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U.S. Transhumanist Party Q&A Session – October 21, 2017

U.S. Transhumanist Party Q&A Session – October 21, 2017

G. Stolyarov II
Martin van der Kroon
Sean Singh
B.J. Murphy


In this interactive question-and-answer session, which occurred at 1 p.m. U.S. Pacific Time on Saturday, October 21, 2017, U.S. Transhumanist Party Officers provided an updated view of the Transhumanist Party’s projects, operations, and achievements, in response to audience questions. Because October is Longevity Month, this Q&A session had a life-extension theme but also delved into various other areas, including how to address conspiracy theories and various approaches toward diet, nutrition, and cultural norms regarding food consumption. The Q&A session has been archived on YouTube here.

The following U.S. Transhumanist Party Officers took part in this Q&A session:

– Gennady Stolyarov II, Chairman
– Martin van der Kroon, Director of Recruitment
– Sean Singh, Director of Applied Innovation
– B.J. Murphy, Director of Social Media

The YouTube question/comment chat for this Q&A session has been archived here and is also provided below.

Visit the U.S. Transhumanist Party website here.

Visit the U.S. Transhumanist Party Facebook page here.

See the U.S. Transhumanist Party FAQ here.

Become a member of the U.S. Transhumanist Party for free, no matter where you reside.

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

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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.

Charlie Gard’s Parents Are Forced to Stop Fighting for Their Dying Baby – Article by Marianne March

Charlie Gard’s Parents Are Forced to Stop Fighting for Their Dying Baby – Article by Marianne March

The New Renaissance Hat
Marianne March
July 27, 2017
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I cannot imagine the pain Charlie Gard’s parents are feeling now, as they savor their last moments with their precious child. Charlie is 11 months old and he’s dying.

Chris and Connie have been fighting for months to get treatment for Charlie, ever since he was diagnosed with a rare genetic condition, mitochondrial DNA depletion syndrome. But they have been forced to give up that fight.

I can’t imagine their pain, but I can imagine their fury because I share it.

From the Hospital to the Courts

Charlie is not mine. I’ve never met him or anyone who knows him. Yet I am furious with the British government for refusing to allow his parents to take their dying son to the United States for treatment: a therapy trial, his last and only hope.

No further recourse was available in the UK, but an American doctor was ready to try to help him at Columbia University Medical Center. Charlie’s parents raised £1.4 million through crowdfunding; they had the money to take him to the US by air ambulance.

But doctors at Great Ormond Street Hospital in London didn’t like that idea. They said it wouldn’t help, that the American therapy was experimental. They said the baby’s life support should just stop.

On April 11th, a British High Court judge ruled with the doctors, empowering them to turn off Charlie’s life-support machines. His mother screamed “no” when she heard the verdict.

There was a petition with more than 110,000 names on it. People wrote letters to the Prime Minister, calling on her to release Charlie from Great Ormond Street’s care. The pope said he was praying for Charlie’s parents, “hoping that their desire to accompany and care for their own child to the end is not ignored.”

And now Charlie is out of time.

Even US President Trump tweeted that “If we can help little #CharlieGard, as per our friends in the U.K. and the Pope, we would be delighted to do so.”

Charlie’s parents challenged the decision in the Court of Appeals, the Supreme Court, and the European Court of Human Rights.

All to no avail. The Courts would not allow them to try to save their baby’s life.

Who Can Call This Justice?

And now Charlie is out of time. According to the BBC, “US neurologist Dr. Michio Hirano had said he was no longer willing to offer the baby experimental therapy after he saw the results of a new MRI scan last week.”

It’s possible that Charlie’s doctors were right, that experimental treatment wouldn’t have helped (although his parents don’t think so, nor do American and Italian doctors). But what harm could it have done when he’s dying anyway? And if his parents had the means to give him one last chance, why shouldn’t they exercise their right to do so? They belong to Charlie just as he belongs to them, and no one but Chris and Connie should get the final say on his medical care.

I never really knew what people meant by the phrase “death panels” before. It was just a term bandied about by talking heads and political personalities. It’s chilling how well it applies in this instance: a group of bureaucrats that sits around deciding who is worthy of medical care.

I don’t know how the power slipped away from the individual, whether taken by force or given away with applause, but this is outrageous. And it’s wrong.

