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D.N.A. Congress Announcement by the Institute of Exponential Sciences

D.N.A. Congress Announcement by the Institute of Exponential Sciences

The New Renaissance HatInstitute of Exponential Sciences
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Editor’s Note: The forthcoming D.N.A. Congress in Utrecht, The Netherlands, hosted by the Institute of Exponential Sciences, devoted to discussions of gene therapies, receives the strong endorsement of both The Rational Argumentator and the Nevada Transhumanist Party. The D.N.A. Congress offers a promising venue to discuss the potential for gene therapies to cure diseases, lengthen lifespans, and improve quality of life for millions of people in the coming years and decades.

~ Gennady Stolyarov II, Editor-in-Chief, The Rational Argumentator, June 5, 2016

D.N.A CONGRESS PRESS RELEASE:

The Institute of Exponential Sciences (IES) has a large announcement to make. We are organising D.N.A – The largest European congress on human gene therapies, featuring speakers such as Aubrey de Grey, Liz Parrish, Oliver Medvedik and others.

Our event has been endorsed by LEAF, Heales VZW, BioViva, SENS Research Foundation, Singularity Network, People Unlimited, The Rational Argumentator, and many others. The event will be covered by national media and will be broadcasted online.

To make this vision a reality, we need your support. Share this message and donate today. Thank you!

IES needs your support to help make this vision a reality. Click here to donate to our crowdfunding campaign.

D.N.A – Designing New Advances: The second large Institute of Exponential Sciences event is coming to Utrecht

 

DNADemian Zivkovic

Utrecht – After a successful event last year in May, the grand congress is ready for a second edition. With a new name, we hope to make exponential sciences more approachable to the general public and bring people in the field closer together. The Institute of Exponential Sciences congress 2016 will be held at RASA podium on the 9th of July. The main theme of the event is gene therapies and cutting-edge applications of such therapies, such as health extension and interventions against human aging. To guarantee a great event, we have invited some of the biggest names in the field. Our guest speakers will be as follows:

Opening the event will be Oliver Medvedik, Ph.D, director of scientific programs at Genspace. Dr. Medvedik has earned his Ph.D at Harvard Medical school in the biomedical and biological sciences program. Since graduating from Harvard, he has worked as a biotechnology consultant, taught molecular biology to numerous undergraduates at Harvard, and mentored two of Harvard’s teams for the international genetically engineered machines competition (IGEM) held annually at M.I.T.

Our second speaker is Aubrey David Nicholas Jasper de Grey, Ph.D, an English author, Chief Science Officer of the SENS Research Foundation, and editor-in-chief of the academic journal Rejuvenation Research. Aubrey de Grey is well known for his focus on regenerative medicine and views on human aging. He will take the stage talking about the applications of current and upcoming technologies and studies which hold the potential to greatly extend our healthy lifespan.

Our third speaker is Tatjana Kochetkova, Ph.D, who is a fellow of the Institute of Exponential Sciences and a bioethicist. Dr. Kochetkova will follow up discussing the ethical and philosophical side of the technology and will address questions of what exponential technologies in biotech mean for society.

Our fourth speaker is Elizabeth Parrish, a fellow of the Institute of Exponential Sciences and the Founder and CEO of BioViva Sciences Inc, a Delaware corporation based in Seattle, WA, with labs and participating clinics in South/Central America where the majority of practical work is carried out. BioViva has been noted for being the first corporation in the world to treat a patient with gene therapy to reverse aging. The woman who wants to genetically engineer you will cover the basics of BioViva’s approach and vision for the the future, as well as the potential that gene therapies hold for radically improving our health and lives in the future.

Our fifth speaker will be Keith Comito, who is the founder and president of the Life Extension Advocacy Foundation (LEAF), a 501(c)(3) non-profit organization and a partner of the Institute of Exponential Sciences. Through LEAF, he operates the crowdfunding platform Lifespan.io, which supports biomedical research aimed at extending healthy human lifespan. He also serves as policy coordinator for the Global Healthspan Policy Institute, which facilitates relationships between researchers and government to advance initiatives in support of healthy life extension.

About Institute of Exponential Sciences

The Institute of Exponential Sciences is an international innovation-oriented think tank, outreach organisation, and networking platform based in the Netherlands, in the city of Utrecht. Its main activities include organising lectures and conferences, providing quality consultancy on innovation and exponential technologies, and collaborating with student organisations and universities in educating the public on the importance of exponential technologies.

It was founded by members of its predecessor, the Arma’thwynn society, which was a student group of like-minded young academics in the Netherlands. After organising events and attracting a very diverse and professional team of entrepreneurs, academics, and journalists, the society decided to move past student politics and make the move towards professionalism.

The Institute of Exponential Sciences is the result of that decision. After organising successful events (the largest of which was their symposium in April, 2015), the Institute of Exponential Sciences formalised its mission and reached out towards a process of international collaboration with other entities which share a techno-positive vision. The institute strives towards excellence in providing the best information and resources related to the issues relevant in the rapidly advancing technological society we live in.

The IES approach is focused on providing interdisciplinary education in the fields of exponential technologies such as artificial intelligence, bio-informatics, gene therapies, 3D-printing, augmented reality, and neural interfacing. We also provide a networking platform which allows entrepreneurs, scientists, journalists, and students to get in touch with others with similar ideas so that they may create the technologies of tomorrow. The IES strives not only to improve the speed of development of these technologies, but also to show the public the amazing possibilities technology provides for society.

IES and the IES logo are either registered trademarks or trademarks of IES Foundation in the Netherlands and/or other countries. All other products and/or services referenced are trademarks of their respective entities.

The Two Faces of Aging: Cancer and Cellular Senescence – Article by Adam Alonzi

The Two Faces of Aging: Cancer and Cellular Senescence – Article by Adam Alonzi

The New Renaissance Hat
Adam Alonzi
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This article is republished with the author’s permission. It was originally posted on Radical Science News.

hELA-400x300Multiphoton fluorescence image of HeLa cells.

Aging, inflammation, cancer, and cellular senescence are all intimately interconnected. Deciphering the nature of each thread is a tremendous task, but must be done if preventative and geriatric medicine ever hope to advance. A one-dimensional analysis simply will not suffice. Without a strong understanding of the genetic, epigenetic, intercellular, and intracellular factors at work, only an incomplete picture can be formed. However, even with an incomplete picture, useful therapeutics can be and are being developed. One face is cancer, in reality a number of diseases characterized by uncontrolled cell division. The other is degradation, which causes a slue of degenerative disorders stemming from deterioration in regenerative capacity.

Now there is a new focus on making geroprotectors, which are a diverse and growing family of compounds that assist in preventing and reversing the unwanted side effects of aging. Senolytics, a subset of this broad group, accomplish this feat by encouraging the removal of decrepit cells. A few examples include dasatinib, quercetin, and ABT263. Although more research must be done, there are a precious handful of studies accessible to anyone with the inclination to scroll to the works cited section of this article. Those within the life-extension community and a few enlightened souls outside of it already know this, but it bears repeating: in the developed world all major diseases are the direct result of the aging process. Accepting this rather simple premise, and you really ought to, should stoke your enthusiasm for the first generation of anti-aging elixirs and treatments. Before diving into the details of these promising new pharmaceuticals, nanotechnology, and gene therapies we must ask what is cellular senescence? What causes it? What purpose does it serve?

Depending on the context in which it is operating, a single gene can have positive or negative effects on an organism’s phenotype. Often the gene is exerting both desirable and undesirable influences at the same time. This is called antagonistic pleiotropy. For example, high levels of testosterone can confer several reproductive advantages in youth, but in elderly men can increase their likelihood of developing prostate cancer. Cellular senescence is a protective measure; it is a response to damage that could potentially turn a healthy cell into a malignant one. Understandably, this becomes considerably more complex when one is examining multiple genes and multiple pathways. Identifying all of the players involved is difficult enough. Conboy’s famous parabiosis experiment, where a young mouse’s system revived an old ones, shows that alterations in the microenviornment, in this case identified and unidentified factors in the blood of young mice, can be very beneficial to their elders. Conversely, there is a solid body of evidence that shows senescent cells can have a bad influence on their neighbors. How can something similar be achieved in humans without having to surgically attach a senior citizen to a college freshman?

