Sierra Acai Company
Sierra Acai Company
Open 7 Days a Week
MonaVie Independent Distributor
Distributor Training
Shop Online
Enroll Now
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
Friends
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
08-SEPTEMBER-2008 07:42:01 - Strategies for Engineered Negligible Senescence Strategies for Engineered Negligible Senescence SENS is a medical proposal for periodically repairing all of the age-related tissue damage to the human body, thereby effectively curing human ageing and indefinitely extending the healthy human lifespan.12 Engineered negligible senescence refers to an engineered prevention or reversal of cellular aging referred to as senescence in biology. The expression was coined by British biogerontologist Aubrey de Grey and first appeared in print in his 1999 book The Mitochondrial Free Radical Theory of Aging.3 It was later prefaced with the term strategies in the article Time to Talk SENS: Critiquing the Immutability of Human Aging4 and is used in the context of de Grey's life extension medical proposal, Strategies for Engineered Negligible Senescence SENS. De Grey argues for a goal-directed rather than curiosity-driven5 approach to the science of aging, and to this purpose he identifies what he believes are the seven causes of aging and their potential methods of treatments. De Grey in this sense views medicine as a branch of engineering. He believes the next great social debate will occur when aging research progresses to the point that public funds could be used to accelerate the arrival of effective treatment for aging. The proposal has received widespread media attention, including from the BBC,6 the New York Times,7 and 60 Minutes,8 though it has been questioned by mainstream biologists.8 De Grey has summarized the entire SENS program in his 2007 book Ending Aging: The Rejuvenation Breakthroughs that Could Reverse Human Aging in Our Lifetime.2 Although media sources have occasionally described SENS as Cambridge-based,6 the SENS project is free-standing with no exclusive university affiliation.1 Contents 1 Framework 2 Types of aging damage and treatment schemes 2.1 Cancer-causing nuclear mutations/epimutations-OncoSENS 2.2 Mitochondrial mutations-MitoSENS 2.3 Intracellular junk-LysoSENS 2.4 Extracellular junk-AmyloSENS 2.5 Cell loss and atrophy-RepleniSENS 2.6 Cell senescence-ApoptoSENS 2.7 Extracellular crosslinks-GlycoSENS 3 Scientific controversy 3.1 De Grey Technology Review controversy 4 Social and economic implications 5 SENS meetings 6 Methuselah Foundation 7 See also 8 References 8.1 Footnotes 8.2 Bibliography Framework The arrows with flat heads are a notation meaning inhibits, used in the literature of gene expression and gene regulation. The arrows with flat heads are a notation meaning inhibits, used in the literature of gene expression and gene regulation. The goal of the Strategies for Engineered Negligible Senescence SENS is the complete reversal of all age-related illnesses and indefinite extension of the healthy human lifespan.1 The SENS project consists in implementing a series of periodic medical interventions designed to repair, prevent or render irrelevant all the types of molecular and cellular damage that cause age-related pathology and degeneration, in order to avoid debilitation and death from age-related causes.2 De Grey defines aging as the set of accumulated side effects from metabolism that eventually kills us,9 and, more specifically, as follows: a collection of cumulative changes to the molecular and cellular structure of an adult organism, which result in essential metabolic processes, but which also, once they progress far enough, increasingly disrupt metabolism, resulting in pathology and death.10 As de Grey states, geriatrics is the attempt to stop damage from causing pathology; traditional gerontology is the attempt to stop metabolism from causing damage; and the SENS engineering approach is to eliminate the damage periodically, so keeping its abundance below the level that causes any pathology.1 His approach to biomedical gerontology anti-aging medicine is thus distinctive because of its emphasis on rejuvenation rather than attempting to slow the aging process. He identifies what he believes to be the seven biological causes of senescence.211 According to de Grey, the causes of aging in humans are cell loss