Read with a Box of Tissues

I will leave you with the words of Connie Yates, Charlie’s mom:

Due to the deterioration in his muscles, there is now no way back for Charlie. Time that has been wasted. It is time that has sadly gone against him.

We want people to realise that we have been speaking to parents whose children were just like Charlie before starting treatment and now some of them are walking around like normal children. We wanted Charlie to have that chance too.

All we wanted to do was take Charlie from one world renowned hospital to another world renowned hospital in the attempt to save his life and to be treated by the world leader in mitochondrial disease. We feel that we should have been trusted as parents to do so but we will always know in our hearts that we did the very best for Charlie and I hope that he is proud of us for fighting his corner.

Charlie had a real chance of getting better. It’s now unfortunately too late for him but it’s not too late for others with this horrible disease and other diseases. We will continue to help and support families of ill children and try and make Charlie live on in the lives of others. We owe it to him to not let his life be in vain.

Despite the way that our beautiful son has been spoken about sometimes, as if he not worthy of a chance at life, our son is an absolute WARRIOR and we could not be prouder of him and we will miss him terribly. One little boy has brought the world together and whatever people’s opinions are, no one can deny the impact our beautiful son has had on the world and his legacy will never ever die.

We are now going to spend our last precious moments with our son Charlie, who unfortunately won’t make his 1st birthday in just under 2 weeks’ time, and we would ask that our privacy is respected at this very difficult time.

Mummy and Daddy love you so much Charlie, we always have and we always will and we are so sorry that we couldn’t save you.”

Marianne March is a recent graduate of Georgia State University, where she majored in Public Policy, with a minor in Economics. Follow her on twitter @mari_tweets.

This article was published by The Foundation for Economic Education and may be freely distributed, subject to a Creative Commons Attribution 4.0 International License, which requires that credit be given to the author. Read the original article.

An Interview with Kelsey Moody of Ichor Therapeutics, Bringing a SENS Therapy for Macular Degeneration to the Clinic – Article by Reason

An Interview with Kelsey Moody of Ichor Therapeutics, Bringing a SENS Therapy for Macular Degeneration to the Clinic – Article by Reason

The New Renaissance HatReason
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As I mentioned last week, earlier this year Fight Aging! invested a modest amount in the Ichor Therapeutics initiative to develop a treatment for macular degeneration, joining a number of other amateur and professional investors in helping to get this venture started. The approach taken here is based on the results of research carried out at the Methuselah Foundation and SENS Research Foundation over much of the past decade, funded by philanthropists and the support of our community of longevity science enthusiasts. This is how we succeed in building the future: medical science in the laboratory leads to medical development in startup companies, each new stage bringing treatments capable of repairing specific forms of age-related molecular damage that much closer to the clinic.

Ichor Therapeutics is one of a growing number of success stories to emerge from the SENS rejuvenation research community. Young scientists, advocates, and donors involved in earlier projects – years ago now – have gone on to build their own ventures, while retaining an interest in stepping up to do something meaningful to help bring an end to aging. Back in 2010, Kelsey Moody worked on the LysoSENS project to find ways to break down damaging metabolic waste in old tissues; fast-forward six years, and he is the now the CEO of a successful small biotechnology company with a great team, taking that very same technology and putting it to good use. I recently had the chance to ask Kelsey a few questions about the future of SENS rejuvenation research, as well as how the Ichor scientists intend to construct a new class of therapy for macular degeneration, one based on removing one of the root causes of the condition.

Quote:

Who are the people behind Ichor Therapeutics? How did you meet and decide that this was the thing to do? Why macular degeneration as a target?

People have always been the focus of Ichor. Since day one we have worked to create a positive environment that cultivates a product-oriented research focus and emphasizes autonomy and personal accountability for work. As a result, ambitious self-starters tend to find their way to Ichor and remain here. However, we recognized early on that just filling a lab with a bunch of blue-eyed bushy tailed young up-and-comers is not sufficient to develop a robust, mature, translational pipeline. We have augmented our team with a number of critical staff members who are seasoned pharma operators, including our Quality Assurance Director and General Counsel.