By halting its own division, a senescent cell removes itself as an immediate tumorigenic threat. Yet the accumulation of nondividing cells is implicated in a host of pathologies, including, somewhat paradoxically, cancer, which, as any life actuary’s mortality table will show, is yet another bedfellow of the second half of life. The single greatest risk factor for developing cancer is age. The Hayflick Limit is well known to most people who have ever excitedly watched the drama of a freshly inoculated petri dish. After exhausting their telomeres, cells stop dividing. Hayflick et al. astutely noted that “the [cessation of cell growth] in culture may be related to senescence in vivo.” Although cellular senescnece is considered irreversible, a select few cells can resume normal growth after the inactivation of the p53 tumor suppressor. The removal of p16, a related gene, resulted in the elimination of the progeroid phenotype in mice. There are several important p’s at play here, but two are enough for now.

Our bodies are bombarded by insults to their resilient but woefully vincible microscopic machinery. Oxidative stress, DNA damage, telomeric dysfunction, carcinogens, assorted mutations from assorted causes, necessary or unnecessary immunological responses to internal or external factors, all take their toll. In response cells may repair themselves, they may activate an apoptotic pathway to kill themselves, or just stop proliferating. After suffering these slings and arrows, p53 is activated. Not surprisingly, mice carrying a hyperactive form of p53 display high levels of cellular senescence. To quote Campisi, abnormalities in p53 and p15 are found in “most, if not all, cancers.” Knocking p53 out altogether produced mice unusually free of tumors, but those mice find themselves prematurely past their prime. There is a clear trade-off here.

In a later experiment Garcia-Cao modified p53 to only express itself when activated. The mice exhibited normal longevity as well as an“unusual resistance to cancer.” Though it may seem so, these two cellular states are most certainly not opposing fates. As it is with oxidative stress and nutrient sensing, two other components of senescence or lack thereof, the goal is not to increase or decrease one side disproportionately, but to find the correct balance between many competing entities to maintain healthy homeostasis. As mentioned earlier, telomeres play an important role in geroconversion, the transformation of quiescent cells into senescent ones. Meta-analyses have shown a strong relationship between short telomeres and mortality risk, especially in younger people. Although cancer cells activate telomerase to overcome the Hayflick Limit, it is not entirely certain if the activation of telomerase is oncogenic.

majormouse

SASP (senescence-associated secretory phenotype) is associated with chronic inflammation, which itself is implicated in a growing list of common infirmities. Many SASP factors are known to stimulate phenotypes similar to those displayed by aggressive cancer cells. The simultaneous injection of senescent fibroblasts with premalignant epithelial cells into mice results in malignancy. On the other hand, senescent human melanocytes secrete a protein that induces replicative arrest in a fair percentage of melanoma cells. In all experiments tissue types must be taken into account, of course. Some of the hallmarks of inflammation are elevated levels of IL-6, IL-8, and TNF-α. Inflammatory oxidative damage is carcinogenic and an inflammatory microenvironment is a good breeding ground for malignancies.

Caloric restriction extends lifespan in part by inhibiting TOR/mTOR (target of rapamycin/mechanistic target of rapamycin, also called  the mammalian target of rapamycin). TOR is a sort of metabolic manager, it receives inputs regarding the availability of nutrients and stress levels and then acts accordingly. Metformin is also a TOR inhibitor, which is why it is being investigated as a cancer shield and a longevity aid. Rapamycin has extended average lifespans in all species tested thus far and reduces geroconversion. It also restores the self-renewal and differentiation capacities of haemopoietic stem cells. For these reasons the Major Mouse Testing Program is using rapamycin as its positive control. mTOR and p53 dance (or battle) with each other beautifully in what Hasty calls the “Clash of the Gods.” While p53 inhibits mTOR1 activity, mTOR1 increases p53 activity. Since neither metformin nor rapamycin are without their share of unwanted side effects, more senolytics must be explored in greater detail.

Starting with a simple premise, namely that senescent cells rely on anti-apoptotic and pro-survival defenses more than their actively replicating counterparts, Campisi and her colleagues created a series of experiments to find the “Achilles’ Heel” of senescent cells. After comparing the two different cell states, they designed senolytic siRNAs. 39 transcripts were selected for knockdown by siRNA transfection, and 17 affected the viability of their target more than healthy cells. Dasatinib, a cancer drug, and quercitin, a common flavonoid found in common foods, have senolytic properties. The former has a proven proclivity for fat-cell progenitors, and the latter is more effective against endothelial cells. Delivered together, they they remove senescent mouse embryonic fibroblasts. Administration into elderly mice resulted in favorable changes in SA-BetaGAL (a molecule closely associated with SASP) and reduced p16 RNA. Single doses of D+Q together resulted in significant improvements in progeroid mice.

If you are not titillated yet, please embark on your own journey through the gallery of encroaching options for those who would prefer not to become chronically ill, suffer immensely, and, of course, die miserably in a hospital bed soaked with several types of their own excretions―presumably, hopefully, those who claim to be unafraid of death have never seen this image or naively assume they will never be the star of such a dismal and lamentably “normal” final act. There is nothing vain about wanting to avoid all the complications that come with time. This research is quickly becoming an economic and humanitarian necessity. The trailblazers who move this research forward will not only find wealth at the end of their path, but the undying gratitude of all life on earth.

Adam Alonzi is a writer, biotechnologist, documentary maker, futurist, inventor, programmer, and author of the novels “A Plank in Reason” and “Praying for Death: Mocking the Apocalypse”. He is an analyst for the Millennium Project, the Head Media Director for BioViva Sciences, and Editor-in-Chief of Radical Science News. Listen to his podcasts here. Read his blog here.

References

Blagosklonny, M. V. (2013). Rapamycin extends life-and health span because it slows aging. Aging (Albany NY), 5(8), 592.

Campisi, Judith, and Fabrizio d’Adda di Fagagna. “Cellular senescence: when bad things happen to good cells.” Nature reviews Molecular cell biology 8.9 (2007): 729-740.

Campisi, Judith. “Aging, cellular senescence, and cancer.” Annual review of physiology 75 (2013): 685.

Hasty, Paul, et al. “mTORC1 and p53: clash of the gods?.” Cell Cycle 12.1 (2013): 20-25.

Kirkland, James L. “Translating advances from the basic biology of aging into clinical application.” Experimental gerontology 48.1 (2013): 1-5.

Lamming, Dudley W., et al. “Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity.” Science 335.6076 (2012): 1638-1643.

LaPak, Kyle M., and Christin E. Burd. “The molecular balancing act of p16INK4a in cancer and aging.” Molecular Cancer Research 12.2 (2014): 167-183.

Malavolta, Marco, et al. “Pleiotropic effects of tocotrienols and quercetin on cellular senescence: introducing the perspective of senolytic effects of phytochemicals.” Current drug targets (2015).

Rodier, Francis, Judith Campisi, and Dipa Bhaumik. “Two faces of p53: aging and tumor suppression.” Nucleic acids research 35.22 (2007): 7475-7484.

Rodier, Francis, and Judith Campisi. “Four faces of cellular senescence.” The Journal of cell biology 192.4 (2011): 547-556.

Salama, Rafik, et al. “Cellular senescence and its effector programs.” Genes & development 28.2 (2014): 99-114.

Tchkonia, Tamara, et al. “Cellular senescence and the senescent secretory phenotype: therapeutic opportunities.” The Journal of clinical investigation 123.123 (3) (2013): 966-972.

Zhu, Yi, et al. “The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs.” Aging cell (2015).

