adipocytes increase genetic expression of 11beta-HSD. This increases local cortisol production from cortisone. This plays a pivotal role in obesity. Question: would this play a role in peripheral hypothyroid? I think so.
higher cholesterol levels associated with a decreased dementia risk in the elderly population. Stop the press!! Yes, basic physiology tells us this. The brain loves cholesterol, cholesterol is needed. The question is: what will be the impact of "neurodegenerative diseases" by the overzealous use of statins?
Study questions the 5-LOX inhibition as the mechanism of action of Boswellia due to its low absorption. However, prostaglandin E production was inhibited. Both have profound antiiflammatory effects and would benefit chronic inflammatory diseases.
knowledge of progesterone and its metabolites are important in the use of hormones. As the authors concluded here: "natural steroids should not be disparaged...an update on endocrinological knowledge and experience is rather mandatory for gynecologists". There in lies the problem. The IOM has shown that the average physician practices at a level of 17 years behind the current scientific knowledge and the environment created by medical governing bodies discourages questions, so as to protect the system.
Estradiol inhibits glutamate mediated influx of calcium and thus cell death in cell line. Glutamate, the principle excitatory neurotransmitter, is involved in neurodegeneration through activation of calcium channels. This study of cell line cultures found that Estradiol inhibits this process. I question whether this is applicable to both men and women. Time will tell.
Prospective study finds that elevated total and free Estradiol levels in the follicular phase and elevated total and free Testosterone levels in both the follicular and luteal phase are associated with increased breast cancer in women. The risk is for pre menopause in this study. This and several other studies point to serious questions about the massive dosing of Testosterone via pellets, injections, and topicals for libido. We appear to be following the same patter as seen with premarin, provera, now Testosterone in men and this may be the next ball to drop. Is the Testosterone therapy merely producing an environment that feeds breast cancer?
Menopausal rats and rats that had ovaries removed have increased low grade inflammatory signaling. This study treated the rats in question with either Estradiol and Losartan and both decreased inflammatory signaling.
Study out of Canada finds that Metformin reduces mortality rates for all-cause and due to prostate cancer in those with diabetes. The key point here is glucose. Metformin is going to inhibit gluconeogenesis and this limit hepatic glucose production feeding the cancer. This is just the abstract and several questions come to mind: what was the glucose control like in these patients? What dietary changes if any were these patients following? A better study would be to compare the effects of a ketogenic diet with restriction of glutamine versus the metformin.
Cochrane review published in 2010 on the efficacy of the flu vaccine. It doesn't work!. Add that it adds additional cases of Guillain-Barre Syndrome and the question should be what are we doing to ourselves.
ER and PR are suggested to play role in colon cancer. The question is do they play a role in carcinogenesis or does the expression of the receptors indicate something else i.e. attempt at differentiation through progesterone. Also, what receptors are involver here: ER alpha or beta. Likewise for the progesterone receptors
study finds prolonged exposure to estrogen associated with increased colorectal cancer risk in postmenopausal women. So many unanswered questions. What was the ER status of these patients? What was the weight of these patients? One cannot simply compare estrogen exposure to colorectal cancer risk and say aha! What is the environment of the individual(s)?!
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New study suggests that intra-uterine exposure effects prefrontal cortex development that leads to autism. This study was conducted of postmortem samples of children with autism ranging from 2 to 15. Intra-pregnancy exposure of what? That is the question. Environmental toxins: whether it is all the xenoestrogens (autism at rate of 5:1 in boys), PCBs, heavy metals, and yes (lead author) preservatives, metals (Al and thermeresol) in vaccines--particularly the flu vaccine which ACOG is almost mandating during pregnancy.
Interesting concept on Androgen deprivation therapy. ADT has significant negative metabolic effects in men. Here Intermittent ADT is evaluated and found to be questionable in its outcome.
Individuals with obesity and type II Diabetes been found to have significantly different gut bacteria populations compared to healthy individuals. This is not new information. The firmicutes:bacteroidetes ratio has been long known to be elevated in obese individuals vs those that are lean. The question here is cause and effect. Is the change in the bacterial population leading to obesity and type II diabetes? Or is diabetes and obesity leading to changes in the bacterial population? A heavy-laden carb diet is know to lead to a change to a more unhealthy gut bacterial population--maybe it is just a product of diet? Maybe it is effected by vaginal delivery vs cesarean delivery? Maybe breast feeding plays a role. Maybe, all the above is required.
The point is that the cause of obesity and type II diabetes may have its origins deep, deep in the...well you know. http://ow.ly/yqDML
Study finds decreased ovarian reserve in women 20-29 with metabolic syndrome compared to controls. They determined this via ovarian volume measurements as FSH, LH, Estradiol, and Progesterone did not differ.
One item of interest was that women with MetS, had significantly higher Testosterone levels compared to controls. This association of MetS and elevated Testosterone in women has been shown consistently in the literature. This should bring great questions to the doping of Testosterone in women today.
Review of the data points to poor quality of evidence dealing with DHEA in post-menopausal women with normal adrenal function. Yet if DHEA is low, which is >95% produced by adrenals in women, then how can the adrenal function be "normal". The meta-analysis found no improvement in libido and/or sexual function, and no improvement in lipids, glucose, weight... was noted. Essentially not positive or negative effects were noted. Abstract only available here, so dosage is a question.