Age-related macular degeneration (AMD) was chosen as a target because we believe it is the closest SENS therapy to the clinic. While we obviously have an interest in providing cures for the patients suffering from AMD and are attracted to the large market opportunities such a treatment could bring, our broader interest is in validating the entire SENS paradigm. We believe that Aubrey de Grey continues to receive excessive criticism because nothing spun out of SENS has ever made it into a legitimate pre-clinical pipeline, much less to the bedside. However, this does not mean he is wrong. Our goal is to be the first group to bring a SENS inspired therapy into the clinic and in doing so, silence critics and generate new energy and capital for this cause.

I understand there’s a lengthy origin story for the approach you are taking to treat AMD; it’d be great to hear some of it.

Our approach to treating AMD is based on the hypothesis that cellular junk that accumulates over the lifespan significantly contributes to the onset and progression of AMD. Our goal is to periodically reduce the burden of the junk so it never accumulates to levels sufficient to induce pathology. The strategy to accomplish this calls for the identification of enzymes that can break down the junk in a physiological setting, and the engineering of these enzymes such that they can break down the target in the correct organelle of the correct cell without appreciable collateral damage to healthy cells or tissue.

Methuselah Foundation and SENS Research Foundation did excellent work in establishing this program nearly a decade ago. They successfully identified a number of candidate enzymes that could break down the molecular junk, but reported that the targeting systems evaluated failed to deliver these enzymes to the appropriate organelles and cells. My group reevaluated these findings, and discovered that these findings were flawed. The delivery failure could be entirely attributed to a subtle, yet highly significant difference between how the target cells behave outside of the body as compared to inside the body. It turned out that the approach was in fact valid, it was the cell based assay that had been used that was flawed. This discovery was striking enough that SENS Research Foundation provided Ichor with funding and a material and technology transfer agreement to reassess the technology, and over $700,000 in directed program investments and grants have been received in the last year or two.

You recently completed a round of funding for the AMD work; what is the plan for the next year or so?

The new funds will allow us to develop a portfolio of enzyme therapy candidates to treat AMD. We will obtain critical data necessary to secure follow-on investment including in vitro studies (cell culture studies to confirm mechanism of action and cytotoxicity) and pivotal proof-of-concept in vivo studies, such as toxicity, PK/PD (how long the enzyme stays in the body and where), and efficacy. We will also be restructuring the company (reincorporating an IP holding company in Delaware, ensuring all contracts are up to date and audited) and ensuring our IP position is on solid footing (licensing in several related patents from existing collaborators, and filing several provisional patents from our intramural work). Collectively, we believe these efforts will position us to obtain series A for investigational new drug (IND) enabling pre-clinical studies.

You’ve been involved in the rejuvenation research community for quite some time now. What is your take on the bigger picture of SENS and the goal of ending aging?

This is a loaded question. What I can say is that the medical establishment has made great progress in the treatment of infectious disease through the development of antibiotics, vaccines, and hygiene programs. However, similar progress has not been realized for the diseases of old age, despite exorbitant expenditures. I have chosen to work in this space because I think a different approach is necessary, and it is here that I believe my companies and I can be the most impactful. I think SENS provides a good framework within which to ask and answer questions.

What do you see as the best approach to getting nascent SENS technologies like this one out of the laboratory and into the clinic?

We need more people who fully understand, in a highly detailed way, what a real translational path looks like. To take on projects like this, being a good scientist is not enough. We need people who can speak business, science, medicine, and legal, and apply these diverse disciplines to a well articulated, focused product or problem. There is no shortage of people who partially understand some of these, but the details are not somewhat important – they are all that matter for success in this space.

Another area is for investors. Some of the projects that come across my desk for review are truly abysmal, yet I have seen projects that are clearly elaborate hoaxes or outright scams (to anyone who has stepped foot in a laboratory) get funded to the tune of hundreds of thousands of dollars or more. While it is perfectly reasonable for high net worth individuals to gamble on moon shots in the anti-aging space (and I am ever grateful for the investors who have taken such a gamble on us) even aggressive development strategies should have some basis in reality. This is especially true as more and more high tech and internet investors move into the space.

If this works stupendously well, what comes next for Ichor Therapeutics?

I really want to get back into stem-cell research, but I basically need a blank check and a strong knowledge of the regulatory path to clinic before I feel comfortable moving into the space. A successful AMD exit would accomplish both of these goals, and position us to pivot to cell-based therapies.