 

25% Median Life Extension in Mice via Senescent Cell Clearance, Unity Biotechnology Founded to Develop Therapies – Article by Reason

25% Median Life Extension in Mice via Senescent Cell Clearance, Unity Biotechnology Founded to Develop Therapies – Article by Reason

The New Renaissance HatReason
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With today’s news, it certainly seems that senescent cell clearance has come of age as an approach to treating aging and age-related conditions. Some of the leading folk in the cellular senescence research community today published the results from a very encouraging life span study, extending life in mice via a method of removing senescent cells. This is much the same approach employed in one of the first tests of senescent cell clearance, carried out in accelerated aging mice a few years ago, but in this case normal mice were used, leaving no room to doubt the relevance of the results. The researchers have founded a new company, Unity Biotechnology, to develop therapies for the clinic based on this technology. Clearance of senescent cells has been advocated as a part of the SENS vision for the medical control of aging for more than a decade now, and it is very encouraging to see the research and development community at last coming round to this view and making tangible progress.

Senescent cells have removed themselves from the cycle of replication in reaction to cell and tissue damage, or a local tissue environment that seems likely to result in cancer. Their numbers accumulate with age. Most are destroyed by the immune system or their own programmed cell death mechanisms, but enough linger for the long term for their growing presence to be one of the contributing causes of the aging process. These cells behave badly, secreting harmful signals that degrade tissue function, generate inflammation, and alter the behavior of surrounding cells as well. Near every common age-related condition is accelerated and made worse by the presence of large numbers of senescent cells. We would be better off without them, aging would be slowed by the regular removal of these errant cells, and the therapies to make that possible are on the near horizon.

The mouse lifespan study is the important news here, as it demonstrates meaningful extension of median life span through removal of senescent cells, the first such study carried out in normal mice for this SENS-style rejuvenation technology. This sort of very direct and easily understood result has a way of waking up far more of the public than the other very convincing evidence of past years. So it looks like Oisin Biotechnology, seed funded last year by the Methuselah Foundation and SENS Research Foundation to bring a senescent cell clearance therapy to market, now has earnest competition. Insofar as the competitive urge in business and biotechnology speeds progress and produces better results, let the games begin, I say.

Scientists Can Now Radically Expand the Lifespan of Mice – and Humans May Be Next

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Researchers have made this decade’s biggest breakthrough in understanding the complex world of physical aging. The researchers found that systematically removing a category of living, stagnant cells (ones which can no longer reproduce) extends the lives of otherwise normal mice by 25 percent. Better yet, scouring these cells actually pushed back the process of aging, slowing the onset of various age-related illnesses like cataracts, heart and kidney deterioration, and even tumor formation. “It’s not just that we’re making these mice live longer; they’re actually stay healthier longer too. That’s important, because if you were going to equate this to people, well, you don’t want to just extend the years of life that people are miserable or hospitalized.” By rewriting a tiny portion of the mouse genetic code, the team developed a genetic line of mice with cells that could, under the right circumstances, produce a powerful protein called caspase when they start secreting p16. Caspase acts essentially as a self-destruct button; when it’s manufactured in a cell, that cell rapidly dies. So what exactly are these circumstances where the p16 secreting cells start to create caspase and self-destruct? Well, only in the presence of a specific medicine the scientists could give the mice. With their highly-specific genetic tweak, the scientists had created a drug-initiated killswitch for senescent cells. In today’s paper, the team reported what happened when the researchers turned on that killswitch in middle-aged mice, effectively scrubbing clean the mice of senescent cells.

Naturally occurring p16Ink4a-positive cells shorten healthy lifespan

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Senescent cells accumulate in various tissues and organs over time, and have been speculated to have a role in ageing. To explore the physiological relevance and consequences of naturally occurring senescent cells, here we use a previously established transgene, INK-ATTAC, to induce apoptosis in p16Ink4a-expressing cells of wild-type mice by injection of AP20187 twice a week starting at one year of age. We show that AP20187 treatment extended median lifespan in both male and female mice of two distinct genetic backgrounds. The clearance of p16Ink4a-positive cells delayed tumorigenesis and attenuated age-related deterioration of several organs without apparent side effects, including kidney, heart and fat, where clearance preserved the functionality of glomeruli, cardio-protective KATP channels and adipocytes, respectively. Thus, p16Ink4a-positive cells that accumulate during adulthood negatively influence lifespan and promote age-dependent changes in several organs, and their therapeutic removal may be an attractive approach to extend healthy lifespan.

Unity Biotechnology Launches with a Focus on Preventing and Reversing Diseases of Aging

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Unity will initially focus on cellular senescence, a biological mechanism theorized to be a key driver of many age-related diseases, including osteoarthritis, glaucoma and atherosclerosis. “Imagine drugs that could prevent, maybe even cure, arthritis or heart disease or loss of eyesight. It’s an incredible aspiration. If we can translate this biology into medicines, our children might grow up in significantly better health as they age. There will be many obstacles to overcome, but our team is committed and inspired to achieve our mission. This has been a long journey, and we’re at the point now where we can start making medicines to achieve in humans what we’ve achieved in mice. I can’t wait to see what happens as we move into the clinic.”

To close this post, and once again, I think it well worth remembering that SENS rejuvenation biotechnology advocates and supporters have been calling for exactly this approach to treating aging for more than a decade. That call was made based on the evidence arising from many fields of medical research, and from a considered perspective of aging as a process of damage accumulation, one that can be most effectively treated by repair of that damage. The presence of senescent cells is a form of damage. SENS was not so long ago derided and considered out on the fringe for putting forward that position, but for several years now it has been very clear that the SENS viewpoint was right all along. I strongly encourage anyone who remains on the fence about the validity of the SENS proposals for the treatment of aging to reexamine his or her position on the science.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.
The Role of Aging in Society – Article by Demian Zivkovic

The Role of Aging in Society – Article by Demian Zivkovic

The New Renaissance HatDemian Zivkovic
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Take the following situation. We discover an extremely contagious virus. It infects you and your loved ones, and quickly propagates through all of mankind. As a result, 150,000 people die every day. It kills more than twice the number killed in the Holocaust every three months, and in 30 years, it will have killed 1.5 billion, around one in six people. How high would this score on a list of global priorities? There’s no doubt the situation would be grave. Most people would demand immediate action.
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But that’s just a thought experiment, right? Not really. Every day, 150,000 people do die from age-related disease. Not only the cost in lives is monumental; societal and economic costs are also on the rise. According to the Dutch Statistics Authority (the CBS), the amount of people older than 65 (retirement age) will have increased to 27% in 2040, from the current 19%. As more people are born, this also means more people die from age-related disease, taking all their knowledge, expertise, and productivity with them. In short: If we don’t do anything about the consequences of our aging population, we face severe consequences.
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So what is the best way to deal with the problem of our society aging?

There is no simple solution. More conventional healthcare barely improves quality of life, while just letting people die is not an ethical option. Rutger Bregman, a Dutch historian and philosopher, argues for thinking more radically about solutions to societal problems. According to his essay “Een pleidooi voor de utopie” (A plea for utopia) in the Dutch magazine “De groene Amsterdammer”, we have lost the ability to think in such a way; We only look at marginal improvements, instead of looking at changes that could radically improve and change our society. So if we do explore more radical solutions, what can we do?

Professor Aubrey de Grey, Ph.D. in biology, Chief Science Officer of the prestigious SENS Research Foundation, and partner at the Gerontological Society of America, argues that we could look at a radical intervention in human aging. According to de Grey, the best way of solving many of these problems is to cure aging at its source. De Grey is not the only one who holds that opinion. Alphabet, Inc.‘s biotechnology subsidiary (Calico) also views the problem from this position. This point of view obviously raises quite a few questions. Critics claim that de Grey’s vision is impossible or undesirable. Proponents point to the massive advantages of curing age-related disease.

