Ethereum co-founder Vitalik Buterin is on a mission to make humans immortal. Buterin, 27, proposes the idea that “aging is an engineering problem.” (Start At: 2:28:50)
He is not alone in his combined interest in Bitcoin and biohacking. Famous biomedical aging researcher Aubrey de Grey, Xanadu architect and Agoric chief scientist Mark Miller, Bitcoin Cash billionaire Roger Ver and former chief technology officer of Coinbase and a16z general partner Balaji Srinivasan, are all fascinated by the pursuit of longevity.
De Grey recently helped launch VitaDAO, a “decentralized collective funding longevity research.” He says:
“I have been gratified since the beginning of blockchain to see the enormous fanbase that I and the longevity movement have in there.”
(Start At: 2:28:50)
Miller, alongside his engineering hall-of-fame accomplishments, is a senior research fellow at the Foresight Institute, a not-for-profit founded in 1986 with the aim of “advancing technology for the long-term benefit of life.”
“I’m very much involved in this new world of crypto commerce, often referred to as the blockchain sector,” he says. “I’m very hopeful about that as creating an ecosystem in which secure software will dominate because insecure software results in massive losses quickly, with no recourse.”
Srinivasan’s Twitter bio describes his vision as: “Immutable money, infinite frontier, eternal life. #Bitcoin.” Srinivasan states that “the ultimate purpose of technology is to eliminate mortality” and “life extension is the most important thing we can invent.”
Blockchain communities are clearly excited about longevity. But what does cryptocurrency have to do with life extension, and where might this future be headed?
It turns out that the link between crypto and cryogenics stretches back to core contributors, and the Cypherpunks mailing list and its links to trans-humanist groups, including the first person to transact Bitcoin with Satoshi, Hal Finney.
If we’re being more open minded about accepting new weird ideas, can I suggest anti-aging research? Aging is a humanitarian disaster that kills as many people as WW2 every two years and even before killing debilitates people and burdens social systems and families. Let’s end it.
Crypto philanthropists are donating significant wealth to this area, which is typically difficult to garner mainstream support for. They may be the only people on the planet optimistic enough to fund tech that currently only exists in sci-fi novels.
According to Buterin, longevity is a battle worth fighting for. Buterin donated $25 million in SHIB cryptocurrency tokens to the Future of Life Institute in June 2021 and has donated over $350,000 to the SENS Research Foundation to “reimagine ageing”.
He discussed the topic in recent podcast interviews with the likes of Lex Fridman and Tim Ferriss saying that “life extension is definitely really important to me.”
“I think I hope to see the concept of seeing your parents and grandparents die just slowly disappear from the public consciousness as a thing that happens over the course of half a century.”
Buterin has emphasized his adherence to the moral philosophy of effective altruism. This value, known to trans-humanists as the moral urgency of saving lives, is perhaps what motivated his donations of dog coins to both COVID-19 relief in India and life-extension.
“Just even the process of aging turning into something that just becomes reversible and it being a regular thing for people to live one and a half, two centuries and then go even further from there,” Buterin states.
Pinned in Buterin’s Twitter is an essay called “The Fable of the Dragon Tyrant” by professor Nick Bostrom, director of the Future of Humanity Institute. It argues that allowing death from old age is unethical. If you view aging as a disease, the urgency to support the trans-humanist project also makes sense.
“While we still lack effective and acceptable means for slowing the aging process, we can identify research directions that might lead to the development of such means in the foreseeable future,” states Bostrom. The key to freeing humanity from the dragon tyrant of aging, is funding. The new riches from crypto are key.
Bitcoin.com founder Roger Ver has already signed up to be cryogenically frozen. “Rather than investing in cryptocurrency stuff, I want to focus on the extreme life extension technologies, because if you die, you can’t enjoy your life anymore,” Ver told Cointelegraph. He’s so confident in the tech, he even considered being cryogenically frozen as a legitimate alternative to going to prison in 2002.
Roger Ver once considered killing himself and going into cryonic suspension to avoid prison.
Now he plans to spend the next phase of his career — and his fortune — making cryonics a reality. https://t.co/IZ1Ham7NEa
DAOs are also taking part in this life extension renewal. “There is a strong overlap of crypto people and longevity people,” Vincent Weisser, core team member at VitaDAO tells Cointelegraph. VitaDAO exceeded its token raise funding target of $490,000 in June 2021.
Now, they are working with popular blockchain crowd-funding platform Gitcoin to include a future funding category for longevity and life extension.
Trans-humanist philanthropy and funding at scale holds the potential to significantly impact longevity research and the trans-humanist project.
What is trans-humanism?
Trans humanism is a loosely defined movement that promotes the use of technology to enhance the human condition. This includes information technology, genetic engineering, and artificial intelligence for radical extension of human lifespan, augmentation of physical and intellectual capacities, space colonization, and super-intelligent machines.
The goal is not just life extension, but “more,” to the point of becoming superhuman. Although the trans-humanist pursuit of post-humanity is often thought of as medical, the gambit of trans-humanist technologies includes economic and social institutional design and cultural development.
Like crypto communities, trans-humanism is grounded in a vision of evolution and individual freedom of choice. In practice, this leads to a sense of personal responsibility for contributing to solutions, such as biohacking or making provisions for being cryogenically frozen and one day hopefully reanimated.
The goal of the trans-humanist project for society is one based on freedom in determining social arrangements, enabled by self-generating systems and spontaneous order. This description of perpetual, open systems is similar to blockchain.
Not everyone thinks eternal life, or the philosophy underpinning it, is a good idea. Political economist Francis Fukuyama calls trans-humanism “the most dangerous idea in the world” and argues it is “a strange libertarian movement” whose “crusaders” want “nothing less than to liberate the human race from its biological constraints.”
He lists the risks of the fraught nature of humankind to want to live forever, the effects on equality between the “haves” and the “have nots,” and that the essence of humanity is mortality. Yet, trans-humanism has a long history in crypto communities.
More Human Than Human
Trans-humanist values are reflected in the ideological underpinnings of blockchain communities around anarchy and autonomy, self-improvement, and a long-term mindset.
Trans-humanist ideas have long existed in the technology communities that pioneered the core tenets of public blockchains. For example, cryptography pioneer Ralph Merkle (inventor of public key distribution and Merkle trees) considered himself a trans-humanist, publishing on such matters as “The Molecular Repair of the Brain.”
Furthermore, there was substantial cross-pollination of ideas between the Cypherpunks mailing list, which discussed ideas on privacy and digital cash throughout the 1990s and 2000s in the lead-up to the invention of Bitcoin in 2008, and the Extropian mailing list.
Extropy is “the extent of a system’s intelligence, information, order, vitality, and capacity for improvement.” According to 1998’s “Principles of Extropy” published by president of the Extropy Institute, Max Moore, extropians are “those who seek to increase extropy.”
The core principles, refined in “The Extropist Manifesto” in 2010, are “endless eXtension,” meaning perpetual growth and progress in all aspects of human endeavor; transcending the restrictions of authoritarianism, surveillance, or social control; overcoming property rights, including IP and money, by sharing knowledge, culture, and resources; intelligence, including independent thinking and personal responsibility; and smart machines, specifically the attainment of “Friendly Artificial Intelligence” that exceeds human ability, through funding and favorable legislation.
Extropians advocate and explore the philosophies of trans-humanism (technological enhancement), extropy (improving the human condition), and the future.
Numerous prominent cypherpunks also subscribed to the Extropian mailing list, including co-founders of the cypherpunk movement Timothy C. May and Eric Hughes.
Another active member of the extropians was Hal Finney. Finney was co-developer of the first anonymous remailer, the first person to transact Bitcoin with Satoshi and the first maintainer of the Bitcoin codebase. He was cryogenically frozen when he passed away in the hope of living in the future alongside his wife, Fran, who noted that “Hal liked the present.
But he looked towards the future.” For this community, technologies like digital cash offered a way of long-term thinking about the future of humanity, trans-humanism, and solutions and preventions for cryogenics, outer space, and catastrophic environmental or societal collapse.
The cypherpunks’ interest in extropianism, and vice versa, was concerned with building infrastructure today that would sustain the future of human evolution. In some ways, this makes sense.
In order for one’s cryogenic suspended animation to be paid for, maintained and reversed to wake them up in the far-flung future where science advances to the point where this aspiration is realized, there needs to be an incentive.
In 1994, Wired magazine reported over 27 frozen people (technically 17 frozen heads and 10 entire bodies) at the Alcor Life Extension Foundation, the same company that Roger Ver has signed up with.
“Immortality is mathematical, not mystical,” stated Mike Perry, their overseer. The hope is that Bitcoin will be a resilient long-term incentive for someone to wake up Hal, Fran and other friends. Herein lies the need for long-term blockchain infrastructure, to last as a secure monetary reward until the century when “unfreezing” is possible.
Among the principles of extropianism set out by Moore is “intelligent technology,” meaning technologies that bring beneficial results, including “genetic engineering, life-extending bio-sciences, intelligence intensifiers, smarter interfaces to swifter computers, neural-computer integration, worldwide data networks, virtual reality, intelligent agents, swift electronic communications, artificial intelligence, neuroscience, neural networks, artificial life, off-planet migration, and molecular nanotechnology.”
“Expect to see more life extension, brain-machine interfaces, limb regeneration, curing deafness, bionic sight and more incredible feats” in the next decade, states Srinivasan. Trans-humanists predict an inevitable “singularity,” when technology becomes intelligent, uncontrollable and irreversible, to occur around 2035. Blockchain is part of this technology stack.
Where Trans-Humanism And Crypto Overlap
The lofty, futuristic ideas of trans-humanists depend on resilience and digital infrastructure. This is especially true for the goal of friendly artificial intelligence, which is seen as an enabling condition for rapid development across all other core principles of the project. Thanks to blockchain technology, and blockchain philanthropy, we are beginning to have the resources to do it.
An immutable “worldwide computer” enables a decentralized autonomous organization to allow our uploaded brain image to automatically coordinate with friendly artificial intelligence in a decentralized, freedom-loving way.
Blockchain’s immutability makes it the perfect long-term infrastructure. Cypherpunks were paranoid about Orwellian dystopias in which authorities would rewrite history to match state propaganda.
The architectural and political decentralization of public blockchains means that no one can tamper with, control or delete the record of history. This makes it the perfect record-keeping infrastructure if we are going to live forever.
This is essential when it comes to your brain image or your Bitcoin balance. In order to document who owns what coins when you are cryogenically frozen and woken up in the next century, you need resilient, long-term, tamper-proof blockchains.
The values of independence and immutability are essential to both crypto enthusiasts and trans-humanists. Buterin states:
“It’s great that we have people trying to upload or improve brain scanning. It’s also great that we have people including cryonics, so we could just go to sleep in the freezer and eventually, hopefully, sometime in the future […] anyone who gets cryogenically frozen will be able to wake up.”
The combination of trans-humanist philosophy, blockchain technology, community obsession and money enable whole new possibilities. The trans-humanist-blockchain vision is that we will all be connected, humans and machine intelligence, through decentralized, automatically executing smart contracts and marketplaces.
Blockchains provide a platform infrastructure to enable a host of technologically advanced human-machine futures. One example is a decentralized marketplace for AI, such as SingularityNET by artificial intelligence researcher, trans-humanist, and CEO Ben Goertzel. Here, intelligent computational agents buy, sell and barter over work for digital tokens via a blockchain.
In The Trans-humanism Handbook, Melanie Swan predicts that “crypto cloudminds,” in which mind node peers interact through multicurrency pay channels of digital denominations, will algorithmically enforce good behavior between humans and machines through the privacy and transparency of blockchains. According to Srinivasan, this could also lead to “cloud cities,” which allow their members to negotiate with other jurisdictions and crowdfund territories in the physical world.
Trans-humanism, like human beings, is only in its early stages of development.
Trans-humanism, with its focus on superhumans and longevity instead of an afterlife, can be viewed as something akin to a religious impulse. Although many trans-humanists take their worldview to be in opposition to religious outlooks on life, trans-humanism may become the religion of blockchainers. Yet, this doctrine does not come without a clear burden of responsibility.
The Engineer’s Responsibility
While some fear trans-humanism, a core tenet is to ensure that technology produces positive outcomes for humanity. Trans-humanist advocate that the choice to improve human capacities lies with the individual.
Part of the longevity research agenda is figuring out how to measure the risks of friendly artificial intelligence and make it truly friendly to avoid a catastrophe. Trans-humanist want to avoid “X risk,” which is existential risk to humanity of a hypothetical, global, catastrophic future event that could damage human well-being or destroy human civilization.
This is why colonizing outer space is so logical, as Elon and other crypto enthusiasts are pursuing. The “Extropian Principles,v. 3.0” by Max Moore from 1998 emphasizes this, stating that “migration into space will immensely enlarge the energy and resources accessible to our civilization.” Of course, smart machines will also help us explore space because they can handle more gravitational force than humans as they enter the orbit of other planets.
