et al41 showed a trend toward increased cardiovascular mortality associated with lower levels of total testosterone, but statistical significance was not achieved (RR, 1.25
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the authors showed that a decrease of 2.1 standard deviations in levels of total testosterone was associated with a 25% increase in the risk of cardiovascular mortality
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the relative risk of all‐cause mortality in men with lower levels of total testosterone was calculated to be 1.35
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higher risk of cardiovascular mortality is associated with lower levels of bioavailable testosterone
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Existing evidence seems to suggest that lower levels of endogenous testosterone are associated with higher rates of all‐cause mortality and cardiovascular mortality
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studies have shown that lower levels of endogenous bioavailable testosterone are associated with higher rates of all‐cause and cardiovascular mortality
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It may be possible that using bioavailable testosterone to perform mortality analysis will yield more accurate results because it prevents the biologically inactive subfraction of testosterone from playing a potential confounding role in the analysis
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In more recent studies, 3 randomized, placebo‐controlled trials demonstrated that administration of testosterone improves myocardial ischemia in men with CAD
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The improvement in myocardial ischemia was shown to occur in response to both acute and chronic testosterone therapy and seemed to be independent of whether an intravenous or transdermal formulation of testosterone was used.
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There is growing evidence from in vivo animal models and in vitro models that testosterone induces coronary vasodilation by modulating the activity of ion channels, such as potassium and calcium channels, on the surface of vascular smooth muscle cells
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Experimental studies suggest that the most likely mechanism of action for testosterone on vascular smooth muscle cells is via modulation of action of non‐ATP‐sensitive potassium ion channels, calcium‐activated potassium ion channels, voltage‐sensitive potassium ion channels, and finally L‐type calcium ion channels
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Corona et al confirmed those results by demonstrating that not only total testosterone levels are lower among diabetics, but also the levels of free testosterone and SHBG are lower in diabetic patients
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Laaksonen et al65 followed 702 Finnish men for 11 years and demonstrated that men in the lowest quartile of total testosterone, free testosterone, and SHBG were more likely to develop T2DM and metabolic syndrome.
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Vikan et al followed 1454 Swedish men for 11 years and discovered that men in the highest quartile of total testosterone were significantly less likely to develop T2DM
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authors demonstrated a statistically significant increase in the incidence of T2DM in subjects receiving gonadotropin‐releasing hormone antagonist therapy. In addition, a significant increase in the rate of myocardial infarction, stroke, sudden cardiac death, and development of cardiovascular disease was noted in patients receiving antiandrogen therapy.67
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Several authors have demonstrated that the administration of testosterone in diabetic men improves the homeostatic model of insulin resistance, hemoglobin A1c, and fasting plasma glucose
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Existing evidence strongly suggests that the levels of total and free testosterone are lower among diabetic patients compared with those in nondiabetics
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insulin seems to be acting as a stimulant for the hypothalamus to secret gonadotropin‐releasing hormone, which consequently results in increased testosterone production. It can be argued that decreased stimulation of the hypothalamus in diabetics secondary to insulin deficiency could result in hypogonadotropic hypogonadism
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This interaction may be a result of the promotion of lipolysis in abdominal adipose tissue by testosterone, which may in turn cause reduced abdominal adiposity. On the other hand, given that adipose tissue has a higher concentration of the enzyme aromatase, it could be that increased adipose tissue results in more testosterone being converted to estrogen, thereby causing hypogonadism. Third, increased abdominal obesity may cause reduced testosterone secretion by negatively affecting the hypothalamus‐pituitary‐testicular axis. Finally, testosterone may be the key factor in activating the enzyme 11‐hydroxysteroid dehydrogenase in adipose tissue, which transforms glucocorticoids into their inactive form.