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

The New Renaissance Hat
G. Stolyarov II and Demian Zivkovic
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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.

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

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

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

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

D.N.A CONGRESS PRESS RELEASE:

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

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

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

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

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

 

DNADemian Zivkovic

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

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

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

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

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

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

About Institute of Exponential Sciences

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

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

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

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

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

A Most Interesting Data Set Covering the Longevity of Polish Elite Athletes Across Much of the 20th Century – Article by Reason

A Most Interesting Data Set Covering the Longevity of Polish Elite Athletes Across Much of the 20th Century – Article by Reason

The New Renaissance HatReason
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Today I noticed an open access paper in which the authors examine mortality data for Polish Olympic athletes over the past 90 years or so, and compare it with established historical data for the general population. This blends two topics that are occasionally covered here at Fight Aging!: firstly, the growth in human life expectancy in recent history and its causes, and secondly the topic of how regular exercise and life expectancy interact. It is the present consensus that elite athletes, those at the top of their profession, live longer than the rest of us, but it remains open to debate as to whether this is because more exercise is better, or because very robust people who would have lived longer anyway are more likely to enter the world of professional athletics. Researchers want to map the dose-response curve for exercise, in other words. Even though there is very good, very solid evidence for the benefits of regular moderate exercise versus being sedentary, going beyond that to a more nuanced view of what more or less exercise does for health is a challenging goal given the starting point of statistical snapshots of data from various study populations.

Studying the history of life expectancy isn’t much easier, though there the challenges tend to revolve around the ever-decreasing quality of data as you look further back in time. The 20th century marked transitions from hopeful aspiration to solid accomplishment in all fields of medicine, too many profound advances in the capabilities of medical science and practice to list here. As the decades passed, this important progress focused ever more on treatments for age-related conditions. An individual born in the US in 1900 suffered through the end of the era of poor control of infectious disease, prior to modern antibiotics and antiviral drugs, and likely benefited little from later progress towards better control of heart disease and other common age-related diseases. An individual born in the US in 1950, on the other hand, enjoyed a youth with comparatively little fear of disease, and is probably still alive today, with access to far more capable therapies than existed even a couple of decades ago.

Given all of this, one of the interesting things to note in the analysis of the Polish data is that the elite athletes born in the early 20th century appear to have a lower rate of aging than the general population, as determined by a slower rise in mortality over time, but that this difference between athletes and the average individual is greatly diminished for people born in the latter half of the 20th century. This suggests, roughly, that advances in medicine from 1900 to 1950 had a leveling effect, bringing up the average, preventing early deaths, but doing little to address age-related disease. That said, there is a large variation in results across the range of similar studies, both those that look at the history of longevity, and those that look at populations of athletes at a given time. It is wise to consider epidemiological studies in groups rather than one by one, and look for common themes. Still, this one is a fascinating data set for the way in which it combines historical trends and exercise in the study of aging.

Examining mortality risk and rate of ageing among Polish Olympic athletes: a survival follow-up from 1924 to 2012 – by Yuhui Lin, Antoni Gajewski, and Anna Poznańska

Quote:

A sedentary lifestyle is associated with the onset of chronic diseases including ischaemic heart disease, type-II diabetes and neurodegenerative diseases. Frequent exercise is perceived as a major behavioural determinant for improved life expectancy and a slower rate of ageing. There is little doubt that frequent exercise is beneficial for individuals’ well-being, and an active lifestyle reduces the risk for chronic diseases. However, it is still uncertain whether the rate of ageing decelerates in response to frequent and intense physical exercise. Our attempt is the first empirical study to show the application of a parametric frailty survival model to gain insights into the rate of ageing and mortality risk for Olympic athletes.

Our participants for this parametric frailty survival analysis were Polish athletes who had participated in the Olympic Games from 1924 to 2010. We assumed that these athletes were elite in their preferred sports expertise, and that they were engaged in frequent, if not intense, physical exercise. The earliest recorded year of birth was 1875, and the latest was in 1982; total N=2305; male=1828, female=477. For reliable estimates, mortality improvements by calendar events and birth cohort had to be taken into consideration to account for the advancements made in medicine and technology. After the consideration of mortality improvements and the statistical power for parametric survival analysis, we restricted our analysis to male athletes born from 1890 to 1959 (M=1273). For reliable estimates, we preassigned recruited athletes into two categorical cohorts: 1890-1919 (Cohort I); 1920-1959 (Cohort II).