To a trans-humanist, the goal of technology is to amplify our abilities and extend human freedoms. “How could we ensure humanity lives forever and life spreads throughout the universe?” asks Weisser from VitaDAO. “It’s all about probabilities and increasing the probability that humanity will survive,” he says.
A long-term mindset treats aging as an engineering problem. Now, it remains to be seen if the intersection of blockchain philanthropy, VitaDAO’s research collective, and other decentralized, trans-humanist pursuits will be cautiously and collectively propelled forwards with the kind of “long-termism” that will benefit humanity. As Buterin states:
“I hope you guys can […] come to my thousandth birthday party.”
$1B Science Fund Seeks Blockchain Projects To Expand Human Lifespan
Longevity Science Foundation accepts crypto donations and aims to use technology to advance healthy human longevity.
Scientists are continuously pursuing ways to lengthen the human lifespan, and blockchain might have been a missing part of the puzzle. The Longevity Science Foundation, a Swiss entity launched by a consortium of biotech founders, clinicians and leading longevity research institutions, aims to spend more than $1 billion over the next 10 years to find tech-based means to achieve a 120-year human lifespan.
The foundation seeks to fund research, institutions and projects that use blockchain and other next-gen technologies to find new horizons in four critical areas of the field; namely, therapeutics, personalized medicine, artificial intelligence (AI) and predictive diagnostics. The announcement states that such projects can make a significant difference in people’s lives, even within a five-year timeframe.
Applying theoretical longevity concepts to real-world use is a primary goal for the group. The foundation aims to transform scientific findings and technological advances into clinical treatments and solutions through donations.
“By identifying and funding the most promising and cutting-edge advances, the Foundation seeks to address one of the most pressing issues in the science and applicability of longevity medicine radical inequality in accessing and understanding longevity-focused treatment,” the announcement reads.
The foundation’s contributors, who can also make donations with cryptocurrencies, will get voting rights to have a say in deciding which projects receive funding. A visionary board will pre-select and evaluate potential candidates “for their technical soundness and potential impact on human longevity.”
Joining the Visionary Board of the Foundation is Dr. Alex Zhavoronkov, known for his work on longevity tech. Dr. Zhavoronkov is also an advisor to blockchain medical data marketplace Longenesis, which launched a joint project with the Bitfury Group to establish a blockchain-based consent management system for the healthcare industry.
“The Foundation has created a unique and transparent mechanism for boosting early longevity research worldwide and ensuring mass public participation in decision making,” Dr. Zhavoronkov said.
As for how technology can help healthcare research, LongeVC managing partner Garri Zmudze told Cointelegraph that if paired with AI, blockchain can unlock hundreds of terabytes of unstructured hospital data for further analysis.
The Future Of Longevity Lies With Digital Currency Visionaries
Healthcare researchers in collaboration with crypto innovators might prove that a longer and healthier lifespan is an attainable reality.
The promise of a longer and healthier life has dominated both cultural and medical discourse for centuries. From the first accounts of Nicolas Flamel’s philosopher’s stone granting immortality to the latest superfood that promised to reverse aging, we are captivated by the idea of a longer and more vibrant life.
Encouragingly, the longevity sector has proven that a longer and healthier lifespan isn’t just a magazine headline — it is an attainable reality. Humans will not only live longer but will have more active, healthy and engaged years on this Earth.
Research units from all over the world are making discoveries every day. Medical advancements, fueled by intensive research and experimentation, are changing how scientists, doctors and even cultural commentators think about how long and how well we can live. We are, indeed, now in the era of longevity.
What is driving these incredible breakthroughs? Pure creativity and innovation. The advent of artificial intelligence, genetic engineering and a renewed interest in public health stemming from the COVID-19 pandemic are catalyzing discoveries at an unprecedented rate.
To maximize the impact of these researchers, the future of innovation will need to be collaborative and cooperative. It will take a village to make longevity understandable and accessible to medical professionals and average individuals alike.
Where The Future Lies
The best route forward, in my opinion, is to solicit support from true visionaries. Take, for example, the company Longenesis, which I highlighted in my previous article for Cointelegraph.
Its “blockchain toolkit” applies the most compelling features of distributed ledger technology (DLT) to protect sensitive medical data, ensure secure data sharing between numerous partners and provide a pathway for patients to become stakeholders in medical research by contributing their data and participating in clinical trials.
Longenesis could accomplish so much relatively quickly because it had money and support from the highly futuristic and accepting blockchain community. Backed by funding from its joint venture partners, Longenesis achieved its mission of creating a game-changing and blockchain-powered approach to unlocking healthcare data.
This is an increasingly common trend: the Iryo Network relied on support from blockchain professionals to create a token that empowers patients to stake their data and receive payment from research institutions in exchange for data access.
The Texas-based EHRData is working toward a similar goal of decentralized data storage and management by creating an electronic health record built on blockchain that patients can control, share and submit to researchers for staked rewards. These applications were all made possible thanks to blockchain visionaries willing to fund the future of healthcare and longevity.
Early-stage funding can power startups, but it can also support even more foundational innovations by researchers. Genuinely cutting-edge innovation at the laboratory/research stage often requires significant funding for state-of-the-art equipment, materials, operating administration costs, etc., just to get started.
This is a challenge for researchers from smaller institutions, as funding often goes to projects that have access to these resources and, as a result, have already advanced in their discoveries. For these cases, foundational grants can be instrumental in supporting the high upfront fees associated with researching something intended to change the world.
The longevity sector is rich with organizations looking to find and fund the next big idea, but very few organizations are willing to move beyond traditional funding models to make that happen. It is difficult to conceive that an industry with innovation embedded in its very core is lagging in terms of new funding sources, but that is a possible reality facing groundbreaking researchers and institutions.
The time for futurists and visionaries
Luckily, the innovation taking place in the digital currencies sector is spilling over into the biotech and longevity spaces. The community of visionaries who transformed the way money and investing works is here to change how humanity experiences life itself.
Back in 2018, Vitalik Buterin, the co-founder of Ethereum, donated $2.4 million in Ether (ETH) to the SENS Research Foundation, a California-based group working to research, develop and promote comprehensive solutions for aging-related diseases.
Buterin has also donated $25 million in Shiba Inu (SHIB) tokens to the Future of Life Institute to fund Ph.D. fellowships focused on ethical Artificial Intelligence applications and millions to the Methuselah Foundation, an organization researching tissue engineering to reverse aging processes.
The new Longevity Science Foundation will be accepting donations in crypto to contribute to its goal of expanding the human lifespan to 120+ years. The Foundation welcomes crypto visionaries, and all donors (crypto donors both included and encouraged), will receive voting rights in the funding selection process.
VitaDAO aims to extend the human lifespan openly and democratically by researching, financing and commercializing longevity therapeutics. Its decentralized structure is similar to that of many decentralized applications (DApps) and other decentralized autonomous organizations (DAOs), building a new and exciting governance structure.
Its genesis auction raised more than $5 million in funding via purchased VITA governance tokens, attracting approximately 400 new members committed to the DAO’s mission.
The crypto visionaries that have made these accomplishments possible are future-focused collaborators who want a front seat for the cutting-edge science of longevity. They are creating a village that will make longevity care possible and accessible to all, but there is a lot of work still to be done.
There is a significant overlap in the challenges of adopting longevity care and the resistance to blockchain technology and digital currency. By lengthening our lifespans, we create a future that requires the adoption of blockchain and digital currency to be successful.
Digital currencies and blockchain technology changed the way the entire world transacts and uses critical services. They are the foundational technologies for a more fair and efficient society. New applications for DLT are being developed every day, and new investors, adopters and appreciators are drawn to the industry because of its constantly evolving nature.
If we can apply that same entrepreneurial spirit and can-do attitude to the longevity sector, our lives will not only be longer but more enriched, meaningful and digitally enabled.
The longevity sector is working to make sure more people live long enough to enjoy a decentralized and transparent world. To do so, the industry desperately needs the brainpower and experience of the innovators who turned a single white paper into a global and unstoppable movement of transparency and equality. This feat was successful once, let’s make it happen again.
Longevity Genetics – Crypto-Backed Study Seeks 10,000 Centenarians
Dr Nir Barzilai discusses new longevity genetics project funded by crypto investor; expects TAME trial to recruit first patients this year for metformin aging study.
The Institute of Aging Research at the Albert Einstein College of Medicine, and its director, Dr Nir Barzilai, are synonymous with the study of aging.
Led by Barzilai, the Longevity Genes Project and the subsequent LonGenity studies have spanned decades, looking at the genes of people aged over 100, and their offspring, to see what can be learned about the secrets to longevity.
This area of research is about to be greatly scaled up, with a new study aiming to collect longevity genetics data from 10,000 centenarians.
Longevity.Technology: Through his work at Albert Einstein and the American Federation for Aging Research (AFAR), Barzilai is involved in a wealth of research in the longevity field. In addition to learning more about this new project, we also spoke with Barzilai to get an update on the Targeting Aging with Metformin (TAME) trial, which aims to create a template for trials of age targeting therapies.
Barzilai says that, rather than focusing on data gathered from cell or animal studies, pharmaceutical companies are increasingly interested in human longevity genetics data that reveals how certain genetic mutations might be associated with specific diseases and longevity.
“Pharmacogenetics has become very important,” he says. “We’ve already done studies of 750 centenarians and their offspring, which found data on longevity genes that has contributed to the development of at least two drugs. We want to scale this data up, and we are now recruiting 10,000 centenarians and doing their whole genome sequencing.”
Barzilai tells us that the new longevity genetics study has been enabled through an investment from James Fickel, a 26 year old cryptocurrency expert with a growing interest in longevity philanthropy.
“James is really interested in aging and he just wrote a check of $2.8 million to AFAR to support this study,” he says. “In fact, there are lots of young people who are interested in aging. They’re trying to accelerate the field, and I think it’s working.”
Centenarians Live Longer And Healthier
The longevity genetics of centenarians are worth studying, says Barzilai, because not only do they live longer, they usually also stay healthier for longer, and spend less time sick in their final years.
“That’s what we want to achieve – we want people to stay healthy for as long as possible and then die. So we’re going to make a tenfold increase in the number of centenarians that have been sequenced, and we want to find all the longevity genes that allow those people to get over the age of 100 without diseases.”
To support a scale-up of this magnitude, recruitment of centenarians and their offspring will be conducted online, with DNA collection kits sent out and returned by mail.
“There’s a lot of technology that we’re going to use to make it possible to access all these centenarians, their offspring and their grandchildren, so we’re testing to find the best approach,” says Barzilai. “We’re aiming to have 750 samples by the end of the year, see what worked, and then do an acceleration phase that will probably take a couple of years.”
TAME Trial Update
The longevity field has been waiting with bated breath for the TAME trial to begin. Through a series of nationwide, six-year clinical trials at 14 research institutions across the United States, TAME will study more than 3,000 older adults to explore whether taking metformin has an impact on aging.
“When you come into the TAME trial, we don’t care what disease you have, and we don’t care which disease you’re going to get,” says Barzilai. “You’re going to get older, you’re likely going to get a disease or two, but for us, the specific disease means nothing – we’re agnostic. What we’re trying to do is to demonstrate an indication that will relate to the prevention of aging.”
“Okay, the FDA won’t call it prevention of aging, but we’re basically talking about showing that a drug can take a cluster of age-related diseases and delay or postpone them. Whether that means we’re preventing aging or not, let’s leave that aside, but I believe that aging is the mother of all those diseases.”
While there are those in the longevity field that call for aging itself to be considered a disease, Barzilai doesn’t feel this is a helpful way to think of it.
“I’m 66 years old and I‘m in great shape, I don’t have any disease, so I don’t want to told I have a disease!” he says. “AARP and AFAR don’t want to call aging a disease – we should not be antagonising the people we’re trying to help.”
The COVID-19 pandemic hit the TAME trial hard, striking just as the project was about to commence, and putting things on hold.
“TAME isn’t going to start until we can be sure that this pandemic is over,” says Barzilai. “But we’re optimistic, the wheels are in motion, all the protocols are ready, and I hope that the first patients will be recruited this year.”
The Crypto World Should Know About Longevity
Biotech researchers working closely with decentralized tech innovators indicates that there is an appetite for progress in the longevity sector.
As the first month of 2022 drew to a close, the internet was abuzz with trend predictions for the year ahead. Bloggers, Twitter influencers and established business moguls alike were, and still are, incredibly excited about the new opportunities afforded by an explosion of innovation in Web3.
However, something you may have missed in scrolling pages of celebrity-backed NFT drops or speculations about the metaverse was the launch of a new company called Altos Labs, reportedly backed by Amazon’s former CEO Jeffrey Bezos.
The language that followed the launch was largely typical of how many mainstream journalists talk about the longevity sector, words like mysterious and secret. I’ve written in earlier articles that there are a lot of misconceptions around the longevity sector, and this new round of headlines seems to confirm this as still accurate.
