Browsed by
Tag: longevity

Discussion on Life-Extension Advocacy – G. Stolyarov II Answers Audience Questions

Discussion on Life-Extension Advocacy – G. Stolyarov II Answers Audience Questions

Comments 0 Comment
The New Renaissance Hat

G. Stolyarov II

******************************

Gennady Stolyarov II, Chairman of the U.S. Transhumanist Party, answers audience questions regarding life-extension advocacy and possibilities for broadening the reach of transhumanist and life-extensionist ideas.

While we were unable to get into contact with our intended guest, Chris Monteiro, we were nonetheless able to have a productive, wide-ranging discussion that addressed many areas of emerging technologies, as well as trends in societal attitudes towards them and related issues of cosmopolitanism, ideology, and the need for a new comprehensive philosophical paradigm of transmodernism or hypermodernism that would build off of the legacy of the 18th-century Age of Enlightenment.

Become a member of the U.S. Transhumanist Party for free. Apply here.

Nevada Transhumanist Party Interview on the EMG Radio Show – November 7, 2016

Nevada Transhumanist Party Interview on the EMG Radio Show – November 7, 2016

Comments 0 Comment
The New Renaissance HatG. Stolyarov II
******************************

On November 7, 2016, Mr. Stolyarov had his first radio interview as Chief Executive of the Nevada Transhumanist Party. The EMG Radio Show on 91.5 The Rebel HD-2, hosted by Andre’ Haynes, interviewed Mr. Stolyarov for about 10 minutes on the mission of the Nevada Transhumanist Party and transhumanist views on emerging technologies – such as artificial wombs, designer babies, artificial intelligence, and life extension.

The interview begins at 2:00 in the video.

This recording was reproduced with permission from the EMG Radio Show.

Download the interview recording here.

Visit the Nevada Transhumanist Party page here.

Join the Nevada Transhumanist Party Facebook group here.

Find out about Mr. Stolyarov here.

NTP-Logo-9-1-2015

Criticizing Programmed Theories of Aging – Article by Reason

Criticizing Programmed Theories of Aging – Article by Reason

Comments 1 comment
The New Renaissance HatReason
******************************

Today I’ll point out an open-access critique of programmed aging theories by the originator of the disposable soma theory of aging, one of the modern views of aging as accumulated damage rather than programming. The question of how and why we age is wrapped in a lot of competing theory, but of great practical importance. Our biochemistry is enormously complex and incompletely mapped, and thus the processes of aging, which is to how exactly our biochemistry changes over time, and all of the relationships that drive that change, are also enormously complex and incompletely mapped. Nonetheless, there are shortcuts that can be taken in the face of ignorance: the fundamental differences between young and old tissue are in fact well cataloged, and thus we can attempt to reverse aging by treating these changes as damage and repairing them. If you’ve read through the SENS rejuvenation research proposals, well, that is the list. The research community may not yet be able to explain and model how exactly this damage progresses, interacts, and spreads from moment to moment, but that effort isn’t necessary to build repair therapies capable of rejuvenation. You don’t need to build a full model of the way in which paint cracks and peels in order to scrub down and repaint a wall, and building that model is a lot most costly than just forging ahead with the painting equipment.

The engineering point of view described above, simply getting on with the job when there is a good expectation of success, is somewhat antithetical to the ethos and culture of the sciences, which instead guides researchers to the primary goal of obtaining full understanding of the systems they study. In practice, of course, every practical application of the life sciences is created in a state of partial ignorance, but the majority of research groups are nonetheless oriented towards improving the grand map of the biochemistry of metabolism and aging rather than doing what can be done today to create rejuvenation therapies. Knowledge over action. If we had all the time in the world this would be a fine and golden ideal. Unfortunately we do not, which places somewhat more weight on making material progress towards the effective treatment of aging as a medical condition – ideally by repairing its causes.

But what are the causes of aging? The majority view in the research community is that aging is a process of damage accumulation. The normal operation of metabolism produces forms of molecular damage in cells and tissues, a sort of biological wear and tear – though of course the concept of wear and tear is somewhat more nuanced and complex in a self-repairing system. This damage includes such things as resilient cross-links that alter the structural properties of the extracellular matrix and toxic metabolic waste that clutters and harms long-lived cells. As damage accumulates, our cells respond in ways that are a mix of helpful and harmful, secondary and later changes that grow into a long chain of consequences and a dysfunctional metabolism that is a long way removed from the well-cataloged fundamental differences between old and young tissues. An old body is a complicated mess of interacting downstream problems. In recent years, however, a growing minority have suggested and theorized that aging is not caused by damage, but is rather a programmed phenomenon – that some portion of the what I just described as the chain of consequences, in particular epigenetic changes, are in fact the root cause of aging. In the programmed view of aging, epigenetic change causes dysfunction and damage, not the other way around. That these two entirely opposite views can exist is only possible because there is no good map of the detailed progression of aging – only disconnected snapshots and puzzle pieces. There is a lot of room to arrange the pieces in any way that can’t be immediately refuted on the basis of well-known past studies.