or atrophy without replacement,41012 oncogenic nuclear mutations and epimutations,131415 cell senescence Death-resistant cells,1617 mitochondrial mutations,1819 Intracellular junk or junk inside cells lysosomal aggregates,2021 extracellular junk or junk outside cells extracellular aggregates,1617 and random extracellular cross-linking.1617 For each of these problems, de Grey outlines possible solutions, with a research and a clinical component. The clinical component is required because in some of the proposed therapies, feasibility has already been proven, but not completely applied and approved for use by human beings. He believes we will be able to apply these solutions before we completely understand the targeted aging mechanisms, which will take longer.9 He states that the goals work together to eliminate known causes of human senescence, are concrete, seem achievable, and are considered feasible by experts in the applicable fields. The goals were said to be taken from classical literature describing the biological causes of senescence. De Grey proposes that engineered negligible senescence therapies could extend the human lifetime by many centuries or millennia, as early therapies give them enough time to seek more effective therapies later on. He describes an actuarial escape velocity of life extension, when advances in senescence treatment come rapidly enough to save the lives of the oldest beneficiaries of the previous treatments.22 Types of aging damage and treatment schemes Cancer-causing nuclear mutations/epimutations-OncoSENS These are changes to the nuclear DNA nDNA, the molecule that contains our genetic information, or to proteins which bind to the nDNA. Certain mutations can lead to cancer, and, according to de Grey, non-cancerous mutations and epimutations do not contribute to aging within a normal lifespan, so cancer is the only endpoint of these types of damage that must be addressed. A mutation in a functional gene of a cell can cause that cell to malfunction or to produce a malfunctioning product, because of the sheer number of cells, de Grey believes that redundancy takes care of this problem, although cells that have mutated to produce toxic products might have to be disabled. In de Grey's opinion, the effect of mutations and epimutations that really matters is cancer, this is because if even one cell turns into a cancer cell it might spread and become deadly. This would need to be corrected by whole-body interdiction of lengthening telomeres, or any other cure for cancer, if any is ever found. Mitochondrial mutations-MitoSENS Mitochondria are components in our cells that are important for energy production. They contain their own genetic material, and mutations to their DNA can affect a cell's ability to function properly. Indirectly, these mutations may accelerate many aspects of aging. Because of the highly oxidative environment in mitochondria and their lack of the sophisticated repair systems found in cell nucleus, mitochondrial mutations are believed to a be a major cause of progressive cellular degeneration. This would be corrected by moving the DNA for mitochondria completely within the cellular nucleus, where it is better protected. In humans, all but 13 proteins are already protected in this way. De Grey argues that experimental evidence demonstrates that the operation is feasible. Intracellular junk-LysoSENS Our cells are constantly breaking down proteins and other molecules that are no longer useful or which can be harmful. Those molecules which can't be digested simply accumulate as junk inside our cells. Atherosclerosis, macular degeneration and all kinds of neurodegenerative diseases such as Alzheimer's disease are associated with this problem. Junk inside cells might be removed by adding new enzymes to the cell's natural digestion organ, the lysosome. These enzymes would be taken from bacteria, molds and other organisms that are known to completely digest animal bodies. Extracellular junk-AmyloSENS Harmful junk protein can also accumulate outside of our cells. The amyloid plaque seen in the brains of Alzheimer's patients is one example. Junk outside cells might be removed by enhanced phagocytosis the normal process used by the immune system, and small drugs able to break chemical beta-bonds. The large junk in this class can be removed surgically. Junk here means useless