Life Extension Magazine April 2011
As We See It
What We Are Doing To Reverse Your Biological Age
By William Faloon
By William Faloon
Seeking to Vastly Accelerate Aging Research
We live in a fascinating era. Throughout history there were no validated methods to slow human aging, let alone reverse it. Today, scientists are meticulously investigating methods to enable our aging bodies to grow younger. If they succeed, then we might be the last generation to succumb to aging and the horrific diseases that accompany it.
Long before the Nature study was published on November 28, 2010, I brought up a concept while meeting with scientists at a medical conference in December 2008.25
Everyone acknowledged that potential advances might enable us to reverse the aging process we are all suffering. The problem is that no coordinated plan existed amongst the various scientific disciplines to collectively harness this technology into a near-term reality.
I proposed that we emulate what the United States did during World War II to rapidly develop the atomic bomb. I reasoned that if we instill a sense of confidence and urgency, we can collectively implement a “Manhattan Project” aimed at finding ways to reverse the festering aging process.
Several volunteers followed up on my suggestion and put together a “Longevity Summit” that consisted of some of the world’s top anti-aging researchers.
This longevity summit titled The Manhattan Beach Project was held November 13–15, 2009, in Manhattan Beach, CA.26 The expenses were high because we had to fly gerontology experts in from around the world and cover hotel fees and video recording. The Life Extension Foundation funded the entire cost, which amounted to around $60,000.
The first two days of this summit featured presentations by researchers who revealed their scientific roadmap for initiating and achieving age reversal. Some of these scientists had been quietly developing their technologies for many years.
The last day was a roundtable discussion among the wealthy attendees, the scientists, and some very creative minds. The purpose of this brainstorm session was to develop plans to fund these anti-aging research initiatives that our lives so heavily depend on.
The following consensus was reached:
A New “Age-Reversal” Initiative
The first step in implementing the Manhattan Beach Project was to assemble a knowledgeable and experienced Board of Directors to assure that the new company would be competently managed.
The next challenge was lining up the initial seed financing to get this company off the ground. Initially, $2 million was raised, of which the Life Extension Foundation provided $500,000.
The primary motivation for people to be involved with this company is that the research it supports could lead to breakthroughs in the control of human aging that could enable them to live much longer.
What I hope will be different with this company than any other are the expectations of these people. While there is a chance that the development of patented anti-aging therapies could yield considerable profits, that was not the main reason we thought individuals might participate.
From the perspective of most Life Extension members, the development of validated methods that would enable humans to grow biologically younger is far more valuable than all the money in the world.
The company is set up to assist, both financially and technologically, companies that are engaged in research that may lead to the control of human aging.
Not all of these age-reversal initiatives will pan out. But if just one led to the development of a validated method to reverse the course of aging, then every participant (and mankind itself) would benefit.
Age Reversal Was Not Thought Possible
When Life Extension was founded, most people did not believe that reversing human aging could ever happen.
We proved them wrong last year by showing that at least at the cellular level, it is possible to re-program genes to prompt human cells to go back in time. This discovery was announced in the June 2010 issue of Life Extension Magazine.27
If one looks at the rapid technology advances we enjoy today, the probability of conquering aging can be easily analogized. Just think of the progress that has been made in other fields:
One reason we are confident that age reversal is possible in our lifetime is the law of accelerating returns, which means that as scientists reach higher technological milestones, the accumulated knowledge base can be used to rapidly move up the scientific ladder.
At the Manhattan Beach Project summit in November 2009, a number of scenarios for slowing or reversing aging were presented by eminent scientific authorities. The consensus amongst the participants was that it may be possible to cure aging in our lifetime. This prediction was made before the landmark aging-reversal study was published in Nature just one year later (in November 2010).
We reasoned that if we could move up the next big anti-aging breakthrough by even a few years, this will mean the difference between life and death to many of those reading this article. That is why we view this matter with such a sense of urgency.
Where We Stand Today
The challenge we face is turning around public opinion to make aging research the number one priority. We need to overcome the denial about personal extinction that plagues the vast majority of the population. Once this is accomplished, I am certain the collective efforts of the scientific community will deal with aging as efficiently as hand-held computers function today.
Life Extension is currently evaluating several programs aimed at substantially increasing funding to scientists involved in age-reversal research. Your support through membership renewals and product purchases enables us to finance ongoing scientific projects while laying the groundwork for exponential expansion of this research in the not-too-distant future.
For longer life,
1.Jaskelioff M, Muller FL, Paik JH, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature. 2011 Jan 6;469(7328):102-6.
2.von Zglinicki T. Oxidative stress shortens telomeres. Trends Biochem Sci. 2002 Jul;27(7):339-44.
3.Marión RM, Blasco MA. Telomeres and telomerase in adult stem cells and pluripotent embryonic stem cells. Adv Exp Med Biol. 2010;695:118-31.
4.Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, Whooley MA. Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA. 2010 Jan 20;303(3):250-7.
5.Richards JB, Valdes AM, Gardner JP, et al. Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. Am J Clin Nutr. 2007 Nov;86(5):1420-5.
6.Babizhayev MA, Yegorov YE. Telomere attrition in lens epithelial cells - a target for N-acetylcarnosine therapy. Front Biosci. 2010 Jun 1;15:934-56.
7.Shao L, Li QH, Tan Z. L-carnosine reduces telomere damage and shortening rate in cultured normal fibroblasts. Biochem Biophys Res Commun. 2004 Nov 12;324(2):931-6.
