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Published online 28 November 2007 | Nature | doi:10.1038/450603a
Age research: A new angle on 'old'
Are ageing and disease two sides of the same coin? Erika Check Hayden reports from an institute that is betting that they are.
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Why not take a look at an ‘old’ answer to the ‘new’ aging problems? The News Feature article in Nature (vol. 450: 603-605, 2007) presented a grand building and some nice geroscience researchers in the field of aging study. It criticized the isolation of the National Cancer Institute (NCI) and the National Institute on Aging (NIA) into separate buildings and anticipated a better understanding of aging when researchers of the different disciplines are placed under a common roof. However, I wish to point out that the real limitation to the aging study is not the physical separation of researchers or even the lack of an understanding that aging and disease are related part of the same life coin. The real restriction on gero-scientists is actually their conceptual confinement to some dogmas that are fundamentally wrong. One such dogma is that aging is a unique feature of sexual organisms and a result of “trade-off� between germ and soma of multicellular eukaryotes. However, as early as 1990, I have pointed out that aging is a universal feature of all life forms because it is even found in some unicellular asexual prokaryotic organisms such as bacteria. Moreover, biotic aging is actually an evolutionary outcome of abiotic aging. Thus, biotic aging is not intractable but very tractable once its underlying abiotic molecular mechanisms are understood and correctly linked from bottom to top in multilayered organismal hierarchy. As a matter of fact, a linkage between DNA aging and cell aging was offered but relentlessly rejected by Nature. It is a true tragedy in science that my view on aging has been rejected by the mainstream for over a decade. Nevertheless, my views should be known by some aging researchers and other scientists because I have given invited seminars to NCI in 1997 and NIA in 1998, presented posters in ASM in 1997 and AAAS in 1998 and, more importantly, publishing numerous articles in various formats (see http://logibio.com and http://im1.biz) including a peer-reviewed publication in 1999 in Science in China (a very respected journal in China and indexed by SCI) in both English and Chinese, Letters in the official magazine of ASM (ASM News and later Microbe), Science of Aging Knowledge Environment (SAGE KE; http://sageke.sciencemag.org/community/forum/short/sageke_el_307.dtl) and patents disclosures and a granted US patent. Amazingly, aging research communities seemed to have a very limited vision in seeing my views on aging. So to force them to see my views, I spent my own money to travel to Italy in 2006 to make a presentation in the 3rd International Conference on Functional Genomics of Ageing and to engage in communication with some prominent aging researchers. However, my effort achieved no real effect as it is later shown that these aging researchers still ignore my views and even went ahead of claiming some “first� discoveries even though they were clearly told of the publications of some real first discoveries. Why did some aging researchers intentionally ignore the already found answers to their “enigmatic� aging research problems? Why would no gero-scientists be willing to openly challenge my views on aging (http://im1.biz/Aging.htm)? Why would some aging researchers spend more money on “curing� aging or even reversing aging through rejuvenation with “immortal� stem cells rather to acknowledge that no life is immortal and even stem cell will age and die (http://im1.biz/StemCell.htm)? Shi V. Liu Eagle Institute of Molecular Medicine Apex, NC 27502, USA SVL@logibio.com
“Metabonomic research on ageing and disease, the two side of the same coin� The phenomenon of increased life expectancy of world class male athletes (Sarna et al 1993) gives a clue to study the possible mechanism of caloric restriction to extend lifespan since caloric restriction and high intensity training share many many similarities such as chronic disease prevention (Kujala et al 2003, Lynch et al 2007) and immune inhibition(Galassetti et al 2006,Nagatomi 2006), especially in enhancing the quality of energy homeostasis. In other words, there might be a homeostatic mechanism of caloric restriction to extend lifespan so that it might hold for human. The quality of person homeostasis is becoming higher in developing, and lower in ageing. The approaches or drugs to enhance homeostasis quality might enhance performance and prevent the person from chronic diseases, and then extend lifespan. In our metabonomic study of athletes, the sport-specific homeostasis has been found to be represented by metabonomics so that the sport capacity can be precisely predicted. of course, matabonomics has been widely used to study various diseases. Therefore, metabonomics might be used to study the two sides of the same coin, ageing and disease. “Rferences� Galassetti PR, Nemet D, Pescatello A, Rose-Gottron C, Larson J, Cooper DM. 2006. Exercise, caloric restriction, and systemic oxidative stress. J Investig Med. 2006 Mar;54(2):67-75. Kujala UM, Marti P, Kaprio J, Hernelahti M, Tikkan en H, Sarna S. 2003. Occurrence of chronic disease in former top-level athletes. Predominance of benefits, risks or selection effects? Sports Med. 2003;33(8):553-61. Lynch NA, Ryan AS, Evans J, Katzel LI, Goldberg AP. 2007. Older elite football players have reduced cardiac and osteoporosis risk factors. Med Sci Sports Exerc. 2007 Jul;39(7):1124-30. Nagatomi R. 2006. The implication of alterations in leukocyte subset counts on immune function. Exerc Immunol Rev. 2006;12:54-71. Sarna S, Sahi T, Koskenvuo M, Kaprio J. 1993. Increased life expectancy of world class male athletes. Med Sci Sports Exerc. 1993 Feb;25(2):237-44.
The quality of homeostasis is becoming higher in developing and lower in ageing. The age when the homeostasis is of highest quality is defined as optimum age, _h_. The most possible life-span, _y_, of a person might be _y=2h+1_ if the developing and the ageing are supposed to be symmetric. For the detail, please pay attention to the following forum: http://network.nature.com/forums/naturenewsandopinion/906
A system in homeostasis reacts to every change in the environment, or to every random disturbance, through a series of modifications of equal size and opposite direction to those that created the disturbance. The higher the quality of the homeostasis, the stronger the disturbance resistance. Therefore, the longer the life-span, the stronger the disturbance resistance, and then the stronger the capacity of the chronic disease prevention, which might be the cause of two sides of the same coin, ageing and disease. For the detail, please pay attention to the following forum: http://network.nature.com/forums/naturenewsandopinion/906