ER beta appears to be expressed through the menstruation cycle with predominance follicular and early secretory phases. Contrast with ER alpha predominance in late follicular and early secretory phases.
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?
Estradiol increased thyroid papillary and follicular cancer cells via both ER alpha and ER beta in this study. What is also interesting is that estradiol did not increase PR expression.
low Progesterone and progesterone "disturbances" found to be common in juvenile Lupus. The authors in this study proposed it was due to low follicular reserves. The point is that low progesterone increases inflammatory cytokines.
Study finds higher Pb levels in young girls is associated with delayed puberty onset. This occurs through an inverse relationship with inhibin B and follicular development. This relationship was also found with Cadmium. Both of these heavy metals are toxic to the ovaries.
Bisphenol A shown to disrupt ovarian estrogen production from exposure in adults. The point of this that is important is that BPA, a xenoestrogen, can infact disrupt physiologic hormone production in adults, and contribute to ovarian failure. BPA, itself, is 1,000 fold weaker than E2, yet it disrupts ovarian function.
it is clear that serum IGF-1 and or IGFBP-3 can be normal in patients with undisputed GHD
Various investigators have reported normal IGF-1 values in 37–70% of GH deficient adults
The co-administration of arginine and GHRH (the combined test) is a powerful stimulus for GH production and has gained increasing acceptance as a useful method of diagnosing GHD [34]. This test has been advocated as a suitable alternative to ITT
The glucagon stimulation test (GST) is a reliable, safe alternative to the ITT in the diagnosis of GHD
An intravenous infusion of arginine (0.5 g/kg body weight) together with an intravenous bolus of GHRH (1 mcg/kg body weight) is administered [30]. Serum samples for GH are then obtained every 15–30 minutes for two hours.
Obesity, particularly marked obesity, is associated with blunted GH secretion in response to provocative stimuli
It has also been suggested that that even mildly increased BMI (25–30 kg/m2) can result in diminished stimulated GH production in 13% of healthy subjects
Corneli et al. have defined BMI-specific cut-off points for diagnosing adult-onset GHD using GHRH + arginine—11.5 ng/mL for those with BMI < 25 kg/m2, 8.0 ng/mL for BMI 25–30 kg/m2, 4.2 ng/mL for those with BMI > 30 kg/m2
GH levels are higher during the luteal phase in comparison with the follicular phase of the cycle
Oral, in contrast to transdermal oestrogen, lowers IGF-1 levels and is associated with increased GH levels
Adequate pituitary replacement with thyroxine and hydrocortisone are needed for optimal GH production
one cannot rely on a low IGF-1 to diagnose GHD in women taking oral oestrogen preparations.
Numerous GH secretagogues are available with the insulin tolerance test being the gold standard and the glucagon stimulation test or the GHRH + arginine as acceptable alternatives
ain et al. found the GST to be at least as good as the ITT in provoking GH secretion
the GST is safe, with almost no contraindications, it causes nausea and sometimes vomiting in 15–20% of subjects