Many are the plagues of aging and many, if not most, people will suffer the debilitating effects of aging as they transition into a greatly diminished quality of life. Some of the effects are headaches, depression, mood and emotion swings, lethargy, weakness, muscle loss, high blood pressure, unwanted facial hair, great weight gain or loss, loss of memory, loss of sleep, sexual dysfunction, loss of libido, erectile dysfunction, infertility and impotence, irregular menses and hot flashes, lactating breasts, diabetes, joint pain, osteoporosis, urinary incontinence, hair loss, and so on. In most cases these effects are the result of a dysfunctional Pituitary Gland whose hormonal control has lessened its output to less than marginal. Following are excerpts from The Journal of Clinical Endocrinology & Metabolism documenting the research into aging-related disabilities:
Unreplaced Sex Steroid Deficiency, Corticotropin Deficiency, and Lower IGF-I Are Associated with Lower Bone Mineral Density in Adults with Growth Hormone Deficiency
(http://jcem.endojournals.org/cgi/content/abstract/96/5/1516)
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| Growth Hormone Deficiency |
Setting: The study was an international epidemiological survey of more than 15,000 adult GHD patients from 31 countries.
Patients: A total of 1218 subjects with stringently defined GHD of adult onset (641 women and 577 men) who were GH naïve and had BMD measured in the posterior anterior lumbar spine and femoral neck by dual-energy X-ray absorptiometry.
Conclusions: Hormone variables associated with lower sBMD in patients with adult-onset GHD include unreplaced sex steroid deficiency and corticotropin deficiency in the LS and lower IGF-I SDS in the FN.
Plain English Translation: A total of 1218 subjects with Growth Hormone Deficiency (GHD) as a result of aging also had Bone Mineral Deficiency (BMD) (aka osteoporosis) as measured by X-ray in the neck and spine.
Progesterone Prevents Sleep Disturbances and Modulates GH, TSH, and Melatonin Secretion in Postmenopausal Women
(http://jcem.endojournals.org/cgi/content/abstract/96/4/E614)
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| Fragmented Sleep |
Design: Randomized, double-blind, placebo-controlled study. For 3 wk, subjects took daily at 2300 h a capsule of either 300 mg of Progesterone or placebo. Sleep was polygraphically recorded during the last two nights, and blood samples were obtained at 15-min intervals for 24 h.
Results: During the first night (no blood sampling), sleep was similar in both conditions. Under placebo, blood sampling procedure was associated with marked sleep disturbances, which were considerably reduced under Progesterone treatment: mean duration of wake after sleep onset was 53% lower, slow-wave sleep duration almost 50% higher, and total slow-wave activity (reflecting duration and intensity of deep sleep) almost 45% higher under Progesterone than under placebo (P 0.05). Nocturnal GH secretion was increased, and evening and nocturnal TSH levels were decreased under Progesterone (P 0.05).
Conclusions: Progesterone had no effect on undisturbed sleep but restored normal sleep when sleep was disturbed, acting as a "physiologic" regulator rather than as a hypnotic drug. Use of Progesterone might provide novel therapeutic strategies for the treatment of sleep disturbances, in particular in aging where sleep is fragmented and of lower quality.
Progesterone is naturally secreted by the Ovary in the second two weeks of the menstrual cycle. The Ovary is stimulated by Estrogen which is produced by the Uterus, which is stimulated by Luteinizing Hormone (LH) produced by the Pituitary Gland.
Interaction between Testosterone and Growth Hormone on Whole-Body Protein Anabolism Occurs in the Liver
(http://jcem.endojournals.org/cgi/content/abstract/96/4/1060)
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| Loss of Libido |
Patients and Intervention: Eleven hypopituitary men with GH and testosterone deficiency were randomized to 2-wk treatments with transdermal testosterone (10 mg) or oral testosterone (40 mg), with or without GH replacement (0.6 mg/d). The dose of testosterone administered orally achieves physiological portal testosterone concentrations without spillover into the systemic circulation.
Results: In the absence of GH, neither transdermal nor oral testosterone affected LRa or Lox. GH therapy significantly increased LRa, an effect equally reduced by transdermal and oral testosterone administration. GH replacement alone did not significantly change Lox, whereas addition of testosterone treatment reduced Lox, with the effect not significantly different between transdermal and oral testosterone.
Conclusions: In the doses used, testosterone stimulates protein anabolism by reducing protein breakdown and oxidation only in the presence of GH. Because the net effect on protein metabolism during GH therapy is not different between systemic and solely hepatic testosterone administration, we conclude that the liver is the primary site of this hormonal interaction.