Our findings suggest that Polish elite athletes in Cohort I born from 1890-1919 experienced a slower rate of ageing, and had a lower risk for mortality and a longer life-expectancy than the general population from the same birth cohort. It is very unlikely that these survival benefits were gained within a short observational time. Therefore, we argue that participation in frequent sports from young adulthood reduces mortality risk, increases life-expectancy and slows the rate of ageing. The age-specific mortality trajectories of Cohort I elite athletes also suggest frequent exercise can decelerate the rate of ageing by 1% with an achievement of threefold risk reduction in mortality. In comparison with those of the general population, the differences in energy expenditure, behavioural habits, body mass and sports expertise were likely to be the contributing factors to the higher variance in lifespan among elite athletes.

In Cohort II, the estimated rate of ageing is highly similar between elite athletes and the general population, which contradicts our estimates for Cohort I. This may be attributed to mortality improvements from year 1920 onwards in Poland. These mortality improvements have changed individuals’ susceptibilities for different causes of death, which has resulted in an increased variation in lifespan both in the general population and for elite athletes. Interestingly, the comparison of the rate of ageing of elite athletes in Cohort I and II shows a similar rate of ageing. Among the elite athletes, the estimates suggest that Cohort II individuals benefited from a 50% mortality risk reduction as compared with individuals born in Cohort I. The estimated overall mortality risk of the Polish general population is 29% lower in Cohort II than in I.

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

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

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

hELA-400x300Multiphoton fluorescence image of HeLa cells.

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

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

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

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

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

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

majormouse

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

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

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

 

CBO: Tangled Web of Welfare Programs Creates High Tax Rates on Participants – Article by Charles Hughes

CBO: Tangled Web of Welfare Programs Creates High Tax Rates on Participants – Article by Charles Hughes

The New Renaissance HatCharles Hughes
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The dozens of different programs that form our tangled welfare system often impose high effective marginal tax rates that make it harder for low-income people to transition out of these programs and lift of those programs and into the middle class. As the people in these programs enter the workforce, get a promotion, or work more hours, they can lose a significant portion of those earnings through reduced benefits and increased taxes. A new report from the Congressional Budget Office (CBO) illustrates this predicament: many households hovering around the poverty level face steeper effective marginal tax rates than even the highest earners. These prohibitively high tax rates can discourage work and limit their prospects, ultimately making them less likely to escape poverty.

Marginal Tax Rates at the Median and 90th Percentiles by Earnings Group, 2016

cbo_tableau_marginal

Source: Congressional Budget Office, “Effective Marginal Tax Rates for Low- and Moderate-Income Workers in 2016,” November 19, 2015.

Note: Figure created using Tableau. 

CBO’s analysis looks at the range of effective marginal tax rates households face at different levels of income. The median marginal tax rate for households just above the poverty level is almost 34 percent, the highest for any income level. Some households that receive larger benefits or higher state taxes have even higher effective rates: 10 percent of households just above the poverty line face a marginal rate higher than 65 percent. For each additional dollar earned in this range, these households would lose almost two-thirds to taxes or lost benefits. The comparable rate for the highest earners, households above 400 percent of the poverty level, is only 43.4 percent. If anything this analysis might understate how steep the effective marginal rates are for some households. CBO only considers the combined effect of income taxes, payroll taxes, SNAP and ACA exchange subsidies, so households that participate in other programs like TANF or housing assistance could face even higher rates. These results mirror some of Cato’s past work investigating the issues and trade-offs involved with these welfare programs.

The nature of the welfare system contributes to the prevalence of these poverty traps. A House and Ways Human Resources Subcommittee recently held a hearing on issue and released a chart illustrating the complex, labyrinthine nature of the welfare system.

WM-Welfare-Chart-AR-amendment-110215-jpegClick on the image for a full-sized view.

New programs were grafted onto the existing system over time, each intended to address a perceived problem afflicting people in poverty, but they can interact in ways that can deter people from striving to create a better life for their families. That’s part of the reason the status quo system, which the Government Accountability Office estimates spends $742 billion at the federal level each year, has achieved such lackluster results to date.

