This week’s research review focuses on the estrogen-thyroid-adrenal connection with an article by a veterinarian published in Medical Hypothesis. (Plechner 2004)
In the News: “Study shows growth hormone boosts sprint speed” By Shari Roan, May 3, 2010 LA Times
Of interest is that the study was funded by an anti-doping agency. (Meinhardt, Nelson et al. 2010)
An interesting article published in the journal Medical Hypothesis proposed that cortisol abnormalities caused elevated estrogen and immune destabilization. In addition to genetic defects, causes of cortisol deficiency included prolonged stress and toxicity. The adrenal gland is believed to be the most vulnerable organ in the endocrine system to toxins with most of the detrimental effects observed in the cortx, which produces cortisol. (Plechner 2004)
By interfering with cortisol synthesis, estrogen may indirectly impair thyroid function. These combined effects may slow the overall metabolism and interfere with many basic physiologic functions. The author noted several mechanisms: (Plechner 2004)
Estrogen causes an increase in serum thyroxine-binding globulin, which may slow the entry of thyroxine into cells and thereby reduce thyroid hormone action in tissue. (Arafah 2001)
Elevated estrogen may also directly inhibit thyroid glandular release. (Gross, Appleman et al. 1971)
Cortisol appears to be involved in the normal transference of T4 to T3, and the entry of T3 into cells.
Corrective therapy consisted of physiologic dosages sufﬁcient to compensate for deﬁcient cortisol and re-regulate the immune system. These therapeutic dosages are signiﬁcantly lower than standard pharmacologic levels used for short-term treatment and are usually needed for the duration of the patient’s life. This innovative use of a standard medication consistently restores lost immune competence. (Plechner 2004)
Cortisol abnormality as a cause of elevated estrogen and immune destabilization: insights for human medicine from a veterinary perspective
(Plechner 2004) Download Download2 Download3
For more than 35 years the author has treated multiple serious diseases in cats and dogs by correcting an unrecognized endocrine-immune imbalance originating with a deficiency or defect of cortisol. The cortisol abnormality creates a domino effect on feedback loops involving the hypothalamus-pituitary-adrenal axis. In this scenario, estrogen becomes elevated, thyroid hormone becomes bound, and B and T cells become deregulated. Diseases with this aberration as a primary etiological component range from allergies to severe cases of autoimmunity to cancer. The author has consistently identified excess estrogen or "estrogen dominance" as part of an endocrine-immune derangement present in many common diseases of dogs and cats. Ninety-percent of these cases involve spayed females and neutered or intact males, so the elevated estrogen cannot be attributed to ovarian activity. The author identifies the adrenal cortex as a source of the imbalance, which produces a variety of vital hormones. The author has developed an endocrine-immune blood test that measures cortisol, total estrogen, T3 and T4, and IgA, IgG, and IgM antibody levels. The protocol for corrective therapy involves the use of various cortisone medications, either standard pharmaceutical compounds or a natural bio-identical preparation made from an ultra extract of soy. The author's clinical success and the growing clinical applications of low-dosage cortisone therapy for humans strongly argue for sustained research into the nature, magnitude, and impact of cortisol defects, including an associated estrogen-immune problem, in the etiology of disease.
The effects of growth hormone on body composition and physical performance in recreational athletes: a randomized trial
(Meinhardt, Nelson et al. 2010)
BACKGROUND: Growth hormone is widely abused by athletes, frequently with androgenic steroids. Its effects on performance are unclear. OBJECTIVE: To determine the effect of growth hormone alone or with testosterone on body composition and measures of performance. DESIGN: Randomized, placebo-controlled, blinded study of 8 weeks of treatment followed by a 6-week washout period. Randomization was computer-generated with concealed allocation. (Australian-New Zealand Clinical Trials Registry registration number: ACTRN012605000508673) SETTING: Clinical research facility in Sydney, Australia. PARTICIPANTS: 96 recreationally trained athletes (63 men and 33 women) with a mean age of 27.9 years (SD, 5.7). INTERVENTION: Men were randomly assigned to receive placebo, growth hormone (2 mg/d subcutaneously), testosterone (250 mg/wk intramuscularly), or combined treatments. Women were randomly assigned to receive either placebo or growth hormone (2 mg/d). MEASUREMENTS: Body composition variables (fat mass, lean body mass, extracellular water mass, and body cell mass) and physical performance variables (endurance [maximum oxygen consumption], strength [dead lift], power [jump height], and sprint capacity [Wingate value]). RESULTS: Body cell mass was correlated with all measures of performance at baseline. Growth hormone significantly reduced fat mass, increased lean body mass through an increase in extracellular water, and increased body cell mass in men when coadministered with testosterone. Growth hormone significantly increased sprint capacity, by 0.71 kJ (95% CI, 0.1 to 1.3 kJ; relative increase, 3.9% [CI, 0.0% to 7.7%]) in men and women combined and by 1.7 kJ (CI, 0.5 to 3.0 kJ; relative increase, 8.3% [CI, 3.0% to 13.6%]) when coadministered with testosterone to men; other performance measures did not significantly change. The increase in sprint capacity was not maintained 6 weeks after discontinuation of the drug. LIMITATIONS: Growth hormone dosage may have been lower than that used covertly by competitive athletes. The athletic significance of the observed improvements in sprint capacity is unclear, and the study was too small to draw conclusions about safety. CONCLUSION: Growth hormone supplementation influenced body composition and increased sprint capacity when administered alone and in combination with testosterone. PRIMARY FUNDING SOURCE: The World Anti-Doping Agency.
Arafah, B. M. (2001). "Increased need for thyroxine in women with hypothyroidism during estrogen therapy." N Engl J Med 344(23): 1743-9.
Gross, H. A., M. D. Appleman, Jr., et al. (1971). "Effect of biologically active steroids on thyroid function in man." J Clin Endocrinol Metab 33(2): 242-8.
Meinhardt, U., A. E. Nelson, et al. (2010). "The effects of growth hormone on body composition and physical performance in recreational athletes: a randomized trial." Ann Intern Med 152(9): 568-77.
Plechner, A. J. (2004). "Cortisol abnormality as a cause of elevated estrogen and immune destabilization: insights for human medicine from a veterinary perspective." Med Hypotheses 62(4): 575-81.