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Study finds no worsening in cardiovascular biomarkers in women on Testosterone.  The women in this study were chose due to low Testosterone.  Testosterone was given IM at 4 different doses.  This is in contrast to other studies that have looked at endogenous Testosterone level.  Studies have shown increasing endogenous T levels in women is associated with increased CVD.  Studies on exogenous are lacking.  This points to limited risk associated with CVD and T therapy in women.   One caveat.  Two of the authors of this study have ties to the maker of the Testosterone enanthate used in this study.  Why is this important?  Prior studies have shown significant decrease in adverse event reporting in those funded by pharma--bias.

24 week study of 71 women post-hysterectomy finds no increase in cardiovascular biomarkers.  Several problems with this study.  First, there was a large drop out--24%.  Second and most important, the women were pretreated with estrogen prior to Testosterone therapies were initiated.  Other studies have proposed that this protects cardiovascular risk in women on Testosterone.  Previous studies show increasing endogenous Testosterone is associated with increasing cardiovascular disease in women.   This study would be much better if no estradiol was prescribed.  That would give an unbiased view of Testosterone in post-hysterectomy women.  Not much can be taken from this study. If you doctor doesn't know this, find another doctor.  Inherent bias in this study as ties to the manufacturer of the Testosterone was disclosed. This study point to the inherent flaws in so much of the medical literature today.  Most would read the headlines and read no further, but the "further" dispels the headline as flawed.

The risks of estrogen metabolism are not clear cut.  Likely never will be due to the complexity of individual metabolism.  This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer.  Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism.  There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.

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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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This study cannot make the conclusion AT ALL.  They claim to say hormones should not be used to prevent chronic disease. Yet, the study they use to support this statement, the WHI, did not look at hormones.  The WHI looked at premarin and medroxyprogesterone acetate, a progestin.  They are not the hormones the body makes. Second, the WHI looked at women that were 6 years postmenopausal, on average, and then they added in bad drugs, disguised as hormone like, and then were dosed high.   If one desires to truly make a statement of prevention, one needs to pre-empt testing and therapy before disease.  Additionally, the study needs to match the hormones needed at the right physiologic level in the right balance.   One must also ensure proper hormone metabolism and know hormone receptor status.  This study does non of the above and the conclusion of this study is irrelevant.  In fact, I think the authors of this study have undergone scientific malpractice in their conclusions.

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.

animal study finds that fructose increased liver mass, abdominal fat and decreased physical activity when compared to glucose.  The study groups were iso caloric, but one group was fed 18% fructose and the other 18% glucose.

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.  

Nice review of Testosterone levels and some of the evidence linking Diabetes with low T.  However, the conclusion by the authors regarding what is causing the low T in men with Diabetes is baffling.  The literature does not point to one cause, it is clearly multifactorial--obesity, inflammation, high aromatase activity...I would suggest the authors continue their readings in the manner.

Article discusses the expanding evidence of low T and Metabolic syndrome.

Study results suggest that higher Testosterone and lower Estrogen levels provide anti-inflammatory effects in men.  The inflammatory biomarker assessed here was CRP.  Low total and calculated free Testosterone was associated with an increase in CRP.  In contrast, total and free Estrogen was associated with an increase in CRP.  Estradiol increased WBC count and SHBG was inversely related to WBC count in this study.

This study proves the problems rampant in science today.  This study looked at older men with mobility limitations: safe to say, not optimal health.  They give 10 grams of testosterone daily to these men.  Physiologic doses are 5-10 mg.  And they are surprise that there is an increase in side effects, here in this study CVD.  They did look at cytokines, I'll give them that; but they did not look at aromatase activity and E2, E1 levels which have been shown to be the driving forces behind these inflammatory cytokines in men.  Testosterone has in fact been shown to downregulate these inflammatory cytokines.  Poor study.  No conclusion can be taken from this study.

No benefit to memory for post menopause women with estradiol therapy.  This study looked at early and late menopause estrogen therapy.  The study also found no harm.  Only abstract available here.  These studies would do more scientific benefit if they would follow hormone levels.  This study did not touch on dementia; other studies have shown benefit from estrogen therapy  in preventing dementia in women.

There are alot of problems with evidence-based medicine.  Don't for one minute think that a "study" can be without major flaws and biases.  In fact, alot  of the studies reported by the press are based on poorly designed and manipulated studies.  Probably 50% of the studies that I read I disgard after evaluating the study design and statistics.

Study finds that elevated serum Testosterone and androstenedione is associated with an increase risk of breast cancer.  This EPIC study looked at serum hormones in premenopausal women.  This study also found an association with increased breast cancer and low serum progesterone in women.  This was also found in the ORDET study.  This study did not find a link with estrogen.  These are endogenous levels.  Does this translate to exogenous? This theory of elevated androgens and breast cancer was first proposed by Grattarola.

This is a short interview of the author on a recent retrospective review that revealed no increase in cardiovascular events in men.  The author rightly points out his data, which is quite different than the previous JAMA and PLOSone publications which showed an increase in cardiovascular events.   However, the lead author points out the main problem with comparisons:  his study group was younger and healthier.  So, the comparison is apples to oranges.  Studies still point to increased risk of Testosterone therapy in men with pre-existing CVD.  This new study does not refute this point at all.   Another serious flaw here, is that only Testosterone was followed.  This logic is seriously flawed as I have previously documented.  The author points out the flaw in the levels in the JAMA study post treatment.  But he fails to account for the the lack of adequate pathway assessment i.e.aromatazation.  Also, no inflammatory cytokine evaluation was performed in that study.  Both of these should have been highlighted.    In contrast, a positive was the length of follow.