I believe there is a lot more to the longevity sector than secret deals featuring the planet’s wealthiest billionaires. The space is ripe with interested investors, groundbreaking discoveries and development opportunities.
The message is clear — longevity is here to stay. And for the crypto industry, or a world populated with trend-setting, tech-savvy individuals, the time is now to start getting up to speed on this incredible space.
While it was wrapped up in mysterious media discourse, the Altos Labs deal was indicative of the high-level interest in the diverse longevity sector. With a reported $3 billion backing on day one, the deal is believed to be the largest biotech deal to date and has attracted the talent to match.
The first executive team is composed of globally renowned scientists, CEOs and doctors eager to seek new heights in the science of anti-ageing.
The Altos announcement was reminiscent of Calico Labs, another longevity company announced in 2013 by Google co-founder Larry Page. While the Google spin-off has been subject to inquiries about its productivity, it successfully published its first preprint on cell reprogramming in May 2021.
It is not only tech CEOs making headlines about investment: Deals from the past two months alone include areas like stem cell therapy, liver regeneration, senescence targeting, reproductive longevity and more.
It’s clear that the planet’s top innovators are looking to live longer. It’s up to us to make sure that longevity technology is accessible to all when it reaches public use.
Insilico Medicine, a Hong Kong-based drug discovery company, announced a significant milestone at the end of 2021. Their first AI-discovered medicine entered human trials. The medication will be used to treat idiopathic pulmonary fibrosis, a chronic lung disease, and has shown promising early results in first studies. This marks the first AI-discovered drug to reach this stage and is an exciting indication of new inventions to come.
AI is a central area of research in the longevity space, with countless applications in drug discovery and beyond.
Other new and exciting areas include cell regeneration, plant-powered supplements and progress in wearable technology that helps monitor ageing-related diseases. Charitable organizations like VitaDAO and the Longevity Science Foundation are working tirelessly to provide research funding to these early-stage ideas and help them reach public adoption.
Longevity Sector Development
On Deck, a company that offers acceleration programs for top talent across multiple sectors, launched its first Longevity Biotech Fellowship in June 2021. The inaugural cohort boasted participation from top longevity and biotech companies including turn.bio, Juvena Therapeutics, Retro Sciences and more.
Researchers from universities including Yale, University of Washington and ETH Zurich also contributed to the curated community.
On Deck is currently accepting applications for their second cohort, which will kick off later this month. The community claims to push the boundaries of traditional health and is growing the biotech ecosystem one member at a time.
Longevity is also reaching public awareness via international organizations. Martha Deevy, director of the Stanford Center on Longevity, contributed to a World Economic Forum article on the societal implications of living longer lives.
The idea of the multi-generational workplace, for example, has been expanded to include five or six different generations in one office space as a result of employees living longer and retiring later.
Deevy noted that while old age is often seen as a time of dependence and vulnerability, this narrative is changing. New societal approaches should emphasize a lifelong balance between education, work and rest. Deevy’s article said it best: We need to pay attention to the longevity sector because the effects of living longer lives are already showing up in surprising areas of our everyday lives.
Longevity And Crypto
It is clear that the longevity sector has been busy with no signs of slowing down. A recent poll showed that 70% of respondents believed the human lifespan should continue to increase if the necessary medical and technological advancements were in place to support it. Similarly, 68% of respondents reported they would be willing to take anti-ageing drugs if proven effective and free from side effects.
There is an appetite for progress in longevity, and the above examples show that we are on the right path. Still, more can be done — stay tuned for more news about longevity nonfungible tokens (NFTs), crypto investment into this space and other updates.
Scientists Identify The Optimal Number of Daily Steps For Longevity, And It’s Not 10,000
Conventional wisdom would have us believe the journey to a long and healthy life begins with 10,000 steps. Each and every day.
For those living a more sedentary lifestyle, it’s a goal that can take some effort to maintain. We’ve also known for some time it’s also almost certainly wrong.
By analyzing data on tens of thousands of people across four continents compiled between 15 existing studies, a team of researchers has now landed on a more comfortable figure: the optimal number is probably closer to 6,000 steps per day, depending on your age.
Anything more is unlikely to further reduce your chances of stumbling into an early grave.
“So, what we saw was this incremental reduction in risk as steps increase, until it levels off,” says University of Massachusetts Amherst epidemiologist Amanda Paluch.
“And the leveling occurred at different step values for older versus younger adults.”
Humans are essentially built to ambulate. Evolution has honed our physiology to walk long distances, shedding heat easily as we tick-tock back and forth like inverted pendulums across the landscape in search of food and water.
This means our metabolisms, cardiovascular fitness, impact on our bones and muscles, and even our mental health are all tuned to appreciate a good hike. Squeezing just about any kind of stroll into our busy schedule will serve us well by helping us live longer, healthier, happier lives.
This is easier said than done for those pressed for time or lacking motivation, which is why tech companies invented small devices that help us keep track of the number of steps we take each day.
Half a century ago, the Yamasa Clock and Instrument Company in Japan sought to cash in on the buzz left by the 1964 Tokyo Olympics by producing a pedometer they called ‘Manpo-kei’ – a word that translates into 10,000 steps.
Why 10,000? Good old fashioned marketing. It’s a nice, round number that sounds taxing enough to be a goal, but achievable enough to be worth striving for. What it doesn’t have going for it is any scientific backing.
Having a single figure to promote to a general population is certainly useful. “It’s such a clear communication tool for public health messaging,” says Paluch.
But getting that number right could make the difference between encouraging everybody to get enough exercise and putting people off trying altogether.
Last year, Paluch and her team published research based on a cohort of more than 2,000 middle-aged individuals living across the US. They found taking at least 7,000 steps a day reduced chances of premature death by 50 to 70 percent.
Those words ‘at least’ are doing some heavy lifting. With questions remaining over whether more is better, and whether squeezing all those steps into a more rapid pace is in any way useful, the research team widened their net to include previously published research.
Their latest meta-analysis included information collected on the health and step-counts of 47,471 adults from Asia, Australia, Europe, and North America. They found the 25 percent of adults who stepped the most each day had 40 to 53 percent lower chance of dying, compared with those in the bottom 25 percent of step-counts.
For adults aged 60 and older, this reduced risk topped out at around 6,000 to 8,000 steps a day. Pushing further might have other benefits, but a reduced chance of death isn’t one.
The study found that those who are younger could do well to walk a little more, but there wasn’t evidence that they’d necessarily live longer by walking more than 8,000 to 10,000 steps a day.
As for the rate of steps, the team found volume is what really matters.
“The major takeaway is there’s a lot of evidence suggesting that moving even a little more is beneficial, particularly for those who are doing very little activity,” says Paluch.
None of this is to say we wouldn’t benefit from working our bodies harder in other ways.
Researchers Say They’ve Reversed Ageing In Human Cells By 30 Years
Researchers have reversed ageing in human skin cells by 30 years, according to a new study.
Scientists say they have developed a method to time jump human skin cells by three decades – longer than previous reprogramming methods, rewinding the ageing clock without the cells losing their function.
Researchers describe being able to partly restore the function of older cells, as well as renew the biological age.
According to the study, in experiments that simulated a skin wound, the partially rejuvenated cells showed signs of behaving more like youthful cells.
Experts suggest that, while in their early stages, the findings could eventually revolutionise regenerative medicine, especially if it can be replicated in other cell types.
Professor Wolf Reik, a group leader in the Epigenetics research programme who has recently moved to lead the Altos Labs Cambridge Institute, said: “This work has very exciting implications.
“Eventually, we may be able to identify genes that rejuvenate without reprogramming, and specifically target those to reduce the effects of ageing.”
“This approach holds promise for valuable discoveries that could open up an amazing therapeutic horizon.”
Dr Diljeet Gill, a postdoctoral researcher in Prof Reik’s lab at the Babraham Institute who conducted the work as a PhD student, said: “Our results represent a big step forward in our understanding of cell reprogramming.
“We have proved that cells can be rejuvenated without losing their function and that rejuvenation looks to restore some function to old cells.
“The fact that we also saw a reverse of ageing indicators in genes associated with diseases is particularly promising for the future of this work.”
As people age, their cells’ ability to function declines and the genome – DNA blueprint – accumulates marks of ageing.
Regenerative biology aims to repair or replace cells, including old ones.
One of the most important tools in regenerative biology is our ability to create ‘induced’ stem cells.
However, this process essentially wipes the cells of their function and gives them the potential to become any cell type.
The new method, based on the Nobel Prize-winning technique scientists use to make stem cells, overcomes the problem of completely erasing cell identity by stopping reprogramming part of the way through the process.
This allowed researchers to find the precise balance between reprogramming cells, making them biologically younger, while still being able to regain their specialised cell function.
They say the potential applications of this technique are dependent on the cells not only appearing younger but functioning like young cells too.
Experts suggest that, in the future, the research may also open up other therapeutic possibilities.
They observed that their method also had an effect on other genes linked to age-related diseases and symptoms, like the APBA2 gene associated with Alzheimer’s disease, and the MAF gene with a role in the development of cataracts.
The research is published in the journal eLife.
Scientists have been able to find a way to reverse the ageing process in human skin. Through a breakthrough research, a team of Cambridge scientists claims to have made the skin cells of a 53-year-old woman 30 years younger.
This is longer reversal of the ageing clock than any other previous studies without damaging the cells. A study detailing the method has been published in eLife magazine.
The team told the BBC that it can do the same thing with other tissues of the body. Their ultimate aim is to develop treatments for age-related diseases, like diabetes, heart disease and neurological ailment.
“This work has very exciting implications. Eventually, we may be able to identify genes that rejuvenate without reprogramming, and specifically target those to reduce the effects of ageing,” Professor Wolf Reik, a group leader in the Epigenetics research programme, told Sky News.
The findings are still in early stages and if more research is done, the method could revolutionise regenerative medicines, said the scientists.
It is built on the technology used to clone Dolly the sheep more than 25 years ago.
The researchers at Roslin Institute in Scotland cloned Dolly by developing a method that turned the mammary gland cell taken from a sheep into an embryo. The gland was taken from six-year-old Finn Dorset sheep and an egg cell taken from a Scottish Blackface sheep.
Dolly was born on July 5, 1996.
The technique was aimed to create human embryonic stem cells, which could be grown into specific tissues, like muscle, cartilage and nerve cells. These tissues could be used to replace old body parts.
It is the gradual decline in the ability of the cells to function optimally, which leads to tissue dysfunction and disease. Regenerative biology aims to repair these old cells.
The team in Cambridge used the Maturation Phase Transient Reprogramming (MPTR) method, which overcomes the problem of erasing cell identity, allowing the researchers to find the balance of making cells younger while still retaining their specialized cell function.
Live Longer: ‘Amazing’ Technique ‘Reverses’ Ageing By 30 Years And Could Treat Alzheimer’s
A REVOLUTIONARY technique has allowed scientists to de-age individual skin cells by 30 cells while retaining their specialised functions – and it could pave the way to new treatments for age-related conditions like Alzheimer’s disease.
As one gets older, time takes its toll and we find ourselves perhaps less able to do all the things we used to. The same kind of thing happens, albeit on a smaller scale, to our cells. Scientists working in the field of regenerative medicine work to reverse the ravages of time, and other forms of damage, by re-growing, repairing and replacing cells and tissues.
One of their key tools lies in the ability to create so-called induced stem cells, which theoretically have the ability to become any other cell type, by taking regular cells and removing some of the marks that make them specialised.
Unfortunately, we are presently not able at present to reliably recreate all the conditions that turn stem cells into all the particular cell types — meaning that we can effectively make cells young, but in the process, they can lose their identity and function.
In their new study, epigeneticist Dr Diljeet Gill of the Babraham Institute in Cambridge and his colleagues addressed this problem by halting the cellular reprogramming halfway through — effectively making the cells biologically younger, while not actually erasing their specialised cell function.
Their method builds on the 2012 Nobel Prize-winning technique developed by Professor Shinya Yamanaka of Japan’s Kyoto University for turning mature cells with a specific function into stem cells that can become any other cell type.
The cell reprogramming process he developed takes around 50 days to run its full course, and makes use of four key molecules which have been dubbed “the Yamanaka factors”.
What Dr Gill and his team have done, instead, is to expose skin cells to the Yamanaka factors for just 13 days — which strips the cells of all their age-related changes and causes them to temporarily lose their identity.
When these partly-reprogrammed cells were given time to grow under normal conditions, however, the team found that the specific functions that make them skin cells returned.
Under a microscope, the cells were observed to produce collagen, the protein that makes skin resilient and strong and helps heal wounds, while genomic analysis confirmed that the cells had regained all the markers that are characteristic of skin cells.
The researchers were also able to confirm that the cells — which came from three donors aged 38, 53 and 53 respectively — had lost the hallmarks of ageing.