One of the arguments put forward is that short-term thinking causes many economical and societal problems. Economist Joseph Stiglitz speaks about rent-seeking (“Rent-Seeking and the Making of an Unequal Society”, 2014), economically destructive behaviour in which an individual or business enriches itself while harming the entire economy in the process. Environmental concerns are also a very large issue. Since people (if they are lucky) don’t get to live much longer than a hundred years old, many people find it very uninteresting to think about what our behaviour is doing to the environment on the long term. But what will it mean for these problems if we have to let go of short-term thinking, because we live for a much longer time? One thing is for sure: If de Grey’s vision becomes reality, a lot will change in our society.

Economy, Environment, and Overpopulation
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Short-term thinking has a catastrophic effect on our economy and environment.

The previously mentioned economist Joseph Stiglitz claims in his article that our economy is suffering serious problems, since rent-seeking is causing society-wide destruction and inequality. For centuries, economists, philosophers, and ethicists have been considering how to stop such unethical behavior. Usually, they looked at different moral developments, better regulations, or restructuring society as solutions.

In his work “The Power of Context”, Malcolm Gladwell makes the claim that the environment and the context we live in have a large impact on our behaviour. Human life knows a few certainties; one of them is that you will die within a century. One may have children or grandchildren, but very few people are concerned about the fate of their heir several hundred generations down the road. In my interview with him (2014, Nakedbutsafe magazine), Professor de Grey argues that many people would be much more concerned with the long term if they knew they would still be around in several centuries, and there’s a lot to be said about that. Instead of waging a fruitless and hopeless war on selfishness, it may be more prudent to use it to improve the world.

De Grey’s solution essentially means inventing the fountain of youth through advanced biotechnology. He wants to do this through a method called “Strategies for Engineered Negligible Senescence” or SENS. SENS essentially involves periodically repairing accumulated damage from aging, so it never reaches a critical point where it turns into a specific illness. De Grey is not the only one who is looking for a solution for aging: Google Ventures heavily invests in such technology.

In 2013, Google founded a company called Calico, which entered a partnership with AbbVie. With a record investment of two billion dollars, most money ever put into a start-up, the ambitious firm wants to create a fundamental understanding of aging and use said understanding to eventually cure said aging. Bill Maris, president of Google Ventures, has already made the famous claim we will be able to have technology to live 500 years within our lifetimes. Another actor in the corporate sector is BioViva, whose CEO, Elizabeth Parrish, has become the first human on the planet to get treated with a combination of in vivo gene therapies to slow down aging.

The approaches of Calico, SENS, and BioViva look at the problem from different angles, but they have one thing in common: they are not looking at ways to extend the lives of sick, disabled seniors. Instead, they are looking at a method to not simply extend life, but to extend health. They are looking at methods to stop this biological aging from happening. Life extension is merely a side effect. After all, if a 200-year-old has the vitality of a 40-year-old, why would an aging population be a problem? Even though the population will age, the percentage of “elderly” people will decrease, and so will age-related suffering and related economic pressure.

However, not everyone is optimistic about these changes. Critics are concerned about what a radically extended life will mean for overpopulation. They argue that if nobody dies, we will have so many people that we will either have to kill people, or make reproduction illegal. While such a top-down approach may seem like “common sense”, there’s a lot to be said about why such drastic top-down measures will be unnecessary. Steven Johnson, a best-selling popular science author and media theorist, introduces the concept of emergence (Emergence: The Connected Lives of Ants, Brains, Cities, and Software, 2001). Emergence refers to patterns in complex systems which can’t be reduced to the properties or behaviours of an individual element of the system. Johnson uses the ant colony as an example: while no single ant coordinates the behaviour of the colony, the entire system is self-organizing and thus functions perfectly. An ant colony, but even more so human society, is a good example of an emergent system.

A simple example of this self-organization is the distribution of bread. There is no central authority that plants where bakeries should be located, how much grain should be produced, what logistic solutions should be used for bread transport to people’s homes, or what bread prices ought to be. In fact, such central planning has been tried several times in history. In communist dictatorships such as the Soviet Union and North Korea, centralized attempts at steer society have had catastrophic results. However, if emergence of self-organisation does its job, a society flourishes. We can see this same effect work on overpopulation and birth rates. According to the World Health Organisation, the fertility rates plummet as life expectancy skyrockets. Countries that have the highest life expectancies have the lowest birth rates. Japan, which has one of the highest life expectancies has a negative birth rate; its population is in decline, even though no central planning has intervened in any way.

This hypothesis is also supported by virtually all historic trends. Every widespread average life-expectancy spike was met with a plummet in birth rates. When our life expectancy went up because of the invention of antibiotics, our birth rates hit historic lows. We see the opposite in countries where life expectancy is very low. The country with the highest birth rate is Nigeria, while it’s one of the poorest countries in the world. The average life expectancy in Nigeria is below 55. According to the United Nations, countries with low life expectancy have by far the largest effect on overpopulation.

Regulation of population is therefore unnecessary; a complex system such as modern society self-regulates and corrects itself. This idea is in line with Gladwell’s theory of context-dependent behavior; the context largely defines our behavior. And as a self-organizing system, society demonstrably changes the context to steer our behavior in effective patterns. A dystopia where government has to regulate reproduction or death is very unlikely.

Philosophical Arguments

If Gladwell is right about context as catalyst of behaviour, what will the effects of a society devoid of biological aging be on our humanity? Not all arguments against radical life extension are pragmatic in nature. The conservative bioethicist Leon Kass is one of the opponents of radical life extension pondering this question. He argues that indefinite life extension is unnatural and thus undesirable. Kass also claims that we won’t appreciate life if we life “forever.”

“Time is a gift, but the perception of endless time or of time without bound in fact has the possibility of undermining the degree to which we take time seriously and make it count.”

~ Leon Kass (Aging Research, 2004).

Kass makes a comparison with the ancient Greek gods to argument why life’s shortness gives it purpose.

Homer in The Iliad and The Odyssey presents human beings whom he names as mortals. That is their definition in contrast to the immortals. And the immortals for their agelessness and their beauty live sort of shallow and frivolous lives. Indeed, they depend for their entertainment on watching the mortals who, precisely because they know that their time is limited, and that they go around only once, are inclined to make time matter and to aspire to something great for themselves.

~ Leon Kass (Aging Research, 2004)

While these arguments may seem somewhat of a philosophical take on many common criticisms, they are easily debunked. Elizabeth Parrish, CEO of BioViva and a pioneering entrepreneur in the field of gene therapy, argues against the idea that we should accept something because it’s considered “normal.” (“Liz Parrish speaks at People Unlimited on transcending the aging paradigm with gene therapy”, 2015). She argues that “normal” is a situational opinion which constantly changed throughout the entirety of history. In 1665, dying of infectious disease was normal. During this time only one percent of all humans died from aging: Infectious diseases were responsible for more than three quarters of all deaths before we developed the first immunization therapies – the development of which is similar to the process to defeat aging with gene therapy today. Just like today, there was criticism of the development of vaccines and antibiotics, even though lifespans and health were greatly improved by the use of these advancements – and the arguments have stayed very much the same.

Parrish is not the only one who provides a strong argument against the vision of Kass. Reason, creator of the Fight Aging! blog, is another intellectual who is very skeptical about Kass’s position. In his rebuttal of Kass (“Leon Kass, Mystic” by Reason, 2004), he compares Kass with an alchemist, a modern mystic:

“The alchemists of old stood atop what little knowledge of chemistry they had and built a speculative religion of hermetic magic, transient wishes, celestial signs and hidden gold. Leon Kass stands atop what little biotechnology we have today (and seems to have a good grasp thereof), building his own structures of fanciful thought, equally disconnected from the real world. 

All of Kass’ arguments against longer, healthier lives are essentially mystical and devoid of real substance.”

In “Leon Kass, Mystic” (2004), Reason wonders if Kass’s philosophical musings are enough of a reason to condemn billions of people to a slow and painful death. Just like the alchemists, Reason argues, Kass’s vision is based upon ancient texts and his own subjective knee-jerk reactions, instead of researching the world around him. Reason postulates that this is the fundamental difference between a mystic and a scientist: The mystic is immune to impractical facts, consequences, and reality.

