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Nice, more recent analysis, of HGH testing.

the Glucagon Stim test is a useful alternative to the ITT for HGH deficiency evaluation.

Progesterone decreased melanoma cell growth in cell line study.  This inhibition occurred through non-progesterone receptor pathways.

Exercise is not just for calories out.  Exercise increases growth hormone, IGF-1, glucagon-like peptide 1, IL-6, and IL-1ra.  The effect is to GH increases beta islet cell mass and protects beta cell lines against IL-1beta, Interferon-gamma and TNF-alhpa induced apoptosis.  IL-6 increased production increases GLP-1 and IL-1ra which counters IL-1beta.  Interleukin-1beta induces islet cell apoptosis and thus IL-1ra counters this pro-inflammatory signal.

another awesome article dealing with hormone metabolites. Physicians that don't understand metabolites and receptors may be doing more harm than good.   One of the mainstays of the treatment of metastatic prostate disease is androgen deprivation therapy.  This article requires a reassessment of this due to the DHT metabolite 3-beta androstanediol.  This metabolite is produced from DHT production via the enzyme 3beta HSD.  This metabolite binds to ER beta, an estrogen receptor, and inhibits proliferation, migration, promotes adhesion (limits spreading), and stimulates apoptosis.  This is contrast to 3-alpha androstanediol.  Androgen deprivation therapy will decrease 3-beta androstanediol.  This is the likely reason for the increased aggressive prostate cancer found in those men using 5 alpha reductase inhibitors.

GHRH, for 20 weeks shown to subjectively and objectively improve cognitive function in adults.  

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.

Great read on the different mechanisms by which GH promotes carcinogenesis and growth via STATs, P13K/Akt, mTOR, IGF-1...

This is a dissertation, but they found ER alpha expression in all meningioma samplings. This is in contrast to previous studies. As further research has come with meningiomas, more ER presence is found, likely due to improved testing techniques. What is interesting here is that Low/no PR status was associated with Increased ER alpha status. This has been shown to be a more pro-inflammatory/pro-growth picture in disease states, such as breast and prostate CA.

small study, but males with pancreatic cancer were found to have higher levels of FSH (p < 0.01), LH and oestradiol (p < 0.001) and lower levels of progesterone (p < 0.01) and testosterone (p < 0.05) than the controls. Female patients with pancreatic cancer were found to have higher levels of oestradiol (p < 0.001) and lower levels of LH, FSH and progesterone.  Though cause and effect is not known, the expression of ER alpha in pancreatic cancer is known and the inflammatory and pro-growth signal of ER alpha is known, thus heavy stimulation would be unwise.

Retrospective study finds that 2 years of Testosterone and GH do not change metabolic biomarkers, PSA, or disease risk.  LDL and TC were in fact decreased in the study arm without statin therapy.

HGH treatment preoperatively preserved muscle mass and reduced postoperative fatigue.

The effects of T3 on cancer cell lines varies.  All cell lines came from the same tissue. It doesn't appear that simply stating T3 promotes cellular metabolism and thus provides an increase in cancer progression risk.  Some cell lines studies actually had an inhibition of cell growth, whereas others saw an increase.  

GH plays a key regulating role in obesity.  GH deficiency promotes increased cortisone to cortisol production in adipose tissue and liver.  This promotes insulin resistance and obesity. 

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.

In vivo study finds melatonin reduced tumor growth, proliferation, and inhibited angiogenesis in breast cancer model.

DIM, from cruciferous veggies often used to aid estrogen metabolism, is found to decrease PSA transcription and function as an androgen receptor antagonist in prostate cancer cell lines.

Progesterone shown to stimulate growth and migration of astrocytes in the brain.  The has both implications in cancer, such as in astrocytomas, but also in TBI.  The study also found that the Progesterone antagonist RU486 inhibited this effect.  A more thorough evaluation would have included the pregnane metabolites.

Elevated GH levels favor carcinogenesis and spread of colorectal cancer.