Dr Gill said: “Our understanding of ageing on a molecular level has progressed over the last decade, giving rise to techniques that allow researchers to measure age-related biological changes in human cells.
“We were able to apply this to our experiment to determine the extent of reprogramming our new method achieved.”
In fact, after checking both the cells’ “epigenetic clock” — which works by assessing the presence of chemical tags throughout the genome that indicate age — and all the gene readouts produced by the cell, the “transcriptome”, the researchers found that their process had effectively de-aged the skin cells be around 30 years.
The key to this research is that the cells do not just look three decades younger, but are able to act like it as well.
According to the team, the rejuvenated skin cells were able to produce collagen faster than cells of the same actual age that had not undergone the procedure.
Experiments involving creating artificial cuts in a layer of cells in a petri dish also showed that the rejuvenated skin cells moved faster to fill the gap.
The researchers said that this suggests their findings could be developed to create cells that are more efficient at healing wounds.
The team also reported that their “maturation phase transient reprogramming” method also appeared to have a potentially useful effect on genes related to age-related diseases.
For example, both the APBA2 gene — which is associated with Alzheimer’s disease — and the MAF gene which has been linked to the development of cataracts were found to show changes towards more youthful levels of transcription after the reprogramming process.
Dr Gill said: “We have proved that cells can be rejuvenated without losing their function and that rejuvenation looks to restore some function to old cells.
“The fact that we also saw a reverse of ageing indicators in genes associated with diseases is particularly promising for the future of this work.”
The team said that, while the technique is in its early stages, it has the potential to “revolutionize” regenerative medicine.
Paper co-author and epigeneticist Professor Wolf Reik, formerly also of the Babraham Institute, added: “This work has very exciting implications.
Senolytics Improve Resistance Training In Old Mice
A senolytic combination only improved muscles with resistance training, not without it.
In this paper, the researchers cite their prior research showing that the SASP, in conjunction with its known inflammatory effects, harms the ability of muscle progenitor cells to proliferate, thus depleting the ability of muscle to regenerate.
That paper showed that removing senescent cells through the senolytic combination of dasatinib and quercetin (D+Q) allowed for muscle regeneration in old mice, although it did not benefit old mice.
In this new research, the research sought to determine whether this also applied to muscle hypertrophy: that is, whether senolytics can help older organisms to build muscle through resistance training.
Resistance Training For Mice
Unfortunately, it isn’t possible to get mice to the gym. Therefore, the researchers used an established technique of removing “synergistic” muscle tissue (in this case, of the soleus and the gastrocnemius) in order to spur the development of the targeted muscle (in this case, the plantaris) . Sham surgeries, in which no tissue was actually removed, were performed on a control group.
The plantaris muscles of both young (5 to 6 months) and old (23 to 24 months) mice increased slightly compared to their respective control groups, although young mice had significantly more muscle mass both before and afterwards, and while older mice stopped growing plantaris muscle tissue after a week, younger mice continued to grow it for two weeks.
As expected, senescent cells, which increase in muscle tissue after exercise, were found in substantially greater numbers in the older mice, especially after 14 days.
While their numbers varied wildly from mouse to mouse, older mice had substantially and significantly more senescent cells than younger animals did, according to tests for the known senescent biomarkers p21 and SA-ß-gal.
The Effects Of Senolytics
The effects of D+Q on senescent cells were significant, in line with previous murine studies. Cells expressing SA-ß-gal were decreased to a third of their previous level, while cells expressing p21 were approximately halved.
The researchers’ main hypothesis, that D+Q would increase muscle mass upon resistance training, was shown to be correct: older mice given this senolytic combination and the surgery had greater plantaris muscle mass and superior fiber characteristics to the older mice given only the surgery.
However, this comes with an important caveat. Older mice that received D+Q but only received the sham surgery, which did not impart resistance effects on their plantaris muscles, actually had muscles that were weaker or equal to the mice that did not receive D+Q at all.
In other words, in the absence of resistance training, senolytics were not shown to be of any benefit and may have even have caused harm below the level of statistical significance.
Senescent Cells In Human Volunteers
Fortunately, it is possible to get people to the gym. In a cohort of human volunteers between 20 and 39 years old, nearly no senescent cells were found in muscle tissue; however, after resistance exercise, p21 and SA-ß-gal tests found the presence of these senescent cell biomarkers, although their numbers varied wildly as they did in mice.
This data suggests that the results found in mice may apply to human beings, although this was not a human trial.
The finding that senolytics may only have value in building muscle when combined with resistance exercise is a very important one that will certainly guide future trial design. If the results found in mice are recapitulated in human beings, a senolytic and exercise combination may be prescribed in the near future in order to give older people back some of their mobility and fight back against frailty.
 Dungan, C. M., Murach, K. A., Zdunek, C. J., Tang, Z. J., VonLehmden, G. L., Brightwell, C. R., … & Peterson, C. A. (2022). Deletion of SA ß-Gal+ cells using senolytics improves muscle regeneration in old mice. Aging Cell, e13528.
 Kirby, T. J., McCarthy, J. J., Peterson, C. A., & Fry, C. S. (2016). Synergist ablation as a rodent model to study satellite cell dynamics in adult skeletal muscle. In Skeletal Muscle Regeneration in the Mouse (pp. 43-52). Springer, New York, NY.
How Old Are You Really? Meet Your ‘Biological Age’
Biological age won’t help you live forever, but a ‘credit score for your body’ might prolong your lifespan, some scientists say.
Biological age—a measure of health that can be more or less than your chronological age—might help determine your quality of life as you get older, scientists say.
The idea behind biological age is that your cells and organs have ages that vary from your regular age. Many aging-research scientists believe that knowing your biological age could help you postpone or avoid Alzheimer’s, cancer, cardiovascular disease or other age-related illnesses. Some also believe biological age can better predict an individual’s lifespan.
Other scientists agree that biological age is important but disagree that it can predict your life. They say there is no standard way to measure biological age and many of the tools in development aren’t yet proven.
At the center of the debate are hopes that people can prolong their lives by changing their behaviors; a crop of companies are betting on it.
David Sinclair, professor of genetics and co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School, is among the researchers and entrepreneurs promoting the notion of a biological age. He describes it as “like a credit score for your body.”
Dr. Sinclair is 52 chronologically but says he is biologically more like 42. Dr. Sinclair is a co-founder of a new company that is developing a biological-age test.
Some scientists calculate the metric by analyzing biomarkers in blood or saliva; other scientists and engineers do it by comparing individuals with broader aging patterns.
The activities that influence biological age—such as sleep, exercise and diet—are essentially the good habits we already know about.
But since everybody’s genes are different, tracking your biological age could help determine which habits are most helpful and how to customize them. For one person, 10,000 steps a day could be optimal, while it is 6,000 for someone else.
People also can attempt to lower their biological age through meditation, yoga or other ways of effectively managing stress. Some, including Dr. Sinclair, use supplements to try to make themselves younger.
Scientists studying aging hope that eventually, individuals will be able to accurately measure their biological age and uncover the steps that influence it to forestall chronic disease and possibly live longer.
‘Your choices have a much more profound effect than just changing whether your heart is beating fast or slow.’
— Michael Roizen, an anesthesiologist
Even so, some scientists are skeptical of the process. Some think that even if you do know your biological age, it is a stretch to believe that you could use the concept to help you live longer.
Alex Zhavoronkov, chief executive of Insilico Medicine, which uses artificial intelligence to develop drugs targeting age-related diseases, says biological age is a useful concept for drug development. But he says he doubts that people will be able to use behaviors to live longer, based on studies of lifespan in different countries around the world.
“Extreme optimization of sleep, exercise and diet is unlikely to result in dramatic lifespan increases,” he says.
Growing interest in biological age is fueled by advances in the field of epigenetics, the study of how gene expression is affected by behaviors and the environment.
Dr. Sinclair at Harvard is developing a biological-age test based on chemical changes on DNA found in cells from the side of the cheek taken in a swab you do at home. He plans to launch it with a new company called Tally Health.
Dr. Sinclair has been criticized by other scientists for hyping the results of some of his findings, like the antiaging effects found in the compound resveratrol, claims he rebuts.
He says that he doesn’t overstate his research findings and that the resveratrol research was published in leading scientific journals. He has co-founded more than a dozen biotech companies and is invested in most of them, including some that are developing therapeutics that target the biology of aging.
Segterra Inc.’s InsideTracker, a personalized-nutrition company founded by scientists from Harvard, Tufts University and the Massachusetts Institute of Technology, calculates biological age by having users take blood tests and analyzing the samples for markers of conditions like inflammation, heart health and liver or kidney disorder.
Those who test as older than their years get recommendations to adjust diet, exercise and supplements.
Many other health startups are offering testing that purports to calculate biological age, sometimes with little scientific backing, and designing supplements aimed at boosting youthfulness.
Stephen Roberts, a winery owner in France, tested himself earlier this year with an at-home blood test by U.K.-based biotech company GlycanAge Ltd. The test was part of an effort by Mr. Roberts to improve his health at age 51.
“I drink. I sometimes smoke and party and eat what I want,” he says, so he expected his biological age to be a lot older than his calendar age.
He says he was shocked when test results reported his biological age was 24.
“My first reaction was: ‘This is wrong.’” He says he hasn’t made any changes as a result of the test but plans to test again later this year.
Gordan Lauc, professor of biochemistry and molecular biology at the University of Zagreb, in Croatia, and chief scientific officer of GlycanAge, says the results make sense given Mr. Roberts’s genetics—longevity runs in his family—and lifestyle, which is likely lower-stress than most.
Michael Roizen, an anesthesiologist and chief wellness officer emeritus at the Cleveland Clinic, created one of the first biological age calculators 25 years ago based on a questionnaire. He sold it to digital health company Sharecare Inc., where he receives stock options as a member of its scientific advisory board.
Dr. Roizen now has a book and website due out in the fall, part of a new company he says will be aimed at helping people understand how to live longer.
Exercise, for instance, does more than strengthen your heart, he says. Working out switches on a gene that starts a chain reaction that increases secretion of a protein that improves memory, studies show. Your methods of managing stress can switch on or off the functioning of more than 250 genes, Dr. Roizen says.
“Your choices have a much more profound effect than just changing whether your heart is beating fast or slow,” says Dr. Roizen.
Why Longevity Matters To Everyone: Living Longer Lives In The World Of Web3
Physicians and founders are rallying behind longevity medicine, and here is what a longer, healthier human lifespan means for the crypto community.
Expected to reach a market size of $128 billion by 2028, the longevity sector is no longer something that those outside the medical world can ignore. In the next few years, life-extending technologies and treatments for aging-related diseases will reach human trials.
There is an exciting wave of development happening in research labs and technology centers across the globe, with more and more early adopters embarking on their longevity journeys.
Longevity not only incorporates disruptive technologies, such as artificial intelligence and distributed ledger technologies but also has a visionary spirit and is supported by stakeholders dedicated to improving the human aging experience.
To share more about this up-and-coming sector, I spoke with three individuals about their alignment with longevity science and why they want you to know about the opportunities afforded by embracing longevity.
The sector has already shown tremendous support in favor of the industry. The insights from one of the world’s foremost longevity physicians, the founder of the world’s leading full-service blockchain technology company, are unique but share a common theme: It is time for the world to pay attention to what the future holds for human lifespans.
Evelyne Yehudit Bischof, Chair Of The Longevity Science Foundation Visionary Board
“As a longevity physician, my goal is to maintain or even improve the quality of life for someone. But the term ‘longevity’ conjures images of living longer. But it’s more than just that. Life has to be fulfilling. It has to be fun. In longevity medicine, it is essential to focus on physical health as well as behavioral and mental health. All these pieces fit to make a healthy human.”
“In general, I am not a fan of sweeping recommendations. I like personalization. I like structure. I especially like structure when developing treatment trajectories for a patient. Of course, there is a foundation of longevity that incorporates common themes. However, I do not have typical recommendations for everybody.”
“I look at the unique characteristics of each patient in several different categories. The first category is metabolic optimization. This category encompasses nutritional improvements, exercise and hormones. Some people are athletes, and I also work with pre- and post-menopausal women. Some patients are preparing for pregnancy. These unique characteristics factor into the recommendations.”
“The second category is sleep. Many people underestimate how important sleep is to maintaining healthy bodily functions. As part of patient evaluation, I look at how easily the patient falls asleep and how optimal the sleep is based on oxygen levels, the number of apnea episodes, and more.”
“The third optimization area is cognition. Neurodegeneration is a significant concern for individuals as they age, and optimizing this area requires early prevention of any cognitive decline or neurosurgical health. Cognition also includes mental health. I am trained in psychiatry, so mental health is essential to me. A lot of people are already on antipsychotics or antidepressants. I meet patients where they are and help them achieve their goals of improving mental health.”