De Grey also argues against the bioconservative position. He rejects the idea that longer lives will somehow lower our appreciation of life. We will be able to start a new major when we are fifty years old, or a new career when we’re a hundred and fifty. The very fact that we have so little time causes us to experience “lock-in” in our careers and choices. This causes boredom and stress. The amount of time we lose switching to doing something we may enjoy a lot more is too radical, because we have so little time to begin with. Radical life extension seems more likely to actually cure the problems its critics claim it will cause (such as boredom, stress, or disenchantment with life).

Conclusion

Treatments for age-related diseases are on their way, and curing aging is big business. The first people are already getting early treatments, and the prognoses are positive. Society will have to adapt to the changes that come with these treatments. It is very important to explore options for adequately engaging public opinion in favor of curing age-related disease, to mitigate massive economic and human losses that these diseases currently cause, and to create the legislation and framework needed to implement these technologies in a fair, responsible, and sane way.

Bibliography

Bregman, Rutger (2013). Dromen is niet eng; Essay Pleidooi voor de utopie. De Groene Amsterdammer, jaar 137, week 20. https://www.groene.nl/artikel/pleidooi-voor-de-utopie.

Gladwell, Malcolm (2000). The Power of Context. In R.E. Miller & Spellmeyer (Eds.), The New Humanities Reader (Fifth Edition, pp. 148-167). Print.
 *** 
Stiglitz, J. E. (2012). Rent Seeking and the Making of an Unequal Society. In R.E. Miller & Spellmeyer (Eds.), The New Humanities Reader (Fifth Edition, pp. 148-167). Print.
 *** 

Johnson, Steven. ‘Emergence: The connected Lives of Ants, Brains, Cities, and Software’, 2001. In ‘The New Humanities Reader’, Richard E. Miller, Kurt Spellmeyer, Wadsworth, 2011, pp. 151 – 165

De Grey, Aubrey D. N. J. (2005). Resistance to debate on how to postpone ageing is delaying progress and costing lives. EMBO Reports, 6(Suppl 1), S49–S53. http://doi.org/10.1038/sj.embor.7400399

Kass, Leon (2004). Aging Research.  http://agingresearch.org/sage/Default.aspx?tabid=60

Reason (2004). Leon Kass, Mystic. FightAging.org. https://www.fightaging.org/archives/2004/04/leon-kass-mysti.php
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Parrish, Elizabeth (2015). Liz Parrish speaks at People Unlimited on transcending the aging paradigm with gene therapy. https://www.youtube.com/watch?v=87OUb8TBwX0
 *** 

Demian Zivkovic is the president of the Institute of Exponential Sciences  (Facebook  / Meetup) – an international transhumanist think tank / education institute comprised of a group of transhumanism-oriented scientists, professionals, students, journalists, and entrepreneurs interested in the interdisciplinary approach to advancing exponential technologies and promoting techno-positive thought. He is also an entrepreneur and student of artificial intelligence and innovation sciences and management at the university of Utrecht.

Demian and the IES have been involved in several endeavors, such as organizing lectures on exponential sciences, interviewing experts such as Aubrey de Grey, joining several of Mr. Stolyarov’s futurism panels, and spreading Death is Wrong – Mr. Stolyarov’s illustrated children’s book on indefinite life extension – in The Netherlands.

Demian Zivkovic is a strong proponent of healthy life extension and cognitive augmentation. His interests include hyperreality, morphological freedom advocacy, postgenderism, and hypermodernism. He is currently working on his ambition of raising enough capital to make a real difference in life extension and transhumanist thought.

“A Morte é um Erro” – Portuguese Translation of “Death is Wrong” – Translated by Eric Pedro Alvaro – Post by G. Stolyarov II

“A Morte é um Erro” – Portuguese Translation of “Death is Wrong” – Translated by Eric Pedro Alvaro – Post by G. Stolyarov II

The New Renaissance Hat
G. Stolyarov II
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A free PDF version of A Morte é um Erro – the Portuguese translation of Death is Wrong – is now available for download from The Rational Argumentator. You can obtain your copy here and may spread it to Portuguese-speaking audiences as widely as you wish.

A Morte é um Erro was generously translated into Portuguese by Eric Pedro Alvaro.

Death_is_Wrong_Portuguese_CoverPaperback copies of A Morte é um Erro can be purchased in the following venues:

Createspace

Amazon

Kindle copies of A Morte é um Erro can be purchased on Amazon for $0.99.

***

Se você já se perguntou, “Por que as pessoas morrem?” então este livro é para você. A resposta é que não, a morte não é necessária, inevitável ou boa. Na verdade, a morte é um erro. A morte é uma inimiga de todos nós, que deve ser combatida com ciência, medicina e tecnologia. Este livro lhe apresenta os maiores, mais desafiantes e mais revolucionários movimentos para prolongar radicalmente o tempo de vida humano, para que você então simplesmente não precise morrer.

Você aprenderá sobre algumas plantas e animais com um tempo de vida incrivelmente longo, sobre recentes descobertas científicas em relação a ampliação do tempo de vida em humanos, e sobre simples e poderosos argumentos que podem refutar as comuns desculpas para a morte. Se você alguma vez já pensou que a morte é injusta e que ela deve ser derrotada, você não está sozinho. Leia este livro, e se torne parte desta importante busca na história da humanidade.

Este livro foi escrito pelo filósofo e futurólogo Gennady Stolyarov II e ilustrado pela artista Wendy Stolyarov. Com o intuito de lhe mostrar que, não importa quem é você e o que você pode fazer, sempre há uma forma de ajudar humanidade em sua batalha contra morte.

Refuting Ayn Rand’s “Immortal Robot” Argument – Article by G. Stolyarov II

Refuting Ayn Rand’s “Immortal Robot” Argument – Article by G. Stolyarov II

The New Renaissance HatG. Stolyarov II

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Here I refute an argument that has been leveled against proponents of indefinite human longevity from a surprising direction – those sympathetic to the Objectivist philosophy of Ayn Rand. Some advocates of Ayn Rand’s philosophy believe that indefinite life would turn human beings into “immortal, indestructible robots” that, according to Ayn Rand, would have no genuine values. Both of these claims are false. Indefinite life would not turn humans into indestructible robots, nor would an indestructible robot with human abilities lack values or motivation for doing great things. In Ayn Rand’s own words, “Achieving life is not the equivalent of avoiding death.” (John Galt’s speech in For the New Intellectual, p. 135)

Rand’s “immortal robot” argument is found in “The Objectivist Ethics” (The Virtue of Selfishness, p. 15): “To make this point fully clear, try to imagine an immortal, indestructible robot, an entity which moves and acts, but which cannot be affected by anything, which cannot be changed in any respect, which cannot be damaged, injured or destroyed. Such an entity would not be able to have any values; it would have nothing to gain or to lose; it could not regard anything as for or against it, as serving or threatening its welfare, as fulfilling or frustrating its interests. It could have no interests and no goals.”

The “immortal robot” argument needs to be challenged because it originates from Ayn Rand, who otherwise espouses numerous rational ideas. I myself agree with most of the fundamental principles that Ayn Rand advocates. However, in some of her particular reasoning – at least, if applied to the wrong context – she can be off-target in such a way as to retard further progress. The often-leveled argument, derived by contemporary non-transhumanist Objectivists from the above-quoted passage, is that achieving indefinite longevity would turn human beings into Ayn Rand’s description of the “immortal, indestructible robot”.