There are two ways to settle the debate of aging as damage versus aging as evolved program. The first is to produce that grand map of metabolism and aging, something that I suspect is at the least decades and major advances in life science automation removed from where we stand now. The other is to build therapies that produce large degrees of rejuvenation, enough of a difference to put it far beyond argument that the approach taken is the right one. That is not so far away, I believe, as the first SENS rejuvenation therapies are presently in the early stages of commercial development. I think that, even with the comparative lack of funding for this line of development, ten to twenty years from now the question will be settled beyond reasonable doubt. Meanwhile, the programmed-aging faction has become large enough and their positions coherent enough that the mainstream is beginning to respond substantially to their positions; I expect that this sort of debate will continue all the way up to and well past the advent of the first meaningful rejuvenation therapies, which at this point look to be some form of senescent cell clearance.

Can aging be programmed? A critical literature review – by Axel Kowald and Thomas B. L. Kirkwood

Quote:

Many people, coming new to the question of why and how aging occurs, are attracted naturally to the idea of a genetic programme. Aging is necessary, it is suggested, either as a means to prevent overcrowding of the species’ environment or to promote evolutionary change by accelerating the turnover of generations. Instead of programmed aging, however, the explanation for why aging occurs is thought to be found among three ideas all based on the principle that within iteroparous species (those that reproduce repeatedly, as opposed to semelparous species, where reproduction occurs in a single bout soon followed by death), the force of natural selection declines throughout the adult lifespan. This decline occurs because at progressively older ages, the fraction of the total expected reproductive output that remains in future, on which selection can act to discriminate between fitter and less-fit genotypes, becomes progressively smaller. Natural selection generally favours the elimination of deleterious genes, but if its force is weakened by age, and because fresh mutations are continuously generated, a mutation-selection balance results. The antagonistic pleiotropy theory suggests that a gene that has a benefit early in life, but is detrimental at later stages of the lifespan, can overall have a net positive effect and will be actively selected. The disposable soma theory is concerned with optimizing the allocation of resources between maintenance on the one hand and other processes such as growth and reproduction on the other hand. An organism that invests a larger fraction of its energy budget in preventing accumulation of damage to its proteins, cells and organs will have a slower rate of aging, but it will also have fewer resources available for growth and reproduction, and vice versa. Mathematical models of this concept show that the optimal investment in maintenance (which maximizes fitness) is always below the fraction that is necessary to prevent aging.

In recent years, there have been a number of publications claiming that the aging process is a genetically programmed trait that has some form of benefit in its own right. If this view were correct, it would be possible experimentally to identify the responsible genes and inhibit or block their action. This idea is, however, diametrically opposed to the mainstream view that aging has no benefit by its own and is therefore not genetically programmed. Because experimental strategies to understand and manipulate the aging process are strongly influenced by which of the two opinions is correct, we have undertaken here a comprehensive analysis of the specific proposals of programmed aging. On the principle that any challenge to the current orthodoxy should be taken seriously, our intention has been to see just how far the various hypotheses could go in building a convincing case for programmed aging.

This debate is not only of theoretical interest but has practical implications for the types of experiments that are performed to examine the mechanistic basis of aging. If there is a genetic programme for aging, there would be genes with the specific function to impair the functioning of the organism, that is to make it old. Under those circumstances, experiments could be designed to identify and inhibit these genes, and hence to modify or even abolish the aging process. However, if aging is nonprogrammed, the situation would be different; the search for genes that actively cause aging would be a waste of effort and it would be too easy to misinterpret the changes in gene expression that occur with aging as primary drivers of the senescent phenotype rather than secondary responses (e.g. responses to molecular and cellular defects). It is evident, of course, that genes influence longevity, but the nature of the relevant genes will be very different according to whether aging is itself programmed or not.

For various programmed theories of aging, we re-implemented computational models, developed new computational models, and analysed mathematical equations. The results fall into three classes. Either the ideas did not work because they are mathematically or conceptually wrong, or programmed death did evolve in the models but only because it granted individuals the ability to move, or programmed death did evolve because it shortened the generation time and thus accelerated the spread of beneficial mutations. The last case is the most interesting, but it is, nevertheless, flawed. It only works if an unrealistically fast-changing environment or an unrealistically high number of beneficial mutations are assumed. Furthermore and most importantly, it only works for an asexual mode of reproduction. If sexual reproduction is introduced into the models, the idea that programmed aging speeds up the spread of advantageous mutations by shortening the generation time does not work at all. The reason is that sexual reproduction enables the generation of offspring that combine the nonaging genotype of one parent with the beneficial mutation(s) found in the other parent. The presence of such ‘cheater’ offspring does not allow the evolution of agents with programmed aging.

In summary, all of the studied proposals for the evolution of programmed aging are flawed. Indeed, an even stronger objection to the idea that aging is driven by a genetic programme is the empirical fact that among the many thousands of individual animals that have been subjected to mutational screens in the search for genes that confer increased lifespan, none has yet been found that abolishes aging altogether. If such aging genes existed as would be implied by programmed aging, they would be susceptible to inactivation by mutation. This strengthens the case to put the emphasis firmly on the logically valid explanations for the evolution of aging based on the declining force of natural selection with chronological age, as recognized more than 60 years ago. The three nonprogrammed theories that are based on this insight (mutation accumulation, antagonistic pleiotropy, and disposable soma) are not mutually exclusive. There is much yet to be understood about the details of why and how the diverse life histories of extant species have evolved, and there are plenty of theoretical and experimental challenges to be met. As we observed earlier, there is a natural attraction to the idea that aging is programmed, because developmental programming underpins so much else in life. Yet aging truly is different from development, even though developmental factors can influence the trajectory of events that play out during the aging process. To interpret the full complexity of the molecular regulation of aging via the nonprogrammed theories of its evolution may be difficult, but to do it using demonstrably flawed concepts of programmed aging will be impossible.