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increasing age may alter the association between testosterone and CRP. Another possible explanation for the association between testosterone level and CRP is central obesity and waist circumference
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Bai et al have provided convincing evidence that testosterone might be able to shorten the QTc interval by augmenting the activity of slowly activating delayed rectifier potassium channels while simultaneously slowing the activity of L‐type calcium channels
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Intima‐media thickness (IMT) of the carotid artery is considered a marker for preclinical atherosclerosis
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Studies have shown that levels of endogenous testosterone are inversely associated with IMT of the carotid artery,126–128,32,129–130 as well as both the thoracic134 and the abdominal aorta
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1 study has demonstrated that lower levels of free testosterone are associated with accelerated progression of carotid artery IMT
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another study has reported that decreased levels of total and bioavailable testosterone are associated with progression of atherosclerosis in the abdominal aorta
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These findings suggest that normal physiologic testosterone levels may help to protect men from the development of atherosclerosis
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Czesla et al successfully demonstrated that the muscle specimens that were exposed to metenolone had a significant shift in their composition toward type I muscle fibers
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Type I muscle fibers, also known as slow‐twitch or oxidative fibers, are associated with enhanced strength and physical capability
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It has been shown that those with advanced CHF have a higher percentage of type II muscle fibers, based on muscle biopsy
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Studies have shown that men with CHF suffer from reduced levels of total and free testosterone.137 It has also been shown that reduced testosterone levels in men with CHF portends a poor prognosis and is associated with increased CHF mortality.138 Reduced testosterone has also been shown to correlate negatively with exercise capacity in CHF patients.
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Testosterone replacement therapy has been shown to significantly improve exercise capacity, without affecting LVEF
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the results of the 3 meta‐analyses seem to indicate that testosterone replacement therapy does not cause an increase in the rate of adverse cardiovascular events
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Data from 3 meta‐analyses seem to contradict the commonly held belief that testosterone administration may increase the risk of developing prostate cancer
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One meta‐analysis reported an increase in all prostate‐related adverse events with testosterone administration.146 However, when each prostate‐related event, including prostate cancer and a rise in PSA, was analyzed separately, no differences were observed between the testosterone group and the placebo group
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the existing data from the 3 meta‐analyses seem to indicate that testosterone replacement therapy does not increase the risk of adverse cardiovascular events
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the authors correctly point out the weaknesses of their study which include retrospective study design and lack of randomization, small sample size at extremes of follow‐up, lack of outcome validation by chart review and poor generalizability of the results given that only male veterans with CAD were included in this study
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the studies that failed to find an association between testosterone and CRP used an older population group
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low testosterone may influence the severity of CAD by adversely affecting the mediators of the inflammatory response such as high‐sensitivity C‐reactive protein, interleukin‐6, and tumor necrosis factor–α
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Good review of Testosterone and CHD. Low T is associated with increased all cause mortality and cardiovascular mortality, CAD, CHF, type II diabetes, obesity, increased IMT, increased severity of CAD and CHF. Testosterone replacement in men with low T has been shown to improve exercise tolerance in CHF, improve insulin resistance, improve HgbA1c and lower BMI in the obese.
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shared by Nathan Goodyear on 03 Dec 13
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Effect of acute testosterone on myocardial isch... [Am J Cardiol. 1999] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...10072236
Testosterone therapy cardiovascular disease men male hormone hormones
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Natural progesterone, but not medroxyprogesterone acetate, enhances the beneficial effe... - 0 views
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Association between increased levels of reverse tr... [Am J Med. 2001] - PubMed result - 0 views
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CONCLUSION: Determination of reverse T3 levels may be a valuable and simple aid to improve identification of patients with myocardial infarction who are at high risk of subsequent mortality.
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ScienceDirect - Clinical Biochemistry : Correlation between total homocysteine, low-den... - 0 views
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usefulness of LDL-C, HDL-C and serum total homocysteine as prognostic markers in myocardial infarction patients
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Effect of calcium supplements on risk of myocardial infarction and cardiovascular event... - 0 views
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Calcium supplements (without coadministered vitamin D) are associated with an increased risk of myocardial infarction.
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Exercise-induced right ventricular dysfunction and structural remodelling in endurance ... - 0 views
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In a cohort of well-trained athletes, we demonstrated that intense endurance exercise causes an acute reduction in RV function that increases with race duration and correlates with increases in biomarkers of myocardial injury
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focal gadolinium enhancement and increased RV remodelling were more prevalent in those athletes with a longer history of competitive sport, suggesting that repetitive ultra-endurance exercise may lead to more extensive RV change and possible myocardial fibrosis
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Greater reductions in RV function occurred in those athletes competing for a longer duration, suggesting that the heart has a finite capacity to maintain the increased work demands of exercise
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We enrolled elite and subelite athletes and found a significant association between fitness (VO2max) and the reduction in post-race RVEF
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Previous investigators have documented reductions in RV function in less trained subjects over the marathon distance
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The focus on well-trained athletes may be of particular relevance, given that they perform exercise of highest intensity and duration most frequently, and, thus, may be at a greater risk of cumulative injury.
