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The U.S. Transhumanist Party – Four Years of Advocating for the Future – Gennady Stolyarov II Presents at RAAD Fest 2018

The U.S. Transhumanist Party – Four Years of Advocating for the Future – Gennady Stolyarov II Presents at RAAD Fest 2018

Gennady Stolyarov II


This is the video that American voters need to see prior to the 2018 elections. Watch it here.

On October 7, 2018, the U.S. Transhumanist Party marked its four-year anniversary. On September 21, 2018, at RAAD Fest 2018 in San Diego, CA, Chairman Gennady Stolyarov II spoke in advance of this occasion by highlighting the U.S. Transhumanist Party’s recent achievements – including a doubling in membership over the past year, the revived Enlightenment Salons, a Platform that rivals those of the two major political parties, and Mr. Stolyarov’s own candidacy in 2018.

Join the U.S. Transhumanist Party for free, no matter where you reside. Fill out our free Membership Application Form. It takes less than a minute!

Visit the U.S. Transhumanist Party Values page.

See the U.S. Transhumanist Party Platform.

See the Transhumanist Bill of Rights, Version 2.0.

Watch the U.S. Transhumanist Party’s subsequent meeting at RAAD Fest 2018 on September 22, 2018 here.

View Mr. Stolyarov’s official page for his candidacy for the Indian Hills General Improvement District (IHGID) Board of Trustees.

What It Will Be Like to Be an 85-Year-Old in the 2070s – Article by Scott Emptage

What It Will Be Like to Be an 85-Year-Old in the 2070s – Article by Scott Emptage

Scott Emptage


I will be 85 sometime in the early 2070s. It seems like a mirage, an impossible thing, but the future eventually arrives regardless of whatever you or I might think about it. We all have a vision of what it is to be 85 today, informed by our interactions with elder family members, if nothing else. People at that age are greatly impacted by aging. They falter, their minds are often slowed. They are physically weak, in need of aid. Perhaps that is why we find it hard to put ourselves into that position; it isn’t a pleasant topic to think about. Four decades out into the future may as well be a science-fiction novel, a faraway land, a tale told to children, for all the influence it has on our present considerations. There is no weight to it.

When I am 85, there will have been next to no senescent cells in my body for going on thirty years. I bear only a small fraction of the inflammatory burden of older people of past generations. I paid for the products of companies descended from Oisin Biotechnologies and Unity Biotechnology, every few years wiping away the accumulation of senescent cells, each new approach more effective than the last. Eventually, I took one of the permanent gene therapy options, made possible by biochemical discrimination between short-term beneficial senescence and long-term harmful senescence, and then there was little need for ongoing treatments. Artificial DNA machinery floats in every cell, a backup for the normal mechanisms of apoptosis, triggered by lingering senescence.

When I am 85, the senolytic DNA machinery will be far from the only addition to my cells. I underwent a half dozen gene therapies over the years. I picked the most useful of the many more that were available, starting once the price fell into the affordable-but-painful range, after the initial frenzy of high-cost treatments subsided into business as usual. My cholesterol transport system is enhanced to attack atherosclerotic lesions, my muscle maintenance and neurogenesis operate at levels far above what was once a normal range for my age, and my mitochondria are both enhanced in operation and well-protected against damage by additional copies of mitochondrial genes backed up elsewhere in the cell. Some of these additions were rendered moot by later advances in medicine, but they get the job done.

When I am 85, my thymus will be as active as that of a 10-year-old child. Gene and cell therapies were applied over the past few decades, and as a result my immune system is well-gardened, in good shape. A combination of replacement hematopoietic stem cells, applied once a decade, the enhanced thymus, and periodic targeted destruction of problem immune cells keeps at bay most of the age-related decline in immune function, most of the growth in inflammation. The downside is that age-related autoimmunity has now become a whole lot more complex when it does occur, but even that can be dealt with by destroying and recreating the immune system. By the 2030s this was a day-long procedure with little accompanying risk, and the price fell thereafter.

When I am 85, atherosclerosis will be curable, preventable, and reversible, and that will have been the case for a few decades. There are five or six different viable approaches in the marketplace, all of which basically work. I used several of their predecessors back in the day, as well. Most people in the wealthier parts of the world have arteries nearly free from the buildup of fat and calcification. Cardiovascular disease with age now has a very different character, focused more failure of tissue maintenance and muscle strength and the remaining small portions of hypertension that are still problematic for some individuals. But that too can be effectively postponed through a variety of regenerative therapies.