Given that the author here has in the past been among those who dismissed the SENS initiative as an approach to treating aging by repairing damage, it is perhaps a little amusing to see him putting forward points such as this one: “despite the cogent arguments that aging is not programmed, efforts continue to be made to establish the case for programmed aging, with apparent backing from quantitative models. It is important to take such claims seriously, because challenge to the existing orthodoxy is the path by which science often makes progress.” Where was this version of the fellow ten years ago?

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.
Towards a Greater Knowledge of Mitochondrial DNA Damage in Aging – Article by Reason

Towards a Greater Knowledge of Mitochondrial DNA Damage in Aging – Article by Reason

Comments 0 Comment
The New Renaissance HatReason
******************************

Today I’ll point out a very readable scientific commentary on mutations in mitochondrial DNA (mtDNA) and the importance of understanding how these mutations spread within cells. This is a topic of some interest within the field of aging research, as mitochondrial damage and loss of function is very clearly important in the aging process. Mitochondria are, among many other things, the power plants of the cell. They are the evolved descendants of symbiotic bacteria, now fully integrated into our biology, and their primary function is to produce chemical energy store molecules, adenosine triphosphate (ATP), that are used to power cellular operations. Hundreds of mitochondria swarm in every cell, destroyed by quality control processes when damaged, and dividing to make up the numbers. They also tend to promiscuously swap component parts among one another, and sometimes fuse together.

Being the descendants of bacteria, mitochondria have their own DNA, distinct from the nuclear DNA that resides in the cell nucleus. This is a tiny remnant of the original, but a very important remnant, as it encodes a number of proteins that are necessary for the correct operation of the primary method of generating ATP. DNA in cells is constantly damaged by haphazard chemical reactions, and equally it is constantly repaired by a range of very efficient mechanisms. Unfortunately mitochondrial DNA isn’t as robustly defended as nuclear DNA. Equally unfortunately, some forms of mutation, such as deletions, seem able to rapidly spread throughout the mitochondrial population of a single cell, even as they make mitochondria malfunction. This means that over time a growing number of cells become overtaken by malfunctioning mitochondria and fall into a state of dysfunction in which they pollute surrounding tissues with reactive molecules. This can, for example, increase the level of oxidized lipids present in the bloodstream, which speeds up the development of atherosclerosis, a leading cause of death at the present time.

The question of how exactly some specific mutations overtake a mitochondrial population so rapidly is still an open one. There is no shortage of sensible theories, for example that it allows mitochondria to replicate more rapidly, or gives them some greater resistance to the processes of quality control that normally cull older, damaged mitochondria. The definitive proof for any one theory has yet to be established, however. In one sense it doesn’t actually matter all that much: there are ways to address this problem through medical technology that don’t require any understanding of how the damage spreads. The SENS Research Foundation, for example, advocates the path of copying mitochondrial genes into the cell nucleus, a gene therapy known as allotopic expression. For so long as the backup genes are generating proteins, and those proteins make it back to the mitochondria, the state of the DNA inside mitochondria doesn’t matter all that much. Everything should still work, and the present contribution of mitochondrial DNA damage to aging and age-related disease would be eliminated. At the present time there are thirteen genes to copy, a couple of which are in commercial development for therapies unrelated to aging, another couple were just this year demonstrated in the lab, and the rest are yet to be done.

Still, the commentary linked below is most interesting if you’d like to know more about the questions surrounding the issue of mitochondrial DNA damage and how it spreads. This is, as noted, a core issue in the aging process. The authors report on recent research on deletion mutations that might sway the debate on how these mutations overtake mitochondrial populations so effectively.

Expanding Our Understanding of mtDNA Deletions

A challenge of mtDNA genetics is the multi-copy nature of the mitochondrial genome in individual cells, such that both normal and mutant mtDNA molecules, including selfish genomes with no advantage for cellular fitness, coexist in a state known as “heteroplasmy.” mtDNA deletions are functionally recessive; high levels of heteroplasmy (more than 60%) are required before a biochemical phenotype appears. In human tissues, we also see a mosaic of cells with respiratory chain deficiency related to different levels of mtDNA deletion. Interestingly, cells with high levels of mtDNA deletions in muscle biopsies show evidence of mitochondrial proliferation, a compensatory mechanism likely triggered by mitochondrial dysfunction. In such circumstances, deleted mtDNA molecules in a given cell will have originated clonally from a single mutant genome. This process is therefore termed “clonal expansion.”