“As you can see, we very much focus on the granular level in longevity treatment. We focus on all aspects of a person to ensure treatments work in harmony. Physicians and patients need to remember that flexibility is key for any medical success. Longevity treatment should be just as flexible.”
Val Vavilov, Founder And Chief Visionary Officer Of Bitfury And Member Of The Longevity Science Foundation Patrons Board
“My interest in longevity began as a personal one. Running a global, billion-dollar company takes a toll on you. To achieve our mission, I realized that I needed to optimize not only my health but also my physical, emotional, mental and spiritual development. Health is usually one of the first things people neglect when they are focused elsewhere.”
“I started reading about everything that was considered cutting-edge in the field, from intermittent fasting to veganism. I even went as detailed to evaluate the micronutrients of different fruits and vegetables I was eating to balance them. When you start researching these things, you will eventually come to the field of longevity because longevity is all about the optimization of your life and health. That speaks to the engineer in me. We look at what we can optimize and how to do it. I spent more than a year optimizing my health, food, sleep — everything. And now, I feel better than I did in my 20s!”
“I became a patron of the Longevity Science Foundation because I genuinely believe longevity should not just belong to one group of people. Everyone deserves access to the tools and science to live longer and healthier lives. I support the mission of the foundation to democratize access to this information because everyone has the right to it. Longevity should be shared.”
“What is the point of living a longer and healthier life if you are the only person benefiting from it? What kind of a world will you inherit? How can you build a better one if you are alone? Longevity is a crucial piece of our collective future. Crypto, blockchain and Web3 make it easier for us to work together and support each other — while protecting ourselves. Longevity science means we can do that while living longer, being healthier and being happier. In other words: A better existence is out there for humans if we collaborate and create more open systems accessible to everyone.”
Maja Vujinovic, Managing Director Of Ogroup And Member Of The Longevity Science Foundation Patrons Board
“I’ve been an early pioneer in emerging technologies since 2005, entering spaces, such as mobile payments, renewable energy, the Internet of Things, CRISPR and cryptocurrencies, years before they reached mainstream understanding and recognition. Working at this leading edge requires one to constantly question the status quo and to search for optimization. I’m bringing the same pioneering attitude to longevity: There is more to longevity medicine than the extension of life. It’s about nudging our evolutionary engine. It is a challenging yet thrilling quest.”
“Our ancestors had countless challenges to overcome as we moved from caves to dwellings to tribes to cities to where we are now. We had to deal with predators, disease, famine, war, infection. While many of these challenges still exist, we have defenses against many of them. These are defenses that we developed outside of ourselves. There was nothing evolutionary about them. Today, it is a combination of internal and external development that is furthering society. Thanks to incredible technological breakthroughs, we are able to access products that aid in our evolutionary process.”
“However, our biological evolution has been outpaced by a technological revolution. Simply put, the human brain cannot advance with the same inertia as current technological progress. This might seem like a scary concept, but it’s also an exciting one. This unprecedented progress is inspiring. I see this spirit in the crypto community, and I see it again in longevity medicine. There is a powerful movement to improve the way existing systems like the financial sector function by disrupting and democratizing them. I see the longevity thesis as a disruptor of the way we age.”
“Longevity medicine is about the balance of technology and our own awareness to be more present and a reminder of the basics. In some aspects, our quality of life is even worse than that of our ancestors, as we have less time to do the things we love. Our appetite for connection is decreasing as a result of constant technology usage and less human interaction. Thus, longevity is about making a plan for yourself that looks beyond a pill, injection, hyperbaric chamber or an expensive health spa. Instead, it is about establishing a daily routine and lasting, sustained change versus mindless, endless growth for the sake of growth. It requires planning, restrategizing our healthcare costs, and upgrading where it makes sense.”
“You commit to that in your work. Are you ready to do that for your life?”
New Study Pinpoints Eight Foods That May Hold The Key To Illness-Free Old Age
LIFE expectancy tends to differ between the sexes, with women living longer than men on average. However, this superiority comes at a cost for women – they tend to have higher rates of illness. Now, a new study has pinpointed eight foods that can help to shield women against illness as they age.
On average, women live longer than men. In fact, “57 percent of all those ages 65 and older are female. By age 85, 67 percent are women”, according to Harvard Health.
That is not to say those added years are an unalloyed benefit – women tend to have higher rates of illness. However, new research suggests women can reduce their exposure to illness by improving their diet.
Researchers found a diet high in pigmented carotenoids such as yams, kale, spinach, watermelon, bell peppers, tomatoes, oranges and carrots can help to shield the body against illness.
These bright-coloured fruits and vegetables are particularly important in preventing visual and cognitive loss.
“The idea is that men get a lot of the diseases that tend to kill you, but women get those diseases less often or later so they perseverate but with illnesses that are debilitating,” said Billy R. Hammond, a professor in UGA’s Franklin College of Arts and Sciences department of psychology behavioral and brains sciences program and co-author of the study.
“For example, of all of the existing cases of macular degeneration and dementia in the world, two-thirds are women … these diseases that women suffer for years are the very ones most amenable to prevention through lifestyle.”
The study, which reviewed and analysed data from previous studies, detailed several degenerative conditions, from autoimmune diseases to dementia that, even controlling for lifespan differences, women experience at much higher rates than men.
“If you take all the autoimmune diseases collectively, women account for nearly 80 percent. So, because of this vulnerability, linked directly to biology, women need extra preventive care,” Professor Hammond said.
What Accounts For This Asymmetry Between The Sexes?
One of the reasons for this vulnerability has to do with the way women store vitamins and minerals in their bodies.
Professor Hammond points out that women have, on average, more body fat than men.
Body fat serves as a significant sink for many dietary vitamins and minerals, which creates a useful reservoir for women during pregnancy.
This availability, however, means less is available for the retina and the brain, putting women at more risk for degenerative problems.
Dietary intake of pigmented carotenoids act as antioxidants for humans. Two specific carotenoids, lutein and zeaxanthin, are found in specific tissues of the eye and brain and have been shown to directly improve central nervous system degeneration.
“Men and women eat about the same amount of these carotenoids, but the requirements for women are much higher,” said Professor Hammond.
“The recommendations should be different, but there are, generally, not any recommendations for men or women for dietary components that are not directly linked to deficiency disease (like vitamin C and scurvy),” Professor Hammond said.
“Part of the idea for the article is that recommendations need to be changed so that women are aware that they have these vulnerabilities that they have to proactively address, so they don’t have these problems later in life.”
Carotenoids are also available via supplements, and the National Institutes of Health has focused resources on specific carotenoids through the National Eye Institute program.
And though supplements of lutein and zeaxanthin are a way of increasing intake, Professor Hammond said getting them through food is a much better strategy.
“Components of diet influence the brain, from things like personality to even our concept of self. I don’t think people quite realise what a profound effect diet has on basically who they are, their mood, even their propensity to anger,” Professor Hammond said.
“And now of course this is extended to the microbiome and the bacteria that make up your gut – all of these components work together to create the building blocks that compose our brain and the neurotransmitters that mediate its use.”
You Can Boost Your Body’s Natural Healing With Platelet-Rich Plasma Therapy
The body comes with incredible power to heal itself, but sometimes it needs an added boost. Platelet-rich plasma therapy offers an innovative form of regenerative medicine to accelerate tendon healing and decrease arthritic pain.
“The idea is that a lot of injuries don’t heal well because they don’t receive adequate blood flow. Blood contains certain markers that let our bodies know an injury needs attention and help; so less blood flow means less healing,” explained Dr. Tyler Hedin, physical medicine and rehabilitation specialist at the East Falls Clinic.
“Our tendons and joints are notorious for not getting a lot of blood flow. That’s why we’re bringing platelet-rich plasma, a mixture from the patient’s own blood, directly to the problem areas.”
Regenerative medicine focuses on regrowing, repairing or replacing damaged cells. With platelet-rich plasma therapy, that revival occurs as physicians inject the body’s own plasma, enriched with a dense number of blood cells that cause clotting and other needed growth and healing functions.
Dosing the injuries with mass platelets provides a callout for internal attention and action.
A Regenerative Approach: The Future Of Medicine
For the past five years, Dr. Hedin has offered the procedure, where he draws a patient’s blood, mixes it in a high-quality centrifuge machine that concentrates the platelets, then injects the enriched liquid directly into the wounded tendon or musculoskeletal area.
“Regenerative medicine is very up and coming and likely the future of medicine, and I’ve seen great successes with platelet-rich plasma injections,” Dr. Hedin said.
Platelet-rich plasma therapy works well with chronic tennis elbow, rotator cuff and Achilles’ tendon injuries, as well as mild to moderate arthritis in the knees, hips and shoulders.
For example, one of Dr. Hedin’s patients suffered from a work-related shoulder injury. With two rotator cuff tears and a tear along the ring of cartilage in the shoulder joint (also known as a shoulder labral tear), the patient figured surgery was imminent – until he heard about platelet-rich plasma therapy.
“That patient had a lot going on, but we avoided surgery by injecting platelet-rich plasma in all three sites at the same time. I saw the patient a month later, and the pain had decreased significantly; by six weeks, he had full range of shoulder motion and no pain at all,” Dr. Hedin said.
Another patient dealt with a chronic hamstring injury that refused to respond to physical therapy or any other treatment plans. Sitting caused the patient great pain and driving more than 30 minutes became excruciating.
One month after an injection of platelet-rich plasma to the hamstring tendon, the patient could be in the car for longer durations; by two months, the pain had completely dissipated.
Choosing Quality Care For Quality Results
Although Dr. Hedin regularly witnesses the positive results of platelet-rich plasma therapy, research often reports varied reviews. Dr. Hedin believes that’s because not all medical physicians and equipment are created equal.
“Anyone can buy a centrifuge machine online and say they offer platelet-rich plasma therapy – but it needs to be done the right way to get the best results. I advise patients to research not only the amount of experience a physician has, but the quality of equipment used,” Dr. Hedin said.
“I also encourage my patients to pair platelet-rich plasma therapy with physical therapy in order to get the best results, as the stretching and strategic exercises can also increase blood flow.”
Once patients feel comfortable with their physician, facility and treatment plan, Dr. Hedin says they can expect an initial increase in swelling and soreness directly after an injection of platelet-rich plasma, and then the injury gradually improves.
“Usually within three to four weeks, patients notice a decrease in pain; by six to eight weeks the results really shine. Though this isn’t an instant fix, it offers long-term healing without surgery. I like offering patients a way they can save costs and avoid trauma and potential complications from a surgical procedure,” Dr. Hedin said.
“I think prompting the body to fix injuries on its own is incredibly rewarding – especially as patients get back to living life and the things they love to do. That’s the whole nature of my specialty.”
Scientists Aim To Grow Billions Of Stem Cells Aboard The International Space Station
Stem Cell Growth In Space
Stem cells can be used to generate nearly any type of cell in the body. Due to their impressive adaptability, they have great potential as a key tool in developing a wide array of treatments for diseases, including Parkinson’s and heart disease.
This is the latest effort to overcome one of the key hurdles for widespread stem cell therapies.
Scientists from Cedars-Sinai Medical in Los Angeles are investigating how to grow large batches of a specific type of stem cell.
Their mission has taken them orbital — to the International Space Station — and it could help unlock a whole host of stem cell therapies to combat deadly diseases.
One of the researchers, Dhruv Sareen, even donated his own stem cells for the experiment, a press statement reveals. If all goes to plan, the scientists hope to eventually grow billions of stem cells in space.
Sareen’s cells arrived aboard a SpaceX resupply mission — the SpX-25 dragon cargo mission — to the ISS over the weekend. “I don’t think I would be able to pay whatever it costs now” to travel to space as a tourist, Sareen said. “At least a part of me in cells can go up!”
Several stem cell experiments have been conducted aboard the ISS in the past, as the microgravity conditions aboard the orbital space station provide a wildly different environment in which to investigate new methods and applications.
Though most stem cell therapies are still some way off from coming to consumers, space could help overcome one of the main logistical hurdles when it comes to mass production.
A Stem Cell Rideshare Mission To Space
In the future, stem cell therapy patients could require billions of cells depending on their treatment. Earth’s gravity makes it difficult to grow the vast quantities of stem cells needed for therapies, so that’s where the ISS comes in.
“With current technology right now, even if the FDA instantly approved any of these therapies, we don’t have the capacity to manufacture,” Jeffrey Millman, a biomedical engineering expert at Washington University in St. Louis, explained.
This is because, on Earth, large bioreactors are required to grow stem cells. The cells need to be stirred vigorously, so they don’t clump together or fall to the bottom of the tank.
However, the stirring itself can damage the cells. In microgravity, there’s no force on the cells so that they can grow via a different method.
The Cedars-Sinai team sent up a shoebox-sized container holding pluripotent stem cells for their NASA-funded experiment. It contains pumps and chemical solutions required to keep the stem cells alive for four weeks. The same experiment will be carried out on Earth for comparison.