things accumulated by a body, but which cannot be digested or removed by its processes, such as the amyloid plaques characteristic of Alzheimer's disease. The oft-mentioned toxins that are identified as causes of many diseases most likely fit under this class. Cell loss and atrophy-RepleniSENS Some of the cells in our bodies cannot be replaced, or can only be replaced very slowly-more slowly than they die. This decrease in cell number causes the heart to become weaker with age, and it also causes Parkinson's disease and impairs the immune system. Cell depletion can be partly corrected by therapies involving exercise and growth factors. But stem cell therapy is almost certainly required for any more than just partial replacement of lost cells. De Grey points out that this research involves a large number of details, and is already occurring on many fronts. Cell senescence-ApoptoSENS This is a phenomenon where the cells are no longer able to divide, but also do not die and let others divide. They may also do other things that they are not supposed to do, like secreting proteins that could be harmful. Immune senescence and type 2 diabetes are caused by this. Cells sometimes enter a state of resistance to signals that should cause them to destroy themselves, a process called apoptosis; an example is the state known as cellular senescence. These cells could be eliminated might be corrected by forcing such cells to apoptose. Cell killing with suicide genes or vaccines is suggested for making the cells undertake apoptosis. Healthy cells would multiply to replace them. Extracellular crosslinks-GlycoSENS Cells are held together by special linking proteins. When too many cross-links form between cells in a tissue, the tissue can lose its elasticity and cause problems including arteriosclerosis and presbyopia.9 These are chemical bonds between structures that are part of the body, but not within a cell. In senescent people many of these become brittle and weak. De Grey proposes to further develop small-molecular drugs and enzymes to break links caused by sugar-bonding glycation, and other common forms of chemical linking. Scientific controversy SENS has been a highly controversial proposal, with many critics arguing that the SENS agenda is fanciful and the highly complicated biomedical phenomena involved in the aging process contain too many unknowns for SENS to be scientific or implementable in the foreseeable future. In November 2005, 28 biogerontologists published a statement of criticism in EMBO reports, Science fact and the SENS agenda: what can we reasonably expect from ageing research?,23 arguing each one of the specific proposals that comprise the SENS agenda is, at our present stage of ignorance, exceptionally optimistic,23 and that some of the specific proposals will take decades of hard work to be medically integrated, if they ever prove to be useful.23 The researchers argue that while there is a rationale for thinking that we might eventually learn how to postpone human illnesses to an important degree,23 increased basic research, rather than the goal-directed approach of SENS, is presently the scientifically appropriate goal. This article was written in response to a July 2005 EMBO reports article previously published by de Grey24 and a response from de Grey was published in the same November issue.25 De Grey summarizes these events in The biogerontology research community's evolving view of SENS, published on the Methuselah Foundation website.26 De Grey Technology Review controversy Main article: De Grey Technology Review controversy In February 2005, Technology Review, which is owned by the Massachusetts Institute of Technology, published an article by Sherwin Nuland, a Clinical Professor of Surgery at Yale University and the author of How We Die,27 that drew a skeptical portrait of Aubrey de Grey, at the time a computer associate in the Flybase Facility of the Department of Genetics at the University of Cambridge.28 While admiring de Grey's intelligence, Nuland concluded that he would surely destroy us in attempting to preserve us29 because living for such long periods would undermine what it means to be human.29 In the same issue of the magazine, Jason Pontin, the or in chief and publisher of Technology Review, criticised de Grey. Writing an or's letter, titled Against Transcendence, he questioned the