The accumulation of high levels of mtDNA deletions is challenging to explain, especially given that mitophagy should provide quality control to eliminate dysfunctional mitochondria. Studies in human tissues do not allow experimental manipulation, but large-scale mtDNA deletion models in C. elegans have proved to be helpful, showing some conserved characteristics that match the situation in humans, as well as some divergences. Researchers have used a C. elegans strain with a heteroplasmic mtDNA deletion to demonstrate the importance of the mitochondrial unfolded protein response (UPRmt) in allowing clonal expansion of mutant mtDNAs to high heteroplasmy levels. They demonstrate that wild-type mtDNA copy number is tightly regulated, and that the mutant mtDNA molecules hijack endogenous pathways to drive their own replication.

The data suggests that the expansion of mtDNA deletions involves nuclear signaling to upregulate the UPRmt and increase total mtDNA copy number. The nature of the mito-nuclear signal in this C. elegans model may have been the transcription factor ATFS-1 (activating transcription factor associated with stress-1), which fails to be imported by depolarized mitochondria, mediates UPRmt activation by mtDNA deletions. A long-standing hypothesis proposes that deleted mtDNA molecules clonally expand because they replicate more rapidly due to their smaller size. To address this question, researchers examined the behavior of a second, much smaller mtDNA deletion molecule. They found no evidence for a replicative advantage of the smaller genome, and clonal expansion to similar levels as the larger deletion. In human skeletal muscle, mtDNA deletions of different sizes also undergo clonal expansion to the same degree. Furthermore, point mutations that do not change the size of the total mtDNA molecule also successfully expand to deleterious levels, indicating that clonal expansion is not driven by genome size. Thus, similar mechanisms may be operating across organisms. In the worm, this involves mito-nuclear signaling and activation of the UPRmt.

There is some debate over interpretation of results. One paper indicates that UPRmt allows the mutant mtDNA molecules to accumulate by reducing mitophagy. Another demonstrates that the UPRmt induces mitochondrial biogenesis and promotes organelle dynamics (fission and fusion). Both papers show that by downregulating the UPRmt response, mtDNA deletion levels fall, which may allow a therapeutic approach in humans. Could there be a similar mechanism in humans, especially since some features detected in C. elegans are also present in human tissues, including the increase in mitochondrial biogenesis and the lack of relationship between mitochondrial genome size and expansion? It is likely that there will be a similar mechanism to preserve deletions since, as in the worm, deletions persist and accumulate in human tissues, despite an active autophagic quality-control process. Although the UPRmt has not been characterized in humans as it has in the worm, and no equivalent protein to ATFS-1 has been identified in mammals, proteins such as CHOP, HSP-60, ClpP, and mtHSP70 appear to serve similar functions in mammals as those in C. elegans and suggest that a similar mechanism may be present.

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.
It’s Time to Postpone Your Appointment with the Grim Reaper – Article by Gerrard Jayaratnam

It’s Time to Postpone Your Appointment with the Grim Reaper – Article by Gerrard Jayaratnam

Comments 1 comment
The New Renaissance HatGerrard Jayaratnam
******************************

How long would you like to live for? Is there a limit to how long we can live for? These are not questions you hear often, but do not be surprised if they are repeated more frequently in the future. The reason? Life extension. It is the concept of living well beyond the average lifespan. [1]

Humans are already living longer due to vaccines and improvements in sanitation. [2] The World Health Organization reported that the average life expectancy at birth increased from 48 years in 1955 to 65 years in 1995, and is projected to rise to 73 years by 2025. [3] As medical techniques continue to improve, we are more inclined than ever to pursue life extension. [1] Indeed, from the Epic of Gilgamesh to China’s First Emperor, prolonging life has been an ever-present thought in society. [4, 5] Both individuals failed to escape death, but the idea of life extension ironically lives on. Even so, is it truly possible and what should upcoming doctors and scientists consider if they are to join the most ambitious of quests?

The “Horcruxes” of reality 

In the fictional Harry Potter series, “Horcruxes” were objects where people could hide a fragment of their soul in an attempt to take one step towards immortality. [6] Of course, humans cannot split their souls and hide them in objects, but there are several proposed means by which life extension may be achieved. [1] This is a testimony to the progress within the life extension field, but there remains much room for improvement.

Eat less, live more

Caloric restriction (CR) is one proposed method for life extension. [1] In the CALERIE (Comprehensive Assessment of Long term Effects of Reducing Intake of Energy) trial, 218 non-obese humans were randomised to either a control group or an intervention group. The latter aimed for a 25% reduction from baseline energy intake. At the end of the 2-year study period, the intervention group had significantly greater reductions in circulating levels of TNF-α – an inflammatory marker involved in many age-related diseases. [7] Dr Alexander Miras, winner of the 2014 Nutrition Society Cuthbertson Medal for his research on bariatric surgery, acknowledges that the study was a “good first step,” but argues that “the evidence in humans is lacking.” “A definitive RCT (randomised controlled trial),” Dr Miras continues, “would be very hard, if not impossible.” He also spots a glaring consequence of CR. “My personal approach is to avoid caloric restriction as this leads to hunger which is an unpleasant feeling. I would rather live a shorter life, but enjoy my food.”

Manipulating telomerase

One alternative is modulating telomerase activity – as attempted with the anti-ageing TA-65MD® supplement. [8] Telomeres protect the ends of chromosomes [9]; they resemble the aglets on the ends of shoelaces. Just as shoelaces would unravel without the aglet, chromosomes would lose vital DNA sequences in the absence of telomeres. [9] Our cells divide over time, causing telomeres to shorten. Once the telomere becomes too short, cell division ceases, and short telomeres correlate with cellular ageing. [10] Telomerase is an enzyme that can oppose telomere shortening [10] – it was what Hamlet was to King Claudius; what exercise is to obesity; and what junior doctors, in England, will be to Jeremy Hunt.