When I am 85, there will be an insignificant level of cross-linking in most of my tissues, as was the case since my early 60s. My skin has the old-young look of someone who went a fair way down the path before being rescued. Not that I care much about that – I’m much more interested in the state of my blood vessels, the degree to which they are stiff and dysfunctional. That is why removal of cross-links is valuable. That is the reason to keep on taking the yearly treatments of cross-link breakers, or undergo one of the permanent gene therapies to have your cells produce protective enzymes as needed.

When I am 85, I will have a three-decade patchwork history of treatments to partially clear this form of amyloid or that component of lipofuscin. I will not suffer Alzheimer’s disease. I will not suffer any of the common forms of amyloidosis. They are controlled. There is such a breadth of molecular waste, however: while the important ones are addressed, plenty more remain. This is one of the continuing serious impacts to the health of older individuals, and a highly active area of research and development.

When I am 85, I will be the experienced veteran of several potentially serious incidences of cancer, all of which were identified early and eradicated by a targeted therapy that produced minimal side-effects. The therapies evolve rapidly over the years: a bewildering range of hyper-efficient immunotherapies, as well as treatments that sabotage telomere lengthening or other commonalities shared by all cancer cells. They were outpatient procedures, simple and quick, with a few follow-up visits, so routine that they obscured the point that I would be dead several times over without them. The individual rejuvenation technologies I availed myself of over the years were narrowly focused, not perfect, and not available as early as I would have liked. Cancer is an inevitable side-effect of decades of a mix of greater tissue maintenance and unrepaired damage.

Do we know today what the state of health of a well-kept 85-year-old will be in the 2050s? No. It is next to impossible to say how the differences noted above will perform in the real world. They are all on the near horizon, however. The major causes of age-related death today will be largely controlled and cured in the 2050s, at least for those in wealthier regions. If you are in your 40s today, and fortunate enough to live in one of those wealthier region, then it is a given that you will not die from Alzheimer’s disease. You will not suffer from other common age-related amyloidosis conditions. Atherosclerosis will be reliably controlled before it might kill you. Inflammatory conditions of aging will be a shadow of what they once were, because of senolytic therapies presently under development. Your immune system will be restored and bolstered. The stem cells in at least your bone marrow and muscles will be periodically augmented. The cross-links that cause stiffening of tissues will be removed. Scores of other issues in aging process, both large and small, will have useful solutions available in the broader medical marketplace. We will all live longer and in better health as a result, but no-one will be able to say for just how long until this all is tried.

Scott Emptage is an anti-aging activist in the United Kingdom. 

U.S. Transhumanist Party Chairman Gennady Stolyarov II Answers Common Interview Questions

U.S. Transhumanist Party Chairman Gennady Stolyarov II Answers Common Interview Questions

Gennady Stolyarov II


Gennady Stolyarov II, Chairman of the U.S. Transhumanist Party and Chief Executive of the Nevada Transhumanist Party, answers questions posed by Francesco Sacco, which are representative of common points of inquiry regarding transhumanism and the Transhumanist Party:

1. What is Transhumanism and what inspired you to follow it?
2. What are the long-term goals of the Transhumanist party?
3. What are your thoughts on death and eternal life through technological enhancements?
4. Do you feel there are any disadvantages to having access to the cure for death? What advantages are there?

Become a member of the U.S. Transhumanist Party for free, no matter where you reside. Fill out our Membership Application Form here.

See Mr. Stolyarov’s presentation, “The U.S. Transhumanist Party: Pursuing a Peaceful Political Revolution for Longevity“.

I am the Lifespan – Video by G. Stolyarov II

I am the Lifespan – Video by G. Stolyarov II

G. Stolyarov II


Gennady Stolyarov II, Chairman of the United States Transhumanist Party, discusses why longevity research is crucial, and how our generation stands on the threshold of finally dealing a decisive blow to the age-old enemies of aging and death, which have destroyed great human minds since the emergence of our species.

This video is part of the #IAmTheLifespan campaign, coordinated by Lifespan.io and the Life Extension Advocacy Foundation (LEAF) for Longevity Month, October 2017. Read more about this campaign here.

Become a member of the U.S. Transhumanist Party for free, no matter where you reside. Fill out our Membership Application Form here.

Become a Foreign Ambassador for the U.S. Transhumanist Party. Apply here.

Visit the website of the U.S. Transhumanist Party here.