In roughly five weeks, the box in space will be returned to Earth in the same SpaceX capsule it was carried up on. The rideshare mission will allow the scientists to directly evaluate the results in space and on Earth within a short timeframe. This will provide valuable new data that could help unlock a promising new field of medical research.
Can A ‘Magic’ Protein Slow The Aging Process?
Several years ago, scientists studying aging at the Harvard Stem Cell Institute used a somewhat Frankensteinian technique known as parabiosis — surgically joining a young mouse and an old mouse so that they share blood — to see what would happen to the heart and skeletal muscle tissue.
They knew from previous research that putting young blood in old mice caused them to grow biologically younger, and that young mice exposed to old blood aged faster.
The Harvard researchers, Amy Wagers and Dr. Richard Lee, found that the old mouse’s heart tissue had been repaired and rejuvenated, becoming young again. In fact, the size of the old mouse’s heart had reduced to that of a young heart.
“We all wondered, what’s the magic stuff in the blood?” said Lee Rubin, a professor of stem cell and regenerative medicine at Harvard and the co-director of the neuroscience program at the Stem Cell Institute. The “magic” they identified was a protein, GDF11, one of tens of thousands produced in the human body.
Dr. Rubin’s lab also found that GDF11 in mice stimulated the growth of new blood vessels in the brain and neurons in the hippocampus, a part of the brain associated with learning and memory.
Dr. Wagers’s lab found that GDF11 rejuvenated skeletal muscle tissue, too. The scientists’ discoveries were published in the journals Cell and Science in 2013 and 2014.
The obvious next question: Could GDF11 be harnessed to promote regeneration and repair in humans? In 2017, Drs. Rubin, Wagers and Lee, along with five others, founded the pharmaceutical start-up Elevian with the aim of commercializing GDF11-based therapies to stop, slow or reverse diseases associated with aging.
It’s a big step from mice to humans, but one that could have profound consequences.
“We’re interested in proteins like GDF11 that are excreted into the bloodstream because those can cause changes throughout the body,” said Dr. Mark Allen, the chief executive of Elevian. “And those are the kind of changes we want.”
Dr. Allen started his first health care company while in medical school at the University of California, Los Angeles, and he left his residency position in 2000 to start a second.
In early 2017, he and his investment partner, Sebastian Giwa, an economist, were looking to start a new one that would develop therapies targeting the degenerative processes involved in aging. They looked at two dozen potential research projects before deciding on GDF11.
“I had this idea that aging itself could be a target for therapeutic intervention,” Dr. Allen said, “because if we target one aspect of the aging process, then we have the potential to treat many different diseases.”
The initial research into the rejuvenating properties of GDF11 has gotten some pushback from the scientific community.
In 2015, after Dr. Wagers and Dr. Lee had published their results, a group of researchers led by David Glass, the executive director of the Novartis Institutes for Biomedical Research in Cambridge, Mass., at the time, challenged the accuracy of their findings in an article in the journal Cell Metabolism.
The Harvard researchers subsequently countered the Novartis team’s findings in another paper published later that year in the journal Circulation Research, in which the Harvard researchers cited a problem with the Novartis team’s findings.
Dr. Glass, who is now at the biotechnology company Regeneron, said in a recent email that he stands by his original work, which showed that GDF11 inhibits, rather than helps, muscle regeneration. But, he added, “our work still leaves open the possibility that there could be positive effects of GDF11 in particular settings.”
Dr. Allen said that since the original controversy, Elevian’s research team has reproduced and extended its original findings in multiple studies, but none have yet been published in peer-reviewed journals.
However, institutions unrelated to Elevian have conducted and published many preclinical studies demonstrating the therapeutic efficacy of rGDF11 (the form of GDF11 developed in a lab) in treating age-related diseases.
The company is on track to begin human clinical trials in the first quarter of 2023 and has raised $58 million in two rounds of funding, with another round set for mid-2023.
Elevian is one of many companies racing to find ways to increase the human life span by increasing “health span,” the period of life when a person is in generally good health.
About $2 billion in venture capital was invested in pharmaceutical companies focused on anti-aging in 2021, according to Longevity Technology, a market research company and investment platform focused on the longevity sector.
For years, researchers have been looking for drugs that can extend life span and health span. The Interventions Testing Program at the National Institutes of Health began testing drugs — some approved by the Food and Drug Administration, some not — in mice 17 years ago to see if these interventions would extend their lives.
Dr. Richard A. Miller, a professor of pathology at the University of Michigan and the director of the Paul F. Glenn Center for Biology of Aging Research, said anti-aging therapies are often tested on mice because aging in mice is very similar to aging in humans.
“Mice and people share organs, cell biology and most varieties of neurons and neurotransmitters, and they often respond to drugs in similar ways,” he said.
A significant challenge lies ahead for all of these companies: Commercializing a drug for aging is nearly impossible because the F.D.A. doesn’t recognize aging as a disease to be treated.
And even if it were considered a disease, the clinical studies required to prove that a treatment for it worked would take many years.
“It is likely that clinical studies to see if some drug slows aging — and thereby delays the many consequences of aging — would take a long time,” Dr. Miller said.
So Elevian’s founders determined that the fastest way to market for GDF11 was to target a specific medical condition.
“We thought, what’s the worst disease that has no good treatment and that we could treat for the shortest possible duration and show clinical effects?” Dr. Allen said. “We decided that stroke was the right one to target, because it’s the No. 1 cause of long-term disability with very limited treatment options.”
But according to experts, only about 20 percent of stroke victims receive tPA, either because the stroke is not recognized soon enough or because the patient doesn’t qualify because of pre-existing conditions.
Elevian’s researchers said their preclinical (and as yet unpublished) studies have shown that just a few days of treatment with GDF11 can improve recovery after stroke.
They have found that GDF11 reduces inflammation, improves metabolism and stimulates the brain to regenerate blood vessels and neurons.
The next big hurdle for Elevian is scaling its manufacturing, which requires specialized equipment and conditions. So much research is being conducted in biotech that contract manufacturers are “full up,” Dr. Allen said.
“They are busy with Covid-related work, and there has been a lot of funding in biotech generally,” he added. “So it’s a challenge finding the space that meets our specifications.”
And, like almost all other sectors of the economy, biotech research is facing supply chain issues, which make it harder for Elevian to get some of the basic materials it needs to conduct research.
But the company is moving forward as fast as it can, and Dr. Allen said he believed the results of its work would have a profound impact on the way we age and how long we live.
“By targeting fundamental mechanisms of aging, we have the opportunity to treat or prevent multiple aging-related diseases and extend the health span,” he said. “We want to make 100 the new 50.”
3 Underrated Hacks For A Longer Life, From A Longevity MD
Longevity dominates the health and well-being conversation—you can find numerous tips and tricks for a longer life (and you can bet we’ve covered them all!).
Although, because there are so many hacks to consider, it raises the question: Which techniques give you the best return on investment? Or in other words: How do you get the most bang for your buck with longevity?
You’ve likely heard it once or twice before: Your body’s fight-or-flight response is necessary for your survival, but in our modern society, it gets activated way too often. “We get alerted so easily, whether it be somebody leaving a comment you don’t like on your Instagram or somebody cutting you off on the freeway,” says Vuu.
“You’re telling your body there’s a saber-toothed tiger behind you, and if you think that there’s a saber-toothed tiger behind you the majority of your day, you’re going to increase inflammatory markers.”
There isn’t one way to magically eliminate your stress (these tips can help you get started, if you need some inspiration), but Vuu recommends finding the stress-relieving strategies that work best for you. You might even want to invest in a tracker that measures your heart rate variability, which is a metric that reflects your stress levels.
“Heart rate variability is a marker for a parasympathetic state,” says Vuu. “The greater variance you have in your heart rate variability, the more connected you are to your parasympathetic [nervous system, and we want that because parasympathetic is really a state of healing.”
I use my Whoop to track my HRV, but whatever wearable you choose (if any), make sure you don’t stress yourself out trying to reach a specific number. “That ultimately defeats the purpose if you’re getting more stressed by looking at your numbers,” says Vuu.
OK, we just discussed how too much stress can impede longevity—but a little bit of stress is actually a very good thing. “If we’re able to stress our bodies a little bit, our bodies tend to respond in such a way that makes us better,” says Vuu.
It’s a concept called hormesis: Short, intermittent bursts of certain stressors (called “hormetic stressors”) that can trigger a cascade of cellular processes that make you more resilient to future physical and mental stress, thus enhancing longevity.
“For example, when we fast, we stress our bodies, and it turns on these pathways, namely autophagy, where we clean up all the intracellular junk in our bodies and renew them. “We know that has led to longevity. When we expose ourselves to extreme heat or cold, there are benefits to our bodies,” notes Vuu.
When we asked Vuu how to get the biggest bang for your buck in terms of longevity, he responded with a practice that’s 100% free: building awareness. “If you can build more awareness in your life and have a tactical pause before you do anything, you can direct the life that you want to live,” he states.
Allow Him To Explain: “People are a little bit hypnotized [by] this matrix of how they’re living life, and that way of living is really creating disease,” he adds. “When we’re able to take a tactical pause and say, ‘Oh man, I’m craving that cookie right now, but that’s not really good for me. Can I drink some sparkling water instead? Can I go for a walk instead? Boom. You’ve just made a decision toward your health.”
Basically, it’s all too easy to coast through life on autopilot, simply acting upon what we’ve learned from society, our parents, etc. But if you can break out of that cycle and really think about the decisions you’re making, you can ultimately make better choices for your health.
“Create that space, because in that space is who you create yourself to be…in our relationships, our health, and in our businesses,” Vuu continues. And as we mentioned, creating consciousness is completely free of charge.
If you’d like to focus on a few avenues for longevity, Vuu says stressing your body (just not too much!) and implementing self-awareness can give you a lot of bang for your buck.
Make sure to tune in to the full episode to hear more of his longevity-enhancing tricks—plus, some up-and-coming fancy therapies you should have on your radar—but these free hacks can certainly help you get started.
Startup Reveals That It Has Successfully Transplanted Mitochondria And Achieved “Apparent Age Reversal”
Early data from mitochondrial transplantation study indicates longevity potential.
Mitrix Bio adds Dr Thomas Rando to advisory board as bioreactor-grown mitochondria collaboration shows promise in targeting longevity and age-related disease.
Mitochondrial transplantation start-up Mitrix Bio today revealed it has been working on a project with several universities to explore the potential of using mitochondria grown in bioreactors to target a wide range of age-related diseases.
The project involves large-scale mitochondrial transplantation in animal disease models and in vitro human cells. Mitrix said today that “early results suggest broad efficacy for targeting the immune system, brain, retina, liver, skin, and systemic anti-aging.”
The company also recently announced the appointment of UCLA professor Thomas Rando to its advisory board. The former Stanford professor is one of the longevity field’s leading scientists, with decades of research spanning stem cell aging and epigenetic rejuvenation, tissue engineering, muscle stem cell biology and muscular dystrophies.
Rando joins existing Mitrix advisors, including Professor Michael Snyder, Chair of Genetics and Director of Genomics and Personalized Medicine at Stanford University.
Longevity.Technology:Mitochondria, the power generators within our cells, are heavily implicated in the aging process, and their dysfunction is linked to a wide range of age-related diseases. The “mitlets” technology being developed at Mitrix, and the longevity potential of mitochondrial transplantation, are fascinating. While the company is still at an early stage and the “results” mentioned today are yet to be published, Mitrix says that a series of peer-reviewed papers will be released in the coming months, and the addition of Dr Rando to its advisory board certainly catches the eye.
While mitochondrial transplantation has been explored for several years, Mitrix says that studies have been confined mainly to rare paediatric diseases and surgery.
This is due to scarce supplies of donor mitochondria, which the company aims to address with its approach to growing mitochondria in bioreactors.
Mitrix’s 18-month project focused on adult diseases and longevity, involving researchers from the University of Connecticut Technology Incubation Program, Stanford University, Université Laval Quebec, and Nova Southeastern University.
A series of mitochondrial transplantations were performed in brain, eye, liver, immune system, and skin tests.
In these tests, “young” highly functional mitochondria were grown in prototype bioreactors and transfused into the bloodstream, with the aim that they are absorbed by cells to help supplement old, dysfunctional mitochondria and reverse energetic decline.
Future Therapies For Age-Related Disease
Mitrix says that the tests showed “apparent age reversal in multiple endpoints” in both animal disease models in vivo and human cells in vitro.
The company believes the results seen indicate potential future therapies for age-related diseases such as Alzheimer’s, macular degeneration, cardiovascular disease, frailty and immune senescence.
Beyond specific diseases, Mitrix also says that antiaging effects were also observed on animals’ strength, cognition and appearance.
“These are still early results, and more work remains to be done in human tests, but we think the data points to a potential breakthrough in longevity… in a shorter timeframe compared to other longevity treatments,” said Mitrix Bio CEO Tom Benson.