Reactivating telomerase in telomerase-deficient mice reversed both neurodegeneration and degeneration of other organs. [11] This proved the concept that boosting telomerase activity could have anti-ageing effects, but there is little proof that this occurs in humans. While the mice were telomerase-deficient, humans normally have some telomerase activity. It is like giving food to someone who has been fasting for hours and to someone who has just eaten a three-course meal – the starved individual would unquestionably benefit more. A 12-month long RCT, involving 117 relatively healthy individuals (age range: 53-87), found that low-dose TA-65 significantly increased telomere length when compared to placebo. High-dose TA-65, however, failed to do so. [12]

Dancing with the devil

What is more worrying than treatments that may be ineffective? Side effects. Telomerase is a double-edged sword and by reducing telomere attrition, it can promote unlimited cell division and cancer. [9] Elizabeth Blackburn, co-winner of the 2009 Nobel Prize in Physiology or Medicine for her role in the discovery of telomerase, has doubts about exploiting the enzyme. Speaking to TIME magazine, she said, “Cancers love telomerase, and a number of cancers up-regulate it like crazy. . . . My feeling would be that if I take anything that would push my telomerase up, I’m playing with fire.” [13]

A cauldron of rewards

CR and boosting telomerase activity are just a small sample of life extending techniques, yet there is the notion that such techniques will be intertwined with risks. However, risks are always weighed against rewards, and Gennady Stolyarov, editor-in-chief of The Rational Argumentator and Chief Executive of the Nevada Transhumanist Party, believes life extension would bring “immense and multifaceted” rewards. “The greatest benefit is the continued existence of the individual who remains alive. Each individual has incalculable moral value and is a universe of ideas, experiences, emotions, and memories. When a person dies, that entire universe is extinguished . . . This is the greatest possible loss, and should be averted if at all possible.” Stolyarov also envisages “major savings to healthcare systems” and that “the achievement of significant life extension would inspire many intelligent people to try to solve other age-old problems.”

Former chairman of the President’s Council on Bioethics, Leon Kass, disagrees with this view and argues that mortality is necessary for “treasuring and appreciating all that life brings.” [14] Hence, increased longevity could lead to an overall reduction in productivity over one’s lifetime. Perhaps Kass is correct, but the array of potential benefits makes it seem unwise to prematurely dismiss life extension. In fact, a survey, which examined the opinions of 605 Australians on life extension, highlighted further benefits – 23% of participants said they could “spend more time with family” and 4% cited the opportunity to experience future societies. [15]

Learning from our mistakes

Conversely, life extension may result in people enduring poor health for longer periods. 28% of participants in the Australian survey highlighted this concern. [15] Current trends in life expectancy reinforce their fears. Professor Janet Lord, director of the Institute of Inflammation and Ageing at the University of Birmingham, explains, “Currently, in most countries in the developed world, life expectancy is increasing at approximately 2 years per decade, but healthspan (the years spent in good health) is only increasing at 1.7 years. This has major consequences . . . as more of later life is spent in poor health.” This is a consequence of treating “killer diseases” – according to Dr Felipe Sierra, director of the Division of Aging Biology at the National Institute on Aging. “The current model in biomedicine,” says Dr Sierra, “is to treat one disease at a time. Let’s imagine you have arthritis; cancer; and are starting to develop Alzheimer’s disease. So what do we do? We treat you for cancer. You now live longer with Alzheimer’s disease and arthritis.” A better approach is clear to Dr Sierra who stresses the importance of compression of morbidity – “the goal is to live longer with less time spent being sick.”

Learning from our successes

Even with Dr Sierra’s approach, individual boredom and social implications, including overpopulation, would still be problems.[16] According to Stolyarov, the boredom argument does not hold up when facing “human creativity and discovery.” He believes humans could never truly be bored as “the number of possible pursuits increases far faster than the ability of any individual to pursue.”

In his novel Death is Wrong, Stolyarov explained that the idea that society could not cope with a rapidly expanding population was historically inaccurate. The current population “is the highest it has ever been, and most people live far longer, healthier, prosperous lives than their ancestors did when the Earth’s population was hundreds of times smaller.” [16] If it has been achieved in the past, who is to say our own society – one far more advanced than any before it – cannot adapt?

The verdict

Life extension research is quietly progressing, and there is a good chance that it will eventually come to fruition. Although there are doubts about current techniques, Dr Sierra draws attention to novel interventions, such as rapamycin, which “delay ageing in mice.” He concludes that the next challenge is to “develop measures than can predict whether an intervention works in a short-term assay.” Such measures would provide the scaffolding for future clinical trials that test life extension techniques.

Given what may be gained, it is no surprise that artificially prolonging life is exciting some in the same way the Tree of Knowledge tempted Eve. The impact on society? Impossible to predict. It would undoubtedly be a big risk, but perhaps in this complex and uncertain scenario, we ought to remember the words of the poet Thomas Stearns Eliot: “Only those who will risk going too far can possibly find out how far one can go.” [17]

Gerrard Jayaratnam is a student of Biomedical Science at Imperial College London.

