Get the Federal Government To Extend Your Lifespan

http://www.grg.org/resources/TheScientist.htm(((Okay, so let's, like, extend the human lifespan already. I like it that this is an actual FEDERAL FUNDING PITCH. That there's a BUSINESS MODEL for this idea.)))WHY ACT NOW? Consider what is likely to happen if we don’t. Take, for instance, the impact of just one age-related disorder – Alzheimer disease (AD). For no other reason than inevitable shifting demographics, the number of Americans stricken with AD will rise from 4 million today to as many as 16 million by mid-century.4 This means there will be more people with AD in the US by 2050 than the entire current population of Australia. Globally, AD prevalence is expected to rise to 45 million by 2050, with three of every four AD patients living in a developing nation.5 The US economic toll is currently $[80 - 100] billion, but by 2050 more than $1 trillion will be spent annually on AD and related dementias. The impact of this single disease will be catastrophic, and this is just one example.THE TARGET What we have in mind is not the unrealistic pursuit of dramatic increases in life expectancy, let alone the kind of biological immortality best left to science fiction novels.20 (((Aw c'mon Prof, we sci fi novelists are doing the best we can, given our limited liefspans. Ars longa, vita brevis, and all that.)))Rather, we envision a goal that is realistically achievable: a modest deceleration in the rate of aging sufficient to delay all aging-related diseases and disorders by about seven years.21 This target was chosen because the risk of death and most other negative attributes of aging tends to rise exponentially throughout the adult lifespan with a doubling time of approximately seven years.22 Such a delay would yield health and longevity benefits greater than what would be achieved with the elimination of cancer or heart disease.23 And we believe it can be achieved for generations now alive. If we succeed in slowing aging by seven years, the age-specific risk of death, frailty, and disability will be reduced by approximately half at every age. People who reach the age of 50 in the future would have the health profile and disease risk of today’s 43-year-old; those aged 60 would resemble current 53-year-olds, and so on. Equally important, once achieved, this seven-year delay would yield equal health and longevity benefits for all subsequent generations, much the same way children born in most nations today benefit from the discovery and development of immunizations. A growing chorus of scientists agrees that this objective is scientifically and technologically feasible. How quickly we see success depends in part on the priority and support devoted to the effort. Certainly such a great goal – to win back, on average, seven years of healthy life – requires and deserves significant resources in time, talent and treasury. But with the mammoth investment already committed in caring for the sick as they age, and the pursuit of ever-more expensive treatments and surgical procedures for existing fatal and disabling diseases, the pursuit of the Longevity Dividend would be modest by comparison. In fact, because a healthier, longer-lived population will add significant wealth to the economy, an investment in the Longevity Dividend would likely pay for itself. THE RECOMMENDATION The National Institutes of Health is funded at $28 billion in 2006, but less than 0.1% of that amount goes to understanding the biology of aging and how it predisposes us to a suite of costly diseases and disorders expressed at later ages. We are calling on Congress to invest 3 billion dollars annually to this effort; or about 1% of the current Medicare budget of $309 billion; and to provide the organizational and intellectual infrastructure and other related resources to make this work.Specifically, we recommend that one-third of this budget ($1 billion) be devoted to the basic biology of aging with a focus on genomics and regenerative medicine as they relate to longevity science.(((And, unlike sci-fi novels about life extension, this scientific plan has FOOTNOTED REFERENCES!)))References:1. Huber Warner, Twenty Years of Progress in Biogerontology, National Institute on Aging (2005).2. Richard M. Miller, “Extending Life: Scientific Prospects and Political Obstacles,” The Milbank Quarterly, Vol. 80, No. 1, pp. 155-74 (2002).3. PublicAgenda. “The Science of Aging Gracefully: Scientists and the Public Talk about AgingResearch,” The Alliance for Aging Research and the American Federation for Aging Research(2005).4. E. Liesi, et al., “Alzheimer Disease in the US Population: Prevalence Estimates Using the 2000 Census,” Arch Neurol, Vol. 60, pp. 1119-22 (2003).5. Alzheimer’s Disease Annual Report, Alzheimer’s Disease International. 2004-2005. And http://www.frost.co m/prod/servlet/dsd-fact-file.pag?docid=38565311 6. Robert N. Butler, et al., “The Aging Factor in Health and Disease: the Promise of Basic Research on Aging,” Special Report Aging Clinical and Experimental Research, Vol.16, pp. 104-112 (2004).7. D. Bloom and D. Canning, “The Health and Wealth of Nations,” Science, Vol. 287, pp. 1207-9 (2000).8. M. Vergara, et al., “Hormone-Treated Snell Dwarf Mice Regain Fertility But Remain Long-Lived and Disease Resistant,” J. Gerontol. Biol. Sci., Vol. 59, pp. 1244-50 (2004).9. Richard A. Miller and Stephen N. Austad “Growth and Aging: Why Do Big Dogs Die Young?” in Handbook of the Biology of Aging, E. J. Masoro, S. N. Austad, Eds. (Academic Press, NY) Chap. 19, pp. 512-33 (2006).10. David Sinclair and Leonard Guarente, “Unlocking the Secrets of Longevity Genes” Scientific American, Vol. No., pp. 48-57 (March 2006).11. M. Tatar, et al., “The Endocrine Regulation of Aging by Insulin-Like Signals,” Science, Vol. 299, pp. 1346-51 (2003).12. R. Weindruch, R.S. Sohal, “Seminars in Medicine of the Beth Israel Deaconess Medical Center: Caloric Intake and Aging,” New Engl. J. Med., Vol. 337, pp. 986-94 (1997).13. H. M. Brown-Borg, et al., “Dwarf Mice and the Aging Process,” Nature, Vol. 384, p. 33 (1996). 14. K. Flurkey, et al., “Lifespan Extension and Delayed Immune and Collagen Aging in Mutant Mice with Defects in Growth Hormone Production,” Proc. Natl. Acad. Sci., Vol. 98, pp. 6736-41 (2001).15. B. P. Yu, et al., “Nutritional Influences on Aging of Fischer 344 Rats: I. Physical, Metabolic, and Longevity Characteristics,” J. Gerontol, Vol. 40, pp. 657-70 (1985). 16. Richard Weindruch and Roy L. Walford, The Retardation of Aging and Disease by Dietary Restriction (Charles C Thomas, Springfield, IL, 1988).17. B. J. Geesaman, et al., “Haplotype-Based Identification of a Microsomal Transfer Protein Marker Associated with the Human Lifespan,” Proc. Natl. Acad. Sci., Vol. 100, pp. 14115-20 (2003).18. D. E. Arking, et al., “Association between a Functional Variant of the KLOTHO Gene and High-Density Lipoprotein Cholesterol, Blood Pressure, Stroke, and Longevity,” Circ. Res., Vol. 96, p. 412 (2005).19. N. Barzilai, et al., “Unique Lipoprotein Phenotype and Genotype Associated with Exceptional Longevity,” JAMA, Vol. 290, pp. 2030-40 (2003).20. Huber Warner, et al., “Science Fact and the SENS Agenda,” EMBO Reports, Vol. 6, pp.1106-8 (2005).21. S. Jay Olshansky, “Can We Justify Efforts To Slow the Rate of Aging in Humans?” Presentation before the Annual Meeting of the Gerontological Society of America (2003).22. Robert N. Butler, J.A. Brody, Eds., Delaying the Onset of Late-Life Dysfunction (Springer Publishing Company, New York; 1995).23. S. Jay Olshansky, “Simultaneous/Multiple Cause Delay: An Epidemiological Approach to Projecting Mortality,” J. Gerontol, Vol. 42, pp. 358-65 (1987).