Browsed by
Tag: indefinite life extension

Highlights #1 – First Virtual Debate Among U.S. Transhumanist Party Presidential Candidates – July 6, 2019

Highlights #1 – First Virtual Debate Among U.S. Transhumanist Party Presidential Candidates – July 6, 2019

Rachel Haywire
Johannon Ben Zion
Charles Holsopple
Moderated by Gennady Stolyarov II


Watch highlights from the first virtual debate among U.S. Transhumanist Party / Transhuman Party (USTP) candidates for President of the United States, which took place on Saturday, July 6, 2019, at 3 p.m. U.S. Pacific Time.

Candidates Rachel Haywire, Johannon Ben Zion, and Charles Holsopple provided their introductory statements and discussed how their platforms reflect the Core Ideals of the USTP.

This highlights reel was created by Tom Ross, the USTP Director of Media Production. Watch the full 3-hour debate here.

Learn about the USTP candidates here.

View individual candidate profiles:

Johannon Ben Zion
Rachel Haywire
Charles Holsopple

Join the U.S. Transhumanist Party / Transhuman Party for free, no matter where you reside. Apply in less than a minute here.

Those who join the USTP by August 10, 2019, will be eligible to vote in the Electronic Primary on August 11-17, 2019.

First Virtual Debate Among U.S. Transhumanist Party Presidential Candidates – July 6, 2019

First Virtual Debate Among U.S. Transhumanist Party Presidential Candidates – July 6, 2019

Rachel Haywire
Johannon Ben Zion
Charles Holsopple
Moderated by Gennady Stolyarov II


The first virtual debate among U.S. Transhumanist Party / Transhuman Party candidates for President of the United States took place on Saturday, July 6, 2019, at 3 p.m. U.S. Pacific Time. Watch the debate on YouTube here.

Candidates Rachel Haywire, Johannon Ben Zion, and Charles Holsopple discussed how their platforms reflect the Core Ideals of the USTP and also answered selected questions from the public.

Learn about the USTP candidates here.

View individual candidate profiles:

Johannon Ben Zion
Rachel Haywire
Charles Holsopple

Join the U.S. Transhumanist Party / Transhuman Party for free, no matter where you reside. Apply in less than a minute here.

Those who join the USTP by August 10, 2019, will be eligible to vote in the Electronic Primary on August 11-17, 2019.

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

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

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

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
******************************
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.