References

  1. Stambler I. A History of Life-Extensionism in the Twentieth Century. Ramat Gan: CreateSpace Independent Publishing Platform; 2014.
  2. National Institute on Aging. Living Longer. 2011. https://www.nia.nih.gov/research/publication/global-health-and-aging/living-longer.
  3. World Health Organization. 50 Facts: Global Health situation and trends 1955-2025. 2013. http://www.who.int/whr/1998/media_centre/50facts/en/.
  4. Encyclopaedia Britannica. Epic of Gilgamesh. 2016. http://www.britannica.com/topic/Epic-of-Gilgamesh.
  5. Lloyd DF. The Man Who Would Cheat Death and Rule the Universe. Vision. 2008. http://www.vision.org/visionmedia/history-shi-huang-emperor-china/5818.aspx.
  6. Rowling JK. Harry Potter and the Half-Blood Prince. London: Bloomsbury Publishing; 2005.
  7. Ravussin E, Redman LM, Rochon J, et al. A 2-Year Randomized Controlled Trial of Human Caloric Restriction: Feasibility and Effects on Predictors of Health Span and Longevity. J Gerontol A Biol Sci Med Sci 2015;70:1097-1104.
  8. A. Sciences. What is TA-65®? (n.d.) [Accessed 3rd April 2016]. https://www.tasciences.com/what-is-ta-65/.
  9. De Jesus BB, Blasco MA. Telomerase at the intersection of cancer and aging. Trends Genet 2013;29:513-520.
  10. A. Sciences. Telomeres and Cellular Aging. (n.d.) [Accessed 3rd April 2016]. https://www.tasciences.com/telomeres-and-cellular-aging/.
  11. Jaskelioff M, Muller FL, Paik JH, et al. Telomerase reactivation reverses tissue degeneration in aged telomerase deficient mice. Nature 2011;469:102-106.
  12. Salvador L, Singaravelu G, Harley CB, et al. A Natural Product Telomerase Activator Lengthens Telomeres in Humans: A Randomized, Double Blind, and Placebo Controlled Study. Rejuvenation Res 2016; ahead of print. doi:10.1089/rej.2015.1793.
  13. Kluger J. The antiaging power of a positive attitude. TIME. 2015.
  14. Than K. The Psychological Strain of Living Forever. Live Science. 2006. http://www.livescience.com/10469-psychological-strain-living.html.
  15. Partridge B, Lucke J, Bartlett H, et al. Ethical, social, and personal implications of extended human lifespan identified by members of the public. Rejuvenation Res 2009;12:351-357.
  16. Stolyarov II G. Death is Wrong. 2nd ed. Carson City, Nevada: Rational Argumentator Press; 2013.
  17. The Huffington Post. 11 Beautiful T.S. Eliot Quotes. 2013. http://www.huffingtonpost.com/2013/09/26/ts-eliot-quotes_n_3996010.html.
Crowdfunding Longevity Science: An Interview with Keith Comito of Lifespan.io – Article by Reason

Crowdfunding Longevity Science: An Interview with Keith Comito of Lifespan.io – Article by Reason

Comments 0 Comment
The New Renaissance HatReason
******************************

Keith Comito leads the volunteers of the non-profit Life Extension Advocacy Foundation (LEAF) and the crowdfunding initiative Lifespan.io, a site I’m sure you’ve seen at least in passing by now. The LEAF crew have put in a lot of effort to help make fundraisers for rejuvenation research projects a success both last year and this year. Two such crowdfunding campaigns are running right now, firstly senolytic drug research at the Major Mouse Testing Program with just a few days left to go, and in its stretch goals, and secondly the recently launched drug discovery for ALT cancers at the SENS Research Foundation. Both tie in to the SENS portfolio of research programs aimed at effective treatment of aging and all age-related conditions. These are large projects when taken as a whole, but the way forward in this as in all things is to pick out smaller, achievable goals, and set out to get them done. Then repeat as necessary.

I recently had the chance to ask Keith Comito a few questions about Lifespan.io, the state of funding for the interesting end of longevity science, and what he envisages for the years ahead. This is an interesting, revolutionary time for the life sciences, in which progress in biotechnology has made early stage research very cheap. A great deal can be accomplished at the cutting edge of medical science given access to an established lab, administrators who can break out small initiatives from the larger goals, smart young researchers, and a few tens of thousands of dollars. It is an age in which we can all help to advance the research we care about, by collaborating and donating, and it has never been easier to just reach out and talk to the scientists involved. If you haven’t taken a look at Lifespan.io and donated to one of the projects there, then you really should. This is a way to move the needle on aging research, and advance that much closer to effective treatments for the causes of aging.

Quote:

What is the Lifespan.io story in brief? What was the spur that made you come together and decide to do your part in the fight against aging?