While these shortcomings would seem to indicate that the welfare system is in need of reform, this tangled web has proved resistant to change. One of the last major reforms happened in 1996, when Temporary Assistance for Needy Families (TANF) replaced Aid to Families with Dependent Children (AFDC). Even that reform only addressed one strand of the dozens that make up our tangled system, so while it might have improved that one aspect the larger flaws with the welfare system as a whole have to some extent continued unabated. Even within this one strand there has been little discussion of reform in the past two decades, TANF hasn’t even been properly reauthorized since the Deficit Reduction Act of 2005, it is usually thrown into short-term continuing resolutions or broader omnibus appropriations acts that do not incorporate any meaningful attempts to address the program’s problems. Absent comprehensive, the flawed current system will continue to fall short even as the government funnels hundreds of billions of dollars into it each year.

If the federal government is going to finance a welfare system, it should foster an environment that encourages work and makes it easier for participants to transition out of these programs as they strive to create a better life. The current system falls far short in that regard and needs comprehensive reforms.

Charles Hughes is a research associate at the Cato Institute, where he focuses on federal budget policy, poverty, entitlement reform, and general economics.  Originally from Texas, Hughes joined Cato in 2011 after graduating from the University of Chicago with degrees in Economics and Public Policy.

This work by Cato Institute is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.

Are We Entering The Age of Exponential Growth? – Article by Marian L. Tupy

Are We Entering The Age of Exponential Growth? – Article by Marian L. Tupy

The New Renaissance HatMarian L. Tupy
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In his 1999 book The Age of Spiritual Machines, the famed futurist Ray Kurzweil proposed “The Law of Accelerating Returns.” According to Kurzweil’s law, “the rate of change in a wide variety of evolutionary systems (including but not limited to the growth of technologies) tends to increase exponentially.” I mention Kurzweil’s observation, because it is sure beginning to feel like we are entering an age of colossal and rapid change. Consider the following:

According to The Telegraph, “Genes which make people intelligent have been discovered [by researchers at the Imperial College London] and scientists believe they could be manipulated to boost brain power.” This could usher in an era of super-smart humans and accelerate the already fast process of scientific discovery.

Elon Musk’s SpaceX Falcon 9 rocket has successfully “blasted off from Cape Canaveral, delivered communications satellites to orbit before its main-stage booster returned to a landing pad.” Put differently, space flight has just become much cheaper since main-stage booster rockets, which were previously non-reusable, are also very expensive.

The CEO of Merck has announced a major breakthrough in the fight against lung cancer. Keytruda “is a new category of drugs that stimulates the body’s immune system.” “Using Keytruda,” Kenneth Frazier said, “will extend [the life of lung cancer sufferers] … by approximately 13 months on average. We know that it will reduce the risk of death by 30-40 percent for people who had failed on standard chemo-therapy.”

Also, there has been massive progress in the development of “edible electronics.” New technology developed by Bristol Robotics Laboratory “will allow the doctor to feel inside your body without making a single incision, effectively taking the tips of the doctor’s fingers and transplant them onto the exterior of the [edible] robotic pill. When the robot presses against the interior of the intestinal tract, the doctor will feel the sensation as if her own fingers were pressing the flesh.”

Marian L. Tupy is the editor of HumanProgress.org and a senior policy analyst at the Center for Global Liberty and Prosperity. He specializes in globalization and global wellbeing, and the political economy of Europe and sub-Saharan Africa. His articles have been published in the Financial Times, Washington Post, Los Angeles Times, Wall Street Journal, U.S. News and World Report, The Atlantic, Newsweek, The U.K. Spectator, Weekly Standard, Foreign Policy, Reason magazine, and various other outlets both in the United States and overseas. Tupy has appeared on The NewsHour with Jim Lehrer, CNN International, BBC World, CNBC, MSNBC, Al Jazeera, and other channels. He has worked on the Council on Foreign Relations’ Commission on Angola, testified before the U.S. Congress on the economic situation in Zimbabwe, and briefed the Central Intelligence Agency and the State Department on political developments in Central Europe. Tupy received his B.A. in international relations and classics from the University of the Witwatersrand in Johannesburg, South Africa, and his Ph.D. in international relations from the University of St. Andrews in Great Britain.

This work by Cato Institute is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.