Activating Transhumanism – James Strole Interviews G. Stolyarov II on RAAD Fest

Activating Transhumanism – James Strole Interviews G. Stolyarov II on RAAD Fest

The New Renaissance Hat
G. Stolyarov II and James Strole
June 24, 2017
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U.S. Transhumanist Party Chairman Gennady Stolyarov II was interviewed by James Strole regarding the forthcoming RAAD Fest 2017 in San Diego, California, which will occur on August 9-13, 2017. This interview addressed Mr. Stolyarov’s impressions of RAAD Fest 2016, his goals for the transhumanist movement in politics, and how various perspectives within the transhumanist and life-extensionist movement can benefit from interfacing with one another. Watch the video of the interview on YouTube or below.

At RAAD Fest 2017, Mr. Stolyarov will be moderating a panel consisting of transhumanist philosophers, researchers, and activists – including Zoltan Istvan, Dr. Ben Goertzel, Dr. Max More, and Dr. Natasha Vita-More. You can see the full RAAD Fest schedule here.

The panel moderated by Mr. Stolyarov will occur at 10 a.m.  on Friday, August 11, 2017. Machine augmentation of human bodies and minds will be one topic of discussion; transhumanist politics will be another. As previously announced, Mr. Stolyarov will inaugurate the panel with a brief presentation entitled “The U.S. Transhumanist Party: Pursuing a Peaceful Political Revolution for Longevity”.

Members of the U.S. Transhumanist Party: When registering for RAAD Fest, you can use the special discount code TRANSHUMAN, which will now reduce the cost of registration to $497.

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

The New Renaissance HatReason
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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.
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

The New Renaissance Hat
G. Stolyarov II
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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

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

The New Renaissance HatEdward Hudgins
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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.

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

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

The New Renaissance Hat
G. Stolyarov II
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As a proponent of attaining indefinite human longevity through the progress of medical science and technology, I am frequently asked to address key questions about the effects that indefinite life extension would have on human incentives, behaviors, and societies. Here, I offer my outlook on what some of these impacts would be.

What would be the benefits of life extension?

(1) The greatest benefit of life extension is the continued existence of the individual who remains alive. Each individual – apart from the worst criminals – has incalculable moral value and is a universe of ideas, experiences, emotions, and memories. When a person dies, that entire universe is extinguished, and, to the person who dies, everything is lost and not even a memory remains. It is as if the individual never existed at all. This is the greatest possible loss and should be averted if at all possible. The rest of us, of course, also lose the possible benefits and opportunities of interacting with that individual.

(2) People would be able to accomplish far more with longer lifespans. They could pursue multiple careers and multi-year personal projects and could reliably accumulate enough resources to sustainably enjoy life. They could develop their intellectual, physical, and relational capabilities to the fullest. Furthermore, they would exhibit longer-term orientations, since they could expect to remain to live with the consequences of decisions many decades and centuries from now. I expect that a world of longer-lived individuals would involve far less pollution, corruption, fraud, hierarchical oppression, destruction of other species, and short-term exploitation of other humans. Prudence, foresight, and pursuit of respectful, symbiotic interactions would prevail. People would tend to live in more reflective, measured, and temperate ways instead of seeking to haphazardly cram enjoyment and activity into the tiny slivers of life they have now. At the same time, they would also be more open to experimentation with new projects and ideas, since they would have more time to devote to such exploratory behaviors.

(3) Upon becoming adults, people would no longer live life in strict stages, and the normative societal expectations of “what one should do with one’s life” at a particular stage would relax considerably. If a person at age 80 is biologically indistinguishable from a person at age 20, the strict generational divides of today would dissipate, allowing a much greater diversity of human interactions. People will tend to become more tolerant and cosmopolitan, having more time to explore other ways of living and to understand those who are different from them.

(4) Technological, scientific, and economic progress would accelerate rapidly, because precious intellectual capital would not be lost to the ravages of death and disease. Longer-lived humans would be more likely to invest in projects that would materialize over the course of decades, including space travel and colonization, geo-engineering and terraforming, prevention of asteroid impacts and other natural disasters, safe nuclear disarmament and disposal of nuclear waste, and long-term preservation of the human species. The focus of most intelligent people would shift from meeting quarterly or annual business earnings goals and toward time- and resource-intensive projects that could avert existential dangers to humankind and also expand humanity’s reach, knowledge, and benevolence. The achievement of significant life extension would inspire many intelligent people to try to solve other age-old problems instead of resigning to the perception of their inevitability.

(5) Major savings to health-care systems, both private and governmental, would result if the largest expenses – which occur in the last years of life today, in the attempt to fight a losing battle against the diseases of old age – are replaced by periodic and relatively inexpensive rejuvenation and maintenance treatments to forestall the advent of biological senescence altogether. Health care could truly become about the pursuit of sustainable good health instead of a last-ditch effort against the onslaught of diseases that accompanies old age today. Furthermore, the strain on public pensions would be alleviated as advanced age would cease to be a barrier to work.