“There are plenty of common-sense ways to protect mitochondrial function, like exercise and good nutrition, but none of those are likely to stop mitochondrial decline at 80 years old. With mitochondrial transplantation, we’re not just tinkering around the edges – this replaces mitochondria entirely, like replacing the engine in your car to get another 100,000 miles.”
“All things considered, having improved bioenergetics trumps many of the negative impacts of aging,” said Benedict Albensi, PhD, mitochondria expert and principal investigator for Mitrix Bio. “Even if improvement from mitochondrial transplantation is indirect, it buys time, and that is what longevity is all about.”
Addressing The “Energetics Gap”
With billions currently being poured into development of longevity therapeutics, Benson tells us he believes that failing to address mitochondrial dysfunction would be a grave mistake.
“We call it “the energetics gap” and it’s an obstacle to all longevity therapies going forward,” he says. “The tissues of an elderly person are chronically energy depleted. The aging human body is a classic picture of declining energy… inevitable and eventually fatal.”
While mitochondrial dysfunction is thought of as one of the pillars or hallmarks of aging, Benson believes that it impacts on ALL the other hallmarks as well.
“Less energy causes stem calls to fail, causes an increase in DNA replication errors, causes cells to go senescent, causes decline of the immune system, and so on,” he says. “Declining energetics is the villain lurking behind many of the major aging problems.”
“The only way to fill that energetics gap, that we know of, is to supply entirely new mitochondria, with entirely new mitochondrial DNA, to the body. Fixing them in-place (in the body) while they are operating, is really difficult and dangerous if not impossible.
Much simpler to grow them externally, in a bioreactor where we can have all kinds of quality control mechanisms and arbitrary amounts of energy input, then transfuse them into the body.”
Longevity Linked To Proteins That Calm Overexcited Neurons
New research makes a molecular connection between the brain and aging — and shows that overactive neurons can shorten life span.
A thousand seemingly insignificant things change as an organism ages. Beyond the obvious signs like graying hair and memory problems are myriad shifts both subtler and more consequential: Metabolic processes run less smoothly; neurons respond less swiftly; the replication of DNA grows faultier.
But while bodies may seem to just gradually wear out, many researchers believe instead that aging is controlled at the cellular and biochemical level.
They find evidence for this in the throng of biological mechanisms that are linked to aging but also conserved across species as distantly related as roundworms and humans.
Whole subfields of research have grown up around biologists’ attempts to understand the relationships among the core genes involved in aging, which seem to connect highly disparate biological functions, like metabolism and perception.
If scientists can pinpoint which of the changes in these processes induce aging, rather than result from it, it may be possible to intervene and extend the human life span.
So far, research has suggested that severely limiting calorie intake can have a beneficial effect, as can manipulating certain genes in laboratory animals.
But recently in Nature, Bruce Yankner, a professor of genetics and neurology at Harvard Medical School, and his colleagues reported on a previously overlooked controller of life span: the activity level of neurons in the brain.
In a series of experiments on roundworms, mice and human brain tissue, they found that a protein called REST, which controls the expression of many genes related to neural firing, also controls life span. They also showed that boosting the levels of the equivalent of REST in worms lengthens their lives by making their neurons fire more quietly and with more control.
How exactly overexcitation of neurons might shorten life span remains to be seen, but the effect is real and its discovery suggests new avenues for understanding the aging process.
Genetic Mechanisms of Aging
In the early days of the molecular study of aging, many people were skeptical that it was even worth looking into. Cynthia Kenyon, a pioneering researcher in this area at the University of California, San Francisco, has described attitudes in the late 1980s:
“The ageing field at the time was considered a backwater by many molecular biologists, and the students were not interested, or were even repelled by the idea. Many of my faculty colleagues felt the same way. One told me that I would fall off the edge of the Earth if I studied ageing.”
That was because many scientists thought that aging (more specifically, growing old) must be a fairly boring, passive process at the molecular level — nothing more than the natural result of things wearing out.
Evolutionary biologists argued that aging could not be regulated by any complex or evolved mechanism because it occurs after the age of reproduction, when natural selection no longer has a chance to act.
However, Kenyon and a handful of colleagues thought that if the processes involved in aging were connected to processes that acted earlier in an organism’s lifetime, the real story might be more interesting than people realized. Through careful, often poorly funded work on Caenorhabditis elegans, the laboratory roundworm, they laid the groundwork for what is now a bustling field.
A key early finding was that the inactivation of a gene called daf-2 was fundamental to extending the life span of the worms.
“daf-2 mutants were the most amazing things I had ever seen. They were active and healthy and they lived more than twice as long as normal,” Kenyon wrote in a reflection on these experiments. “It seemed magical but also a little creepy: they should have been dead, but there they were, moving around.”
This gene and a second one called daf-16 are both involved in producing these effects in worms. And as scientists came to understand the genes’ activities, it became increasingly clear that aging is not separate from the processes that control an organism’s development before the age of sexual maturity; it makes use of the same biochemical machinery.
These genes are important in early life, helping the worms to resist stressful conditions during their youth. As the worms age, modulation of daf-2 and daf-16 then influences their health and longevity.
These startling results helped draw attention to the field, and over the next two decades many other discoveries illuminated a mysterious network of signal transduction pathways — where one protein binds another protein, which activates another, which switches off another and so on — that, if disturbed, can fundamentally alter life span.
By 1997, researchers had discovered that in worms daf-2 is part of a family of receptors that send signals triggered by insulin, the hormone that controls blood sugar, and the structurally similar hormone IGF-1, insulin-like growth factor 1; daf-16 was farther down that same chain.
Tracing the equivalent pathway in mammals, scientists found that it led to a protein called FoxO, which binds to the DNA in the nucleus, turning a shadowy army of genes on and off.
That it all comes down to the regulation of genes is perhaps not surprising, but it suggests that the processes that control aging and life span are vastly complex, acting on many systems at once in ways that may be hard to pick apart.
But sometimes, it’s possible to shine a little light on what’s happening, as in the Yankner group’s new paper.
Get Plenty of REST
Figuring out which genes are turned on and off in aging brains has long been one of Yankner’s interests. About 15 years ago, in a paper published in Nature, he and his colleagues looked at gene expression data from donated human brains to see how it changes over a lifetime.
Some years later, they realized that many of the changes they’d seen were caused by a protein called REST. REST, which turns genes off, was mainly known for its role in the development of the fetal brain: It represses neuronal genes until the young brain is ready for them to be expressed.
But that’s not the only time it’s active. “We discovered in 2014 that [the REST gene] is actually reactivated in the aging brain,” Yankner said.
To understand how the REST protein does its job, imagine that the network of neurons in the brain is engaged in something like the party game Telephone. Each neuron is covered with proteins and molecular channels that enable it to fire and pass messages.
When one neuron fires, it releases a flood of neurotransmitters that excite or inhibit the firing of the next neuron down the line.
REST inhibits the production of some of the proteins and channels involved in this process, reining in the excitation.
In their study, published in October 2019, Yankner and his colleagues report that the brains of long-lived humans have unusually low levels of proteins involved in excitation, at least in comparison with the brains of people who died much younger.
This finding suggests that the exceptionally old people probably had less neural firing. To investigate this association in more detail, Yankner’s team turned to C. elegans.
They compared neural activity in the splendidly long-lived daf-2 mutants with that of normal worms and saw that firing levels in the daf-2 animals were indeed very different.
“They were almost silent. They had very low neural activity compared to normal worms,” Yankner said, noting that neural activity usually increases with age in worms. “This was very interesting, and sort of parallels the gene expression pattern we saw in the extremely old humans.”
When the researchers gave normal roundworms drugs that suppressed excitation, it extended their life spans.Genetic manipulation that suppressed inhibition — the process that keeps neurons from firing — did the reverse.
Several other experiments using different methods confirmed their results. The firing itself was somehow controlling life span — and in this case, less firing meant more longevity.
Because REST was plentiful in the brains of long-lived people, the researchers wondered if lab animals without REST would have more neural firing and shorter lives. Sure enough, they found that the brains of elderly mice in which the Rest gene had been knocked out were a mess of overexcited neurons, with a tendency toward bursts of activity resembling seizures.
Worms with boosted levels of their version of REST (proteins named SPR-3 and SPR-4) had more controlled neural activity and lived longer. But daf-2 mutant worms deprived of REST were stripped of their longevity.
“It suggests that there is a conserved mechanism from worms to [humans],” Yankner said. “You have this master transcription factor that keeps the brain at what we call a homeostatic or equilibrium level — it doesn’t let it get too excitable — and that prolongs life span. When that gets out of whack, it’s deleterious physiologically.”
What’s more, Yankner and his colleagues found that in worms the life extension effect depended on a very familiar bit of DNA: daf-16. This meant that REST’s trail had led the researchers back to that highly important aging pathway, as well as the insulin/IGF-1 system.
“That really puts the REST transcription factor somehow squarely into this insulin signaling cascade,” said Thomas Flatt, an evolutionary biologist at the University of Fribourg who studies aging and the immune system.
REST appears to be yet another way of feeding the basic molecular activities of the body into the metabolic pathway.
A Biological Balancing Act
Neural activity has been implicated in life span before, notes Joy Alcedo, a molecular geneticist at Wayne State University who studies the connections between sensory neurons, aging and developmental processes. Previous studies have found that manipulating the activity of even single neurons in C. elegans can extend or shorten life span.
It’s not yet clear why, but one possibility is that the way the worms respond biochemically to their environment may somehow trip a switch in their hormonal signaling that affects how long they live.
The new study, however, suggests something broader: that overactivity in general is unhealthy. Neuronal overactivity may not feel like anything in particular from the viewpoint of the worm, mouse or human, unless it gets bad enough to provoke seizures.
But perhaps over time it may damage neurons.
The new work also ties into the idea that aging may fundamentally involve a loss of biological stability, Flatt said. “A lot of things in aging and life span somehow have to do with homeostasis. Things are being maintained in a proper balance, if you will.”
There’s a growing consensus in aging research that what we perceive as the body slowing down may in fact be a failure to preserve various equilibria. Flatt has found that aging flies show higher levels of immune-related molecules, and that this rise contributes to their deaths.
Keeping the levels in check, closer to what they might have been when the flies were younger, extends their lives.
The results may help explain the observation that some drugs used for epilepsy extend life span in lab animals, said Nektarios Tavernarakis, a molecular biologist at the University of Crete who wrote a commentary that accompanied Yankner’s recent paper.
If overexcitation shortens life span, then medicines that systematically reduce excitation could have the opposite effect. “This new study provides a mechanism,” he said.
In 2014, Yankner’s laboratory also reported that patients with neurodegenerative diseases like Alzheimer’s have lower levels of REST. The early stages of Alzheimer’s, Yankner notes, involve an increase in neural firing in the hippocampus, a part of the brain that deals with memory.
He and his colleagues wonder whether the lack of REST contributes to the development of these diseases; they are now searching for potential drugs that boost REST levels to test in lab organisms and eventually patients.
In the meantime, however, it’s not clear that people can do anything to put the new findings about REST to work in extending their longevity. According to Yankner, REST levels in the brain haven’t been tied to any particular moods or states of intellectual activity.
It would be a “misconception,” he explained by email, “to correlate amount of thinking with life span.” And while he notes that there is evidence that “meditation and yoga can have a variety of beneficial effects for mental and physical health,” no studies show that they have any bearing on REST levels.
Why exactly do overexcited neurons lead to death? That’s still a mystery. The answer probably lies somewhere downstream of the DAF-16 protein and FoxO, in the genes they turn on and off.
They may be increasing the organism’s ability to deal with stress, reworking its energy production to be more efficient, shifting its metabolism into another gear, or performing any number of other changes that together add up a sturdier and longer-lived organism.
“It is intriguing that something as transient as the activity state of a neural circuit could have such a major physiological influence on something as protean as life span,”Yankner said.
Cold Exposure Could Make It Harder For Cancer Cells To Grow, Mice Study Shows
Turning down the thermostat seems to make it harder for cancer cells to grow, according to a study in mice by researchers at Karolinska Institutet in Sweden.
The study, published in the journal Nature, found that chilly temperatures activate heat-producing brown fat that consumes the sugars the tumors need to thrive. Similar metabolic mechanisms were found in a cancer patient exposed to a lowered room temperature.
“We found that cold-activated brown adipose tissue competes against tumors for glucose and can help inhibit tumor growth in mice. Our findings suggest that cold exposure could be a promising novel approach to cancer therapy, although this needs to be validated in larger clinical studies.”
Professor Yihai Cao at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, and corresponding author
The study compared tumor growth and survival rates in mice with various types of cancer, including colorectal, breast and pancreatic cancers, when exposed to cold versus warm living conditions.
Mice acclimatized to temperatures of 4 degrees Celsius had significantly slower tumor growth and lived nearly twice as long compared with mice in rooms of 30 degrees Celsius.