Lifespan.io began to take shape at the tail end of 2012, as a result of a loose discussion group based in New York which consisted of citizen scientists such as myself and Dr. Oliver Medvedik, supporters of SENS, as well as a few healthcare practitioners. We began having monthly meetings to discuss what could be done to accelerate longevity research (usually in oddball locations like salad bars or subterranean Japanese restaurants befitting our motley crew) and eventually hit upon the idea of crowdfunding. What drew us to this idea was that it was something tangible: a concrete way to move the needle on important research not only through funds, but through raised awareness. It is fine to talk and rabble-rouse about longevity, but we felt such efforts would be much more effective if they were paired with a clear and consistent call to action – a path to walk the walk, so to speak. As this idea coalesced we formed the nonprofit LEAF to support this initiative, and the rest is history. Not every one from the initial discussions in 2012 remained throughout the intervening years, but we are thankful to all who gave us ideas in those early days of the movement.

I’d like to hear your take on why we have to advocate and raise funds at all – why the whole world isn’t rising up in support of treatments for the causes of aging.

The reasons why people and society at large have not prioritized anti-aging research thus far are myriad: fear of radical change, a history of failed attempts making it seem like a fools errand, long timescales making it a difficult issue for election-focused politicians to support, etc. The reason I find most personally interesting relates to cognitive bias – specifically the fact that our built-in mental hardware is ill-equipped to handle questions like “do you want to live 100 more years?” If instead you ask the questions “Do you want to be alive tomorrow?” and “Given that your health and that of your loved ones remains the same, do you suspect your answer to the first question will change tomorrow?”, the answers tend to be more positive.

This leads me to conclude that the state of affairs is not necessarily as depressing for our cause as it might appear, and that reframing the issue of healthy life extension in a way that will inspire and unite the broader populace is possible. Aubrey de Grey has spoken about “Longevity Escape Velocity” in relation to the bootstrapping of biomedical research, but I think the same idea applies to the public perception of life extension as well. The sooner we can galvanize the public to support therapies that yield positive results the easier it will become to invite others to join in this great work. It is all about jump starting the positive feedback loop, and that is why we believe rallying the crowd behind critical research and trumpeting these successes publicly is so vitally important.

What the future plans for Lifespan.io and the Life Extension Advocacy Foundation?

In addition to scaling up our ability to run successful campaigns on Lifespan.io, we look forward to improving our infrastructure at LEAF by bringing on some staff members to join the team. LEAF has largely been a volunteer effort thus far, and having the support of a staff will allow us to take on more campaigns as well as further improve the workflow to create and promote them. This will also free me up personally to more actively pursue potential grand slams for the movement, such as collaborations with prominent YouTube science channels to engage the public and policy related goals like the inclusion of a more useful classification of aging in the ICD-11.

Do you have any favored areas in research at the moment? Is there any particular field for which you’d like to see researchers approaching you for collaboration?

Senolytics is certainly an exciting area of research right now (congratulations Major Mouse Testing Program!), and a combination of successful senolytics with stem cell therapies could be a potential game changer. That being said I’d also like to see projects which address the truly core mechanics of aging, such as how damage is aggregated during stem cell division, and the potential differences in this process between somatic and germ cells. How can the germ line renew itself for essentially infinity? The real mystery here is not that we grow old, but how we are born young.

A related question: where do you see aging and longevity research going over the next few years?

In the near future we will likely continue to see the pursuit of compounds which restore bodily systems failing with age to a more youthful state. This will include validating in higher organisms molecules that have shown this sort of promise: rapamycin, metformin, IL-33 for Alzheimer’s, etc. This approach may sound incremental, but it actually signals a great paradigm shift from the old system of mostly ineffective “preventative measures” such as antioxidants. Things like nicotinamide mononucleotide (NMN), IL-33 – if successful these types of therapies can be applied when you are old, and help restore your bodily systems to youthful levels. That would be a pretty big deal.

Funding is ever the battle in the sciences, and especially for aging. Obviously you have strong opinions on this topic. How can we change this situation for the better?

I believe the key to greater funding, both from public and private sources, is to build up an authentic and powerful grassroots movement in support of healthy life extension. Not only can such a movement raise funds directly, but it also communicates to businesses and governments that this is an issue worth supporting. An instructive example to look at here is the work of Mary Lasker and Sydney Farber to bring about the “War on Cancer”. Through galvanizing the public with efforts such as the “Jimmy Fund”, they effected social and political change on the issue, and helped turn cancer from a pariah disease into a national priority. If we all work together to build an inclusive and action-orientated movement, we can do the same.

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.

 

G. Stolyarov II Interviews Demian Zivkovic Regarding the D.N.A. – Gene Therapies Congress

G. Stolyarov II Interviews Demian Zivkovic Regarding the D.N.A. – Gene Therapies Congress

Comments 0 Comment
The New Renaissance Hat
G. Stolyarov II and Demian Zivkovic
******************************

Mr. Stolyarov invited Demian Zivkovic, President of the Institute of Exponential Sciences (IES), to discuss the forthcoming Designing New Advances (D.N.A.) Gene Therapies Congress in Utrecht, The Netherlands.

The interview took place on Sunday, June 19, 2016, at 11 a.m. US Pacific Time. Watch the recording here.

The D.N.A. Congress is scheduled to occur on July 9, 2016, and will feature speakers such as Oliver Medvedik, Aubrey de Grey, Elizabeth Parrish, Keith Comito, and Tatjana Kochetkova. This event receives the strong endorsement of both The Rational Argumentator and the Nevada Transhumanist Party.