usefulness and appropriateness of introducing transcendentalism, or transhumanism, into science.30 The April 2005 issue of Technology Review contained a reply by Aubrey de Grey31 and numerous comments from readers.32 In July of 2005, Pontin announced a $20,000 prize open to any molecular biologist, with a record of publication in biogerontology, who could prove that SENS was so wrong that it is unworthy of learned debate.33 Technology Review received five submissions to its Challenge. In March, of 2006, Technology Review announced that it had chosen a panel of judges for the Challenge.34 Three met the terms of the prize competition. They were published by Technology Review on June 9, 2006. Accompanying the three submissions were rebuttals by de Grey, and counter-responses to de Grey's rebuttals. On July 11, 2006, Technology Review published the results of the SENS Challenge.3536 In the end, no one won the $20,000 prize. The judges felt that no submission met the criterion of the challenge and disproved SENS, although they unanimously agreed that one submission, by Preston Estep and his colleagues, was the most eloquent. Craig Venter succinctly expressed the prevailing opinion: Estep et al. ... have not demonstrated that SENS is unworthy of discussion, but the proponents of SENS have not made a compelling case for it.35 Summarizing the judges' deliberations, Pontin wrote, SENS is highly speculative. Many of its proposals have not been reproduced, nor could they be reproduced with today's scientific knowledge and technology. Echoing Myhrvold, we might charitably say that de Grey's proposals exist in a kind of antechamber of science, where they wait possibly in vain for independent verification. SENS does not compel the assent of many knowledgeable scientists; but neither is it demonstrably wrong.3537 In a letter of dissent dated July 11, 2006 in Technology Review, Estep et al. criticized the ruling of the judges. Social and economic implications De Grey and other scientists in the general field have argued that the costs of a rapidly growing aging population will increase to the degree that the costs of an accelerated pace of aging research are easy to justify in terms of future costs avoided. Olshansky et al. 2006 argue, for example, that the total economic cost of Alzheimer's disease in the US alone will increase from $80-100 billion today to more than $1 trillion in 2050.38 Consider what is likely to happen if we don't invest further in aging research. Take, for instance, the impact of just one age-related disorder, Alzheimer disease AD. For no other reason than the inevitable shifting demographics, the number of Americans stricken with AD will rise from 4 million today to as many as 16 million by midcentury. This means that more people in the United States will have AD by 2050 than the entire current population of the Netherlands. Globally, AD prevalence is expected to rise to 45 million by 2050, with three of every four patients with AD living in a developing nation. 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.38 SENS meetings There have been four SENS roundtables and three SENS conferences held.39 The first SENS roundtable was held in Oakland, California on October, 2000,40 and the last SENS roundtable was held in Bethesda, Maryland on July, 2004.41 The three SENS Conferences were each held at Queens' College of the University of Cambridge in England. All the conferences were organized by de Grey and all featured world-class researchers in the field of biogerontology. The first SENS conference was held in September 2003 as the 10th Congress of the International Association of Biomedical Gerontology42 with the proceedings published in the Annals of the New York Academy of Sciences.43 The second SENS conference was held in September 2005 and was simply called Strategies for Engineered Negligible Senescence SENS, Second Conference44 with the proceedings published in Rejuvenation Research. A third SENS conference was held in September, 2007, also at Queens' College of the University of Cambridge in England and organized by de Grey.45 On March 30-31, 2007 the first North American SENS conference was held in Edmonton, Alberta, Canada as the Edmonton Aging Symposium.4647 Methuselah Foundation Main article: Methuselah Foundation The Methuselah Foundation48 is a non-profit 501c3 volunteer organization