New Research: 'Un-Growth Hormone' Increases Longevity
Editor's ChoiceMain Category: Seniors / Aging
Also Included In: Complementary Medicine / Alternative Medicine
Article Date: 03 Jan 2011 - 0:00 PDT
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A compound which acts in the opposite way as growth hormone can reverse some of the signs of aging, a research team that includes a Saint Louis University physician has shown. The finding may be counter-intuitive to some older adults who take growth hormone, thinking it will help revitalize them.
Their research was published in the Dec. 6 online edition of the Proceedings of the National Academy of Sciences.
The findings are significant, says John E. Morley, M.D., study co-investigator and director of the divisions of geriatric medicine and endocrinology at Saint Louis University School of Medicine, because people sometimes take growth hormone, believing it will be the fountain of youth.
"Many older people have been taking growth hormone to rejuvenate themselves," Morley said. "These results strongly suggest that growth hormone, when given to middle aged and older people, may be hazardous."
The scientists studied the compound MZ-5-156, a "growth hormone-releasing hormone (GHRH) antagonist." They conducted their research in the SAMP8 mouse model, a strain engineered for studies of the aging process. Overall, the researchers found that MZ-5-156 had positive effects on oxidative stress in the brain, improving cognition, telomerase activity (the actions of an enzyme which protects DNA material) and life span, while decreasing tumor activity.
MZ-5-156, like many GHRH antagonists, inhibited several human cancers, including prostate, breast, brain and lung cancers. It also had positive effects on learning, and is linked to improvements in short-term memory. The antioxidant actions led to less oxidative stress, reversing cognitive impairment in the aging mouse.
William A. Banks, M.D., lead study author and professor of internal medicine and geriatrics at the University of Washington School of Medicine in Seattle, said the results lead the team "to determine that antagonists of growth hormone-releasing hormone have beneficial effects on aging."
The study team included as its corresponding author Andrew V. Schally, M.D., Ph.D., a professor in the department of pathology and division of hematology/oncology at the University of Miami Miller School of Medicine.
Source: Saint Louis University
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Banks, et al., may have simply Shifted use of DHEA by Genes
posted by James Michael Howard on 3 Jan 2011 at 5:36 amIt is my hypothesis that evolution selected DHEA because it optimizes replication and transcription of DNA. Therefore DHEA levels affect all tissues and all tissues and genes compete for available DHEA. Furthermore, subordinate to this hypothesis is my hypothesis that DHEA acts with proteins which affect replication and transcription of DNA. The specificity and timing of these hormones will direct sequential gene activity and, therefore, direct growth and differentiation of all tissues. Some of these proteins will affect use of DHEA more than others, that is, some proteins will affect DNA more broadly than others. For example, I think growth hormone acts more broadly than a more specific protein such as a nerve growth factor. A protein that acts more broadly will "use" DHEA more than a more specific transcription factor.
It follows that loss of DHEA accelerates the loss of replication and transcription of DNA, that is, loss of DHEA accelerates ageing and ageing-associated phenomena, including loss of telermerase ("Telomeres, Telomerase, Dehydroepiandrosterone, and Cancer and Aging," at: http://members.cox.net/jmhoward3/Telomeres.htm ).
I suggest the "senescence-accelerated mouse" may exist because of decreased DHEA. The "SAMP8" mouse is considered a possible animal model of Alzheimer's disease. While no research has examined the levels of DHEA in SAMP8 mice, one citation exists which demonstrates that DHEAS, the precursor of DHEA, is "more effective in reversing the cognitive impairments" in a SAMP8 study (Life Sci. 2004 Oct 22;75(23):2775-85). Loosely, this may support low DHEA in this animal model. I first suggested low DHEA as a cause of Alzheimer's disease in 1985 (copyrighted).
When the foregoing is combined, an explanation of Banks, et al., Proc Natl Acad Sci U S A. 2010 Dec 21;107(51):22272-7, "Effects of a growth hormone-releasing hormone antagonist on telomerase activity, oxidative stress, longevity, and aging in mice," may be produced. If SAMP8 mice are deficient in DHEA, then administration of growth hormone will further reduce available DHEA, that is, growth hormone will accelerate ageing, and other problems of loss of DHEA, in individuals of low DHEA. This may explain why "These results strongly suggest that growth hormone, when given to middle aged and older people, may be hazardous." (http://www.medicalnewstoday.com/articles/212470.php). Now, if I am correct, using "growth hormone-releasing hormone (GHRH) antagonist" (previous url) will positively affect SAMP8 mice because reducing the use of DHEA by growth hormone will increase use of DHEA by other, specific growth factors, such as those used by the brain. That is, in the competition among tissues and genes for DHEA, Banks, et al., shifted the "winner."
I suggest this may explain the findings of Banks, et al.
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