In responding to Rand’s argument, several points can be made in relation to prolonging human life indefinitely and lifting the death sentence that hangs over all of us. First, at no point in time will human beings become the “immortal, indestructible robots” that Ayn Rand describes. The simple reason for this is that our existence is physical and contingent on certain physical prerequisites being fulfilled. The moment one of these physical prerequisites is lacking, our existence ceases. This will always be the case, even if we no longer have a necessary upper limit on our lifespans. For instance, biomedical advances that would greatly expand human lifespans – allowing periodic reversions to a more youthful biological state and therefore the possibility of an indefinite existence – would not turn humans into indestructible robots. There would still be the need to actively turn back biological processes of decay, and the active choice to pursue such treatments or not. People who live longer by successfully combating senescence could still get run over by a car or experience a plane crash. They would retain potential vulnerability to certain perils – such as death from accidents – although, as I have explained in “Life Extension and Risk Aversion”, they may be more diligent in seeking to greatly reduce the probability of such outcomes. If it is ever the case that death by senescence and the myriad diseases which kill many human beings today can be averted, then human beings will try to avert the other possibilities of death – for instance, by developing safer modes of transportation or engaging in fewer wars.

It is possible to significantly reduce the likelihood that one can be destroyed, without ever eliminating the theoretical potential of such destruction. Furthermore, because human beings have free will, they always have at least the hypothetical option of choosing to undermine the physical prerequisites of their own lives. In my view, no sane, rational being would actually choose to pursue that option, but the option is there nonetheless. For anybody who seeks to commit suicide by immediate or gradual means, or by refusing to take advantage of life-prolonging techniques once they become available, there is virtually nothing in the world that could prevent this, apart from rational persuasion (which may or may not be successful).

Even with indefinite longevity, human beings will always be vulnerable to some actual or hypothetical perils or poor choices. Moreover, when we manage to avoid one kind of peril, other kinds of perils may become more pressing as they come into the frame of awareness of longer-lived beings. If we do manage to live for hundreds of thousands of years, we will be far more subject to long-term geological changes and fluctuations of the Earth’s climate, such as the cycle of ice ages, whereas today humans do not live long enough to experience these massive shifts. Most of us today do not worry about the consequences of huge glaciers advancing over the continents, but humans who live for millennia will see this as a pressing problem for their own lifetimes. Likewise, the longer we live, the greater the likelihood that we will experience a global cataclysm, such as a supervolcano or an asteroid hitting the Earth. Human ingenuity and resources would need to be devoted toward confronting and even preventing these perils – a highly desirable outcome in general, since the perils exist irrespective of our individual lifespans, but most humans currently lack the long-term vision or orientation to combat them.

Moreover, the need to reject the “immortal robot” argument when discussing indefinite life extension does not stem solely from a desire to achieve philosophical correctness. Rather, we should recognize the potential for actually achieving meaningful, unprecedented longevity increases within our own lifetimes. For instance, the SENS Research Foundation is a nonprofit biogerontological research organization whose founder, Dr. Aubrey de Grey, has outlined an engineering-based approach to reversing the seven principal types of damage that accumulate in the human body with age. (SENS stands for “Strategies for Engineered Negligible Senescence”.) Dr. de Grey has stated that, with proper funding, there is approximately a 50 percent probability of these rejuvenation treatments being developed 20-25 years from now. (The 20-year figure is presented in this transcript from a recent NPR interview of Aubrey de Grey – quoted in “Discussing Science and Aging: Aubrey de Grey and Cynthia Kenyon at NPR” by Reason at FightAging.org.) The SENS Research Foundation is not the only entity pursuing radical life extension. Major commercial efforts toward research into reversing biological aging – such as Calico, created and funded by Google (now Alphabet, Inc.) – have been launched already. Thus, it is premature to conclude that death is a certainty for those who are alive today. Medical advances on the horizon could indeed turn many humans into beings who are still potentially vulnerable to death, but no longer subject to any upper limit on their lifespans.

It is therefore ill-advised to pin any ethical justifications for the ultimate value of human life to the current contingent situation, where it just so happens that human lifespans are finite because we have not achieved the level of technological advancement to overcome senescence yet. If such advances are achieved, common interpretations of the “immortal robot” argument and its derivative claims would suggest that life for human beings would transform from an ultimate value to some lesser value or to no value at all. This implication reveals a flaw in arguments that rely on the finitude of life and the inevitability of death. How is it that, by making life longer, healthier, and of higher quality (with less suffering due to the diseases of old age), humans would, in so doing, deprive life of its status as an ultimate value? If life is improved, it does not thereby lose a moral status that it previously possessed.

Yet another important recognition is that some animals have already attained negligible senescence. Their lifespans are de facto finite, but without a necessary upper limit. Suppose that evolution had taken a different course and rational beings had descended from tortoises rather than from primates. Then these rational beings would have negligible senescence without the need for medical intervention to achieve it. Would their lives thereby lack a type of value which the proponents of the “immortal robot” argument attribute to human lives today? Again, a conclusion of this sort illustrates a flaw in the underlying argument.

But suppose that a true immortal, indestructible robot could exist and be identical to human beings in every other respect. It would possess human biological processes and ways of thinking but be made of extremely strong materials that did not deteriorate or that automatically renewed themselves so as to rapidly, automatically repair any injury. Ayn Rand’s argument would still be mistaken. Even if death were not a possibility for such a being, it could still pursue and enjoy art, music, inventions, games – any activity that is appealing from the perspective of the senses, the intellect, or the general civilizing project of transforming chaos into order and transforming simpler orders into more complex ones.

The fear of death is not the sole motivator for human actions by far. Indeed, most great human accomplishments are a result of positive, not negative motivations. Rand acknowledged this when she wrote that “Achieving life is not the equivalent of avoiding death.” At least in the short term, you do not need to do much to avoid death. You could just sit there, stay out of trouble, eat, drink, keep warm, sleep – and you survive to the next day. But that is not a full life, according to Rand. Obviously, one needs to avoid death to have a full life. Survival is necessary, but it is not sufficient. Many thinkers sympathetic to the Objectivist school, such as Edward Younkins, Tara Smith, Douglas Den Uyl, Douglas Rasmussen, Tibor Machan, George Reisman, and Lester Hunt, have extended this insight to conclude that survival is not enough; one should also pursue flourishing. (Younkins provides an excellent overview of this perspective in “Flourishing and Happiness in a Nutshell”.)

I concur fully with the goal of flourishing and recognize the existence of numerous positive motivations besides mere survival. For example, the desire to see oneself create something, to witness a product of one’s mind become embodied in the physical reality, is a powerful motivation indeed. One can furthermore seek to take esthetic pleasure from a particular object or activity. This does not require even a thought of death. Moreover, to appreciate certain kinds of patterns in existence, which are present in art, in technology, and even in games, does not require any thought of death. Many people play games, even if those games do not contribute anything to their survival. This does not mean, however, that doing so is irrational; rather, it is another creative way to channel the activities of the human mind. Via games, the human mind essentially creates its own field of endeavor, a rule system within which it operates. By operating within that rule system, the mind exercises its full potential, whereas just by sitting there and only doing what is absolutely necessary to survive, the mind would have missed some essential part of its functioning.

Creating art and music, undertaking scientific discoveries, envisioning new worlds – actual and fictional – does not rely on having to die in the future. None of these activities even rely on the threat of death. The immortal, indestructible robot, of course, might not engage in precisely the same activities as we do today. It would probably not need to worry about earning its next meal by working for somebody else, but it could still paint a painting, just because it would like to see its mental processes – in this scenario, processes greatly resembling our own – have some kind of external consequence and embodiment in the external reality. Such external embodiment is a vital component of flourishing.

Fear of death is not the sole motivator for human action, nor the sole prerequisite for value, as Ayn Rand acknowledged. There is more to life than that. Life is not merely about survival and should be about the pursuit of individual flourishing as well. Survival is a necessary prerequisite, but, once it is achieved, an individual is free to pursue higher-order values, such as self-actualization. The individual would only be further empowered in the quest for flourishing and self-actualization in a hypothetical environment where no threats to survival existed.

While we will never be true immortal robots, such immortal robots could nonetheless flourish and truly achieve life. As a result, the “immortal robot” argument fails on multiple counts and is not a valid challenge to indefinite life extension.

This essay may be freely reproduced using the Creative Commons Attribution Share-Alike International 4.0 License, which requires that credit be given to the author, G. Stolyarov II. Find out about Mr. Stolyarov here.

