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Testosterone given to elderly men with low "serum" testosterone shown to increase IGF-1 and increased muscle growth and strength.  So, this study shows that testosterone in men, seems to increase HGH production and thus increase IGF-1 production.  This may be the mechanism by which testosterone promotes muscle growth and increase in strength in men.

very interesting study in rats.  LH induced a dose-dependent increase in testicular estrogen production through aromatase activity.  Yes, LH stimulates the leydig cells to produce testosterone, but there is a point at which LH will actually increase aromatase activity and thus estrogen production at the testicular level.

Great review of the Hypogonadal-obesity-adipocytokine hypothesis.

IL-6 is known to stimulate the HPA and increase cortisol production.  Both, IL-6 and cortisol can decrease TSH production.

This article describes how important glutamine is as an alternative energy source in Glioblastoma. Cancer is a substrate-level dependent energy production disease. If one disrupts glycolysis as a source of energy, then many cancers will use glutamine through glutaminolysis. The cancer cells will do this through glutamate dehydrogenase and glutamate production. This will increase alpha-ketoglutarate which will then feed the substrate-level phosphorylation through the TCA cycle. This study mentioned that EGCG is a way to naturally inhibit glutamate dehydrogenase.

AquaTitanium, Phiten's most commonly utilized AQUA-METAL, is used as a dye-like material and permeated into the fibers of Phiten fabric products becoming a component of the finished product.

progesterone inhibits prostaglandin production

arimidex, also known as anastrozole, is shown to be an effective aromatase inhibitor in men.  These case studies used arimidex to successfully stimulate testosterone production by limiting testosterone to estrogen production.  This was found to be useful in the treatment of gynecomastia.

diabetes associated with increased advanced glycation end products (AGE) in elderly population.  This increase in AGE associated with cognitive decline as evaluated by MMSE.

AGE's, advanced glycation end products, play a role in development/progression of neurodegenerative diseases such as Alzheimer's, Parkinson's...

good article on the biochemistry of COX2 in inflammation.  Particularily with AGE and it the receptors RAGE.  COX2 has been shown to decrease insulin secretion through inhibition of islet cell production, but in the presence of disease level inflammation, COX2 can be a part of a very dangerous autocrine/paracrine loop.

No surprise that progesterone and the synthetic progestin medroxyprogesterone acetate (MPA) have different effects on the vascular endothelium. MPA inhibits NO production, whereas Progesterone maintains NO production.  MPA promoted platelet adhesion whereas Progesterone did not--significant implication in plaque formation.

Good review of the effects of BCAA on ammonia metabolism.  BCAA increase intramuscular NH3 production through the production of alpha-ketoglutarate.

BCAA are low in patients with liver cirrhosis due to increased glutamate production from glutamine.  The addition of BCAA in these patients is not without side effects--increased NH3 production.  The addition of alpha ketoglutarate should alleviate this risk.

This study found that lower TT and E1 associated with more "poor health" as defined by questionnaire.  The conclusion might lead one to think that Estrogen therapy is need in men.  Eightly percent of estrogen production in men occurs from Testosterone.  If Testosterone declines, then estrogen production will likewise decline.  A simple fact that the authors did not comment on.  Also, E1 binds with high affinity to ER alpha, which is pro-inflammatory and pro-proliferative: neither of which is a positive health benefit.   This appears to point more to a broad HPA suppression as an association to the "poor health".

Calorie restriction increases serum Testosterone levels in obese men.  This fits with other research that weight reduction in obese men can resolve low T.  The obvious proposed mechanisms are a reduction in aromatase activity due to a loss of adiposity, a decrease in inflammatory cytokine production thus negatively effecting the HPA, improved HPA signaling and thus improved Testicular production of Testosterone.

Just the abstract here.  Declining estradiol production found to be associated with increased cognitive dysfunction or cognitive decline in those using aromatase inhibitor therapy.  Aromatase inhibition therapy is used to block Testosterone to Estradiol production in women with ER+ breast cancer.

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.

Numerous deletorious effects are seen in high fructose diets: elevated Triglyceride production, fatty liver, insulin resistance, increased VLDL production and secretion, increased deposit of TG in muscle and increased muscle insulin resistance.  Alpha lipoic Acid is shown to counter these effects in rat model.