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The lack of correlation between increases in troponin and changes in LV function seen in this study has been previously interpreted as evidence that post-exercise elevations in cardiac biomarkers are benign.
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a significant correlation between changes in RVEF and post-race biomarker levels and this relationship was even stronger in the athletes who completed the race of longest duration, the ultra-triathlon
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It has been demonstrated that ventricular load increases with exercise intensity and is greater for the RV than the LV,29 thus potentially explaining why the RV is more susceptible to fatigue after prolonged exercise.
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BNP release during intense exercise is associated with greater relative increases in RV systolic pressures, but not LV pressures
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BNP may provide a measure of both acute RV load and the resultant fatigue which occurs when this load is sustained
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The correlations with RVEF, but not LVEF, provide further evidence of the differential effects of intense exercise on RV and LV function
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This study demonstrates, for the first time, an association between endurance exercise of increasing duration and structural, functional, and biochemical markers of cardiac dysfunction in highly trained athletes
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Functional abnormalities were confined to the RV and were largely reversible 1 week following the event
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there remained a significant minority of athletes in whom there was evidence of myocardial fibrosis in the interventricular septum
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RV abnormalities may be acquired through cumulative bouts of intense exercise and provides direction for prospective investigations aimed at elucidating whether extreme exercise may promote arrhythmias in some athletes.
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the acute injury and chronic remodelling of the myocardium both disproportionately affect the RV and it remains possible that the two are linked.
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emerging evidence that intense endurance exercise may be associated with an excess in arrhythmic disorders, the mechanisms for which remain unexplained
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RVEF (and not LVEF) was reduced in athletes with complex ventricular arrhythmias when compared with healthy athletes and non-athletes without arrhythmias
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shared by Nathan Goodyear on 16 Aug 14
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Reverse T3 as a parameter of myocardial functi... [Int J Cardiol. 2010] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...19428128
thyroid hormone hormones reverse T3 fT3_rT3 rT3 heart failure CHF cardiovascular disease.
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shared by Nathan Goodyear on 24 Apr 12
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Dihydrotestosterone treatment in men with coronary artery disease. II. Influence on myo... - 0 views
www.mendeley.com/...al-ischemia-and-left-ventricle
DHT dihydrotestosterone heart cardiac androgen male men androgens
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shared by Nathan Goodyear on 17 Jul 12
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Long-term benefits of testosterone replacement therapy on angina threshold and atheroma... - 0 views
eje-online.org/...443.long
low Testosterone low T heart myocardium ischemia men male testosterone hormone hormones
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shared by Nathan Goodyear on 17 Jul 12
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Low-Dose Transdermal Testosterone Therapy Improves Angina Threshold in Men With Chronic... - 0 views
circ.ahajournals.org/...1906.long
low testosterone low T hormone hormones men male testosterone heart CVD cardiology angina ischemia
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shared by Nathan Goodyear on 21 Nov 13
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Diabetes and Cardiovascular Disease During Androgen Deprivation Therapy: Observational ... - 0 views
jnci.oxfordjournals.org/...39.full
diabetes cardiovascular disease stroke androgen deprivation therapy prostate cancer
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shared by Nathan Goodyear on 03 Dec 13
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Low-Dose Transdermal Testosterone Therapy Improves Angina Threshold in Men With Chronic... - 0 views
circ.ahajournals.org/...1906.abstract
Testosterone therapy angina ST depression heart cardiovascular disease men male hormone hormones
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shared by Nathan Goodyear on 22 Jul 14
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Risk of Myocardial Infarction in Older Men Receiving Testosterone Therapy - 0 views
aop.sagepub.com/...1060028014539918.full
Testosterone men male hormone hormones cardiovascular risk disease MI myocardial infarction heart attack heart disease
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This study appears to fly in the face of the recent studies on the dangers of Testosterone therapy in those with comorbidities. This study was a retrospective cohort. The study found that men in the highest risk for MI, had a reduced MI risk with Testosterone therapy. Men in the lower risk quartiles had no such benefit. Of note, the frequency of injections suggests inadequate dosing i.e. 4.4 in first year and 8.2 in follow up. Most injection regimens will require at least monthly injections, though Testosterone pellets were used. Of special note, no mention of level testing of Testosterone prior to study and/or during study and follow up.