To find out why that is, the researchers analyzed markers in the tissue to study cellular reactions and used imaging tests to examine glucose metabolism. Cancer cells typically need large amounts of glucose, or sugar, to grow.
They found that cold temperatures triggered significant glucose uptake in brown adipose tissue, also known as brown fat, a type of fat that is responsible for keep the body warm during cold conditions.
At the same time, the glucose signals were barely detectable in the tumor cells.
When the researchers removed either the brown fat or a protein crucial for its metabolism called UCP1, the beneficial effect of the cold exposure was essentially wiped out and the tumors grew at a pace on par with those that were exposed to higher temperatures.
Similarly, feeding tumor-bearing mice with a high sugar drink also obliterated the effect of cold temperatures and restored tumor growth.
“Interestingly, high sugar drinks seem to cancel out the effect of cold temperatures on cancer cells, suggesting that limiting glucose supply is probably one of the most important methods for tumor suppression,” Yihai Cao says.
To study the human relevance of the findings, the researchers recruited six healthy volunteers and one patient with cancer undergoing chemotherapy.
Using positron emission tomography (PET) scanning, the researchers identified a significant amount of brown fat activated in the neck, spine and chest area of healthy adults wearing shorts and T-shirts while being exposed to a slightly chilly room temperature of 16 degrees Celsius for up to six hours per day for two weeks.
The patient with cancer wore light clothing while spending time in rooms of 22 degrees Celsius for a week and then in rooms of 28 degrees Celsius for four days.
Prior research has shown that even though there are significant individual differences, 28 degrees Celsius is generally considered a comfortable environmental temperature (the thermoneutral temperature) for most inactive humans.
The imaging scans picked up increased brown fat and lowered tumor glucose uptake during the lower versus the higher temperature.
“These temperatures are considered tolerable by most people,” Yihai Cao says. “We are therefore optimistic that cold therapy and activation of brown adipose tissue with other approaches such as drugs could represent another tool in the toolbox for treating cancer.”
The study was funded by the European Research Council, the Swedish Research Council, the Swedish Cancer Society, the Swedish Childhood Cancer Fund, the Strategic research area in stem cells and regenerative medicine at Karolinska Institutet, the Torsten Söderberg Foundation, the Maud and Birger Gustavsson Foundation, the Novo Nordisk Foundation and the Knut and Alice Wallenberg Foundation.
New Method Mass-Produces Antitumor Cells To Treat Blood Diseases And Cancer
A Purdue University chemical engineer has improved upon traditional methods to produce off-the-shelf human immune cells that show strong antitumor activity, according to a paper published in the peer-reviewed journal Cell Reports.
A Purdue University chemical engineer has improved upon traditional methods to produce off-the-shelf human immune cells that show strong antitumor activity, according to a paper published in the peer-reviewed journal Cell Reports.
Xiaoping Bao, a Purdue University assistant professor from the Davidson School of Chemical Engineering, said CAR-neutrophils, or chimeric antigen receptor neutrophils, and engraftable HSCs, or hematopoietic stem cells, are effective types of therapies for blood diseases and cancer.
Neutrophils are the most abundant white cell blood type and effectively cross physiological barriers to infiltrate solid tumors. HSCs are specific progenitor cells that will replenish all blood lineages, including neutrophils, throughout life.
“These cells are not readily available for broad clinical or research use because of the difficulty to expand ex vivo to a sufficient number required for infusion after isolation from donors,” Bao said. “Primary neutrophils especially are resistant to genetic modification and have a short half-life.”
Bao has developed a patent-pending method to mass-produce CAR-neutrophils from human pluripotent stem cells (hPSCs), that is, cells that self-renew and are able to become any type of human cell.
The chimeric antigen receptor constructs were engineered to express on the surface of the hPSCs, which were directed into functional CAR-neutrophils through a novel, chemically defined protocol.
The method was created in collaboration with Qing Deng at Purdue’s Department of Biological Sciences, Hal E. Broxmeyer, now deceased, at Indiana University School of Medicine, and Xiaojun Lian at the Pennsylvania State University.
“These hPSC-derived neutrophils displayed superior and specific antitumor activities against glioblastoma after engineering with chimeric antigen receptors.”
Bao disclosed the innovation to the Purdue Research Foundation Office of Technology Commercialization, which has applied for an international patent under the Patent Cooperation Treaty system of the World Intellectual Property Organization. The innovation has been optioned to an Indiana-headquartered life sciences company.
“We will also work with Dr. Timothy Bentley, professor of neurology and neurosurgery,and his team at the Purdue College of Veterinary Medicine to run clinical trials in pet dogs with spontaneous glioma,” Bao said.
More Information: Yun Chang et al, Engineering chimeric antigen receptor neutrophils from human pluripotent stem cells for targeted cancer immunotherapy, Cell Reports (2022). DOI: 10.1016/j.celrep.2022.111128
JERUSALEM, Israel — A fountain-of-youth drug could soon make the problems of aging a thing of the past. Researchers in Israel say they have identified a group of molecules that repair the damaged parts of cells which break down over time. That discovery may also lead to a new pill that prevents age-related diseases such as Alzheimer’s.
Scientists from the Hebrew University of Jerusalem note that modern medicine has helped to increase the average life expectancy worldwide.
However, as people live longer, they face more and more problems associated with old age. With that in mind, the team set out to balance the benefits of longevity with a better quality of life in our later years.
During their study, the researchers developed a drug which protects human cells from damage, making it possible for a person’s tissues to retain their proper function for a longer period of time.
Fixing The Power Plants Of Cells
Study authors say a major factor in the aging process is the drop in effectiveness in a cell’s quality-control mechanism. When this system starts to break down, it leads to a buildup of defective mitochondria — the “power plants” of the cells.
“Mitochondria, the cell’s ‘power plants,’ are responsible for energy production. They can be compared to tiny electric batteries that help cells function properly. Although these ‘batteries’ wear out constantly, our cells have a sophisticated mechanism that removes defective mitochondria and replaces them with new ones,” Professor Einav Gross explains in a media release.
However, this mechanism breaks down as people grow older. The result is cell dysfunction and the deterioration in tissue activity — which can cause diseases like Alzheimer’s, Parkinson’s, and heart failure to develop.
The team is hopeful that their study has found an innovative compound that may help treat these diseases. Turned into an easy-to-take pill, the molecules may also act as a preventative measure, repairing cellular aging before it has a chance to trigger disease.
“In the future, we hope we will be able to significantly delay the development of many age-related diseases and improve people’ quality of life,” says co-author Shmuel Ben-Sasson.
The researchers, together with Yissum, Hebrew University’s tech transfer company, have created the startup company Vitalunga to further develop this compound into an anti-aging drug.
“Ben-Sasson’s and Gross’s findings have significant value for the global aging population,” notes Itzik Goldwaser, CEO of Yissum. “As Vitalunga advances towards pre-clinical studies, they’re closer than ever to minimizing the unbearable burden that aging-related diseases, such as Alzheimer’s and Parkinson’s, has on individuals, their families and our health care systems.”
The findings are published in the journal Autophagy.
SuperAgers Initiative – Discovering The Science Behind Exceptional Longevity
SuperAgers are individuals aged 95 and older; they are a promising, living source of scientific knowledge who can provide real-time insights into healthy longevity and what it means to age healthily.
The experience and biology of SuperAgers can open an unique window on aging, offering insights into how we can understand, measure and leverage the correlation between age-related diseases and living an exceptionally long, healthy life.
Longevity.Technology: By studying individuals age 95 and older, the American Federation for Aging Research’s SuperAgers Initiative builds on a foundation of research into the biology of aging and promising therapeutics to extend years of health. It’s an exciting project, and we sat down with Dr Nir Barzilai, AFAR Scientific Director and Director of the Einstein-Institute for Aging Research, to find out more.
The motivation behind the project was trying to answer the question “How do we get science to help us design drugs?”
“We have people who live to 100, and it’s not only living longer, it’s that they are also healthier – maybe 30 extra years of health,” says Barzilai. “Not only are they healthier for longer, but they experience a contract of morbidity – sick for less time at the end of their lives.”
Barzilai explains that what pharmaceutical companies want when it comes to diseases – whether that’s diabetes, cardiovascular, cholesterol-related or whatever – is more information on human genetics.
“We fail when we assume that something that works in mice can necessarily be developed for humans,” he says. “The more human genes we can sequence the better we can understand and tackle diseases.”
Barzilai gives the example of cholesterol drug PCSK9 inhibitor which came about not through animal studies, but because researchers identified mutations in the PCSK9 gene, which provides instructions for making a protein that helps regulate the amount of cholesterol in the bloodstream.
The mutations disrupt the function of PCSK9 and cause hypercholesterolemia – understanding how led to drugs that inhibit PCSK9 and prevent the degradation of cholesterol receptors.
“Pharmaceuticals are looking for genetic proof that drugs work in humans and this triggered the Longevity Genes Study and looking at centenarians,” Barzilai explains. “But for validation purposes, we need more people! By recruiting more SuperAgers and their families and looking at the longevity genes we can design better drugs to slow aging.”
“We found a lot of data with 750 centenarians, but we need ten-fold that number to validate our findings,” says Barzilai. “We’re aiming for 10,000 SuperAgers, 10,000 of their offspring who are likely to live long – and we can come back for more information as time goes on.
Maybe the offspring get married and their spouses act as the control if they don’t have longevity in their family. It’s living data, increasing and evolving. And it’s a more diverse population.”
The American Federation of Aging Research is going to launch a community website to gather as much information as possible, encouraging registrations from SuperAgers and their relatives.
Those willing to participate will be sent a swab kit so their genetics can be added to the data bank and the data will be made available for everyone as soon as possible.
“Previous research has looked at one change in our DNA across thousands of people, or event tens of thousands, to see if it is associated with diabetes, for example,” explains Barzilai. “But we are not built from one change at a time – there are lots of changes.”
Current research is now putting every change into a pathway which is allowing Barzilai and the other researchers to look at effects both downstream and upstream.
“When we look at the pathways of our SuperAgers, we see the pathways that come up are the same as predicted from animal studies – mTOR, insulin, IGF signaling – which is reassuring,” he says.
“But what is rather incredible is that almost 60% of our centenarians have something that prevents the action of growth hormones – it makes sense, as we see from nature that smaller dogs, for examples, live longer than larger breeds and also because bodies need to shift from growth to repair.”
Barzilai references the development of cancer drugs that act on IGF1’s receptor. “When we gave that drug to old animals they lived more healthily, they had better lives. But while aging is not recognised as a disease, we cannot develop these drugs ‘for aging’.”
Instead, says Barzilai, researchers are looking through the data for diseases that are accelerated by aging, but it’s an obstacle.
“The proof of concept is there and the preclinical data is there – we can get extension of lifespan and healthspan in animals, we just don’t have enough data to develop it for aging – yet.”
It all comes down to targets, says Barzilai.
“Now we are identifying targets we can actually wrap our hands around,” he explains. “To reverse aging – the Fountain of Youth – to take an old person and make them young would be very, very difficult. To be Peter Pan – to be young forever – needs interventions that modulate your epigenetics… so maybe in fifty years from now. But for now, there are many targets that are metabolic targets, and the more data we have, the better.”
Find out more about the AFAR’s SuperAgers Initiative HERE.
How To Live Longer: A Certain Type Of Cheese Could Stave Off Bone Thinning
OSTEOPOROSIS is a condition which occurs when the bones in the body begin to thin and weaken.
A part of ageing, bone thinning occurs over several years and is often diagnosed after a fall or broken bone. Scientists from a small study say one dietary change could delay the onset of bone thinning.
Look through all the common accoutrements of an evening meal and one will inevitably find, somewhere in one of the recipes, cheese. Created through the curdling of milk, cheese comes in all shapes and sizes and delights and surprises.
Cheese too, can have health benefits such as lowering blood pressure and inflammation. However, according to recent research, one particular type of cheese could help reduce the delay the onset of bone thinning.
According to research published in the BMJ Nutrition Prevention & Health journal, it could also soon be known to delay the onset of osteoporosis.
Researchers say a small portion of the cheese, 57g, could slow down the progress of bone thinning without an unduly boost levels of harmful cholesterol.
The study was carried out on a small cohort of 66 participants, all of whom were allocated either Jarlsberg or Camembert to add to their diet for six weeks; after this period they swapped cheeses.
While both cheeses are similar, Jarlsberg differs in that it is rich in vitamin K2, one associated with improved skin health and bone metabolism.
Blood tests showed those who ate Jarlsberg experienced a significant boost to their levels of K2 while blood fats increased slightly across both groups.
The researchers concluded: “Daily Jarlsberg cheese consumption has a positive effect on osteocalcin, other [markers of bone turnover], glycated haemoglobin and lipids.”
Professor Sumantra Ray added: “This study shows that while calcium and vitamin D are known to be extremely important for bone health, there are other key factors at play, such as vitamin K2, which is perhaps not as well known.”