Zero-Gravity Orbital Habitation Causes Changes That Are at Least Superficially Similar to Accelerated Aging – Article by Reason

Zero-Gravity Orbital Habitation Causes Changes That Are at Least Superficially Similar to Accelerated Aging – Article by Reason

The New Renaissance HatReason
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That old people will go into orbit to escape the rigors of gravity and thus live longer in their declining years was a staple of golden age and later science fiction. These works were written at a time in which our knowledge of human biochemistry – and the application of that knowledge to medicine – was crude in comparison to today. It is fascinating that we can say that for such a short span of years, a mere short lifetime past, but the differences between the medicine of the 1950s and the medicine of today are profound indeed. The writers of that time largely envisaged a future incorporating great gains in energy generation, and a consequent diaspora from Earth, while computation, medicine and the human condition remained much unchanged; older spacemen in the outer reaches struggling with heart disease in their fifties. Instead we found that expanding the generation, storage, transmission, and application of energy is very hard, and the largely unanticipated information revolution occurred instead. We lost the near future of cheap heavy lift to orbit and the solar system at our beck and call, but gained Moore’s Law, biotechnology, nanotechnology, a pervasive internet, and medical progress that is in the early stages of conquering heart disease and may yet save us from all of degenerative aging.

As it turns out, retreating from the rigors of gravity may well have the opposite effect to that imagined by the authors of the last century. Among the alterations produced by orbital habitation in zero gravity are those that appear, at least superficially, much like accelerated aging of the cardiovascular system. The root causes have yet to be pinned down, since very few people are actually researching this topic, but since the onset of these symptoms is fairly rapid, I’d guess at the cause being more a matter of regulatory dysfunction than increased tissue damage, such as the presence of cross-links related to arterial stiffening in aging. Here I’ll point out a few links to the work of one research group on this topic in recent years:

Waterloo to lead new experiment aboard International Space Station

Quote:

The experiment will link changes in astronauts’ hearts and blood vessels with specific molecules in the blood to determine why astronauts experience conditions that mimic aging-related problems and chronic diseases on earth. The findings will help identify important indicators for chronic disease and assist with the development of early interventions for people on earth. “We know that astronauts return from space with stiffer arteries and resistance to insulin, conditions affecting many adults as they age. For the first time, we will be able to track exactly how – and why – the body’s blood vessels change, and use these findings to potentially improve quality of life and the burden of chronic disease.” “In space, astronauts’ bodies show aging-like changes much faster than on Earth. The International Space Station provides a unique platform to study aging-related conditions providing insights that can be used to help understand some of the biggest health issues affecting society. Our research to date suggests that even though astronauts exercise every day, the actual physical demands of tasks of daily living are greatly reduced due to the lack of gravity. This lifestyle seems to cause changes in the vascular system and in the body’s ability to regulate blood glucose that would normally take years to develop on earth.”

U.Waterloo – Vascular Aging and Space Research Program

Quote:

We study factors related to cardiovascular health with aging. One focus is on blood pressure regulation and its impact on brain blood flow to help us understand some of the factors that could contribute to falls in the elderly, especially those that occur on rising from bed. Another focus is on aging blood vessels. We have reported a strong link between peripheral arterial stiffness and a reduction in brain blood flow. Our space research program is very active. We recently completed the study Cardiovascular and Cerebrovascular Control on Return from the International Space Station (CCISS). We are currently collecting data for the project Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular).

Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular)

Quote:

Cardiovascular Health Consequences of Long-Duration Space Flight (Vascular) investigates the impact of long-duration space flight on the blood vessels of astronauts. Space flight accelerates the aging process, and it is important to understand this process to develop specific countermeasures. Data is collected before, during, and after space flight to assess inflammation of the artery walls, changes in blood vessel properties, and cardiovascular fitness. Spaceflight can cause stiffening of the arteries, affecting the body’s ability to control blood pressure. This investigation assessed the blood vessels of astronauts and found decreased flexibility of the carotid artery during flight. Researchers found no relationship between the level of physical fitness and this decrease. The experiment also provided data on the mechanisms behind increased arterial stiffness from spaceflight. Further research is needed to establish effective ways to counter the cardiovascular consequences of spaceflight and ultimately help treat increased arterial stiffness from aging on Earth, which can cause high blood pressure and organ damage.

Impaired cerebrovascular autoregulation and reduced CO2 reactivity after long duration spaceflight

Quote:

Long duration habitation on the International Space Station (ISS) is associated with chronic elevations in arterial blood pressure in the brain compared with normal upright posture on Earth and elevated inspired carbon dioxide. Although results from short-duration spaceflights suggested possibly improved cerebrovascular autoregulation, animal models provided evidence of structural and functional changes in cerebral vessels that might negatively impact autoregulation with longer periods in microgravity. Seven astronauts (1 woman) spent 147 ± 49 days on ISS. Preflight testing (30-60 days before launch) was compared with postflight testing on landing day or the morning 1 or 2 days after return to Earth. The results indicate that long duration missions on the ISS impaired dynamic cerebrovascular autoregulation and reduced cerebrovascular carbon dioxide reactivity.

Recent findings in cardiovascular physiology with space travel

Quote:

The cardiovascular system undergoes major changes in stress with space flight primarily related to the elimination of the head-to-foot gravitational force. A major observation has been that the central venous pressure is not elevated early in space flight yet stroke volume is increased at least early in flight. Recent observations demonstrate that heart rate remains lower during the normal daily activities of space flight compared to Earth-based conditions. Structural and functional adaptations occur in the vascular system that could result in impaired response with demands of physical exertion and return to Earth. Cardiac muscle mass is reduced after flight and contractile function may be altered. Regular and specific countermeasures are essential to maintain cardiovascular health during long-duration space flight.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries.
This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.
SENS Research Foundation Joins the Global #GivingTuesday Movement – Press Release by SENS Research Foundation

SENS Research Foundation Joins the Global #GivingTuesday Movement – Press Release by SENS Research Foundation

The New Renaissance Hat
SENS Research Foundation
November 28, 2015
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Every Dollar Contributed Up to the First $5,000 Will Be Quadrupled, Turning into $20,000.
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MOUNTAIN VIEW, Calif. — November 24, 2015 — The SENS Research Foundation (SRF), a non-profit organization focused on transforming the way the world researches and treats age-related disease, has joined #GivingTuesday, a global day of giving that harnesses the collective power of individuals, communities and organizations to encourage philanthropy and celebrate generosity worldwide. Every dollar donated to SRF up to the first $5,000 will be quadrupled, making every dollar raised turn into $20,000.

Occurring this year on December 1, #GivingTuesday is held annually on the Tuesday after Thanksgiving (in the U.S.) and the widely recognized shopping events Black Friday and Cyber Monday to kick-off the holiday giving season and inspire people to collaborate in improving their local communities and to give back in impactful ways to the charities and causes they support.

SENS Research Foundation is aiming to reach a goal of $20,000 with the help of contributors who have pledged to match each dollar raised up to the first $5,000. The Croeni Foundation, a philanthropic organization dedicated to giving, the environment and health, has pledged to match the first $5,000 raised dollar for dollar. The foundation gave SRF an unrestricted $5,000 earlier this year, as well. Aubrey de Grey, CSO of SENS Research Foundation, has offered a dollar for dollar matching challenge up to $5,000. And Fight Aging! will match every dollar up to $125,000 through December 31, 2015. Fight Aging! encourages the development of medical technologies, lifestyles, and other means to help people live comfortably, healthily, and capably for as long as they desire.

“We are looking forward to participating in #GivingTuesday for a second year, and offer our thanks to Jan Croeni and the Croeni Foundation, as well as Aubrey de Grey and Fight Aging! for their support,” said Jerri Barrett, vice president of outreach, SENS Research Foundation. “Today’s cost for the treatment and care of chronic diseases of aging costs around $40,000 per second and will only continue to go up, as we spend more money per patient, while the number of patients is increasing. As a society, we need to change our ways and start treating age-related diseases more intelligently. The funds we raise on #GivingTuesday will help facilitate our efforts to do just that, as we work to continue learning how to prevent or reverse age-related diseases.”