What drawbacks would life extension pose?

I do not see true drawbacks to life extension. Certainly, the world and all human societies would change significantly, and there would be some upheaval as old business models and ways of living are replaced by new ones. However, this has happened with every major technological advance in history, and in the end the benefits far outweigh any transitional costs. For the people who remain alive, the avoidance of the greatest loss of all will be well worth it, and the human capacity for adaptation and growth in the face of new circumstances is and has always been remarkable.  Furthermore, the continued presence of individuals from older generations would render this transition far more humane than any other throughout history. After all, entire generations would no longer be swept away by the ravages of time. They could persist and preserve their knowledge and experience as anchors during times of change.

Every day, approximately 150,000 people die, and approximately 100,000 of them die from causes related to senescence. If those deaths can be averted and the advent of indefinite life extension accelerated by even a few days, hundreds of thousands of irreplaceable individual universes would be preserved. This is worth paying even substantial costs in my view, but, fortunately, I think the other – economic and societal – effects that accompany life extension would be overwhelmingly positive as well.

As Death is Wrong, my illustrated children’s book on the prospects for life extension, points out, “Death is the enemy of us all, to be fought with medicine, science, and technology.” The book discusses the benefits of life extension in a language and format accessible to most children of ages 8 or older. Death is Wrong also outlines some common arguments against life extension and reasonable responses to them.  For instance, I respond to the common overpopulation argument as follows: “human population is the highest it has ever been, and most people live far longer, healthier, more prosperous lives than their ancestors did when the Earth’s population was hundreds of times smaller. Technology gives us far more food, energy, and living space than our ancestors had, and the growth in population only gives us more smart people who can create even more technologies to benefit us all. Besides, humans ought to build more settlements on land, on water, underwater, and in space. Space travel could also save the human species if the Earth were hit by a massive asteroid that could wipe out complex life. ” I respond to the boredom argument by stating that, due to human creativity and discovery, the number of possible pursuits increases far faster than the ability of any individual to pursue them. For instance, thousands more books are published every day than a single person could possibly read.

ELFC_Death_is_Wrong

Would governments ban indefinite life extension if it is achieved?

Once life-extending treatments are developed and publicly available, national governments would not be effectively able to ban them, since there will not be a single medicine or procedure that would accomplish indefinite lifespans. Rather, indefinite life extension would be achieved through a combination of treatments, beating back today’s deadliest diseases using techniques that would not be limited in their application to people who explicitly want to live longer. (For instance, people who do not harbor that particular desire but do want to get rid of cancer, heart disease, or Alzheimer’s disease that may afflict them or their loved ones, would also benefit from the same treatments.) These treatments would be as embedded in the healthcare systems of the future as over-the-counter drugs like aspirin and ibuprofen are today; it would be practically impossible to ban them, and countries that did would face massive black markets or people traveling abroad to receive the same treatments.

Furthermore, genuine healthy life extension could be a great fiscal solution for many welfare states today, which are finding themselves with unsustainable burdens pertaining to old-age healthcare and pensions. The majority of health-care costs are expended to keep frail people alive a little bit longer and to fight an expensive and ultimately losing battle against the diseases of old age. The only way dramatic life extension could occur is if regular and relatively inexpensive maintenance (made inexpensive through the exponential progress of information technologies and bio/nanotechnology) prevented the decline of the body to such a stage where expensive, losing battles needed to be fought at all. Replacing the current extremely expensive end-of-life medical care with periodic rejuvenation and maintenance would be a great cost-saver and may avert a major fiscal crisis.

What concerns me is not governments banning life-extension technologies once they are developed, but rather existing political systems (and their associated politically connected established private institutions) creating barriers to the emergence of those technologies in the first place. Most of those barriers are probably inadvertent – for instance, the FDA’s approval process in the United States premised on a model of medicines and treatments that must focus on single diseases rather than the biological aging process as a whole. However, there have been influential “bioethicists”, such as Leon Kass, Daniel Callahan, and Sherwin Nuland, who have explicitly and extensively spoken and written against healthy life extension. It is important to win the contest of ideas so that public opinion does not give encouragement to the “bioconservative” bioethicists who want to use the political process to perpetuate the old cycle of life, death, and decay – where each generation must be swept away by the ravages of senescence. We must stand for life and against age-old rationalizations of our own demise.

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.

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.