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Another ill conceived conclusion by the authors.  IF you are going to study something, know everything about it.  They authors make a major statement about vitamin D, yet they seem to understand a basic understanding of vitamin dosing.  The authors stated that dosing 2,000 IU of vitamin D in those with levels < 50 provided no benefit.  That is of course correct, because 2,000 IU daily won't hold any levels stable, let alone increase levels to 70-80 where they need to be.  The authors of this study are stuck in the traditional RDC thinking here. What is interesting is that low vitamin D was associated with CVD, MS, dyslipidemia, inflammation, glucose dysmetabolism, infections, mood disorders, decline in cognition, impaired physical functioning, and all-cause mortality,  But, vitamin D supplementation is only good for bones.  The authors of this study make a mockery of medicine.

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.

The ignorance of this authors statements is unmeasurable.  Numerous other studies have shown weight loss in men with obesity is associated with increased Testosterone production.  My book highlights the mechanism by which adipose tissue decreased Testosterone production.  The author was quoted as pointed to no Testosterone replacement (even if levels are low????) despite the evidence that Testosterone will improve glucose metabolism, build muscle (reverse sarcopenia obesity), improve cholesterol metabolism,  and significantly aid Diabetes control just to name a few; yet the author says, give surgery instead.  I am sure the author is a surgeon and thus bias might, just might, be present.

Very nice study.  The authors looked at normal prostate, early disease and late stage prostate cancer.  The authors found that ER beta expression, as a general rule, was lost as progression occurred to the high-grade dysplasias and grad 4/5 carcinomas of the prostate.  Early low/moderate dysplasia was associated with an increase in ER beta--the authors propose that this was due to an attempt of the basal epithelium to counter the paracrine effect of ER alpha.   In contrast, androgen receptors appeared to be equally expressed across all.

Study looked at inflammatory markers in RA.  The authors point to high aromatase activity, low androgens, and elevated estrone in synovial fluid as an indicator of a link between aromatase activity and inflammation production through E1 production.  The authors also point to the 16 alpha metabolite pathway as pro-inflammatory as well.  One very interesting point made by the authors is that vitamin D down regulates aromatase activity.  In addition to NK-kappaB inhibition, this may be another mechanism by which vitamin D reduces inflammation.

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.

This is the study that many have used to discredit psa velocity, but that is cherry picking the authors conclusions.  The authors did find an association with a positive psa velocity and + prostate biopsy.  Not useless, but useful in the right context.

Here is where science and particularly conclusions fail the public.  The authors conclusions are that tadalifl improves ED and sexual function irrespective of Testosterone levels.  However, the results say something different.  The group with normal Testosterone responded better versus the low Testosterone group.  This difference didn't reach statistical significance though.  This lack of statistical significance does not exclude the fact that there indeed was a difference.  The authors conlcusions take no part in reporting the whole truth, just that which supports their hypothesis. The diagnosis of low T in this study was < 300 ng/dl

Awesome article on progesterone metabolism in breast cancer.  The author, weibe, describes 2 categories of progesterone metabolites in breast tissue: 5alpha-pregnanes and 4-pregnenes.  The author describes 3 primary enzymes that control the balance between these 2 metabolites--5alpha reductase, 3alpha-HSO, and 20alpha-HSO.  The resultant balance of 5alpha-dihydroprogesterone and 3alpha-dihydroprogesterone helps to determine the cancer potential of breast tissue.

Study worries over the risks of supplements and prescription drugs.  The author should worry more over the lack of knowledge by physicians of the health benefits of supplements.  Instead of focusing on the prescriptions themselves, how about focusing on the supplements to reduce the need for the prescriptions.  This authors focus is all wrong.   Obviously, the patient needs to be forthcoming with his/her physician about all supplements that they are on.  

Study finds heavy presence of xenoestrogens in obese Portuguese women, both pre menopause and post menopause.  This study only looked at obese women; it would be nice to have a control of thin women to contrast the plasma and adipose xenoestrogen levels.  The authors found the presence of xenoestrogens in plasma in pre menopause women to be a 10 year predictor of cardiovascular disease risk in these women.  The authors also found increased Xenoestrogen levels to be associated with metabolic dysfunction and inflammation.

Study finds non-hormonal therapy to manage hot flashes in postmenopausal women--drug them.  The authors of this study, looked to gabapentin, also known as neurontin to treat hot flashes.  Instead of looking at the causes: hormone imbalance, stress... these authors looked to a sedating drug.  The dosing of neurontin was 900 mg.   Most can't stand at this dose.  This study points to the lunacy in the research today.  Very soon, there will be the walking dead among us.  They will be the walking doped instead of dead.

Study reviews the studies of IV vitamin C and cancer.  The authors discuss the mechanism of action of the high dose vitamin C.  The authors are correct in their conclusion that a large body of evidence is lacking and that the majority are case study.  However, to even discount these in the face of the safety and the reduction in side effects associated with chemotherapy by IV vitamin C would be unacceptable. To delay recommendation due to a full lack of understanding would be unacceptable as well.   No deaths have been reported due to IV vitamin C.  Contrast this with chemotherapy.  However, case studies have pointed to IV vitamin C as a positive tool to attach cancer.  

Only abstract available here.  Study of Polish men found lowered Testosterone in men with pre diabetes.  The authors used the term "late onset hypogonadism" here.  An inverse association was found between calculated free Testosteorne and HgbA1c.  The authors conclusion says it all: routine screening of Testosterone in men with pre-diabetes is recommended.

Statin use associated with increased myopathy, liver dysfunction, and type II Diabetes.  The authors conclude that the absolute risk is very low, yet OR was 1.47 for type II Diabetes (translated 47% increased odds of developing Diabetes as a result of statins) and OR of 2.63 in risk of myopathy (translated 163% increased odds of developing myopathy as a result of statins).  Seems the authors "low risk" statement is just applies to those without symptoms/side effects.  Physicians need to do a better job of understanding risks and customizing therapies.

published ahead of print.  The authors conclude that the Testosterone therapy in hypogonadal men with cirrhosis requires further study.  They, the authors, state that the risk of Testosterone and hepatocellular carcinoma is overstated.  This risk is associated with oral Testosterone replacement and thus in that light is not overstated.  The majority of treatment strategies today employ none oral routes of administration which would support their statement.

Authors review the literature behind Testosterone and BPH.  The authors highlight the 4 proposed theories behind BPH: Testosterone, Estrogen, inflammation, and metabolic.   The conclusion is mixed: pointing out that no high level of evidence exists on either side of the debate of Testosterone and BPH.

Data review finds NAC improves pregnancy rates and ovulation rates in women with PCOS against placebo.  Meta-analysis revealed limited studies on the topic.  When compared to metformin, there was no difference found.  Though, one wonders if attacking insulin resistance through proper diet and additional neutraceutical approach would negate that.  The reason?  NAC and metformin are working in different biochemical pathways.  The authors here seem to not realize this. It appears that they think NAC and metormin are both working in the same manner, but they don't.  The fact that there is still benefit found compared to placebo, despited the authors lack of understanding of what NAC is and does is a positive.

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.

Review of the physiology of muscle building.  The authors review the evidence behind the types of muscle building exercises and the physiology responsible for muscle hypertrophy.  The authors point to Schoenfeld's description of mechanical tension, muscle damage, and metabolic stress to build muscle.