Those who are interested in joining SENS Research Foundation’s #GivingTuesday initiative can donate at www.sens.org/donate. To learn more about #GivingTuesday participants and activities or to join the celebration of giving, please visit: http://www.givingtuesday.org/

About SENS Research Foundation (SRF)

SENS Research Foundation is a 501(c)(3) nonprofit that works to research, develop, and promote comprehensive regenerative medicine solutions for the diseases of aging. SRF is focused on a damage repair paradigm for treating the diseases of aging, which it advances through scientific research, advocacy, and education. SENS Research Foundation supports research projects at universities and institutes around the world with the goal of curing such age-related diseases as heart disease, cancer, diabetes and Alzheimer’s disease. Educating the public and training researchers to support a growing regenerative medicine field are also major endeavors of the organization that are being accomplished though advocacy campaigns and educational programs. For more information, visit www.sens.org.

Media Contact:
Jerri Barrett
408-204-7229
jerri.barrett@sens.org

The Immortals Among Us – Article by Reason

The Immortals Among Us – Article by Reason

The New Renaissance Hat
Reason
November 26, 2015
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Let us define immortality as being a state of agelessness, which seems a common colloquial usage these days. More precisely this means that the risk of death due to intrinsic causes such as wear and tear damage of vital organs remains the same over time, perhaps due to advanced medical interventions. Falling pianos are still going to kill you, and a hypothetical biologically young immortal in a hypothetical environment maintaining today’s first world extrinsic mortality rate would have a half-life of 500 years or so, meaning that at any age, there is a 50% chance of evading a life-ending event for another 500 years. There are no human immortals by this criteria of a static intrinsic mortality rate, it seems, though for a while it looked like very old humans might have essentially flat but very high mortality rates in the same way as very old flies do. Immortality in a state of advanced frailty and coupled with a 90% or higher yearly mortality rate isn’t the sort of circumstance that most people would aspire to, of course. It barely improves on the actual circumstance that the oldest of people find themselves in, all too briefly.

However, let us think beyond the box. Consider the small horde of children that you’ll find playing and running in any junior schoolyard here and now. By the time the survivors of their cohorts reach a century of age, the 2100s will have arrived. If the current very slow trend in increasing adult life expectancy continues, adding a year of remaining life expectancy at 60 for every passing decade, then something like 25% of these present children will live to see that centenary. But I don’t for one moment believe that this trend will continue as it has in the past. Past increases in life expectancy were an incidental side-effect of general improvements in medicine across the board, coupled with increasing wealth and all the benefits that brings. Across all of that time, no-one was seriously trying to intervene in the aging process, to address the causes of aging, or to bring aging under medical control. Times are changing, and now many groups aiming to build some of the foundations needed to create exactly this outcome. You may even have donated to support some of them, such as the SENS Research Foundation. The trend in longevity in an age in which researchers are trying to treat the causes of aging will be very different from the trend in longevity in an age in which no such efforts are taking place.

You don’t have to dig very far into the state of the science to see that the first rejuvenation treatments are very close, their advent limited only by funding. If funding were no issue for senescent cell clearance, for example, it would absolutely, definitively be in clinics a decade from now. Other necessary technologies are more distant, but not that much more distant – the 2030s will be an exciting time for the medical sciences. For the occupants of today’s junior playground, it seems foolish to imagine that by age 60 they will not have access to rejuvenation treatments after the SENS model at various stages of maturity, many having having been refined for more than 30 years, at the height of their technology cycle, and just giving way to whatever radical new improvement happens next.

Take a moment for a sober look at the sweeping differences and expanded technological capabilities that exist between today, the 1960s, and the 1910s. So very much has been achieved, and that pace of progress is accelerating. Those junior playground athletes of today will live to see a world even more radically different and advanced than our present time is in comparison to the First World War era. These are the immortals among us. The majority of them will have the opportunity to attain actuarial escape velocity, to keep on using ever-improving versions of rejuvenation treatments until they are gaining life expectancy at a faster rate than they are aging. Their cellular damage, the wear and tear created by the normal operation of metabolism, will be repaired as fast as it is is generated. It is the rest of us, those of us who are no longer spring chickens, who are faced with much more of a race to the goal. The degree to which we can successfully fund and advocate the necessary research is the determinant of whether we can scrape by into the age of rejuvenation treatments, or whether we will gain modest benefits but still age to death – because we were born too soon, and because the rest of the world didn’t get its collective act together rapidly enough in what is now the very tractable matter of building a cure for aging.

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries. 
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This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.

Google Life Sciences to Fund Heart Disease Program – Article by Reason

Google Life Sciences to Fund Heart Disease Program – Article by Reason

The New Renaissance Hat
Reason
November 22, 2015
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An interesting next step from Google Life Sciences: they are putting forward $50 million in search of a laboratory to propose a program that pushes forward the state of the art in research and treatment of heart disease. Spent over ten years, that would produce an organization about the present size of the SENS Research Foundation, or a tenth of the Buck Institute, for purposes of comparison – and smaller than many of the research groups presently dedicated to the study of heart disease. So this is a sizable and welcome investment in medical research, but the significance is overhyped by the reporting organization here; no-one is going to cure heart disease with a $50 million project, since heart disease is caused by aging, and in the most general sense. This is an effort to change the funding landscape, stir things up, and make some progress.

If you walk through the list of forms of cell and tissue damage that causes degenerative aging, near every one of them contributes to structural failure of the cardiovascular system. The loss of stem cell activity and consequent decline in repair of tissues is only one of these: oxidized lipids that contribute to atherosclerosis in blood vessel walls; extracellular cross-links stiffen blood vessel walls and cause hypertension and consequent structural weakening in the heart; senescent cells wreck havoc on all the tissues they accumulate in; transthyretin amyloids that accumulate with age are implicated in heart disease via their ability to clog the cardiovascular system; and the loss of lysosomal function in long-lived cells, including those of the heart, progressively damages their function. Curing heart disease, removing it from the picture, requires treatments that effectively address near all of the causes of aging.

Quote from “Google Aims a $50 Million Moonshot at Curing Heart Disease” by Davey Alba, WIRED, November 16, 2015:

Cardiovascular disease people on Earth than anything else – over 17 million a year, and the number keeps going up. Of those deaths, more than 40 percent is due to coronary heart disease. Medicine has drugs that can treat it and practices that can help prevent it, but nobody really knows what causes it or how to cure it. Now, Google and the American Heart Association aim to change that by dropping a $50 million funding bomb on the problem. And as you might expect from a Silicon Valley giant that believes in moving fast and breaking things – an approach that hasn’t always transferred well to basic scientific research – the company isn’t spreading the money around. Google Life Sciences and the AHA said the money would go to one team over five years. “Traditional research funding models are often incremental and piecemeal, making it difficult to study a long-term, multifaceted subject. AHA and Google Life Sciences have committed to a bold new approach.”

The AHA, already the largest funder of cardiovascular research in the US outside of the federal government, says the program will be its most heavily funded initiative in nearly a century. Applications begin in January and if all goes according to plan, they’ll be due by February 14th. (Valentine’s Day. Get it?) If you want the $50 million, your idea has to fit on a single page. And Google won’t take a financial or intellectual property stake in the results. The organizations hope that the program will accelerate the field of heart research much like Google’s self-driving car eventually compelled the entire automobile industry to follow its lead.

Link: http://www.wired.com/2015/11/google-aims-a-50-million-moonshot-at-curing-heart-disease/

Reason is the founder of The Longevity Meme (now Fight Aging!). He saw the need for The Longevity Meme in late 2000, after spending a number of years searching for the most useful contribution he could make to the future of healthy life extension. When not advancing the Longevity Meme or Fight Aging!, Reason works as a technologist in a variety of industries. 
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This work is reproduced here in accord with a Creative Commons Attribution license. It was originally published on FightAging.org.