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Good deep look into the testosterone and CVD link.

Review of the physiological roles of GH and IGF-1 during exercise.  The focus is on maximizing the normal physiologic response, not supra physiologic.

this study revealed increased breast cancer risk in women on "estrogen" and "testosterone" therapy.  Now, several problems here: first, are these synthetic hormone or bioidentical.  Second, the dosages appear, in what is written, to be supra physiologic.  Third, giving supra physiologic estradiol and testosterone will obviously create imbalances and growth potential.  Fourth, how were the women evaluated prior to starting hormone therapy and then were they remonitered (unlikely), fifth, were hormone metabolites evaluated (too, also unlikely).  This study has serious flaws and very little can be extrapolated other than: don't take supra physiologic hormone levels without appropriate evaluation.  Enough said

great review on performance physiology.  This article reviews  how VO2 max, lactate threshold, performance VO2, and mitochondria contribute to peak endurance performance.

new study finds that men >65 with low libido and Testosterone levels < 275 increase sexual function with Testosterone therapy.  Only libido was improved; no benefit to erectile function was noted--note that is likely due to depleted NO.  Given time that should improve with he increase in NO synthase and thus NO.  I have a fault with on elf the comments on this study: they point out that increased free Testosterone and estradiol levels were associated with improved sexual activity.  This lacks an understanding of the physiology.  In men with low T > 65, the majority are dealing with inflammation and excess weight; all of which increase aromatase activity and thus estradiol activity.  This does not indicate that an increase in estradiol activity is associated with improved libido in men.  How can elevated estrogen levels lead to low T and then increase levels are associated with improved libido?  This is merely a reflection of the body's dysfunctional physiology.  This observation of increased estradiol by no means shows cause and effect.  Scientists need to due a better job in vetting what they write!

This study shows that DHT is a good alternative androgen to Testosterone.  It was shown to have no positive/negative effect on the prostate.  The negative of this study was found to be bone loss from supra physiologic DHT.  The point there is to keep hormone replacement physiologic, as one should with all BHRT.

Study finds that Testosterone regulates glucose metabolism, in part, through adiponectin production.  Early state of low T will slow the use of fats as a source of fuel and this results in an increased energy balance and results in the increased adiponectin production to increase metabolism.  Testosterone and adiponectin exist in an inverse relationship. This study does not mimic normal physiology.  Men with low T are unhealthy with significant metabolic dysfunction.  These young, "healthy" men were induced to a low T state--that is not a clear picture as the physiology of a "young healthy" man is quite different than that of one with low T.   Testosterone conversion to DHT increases GLUT4 and thus glucose uptake--another mechanism of Testosterone's effect on glucose metabolism.

This study confirms what we know about Testosterone, but this study finds that Estradiol aids libido and fat loss.  The conclusion on Estradiol I believe to be extremely premature.  First, it flies in the face of all the accumulative data on estradiol, second, what normal physiology is being replicated with goserelin???  Goserelin has been shown to decrease Prolactin which can effect libido also.  What about the potential there?  The men included in the study were described as "healthy".  So, you are taking "healthy" normal funcitoning men, throwing in a monkey wrench and looking at the effects of your monkey wrench.  Sorry, not physiologic.  In all my practice, I have seen one man with low Estradiol levels.  There is no reference to the hormone levels in the men preceding the suppression with goserelin.  This is a study that lacks application.

This study's conclusion is to evaluate clotting factor i.e. factor V leiden, Factor VIII, and prothrombin prior to giving Testosterone.  This small study found increased clotting in some men on Testosterone. The problem here is the dosing of Testosterone in these men was 50-160 mg.  Physiologic dosing is 5-10 mg.  The problem is doping.  One wonders if physiologic dosing was undertaken if any of the men in this study would develop clotting problems, even though they had undiagnosed hypercoagulabitliy.

data on androgen therapy in women is sparse at best.  The conclusion here is suspect: "evidence supports the short-term efficacy and safety of high physiological doses of T" for women with with hypoactive sexual desire, yet the same authors recommend against long-term therapy.  How do those 2 go together???  They don't.  Support with physiologic Testosterone when appropriate testing reveals low T and symptoms support the same.  This is a practice guideline that lacks evidence to strongly back it up because so little evidence exists.  Practice guidelines are for lazy physicians.

Salivary cortisol as a tool for physiological studies and diagnostic strategies.

great review of vitamin D physiology

Thrombosis and cardiovascular risk is a hot topic in Testosterone therapy in men.  This study showed that topical "physiologic" Testosterone therapy provided no negative effects on the coagulation system.  No changes were documented in tPA, PAI-1, and fibrinogen levels in men with chronic stable angina.  This stands in contrast to supra-physiologic therapy of Testosterone that leads to hypofibrinogenemia.

Good review of data on vitamin D, Vitamin D receptors and cancer risk.  Studies have shown that low Vitamin D levels are associated with increased cancer risk and that higher vitamin D levels are associated with reduced cancer risk.  The ability to fully map out vitamin Ds role in the physiology is probably difficult due to the heterogeneity of cancer development and physiology.

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.

Study finds injectable contraception in men leaves delayed suppressed LH and Testosterone. This drug design is by those devoid of overall knowledge of physiology. Lower Testosterone in men has significant negative metabolic effect, neurotransmitter impact, and what about epigenetics. Some men have epigenetically increased risk of hypogonadism. This contraception is a bad idea physiologically.

Exercise alters gene expression via methylation--the power of epigenetics.  Interestingly, the majority of the methylation was outside the CPG island regions.  This 3 month study found methylation of 5,000 sites across the genome resulting in altered expression of apps 4,000 genes.  The altered muscle changes of the endurance training was linked to DNA methylation changes.

"Ascorbate at physiological concentrations (25 μm) strikingly suppressed HIF-1α protein levels and HIF transcriptional targets, particularly when the system was oncogenically activated in normoxic cells. Similar results were obtained with iron supplementation" Here, physiologic levels of plasma AA decrease HIF-1alpha activity.

Physiologic levels of testosterone shown to induce Calcium channel blockade.  This induces the beneficial cardiovascular vasodilation.  It is known that testosterone binds to the same receptor as the common calcium channel blocker nifedipine.