Read the announcement of the D. N. A. Congress here.

Contribute to the fundraiser for the D. N. A. Congress on Indiegogo  and Generosity.

DNA_Interview_CoverDemian 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.

Impacts of Indefinite Life Extension: Answers to Common Questions – Video by G. Stolyarov II

Impacts of Indefinite Life Extension: Answers to Common Questions – Video by G. Stolyarov II

Comments 0 Comment
The New Renaissance Hat
G. Stolyarov II
******************************

As a proponent of attaining indefinite human longevity through the progress of medical science and technology, Mr. Stolyarov is frequently asked to address key questions about the effects that indefinite life extension would have on human incentives, behaviors, and societies. Here, he offers his outlook on what some of these impacts would be.

The specific questions addressed are the following:
1. What would be the benefits of life extension?
2. What drawbacks would life extension pose?
3. Would governments ban indefinite life extension if it is achieved?

References

– “Impacts of Indefinite Life Extension: Answers to Common Questions” – Essay by G. Stolyarov II
– Death is Wrong – Illustrated Children’s Book by G. Stolyarov II

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

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

Comments 0 Comment
The New Renaissance HatInstitute of Exponential Sciences
******************************
 

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.

Which Culture Can Make 120 Years Old the Prime of Life? – Article by Edward Hudgins

Which Culture Can Make 120 Years Old the Prime of Life? – Article by Edward Hudgins

Comments 0 Comment
The New Renaissance HatEdward Hudgins
******************************
Emma Morano, age 116, is the last person alive born in the nineteenth century. New cutting-edge technologies could mean that more than a few people born at the end of the twentieth century will be in the prime of life when they reach that age. But this future will require a culture of reason that is currently dying out in our world.
emma_morano
Is the secret to a long life raw eggs or genetics?
Signorina Morano was born in Italy on Nov 29, 1899. On the recent passing of Susannah Mushatt Jones, who was born a few months before her, Morano inherited the title of world’s oldest person. She still has a ways to go to best the longevity record of the confirmed oldest person who ever lived, Jeanne Calment (1875-1997) who made it to 122.Every oldster offers their secret to long life. Morano attributes her feat to remaining single, adding that she likes to eat raw eggs. But the reason living things die, no matter what their diet, is genetic. Cellular senescence, the fancy word for aging, means the cells of almost every organism are programmed to break down at some point. Almost, because at least one organism, the hydra, a tiny fresh-water animal, seems not to age.

Defying death
Researches are trying to discover what makes the hydra tick so that they find ways to reprogram human cells so we will stop aging. As fantastic as this sounds, it is just one part of a techno-revolution that could allow us to live decades or even centuries longer while retaining our health and mental faculties. Indeed, the week the Morano story ran, both the Washington Post and New York Times featured stories about scientists who approach aging not as an unavoidable part of our nature but as a disease that can be cured.

Since 2001, the cost of sequencing a human genome has dropped from $100 million to just over $1,000. This is spurring an explosion in bio-hacking to figure out how to eliminate ailments like Parkinson’s and Alzheimer’s. We also see nanotechnology dealing with failing kidneys. New high-tech devices deal with blindness and other such disabilities.

An achievement culture and longevity
But this bright future could be fading. Here’s why.

The source of all human achievement is the human mind, our power to understand our world and thus to control it for our own benefit; Ayn Rand called machines “the frozen form of a living intelligence.”

But America, the country that put humans on the Moon, is becoming the stupid country. Despite increased government education spending, test results in science and most other subjects have remained flat for decades. On international ratings, American students are behind students in most other developed countries. It’s a good thing America still has a relatively open immigration policy! Many of the tech people here come from overseas, especially India, because America still offers enough opportunity to make up for its failing schools.

Apollo_11_nasa-69-hc-916am

The deeper problem is found in the prevailing values in our culture. In the 1950s and ‘60s many young people, inspired by the quest for the Moon, aspired to be scientists and engineers, to train their minds. Many went into the research labs of private firms that became the production leaders of the world. It was a culture that celebrated achievement.

Today, many young people, perverted by leftist dogma, hunger to be political enforcers, to train themselves in power and manipulation. Many go into campaigns and government to wrest wealth from producers to pay for “entitlements,” and to make the country more “equal” by tearing producers down. A growing portion of the culture demonizes achievement and envious of success.

Were they to live for 120 healthy years, individuals with the older, pro-achievement values would find their souls even more enriched by their extended careers of achievement. But individuals in the newer, anti-achievement culture would find their souls embittered as they focused enviously on degrading their productive fellows.

All who want long lives worth living need to not only promote science but also the values of reason and achievement. That’s the way to create a pro-longevity culture.

Explore

Edward Hudgins, “Google, Entrepreneurs, and Living 500 Years.” March 12, 2015.

Edward Hudgins, “How Anti-Individualist Fallacies Prevent Us from Curing Death.” April 22, 2015.

Bradley Doucet, “Book Review: The Green-Eyed Monster.” March 2008.

David Kelley, “Hatred of the Good.” April 2008.

Dr. Edward Hudgins directs advocacy and is a senior scholar for The Atlas Society, the center for Objectivism in Washington, D.C.

Copyright The Atlas Society. For more information, please visit www.atlassociety.org.