co-founded by Aubrey de Grey and David Gobel, which is based in Springfield, Virginia, United States.49 A major activity of the Methuselah Foundation is the Methuselah Mouse Prize, a prize designed to hasten the research into effective life extension interventions by awarding monetary prizes to researchers who stretch the lifespan of mice to unprecedented lengths.49 It's other interests include PR work for the acceptance of and interest in scientific anti-aging research and SENS-based research programs,49 all of which the foundation hopes will lead to a proposed Institute of Biomedical Gerontology.5051 See also Actuarial escape velocity List of basic life extension topics Rejuvenation Research References Footnotes ^ a b c d The SENS Platform: An Engineering Approach to Curing Aging. Methuselah Foundation. Retrieved on June 28, 2008. ^ a b c d de Grey, Aubrey; Rae, Michael September 2007. Ending Aging: The Rejuvenation Breakthroughs that Could Reverse Human Aging in Our Lifetime. New York, NY: St. Martin's Press, 416 pp. ISBN 0312367066. ^ de Grey, Aubrey November 2003. The Mitochondrial Free Radical Theory of Aging. Austin, Texas: Landes Bioscience. ISBN 1587061554. ^ a b de Grey AD, Ames BN, Andersen JK, Bartke A, Campisi J, Heward CB, McCarter RJ, Stock G April 2002. Time to Talk SENS: Critiquing the Immutability of Human Aging. Annals of the New York Academy of Sciences 959: 452-62. PMID 11976218. ^ Bulkes, Nyssa March 6, 2006. Anti-aging research breakthroughs may add up to 25 years to life. The Northern Star. Northern Illinois University DeKalb, USA. ^ a b de Grey, Aubrey December 3, 2004. We will be able to live to 1,000. BBC News. ^ Gorman, James November 1, 2003. High-Tech Daydreamers Investing In Immortality. The New York Times. ^ a b Ferguson, Bruce January 1, 2006. The Quest for Immortality. 60 Minutes. CBS News. ^ a b c Than, Ker April 11, 2005. Hang in There: The 25-Year Wait for Immortality. LiveScience. Imaginova. ^ a b de Grey, Aubrey January 8, 2003. An engineer's approach to the development of real anti-aging medicine. Sci Aging Knowledge Environ. 2003 1: VP1. doi:10.1126/sageke.2003.1.vp1. PMID 12844502. ^ Hooper, Joseph January 1, 2005. The Prophet of Immortality. POPSCI.COM. ^ de Grey, Aubrey 2005. A strategy for postponing aging indefinitely. Stud Health Technol Inform. 118: 209-19. PMID 16301780. ^ de Grey AD, Campbell FC, Dokal I, Fairbairn LJ, Graham GJ, Jahoda CA, Porterg AC June 2004. Total deletion of in vivo telomere elongation capacity: an ambitious but possibly ultimate cure for all age-related human cancers. Ann N Y Acad Sci. 1019: 147-70. doi:10.1196/annals.1297.026. PMID 15247008. ^ de Grey, Aubrey September 1, 2005. Whole-body interdiction of lengthening of telomeres: a proposal for cancer prevention. Frontiers in Bioscience. 10: 2420-29. PMID 15970505. ^ de Grey, Aubrey July-August 2007. Protagonistic pleiotropy: Why cancer may be the only pathogenic effect of accumulating nuclear mutations and epimutations in aging. Mech Ageing Dev. 128 7-8: 456-59. doi:10.1016/j.mad.2007.05.005. PMID 17588643. ^ a b c de Grey, Aubrey February 2003. Challenging but essential targets for genuine anti-ageing drugs. Expert Opinion on Therapeutic Targets. 7 1: 1-5. doi:10.1517/14728222.7.1.1. PMID 12556198. ^ a b c de Grey, Aubrey November 2006. Foreseeable pharmaceutical repair of age-related extracellular damage. Curr Drug Targets. 7 11: 1469-77. ISSN 1389-4501. PMID 17100587. ^ de Grey, Aubrey Fall 2004. Mitochondrial Mutations in Mammalian Aging: An Over-Hasty About-Turn? Rejuvenation Res. 7 3: 171-4. doi:10.1089/rej.2004.7.171. PMID 15588517. ^ de Grey, Aubrey September 2000. Mitochondrial gene therapy: an arena for the biomedical use of inteins. Trends Biotechnol. 18 9: 394-99. doi:10.1016/S0167-77990001476-1. PMID 10942964. ^ de Grey, Aubrey November 2002. Bioremediation meets biomedicine: therapeutic translation of microbial catabolism to the lysosome. Trends Biotechnol. 20 11: 452-5. doi:10.1016/S0167-77990202062-0. PMID 12413818. ^ de Grey AD, Alvarez PJJ, Brady RO, Cuervo AM, Jerome WG, McCarty PL, Nixon RA, Rittmann BE, Sparrow JR August 2005. Medical bioremediation: prospects for the application of microbial catabolic diversity to aging and several major age-related diseases. Ageing Research Reviews. 