Group items tagged

prevalence of MetS in children in US is high.

low SHBG in post-menopausal women correlates with increased risk of metabolic syndrome.  More than that, there is an inverse correlation with SHBG in women and metabolic syndrome components.  Also, Increasing components of MetS was correlated with Testosterone and free androgen index.

Large, randomized, double blind, placebo controlled study of 14,641 men found that daily MVA reduced cancer risk by 8%.  These were just general multivitamins.  Customized would have probably provided better results as they would have met the deficiencies of the individual.

Great review of the Hypogonadal-obesity-adipocytokine hypothesis.

Testosterone therapy is complex in hypogonadism.  Much of the marketing-based medicine of Low T today is in fact doping.  Increasing weight is clearly associated with a declining T level in men.  Testosterone therapy should be approach individually and therapies that use the one size fits all approach never work.  This is the case whether the use of synthetics or natural hormones are employed.  Testosterone has been shown to improve dysglycemia, MetS, reduce fat and increase muscle mass.  

20alpha dihydroprogesterone, a 4 pregnene, has been shown to inhibit breast cancer cell proliferation, decrease mets through increased cell adhesion, and increased apoptosis.  Here, it has been shown to inhibit aromatase activity.  No longer are hormone metabolites to be viewed as waste.  They are biological as active if not more so in many cases.

Good review of the data looking at the relationship between MetS and cancer.

Post menopause women with PCOS have high CVD.  PCOS is essentially metabolic syndrome separated by age.  Both PCOS and MetS in women is associated with an increase in Testosterone levels.

A decrease in the SHBG in post menopause women is associated with increase in free Testosterone, which is associated with increase in MetS and CVD

10 year Cochrane review finds low T associated with aging, obesity, MetS, and poor health.  The authors suggest that low T "may be linked to earlier all-cause and cardiovascular related mortality among men".  This is supported by other studies.  Only abstract available here.

This population study finds increased risk, significantly more for women vs men, of type II Diabetes with gout.  This should come as no surprise as the underlying pathophysiology is the same.  Fructose increases Uric acid.  Uric acid is a biomarker of MetS.  Fructose increases abdominal adiposity and eventually inflammation which leads to diabetes.  

Study finds that leptin, PAI-1, and hsCRP are positively associated with increasing metabolic syndrome components.  Adiponectin was negative associated with increasing MetS.  Not a lot of new info here.

Metabolic Syndrome is associated with CAD.  No surprise here, but increase in # of metabolic syndrome parameters was associated with increasing % of Triple vessel disease.   No surprise that MetS was associated with TNF-alpha, IL-6, IR, and hsCRP.

elevated CRP helps predict metabolic syndrome and cardiovascular disease

low lead levels through oxidative stress contribute to metabolic syndrome

Altered cognitive function found in adolescents with non-IR obesity.  This worsened with MetS and type II Diabetes.  The statement that there is healthy obesity is in error.

Study finds no improvement with glucose control in diabetics.  This study looked at moderately controlled diabetes. Studies have previously shown that poorly controlled diabetes definitely benefits more than those with more mild glucose control problems.  Additionally, the Testosterone levels in this study would not have met the definition of low T by other studies.  So, the question is did these men need T?  Second, did the authors design the study long enough to see changes in the insulin sensitivity and glucose control?  Abstract only available and thus I don't have access to that information.  Third, and this might support the 2nd point, increased lean mass and decreased fat mass was found.  This points to positive metabolic change.  Would this have, given more time, resulted in improved glucose control? No change in visceral adiposity was seen.  This finding, also, is not new.  Testosterone therapy does not improve visceral adiposity.  Though, increasing fat adiposity, low Testosterone, and associated increase in systemic inflammatory cytokine production results in visceral adiposity, Testosterone therapy does reverse the visceral adiposity.  

14% of offensive lineman found to have MetS in small study.