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Low T3 post MI is associated with increased CHF, morbidity and mortality.  Article discusses thyroid hormones and cardiac function/remodeling post infarct.  The article also lays the ground work for a new study of T3 in patients post MI to be followed for 6 months.

Coronary artery calcium is positively associated with CAD risk.  It compares to multiple biomarker assessment, BNP, and homocysteine assessment.

Hg damages the heart muscle.  In this animal study, protection of sulfhidyrl groups prevented this effect.  Examples of sulfhidryl groups is GSH, ALA, cysteine, and NAC.

long standing low T linked to bradycardia and heart failure in case series.  Exact relationship of cause/effect unknown, though low T has been shown to be associated with wide spectrum of increased risk of CVD.

Full thyroid evaluation, not TSH or just T4, is predictive in severity of CHF and heart tachycardia

Low bioavailable Testosterone associated with increased IL-1beta and TNF-alpha in men with CHF.

Animal model finds that Testosterone improves ventricular remodeling and function following myocardial infarction in male rats.  This similar finding has been found in human studies as well.   Testosterone therapy was found to lower BNP in this rat study.

large study of 50,000 postmenopausal women found no significant reduction in CVD with a low fat diet.  The mean dietary time period was 8 years.

Lp(a) is a useful biomarker in the overall assessment of those at moderate to high risk of CVD.

Pb is associated with increased CVD, however, studies are limited and the association is not clear as the exact process by which Pb contributes to CVD is not know.  Oxidative stress and inflammation are proposed as the mechanisms.

Great short review on Fiber and health benefits

Life extesnsions rebuttal to recent JAMA study.  There was several significant flaws in that study and thus limited evidence can be gained by that study.  In fact, I find no useful clinical information from that study. In the rebuttal, there are flaws. The reference the low serum T after treatment and correctly discuss aromatase activity.  But they fail the mention that the less than optimal serum T is likely the result of the high aromatase activity in these men.  Age, stress, and weight are primary causes of increases estrogen production in these men.  These would be why likely high estrogen production occurred and less than optimal serum T resulted.   And, increased E2 will cause an increase in CRP which can precipitate CVD events.

Study finds increased risk of sudden MI in men with low Testosterone and elevated Estradiol.  In converse, increased risk is associated with elevated Estradiol in women.

Hg induces vascular ROS through depletion of glutathione.  This study found that low dose, chronic Hg exposure induced ROS that resulted in vascular dysfunction i.e. hypertension.

Wow, Thyroid replacement after MI, improves heart function and reduces damage

Study looked at hormone levels via serum analysis at the time of sudden cardiac arrest in both men and women.  Low Testosterone and elevated Estrogen levels in  men were associated with increased odds (OR) versus women only had increased odds with elevated Estrogen.   ManBoob nation, my first book, discusses the mechanism behind this for men.  The finding in women really calls into question the Estrogen only model currently employed by physicians for post menopausal women.

Testosterone reduced the vascular benefits of Estrogen (conjugated equine Estrogen) in female rat model.  Testosterone is seeing widespread use in women with very little positive data.  In fact, the majority of data points to poor metabolic effects and poor outcomes.

Testosterone in men with CHF found to improve diastolic function and exercise distance versus placebo.  

resistance/cardio interval training found to improve vascular endothelial function.

low testosterone increases CVD and all-cause mortality in me.