4 3: 315-38. doi:10.1016/j.arr.2005.03.008. PMID 16040282. ^ de Grey, Aubrey June 15, 2004. Escape Velocity: Why the Prospect of Extreme Human Life Extension Matters Now. PLOS Biology 2 6: 723-26. doi:10.1371/journal.pbio.0020187. ^ a b c d Warner H et al. November 2005. Science fact and the SENS agenda. What can we reasonably expect from ageing research?. EMBO reports. 6 11: 1006-1008. doi:10.1038/sj.embor.7400555. PMID 16264422. ^ de Grey, Aubrey July 2005. Resistance to debate on how to postpone ageing is delaying progress and costing lives. EMBO reports. 6 S1: S49-S53. doi:10.1038/sj.embor.7400399. PMID 15995663. ^ de Grey, Aubrey November 2005. Like it or not, life-extension research extends beyond biogerontology. EMBO reports. 6 11: 1000. doi:10.1038/sj.embor.7400565. PMID 16264420. ^ de Grey, Aubrey. The biogerontology research community's evolving view of SENS. Methuselah Foundation. Retrieved on July 1, 2008. ^ Nuland, Sherwin 1994. How We Die: Reflections on Life's Final Chapter. New York: Knopf Random House. ISBN 0679414614. ^ Nuland, Sherwin February 2005. Do You Want to Live Forever?. Technology Review. ^ a b Nuland, Sherwin February 2005. Do You Want to Live Forever?. Technology Review. Page 7. ^ Pontin, Jason February 2005. Against Transcendence, Technology Review. ^ de Grey, Aubrey April 2005. Aubrey de Grey Responds, Technology Review. ^ TR Readers April 2005. LETTERS: Our February cover story on Aubrey de Grey and antiaging science lives on. Technology Review. ^ Pontin, Jason July 28, 2005. The SENS Challenge. Technology Review. ^ Pontin, Jason March 14, 2006. We've picked the judges for our biogerontology prize. Technology Review. ^ a b c Pontin, Jason July 11, 2006. Is Defeating Aging Only A Dream?. Technology Review. ^ SENS Withstands Three Challenges : $20,000 Remains Unclaimed. Methuselah Foundation. Retrieved on July 1, 2008. ^ Garreau, Joel October 31, 2007. Invincible Man. Washington Post. ^ a b Olshansky, S. Jay; Perry, Daniel; Miller, Richard A.; Butler, Robert N. March 2006. In Pursuit of the Longevity Dividend: What Should We Be Doing To Prepare for the Unprecedented Aging of Humanity?. The Scientist. 20 3: 28-36. ^ Conferences. Methuselah Foundation. Retrieved on July 17, 2008. ^ SENS roundtable 1: Biotechnological foreseeability of ENS October 1, 2000. Methuselah Foundation. Retrieved on July 1, 2008. ^ SENS roundtable 4: Enhancing lysosomal catabolic function using microbial enzymes July 26, 2004. Methuselah Foundation. Retrieved on July 1, 2008. ^ The International Association of Biomedical Gerontology 10th Congress September 19-23, 2003. Methuselah Foundation. Retrieved on July 1, 2008. ^ de Grey, Aubrey, Ed. June 2004. Strategies for Engineered Negligible Senescence: Why Genuine Control of Aging May Be Foreseeable. Annals of the New York Academy of Sciences. 1019: xv-xvi; 1-592. PMID 15320311. ^ Strategies for Engineered Negligible Senescence SENS, Second Conference September 7-11, 2005. Methuselah Foundation. Retrieved on July 1, 2008. ^ Strategies for Engineered Negligible Senescence SENS, Third Conference September 6-10, 2007. Methuselah Foundation. Retrieved on July 1, 2008. ^ Program. Edmonton Aging Symposium. Retrieved on July 1, 2008. ^ Presentation Archive. Edmonton Aging Symposium. Retrieved on July 1, 2008. ^ Methuselah Foundation Home Page ^ a b c What is the Methuselah Foundation?. Methuselah Foundation. Retrieved on July 5, 2008. ^ The Institute of Biomedical Gerontology IBG. Methuselah Foundation. Retrieved on July 5, 2008. ^ de Grey, Aubrey. Outline proposal for an Institute of Biomedical Gerontology. Methuselah Foundation. Retrieved on July 5, 2008. Bibliography de Grey, Aubrey; Rae, Michael September 2007. Ending Aging: The Rejuvenation Breakthroughs that Could Reverse Human Aging in Our Lifetime. New York, NY: St. Martin's Press, 416 pp. ISBN 0312367066. Retrieved from http://en..org/wiki/Strategies_for_Engineered_Negligible_Senescence Categories: Aging | Anti-aging | Biomedical engineering | Gerontology | Life extension Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Français Italiano 中文 This page was last modified on 10 August 2008, at 00:47
39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie Video
The Power of You Video
Effects of MonaVie Active on Antioxidant Capacity in Humans
Log into your Wholesale MonaVie Account
So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.
1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.