8.Wang AM, Ma C, Xie ZH, Shen F. Use of carnosine as a natural anti-senescence drug for human beings. Biochemistry (Mosc). 2000 Jul;65(7):869-71.
9.Xu Q. Multivitamin use and telomere length in women. Am J Clin Nutr. 2009 Jun;89(6):1857-63.
10.Puterman E, Lin J, Blackburn E, O’Donovan A, Adler N, Epel E. The power of exercise: buffering the effect of chronic stress on telomere length. PLoS One. 2010 May 26;5(5):e10837.
11.Richter T, von Zglinicki T. A continuous correlation between oxidative stress and telomere shortening in fibroblasts. Exp Gerontol. 2007 Nov;42(11):1039-42.
12.Tanaka Y, Moritoh Y, Miwa N. Age-dependent telomere-shortening is repressed by phosphorylated alpha-tocopherol together with cellular longevity and intracellular oxidative-stress reduction in human brain microvascular endotheliocytes. J Cell Biochem. 2007 Oct 15;102(3):689-703.
13.Condon J, Yin S, Mayhew B, et al. Telomerase immortalization of human myometrial cells. Biol Reprod. 2002 Aug;67(2):506-14.
14.Londoño-Vallejo JA, DerSarkissian H, Cazes L, Thomas G. Differences in telomere length between homologous chromosomes in humans. Nucleic Acids Res. 2001 Aug 1;29(15):3164-71.
15.Allsopp RC, Vaziri H, Patterson C et al. Telomere length predicts replicative capacity of human fibroblasts. Proc Natl Acad Sci U S A. 1992 Nov 1; 89(21):10114-8.
16.Vaziri H, Chapman KB, Guigova A, et al. Spontaneous reversal of the developmental aging of normal human cells following transcriptional reprogramming. Regen Med. 2010 May;5(3):345-63.
17.Available at: http://www.lef.org/featured-articles/Life-Extension-Provides-2-million-dollars-for-Age-Reversal-Study.htm. Accessed January 12, 2011.
18.Bhattacharjee RN, Banerjee B, Akira S, Hande MP. Telomere-mediated chromosomal instability triggers TLR4 induced inflammation and death in mice. PLoS One. 2010 Jul 29;5(7):e11873.
19.Armanios M, Alder JK, Parry EM, Karim B, Strong MA, Greider CW. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am J Hum Genet. 2009 Dec;85(6):823-32.
20.Ilmonen P, Kotrschal A, Penn DJ. Telomere attrition due to infection. PLoS One. 2008 May 14;3(5):e2143.
21.Starr JM, McGurn B, Harris SE, Whalley LJ, Deary IJ, Shiels PG. Association between telomere length and heart disease in a narrow age cohort of older people. Exp Gerontol. 2007 Jun;42(6):571-3.
22.Unryn BM, Hao D, Glück S, Riabowol KT. Acceleration of telomere loss by chemotherapy is greater in older patients with locally advanced head and neck cancer. Clin Cancer Res. 2006 Nov 1;12(21):6345-50.
23.Sastry PS, Parikh P. The earlier age of onset of malignancy in developing world is related to overall infection burden and could be due to the effect on telomere length. Med Hypotheses. 2003 Apr;60(4):573-4.
24.Weng N. Interplay between telomere length and telomerase in human leukocyte differentiation and aging. J Leukoc Biol. 2001 Dec;70(6):861-7.
25.16th Annual International Congress on Anti-Aging Medicine & Regenerative Biomedical Technologies. Las Vegas, Nevada: The Venetian Resort, Hotel, and Casino; December 11-14, 2008.
26.Available at: http://www.maxlife.org/articles/2009/11/progress-for-immortality.asp. Accessed January 14, 2011.
27.Fahy GM, Kent S. Immortal Stem Cells for Anti-Aging Therapies: An Interview with Michael D. West, PhD. Life Extension Magazine®.2010 Jun;16(6): 26-32.
28.Ramagopalan SV, Heger A, Berlanga AJ, et al. A ChIP-seq-defined genome-wide map of vitamin D receptor binding: Associations with disease and evolution. Genome Res. 2010 Oct;20(10):1352-60.
29.John EM, Schwartz GG, Koo J, Van Den BD, Ingles SA. Sun exposure, vitamin D receptor gene polymorphisms, and risk of advanced prostate cancer. Cancer Res. 2005 Jun 15;65(12):5470-9.
30.Welsh J, Wietzke JA, Zinser GM, Byrne B, Smith K, Narvaez CJ. Vitamin D-3 receptor as a target for breast cancer prevention. J Nutr. 2003 Jul;133(7 Suppl):2425S-2433S.
31.Ross TK, Darwish HM, Moss VE, DeLuca HF. Vitamin D-influenced gene expression via a ligand-independent, receptor-DNA complex intermediate. Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9257-60.
32.Barger JL, Kayo T, Vann JM, et al. A low dose of dietary resveratrol partially mimics caloric restriction and retards aging parameters in mice. PLoS One. 2008 Jun 4;3(6):e2264.
33.Jones SB, DePrimo SE, Whitfield ML, Brooks JD. Resveratrol-induced geneexpression profiles in human prostate cancer cells. Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):596-604.
34.Serrero G, Lu R. Effect of resveratrol on the expression of autocrine growth modulators in human breast cancer cells. Antioxid Redox Signal. 2001 Dec;3(6):969-79.