Category Archives: Human Longevity

NEW YORK Dr. Shigeaki Hinohara, who cautioned against gluttony and early retirement and vigorously championed annual medical checkups, climbing stairs regularly, and just having fun advice that helped make Japan the world leader in longevity died July 18 in Tokyo. Dutifully practicing the credo of physician heal thyself, he lived to 105.

When he died, Dr. Hinohara was chairman emeritus of St. Lukes International University and honorary president of St. Lukes International Hospital, both in Tokyo. The cause was respiratory failure, the hospital said.

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He is one of the persons who built the foundations of Japanese medicine, said Yoshihide Suga, Japans chief Cabinet secretary.

Dr. Hinohara ministered to victims of the firebombing of Tokyo during World War II. He was taken hostage in 1970 when Japanese Red Army terrorists hijacked a commercial jet. He was able to treat 640 of the victims of a radical cults subway poison gas attack in 1995 (all but one survived) because he had presciently equipped his hospital the year before to handle mass casualties like an earthquake.

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He also wrote a musical for children when he was 88, and a best-selling book when he was 101. He recently took up golf. Until a few months ago he was still treating patients, and he kept a date book with space for five more years of appointments.

In the early 1950s, Dr. Hinohara pioneered a system of complete annual physicals called human dry-dock that has been credited with helping to lengthen the average life span of Japanese people. Women born there today can expect to live to 87; men, to 80.

In the 1970s, he reclassified strokes and heart disorders commonly perceived as inevitable adult diseases that required treatment to lifestyle ailments that were often preventable.

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Dr. Hinohara insisted that patients be treated as individuals that a doctor needed to understand the patient as a whole as thoroughly as the illness. He also argued that palliative care should be a priority for the terminally ill.

He imposed few inviolable health rules, although he did recommend some basic guidelines: Avoid obesity, take the stairs (he did, two steps at a time), and carry your own packages and luggage. Remember that doctors cannot cure everything. Dont underestimate the beneficial effects of music and the company of animals; both can be therapeutic. Dont ever retire, but if you must, do so a lot later than age 65. And prevail over pain simply by enjoying yourself.

We all remember how as children, when we were having fun, we often forgot to eat or sleep, he often said. I believe we can keep that attitude as adults it is best not to tire the body with too many rules such as lunchtime and bedtime.

Dr. Hinohara maintained his weight at about 130 pounds. His diet was spartan: coffee, milk and orange juice with a tablespoon of olive oil for breakfast; milk and a few biscuits for lunch; vegetables with a small portion of fish and rice for dinner. He would consume 3 2 ounces of lean meat twice a week.

Link:
Dr. Shigeaki Hinohara, 105, longevity expert - The Boston Globe

So it was that Eos, goddess of the dawn, fell in love with Tithonus, a handsome young prince of Troy and, beguiling him with her beauty, brought him to her palace on Mount Olympus.

They lived happily for many years but, being mortal, age eventually overtook Tithonus. In her despair, Eos beseeched Zeus to grant her love immortality. Moved to pity, he granted her request but even the king of Olympus could not bestow eternal youth on a human for that would make him as one of the gods.

As one age passed into the next, Tithonus, withered and shrunken, cried incessantly for release from his torment but Zeus could not undo a wish once granted. It was Eos who eventually provided her poor lover a measure of relief by transforming him into a cicada. Now each summer he emerges from the ground with a fresh body to sing in eternal praise of his beauteous goddess. Or is it rather a lament over his crusted, hollow shell of a body?

Many of the myths and stories we have long told ourselves are cautionary tales against the dangers of hubris, our overconfident pride and arrogance before the gods. Divinity will mete out retribution to those who forget their place in the natural scheme of things. Chief among these absolutes of the human condition is our mortality; we all must die and woe betide any who would seek to have it otherwise.

But consider this statement from the website of the California Life Co. (Calico), a biotechnology firm established in 2013:

Calico is a research and development company whose mission is to harness advanced technologies to increase our understanding of the biology that controls lifespan. We will use that knowledge to devise interventions that enable people to lead longer and healthier lives. Executing on this mission will require an unprecedented level of interdisciplinary effort and a long-term focus for which funding is already in place.

The company is a subsidiary of Alphabet Inc., whose most famous other subsidiary goes by the name of Google. By 2016, Larry Page, Alphabets CEO (and co-founder of Google) had committed the company to contributing $240 million to Calico, with an additional $490 million should it be needed.

Calico is by no means the only Silicon Valley outfit investing big dollars in the life extension sciences field. SENS (Strategies for Engineered Negligible Senescence) Research Foundation, founded in 2009, and Human Longevity Inc., founded in 2014, are two of its better-funded competitors but there are others.

Whats going on here? Lets start with some data. Since 1900, the average human life span has increased by 30 years. But with this, so have the rates of age-related health issues such as cancer, heart disease, stroke, diabetes and dementia. In the U.S., up to age 44 the leading causes of death are accidents and violence. From there to age 65, its cancer and heart disease after that.

Medical advances are making significant inroads on each of these diseases and they may be conquered within your childrens lifetime. What then? Well, epidemiologists suggest a cure for cancer would only add 3.3 years to the average lifespan while the prevention of heart disease would tack on another four years. The elimination of all disease likely would only extend life into the mid-90s.

To go further, the aging process itself must be slowed. Even in the absence of disease, our bodies senesce as our organs, tissues, cells and macromolecules accumulate damage at an ever-increasing rate. Eric Verdin of the Buck Institute for Research on Aging has observed that if you just kept aging at the rate you age between 20-30, youd live to a thousand. But at 30, everything starts to change. Thereafter your risk of mortality doubles every seven years.

Most longevity scientists are health spanners, seeking a healthier life with a compressed morbidity (i.e., a quick and painless death). But immortalists like SENS Research founder Aubrey de Grey and futurist Ray Kurzwell believe science can carry us much further. If aging is encoded in the DNA of our genes, they argue, there should be no technological reason why we couldnt identify and address those parts of our genomes that are responsible for senescence.

Like so much else in modern biology, medical research is increasingly becoming an information science. To find the genetic correlates of aging will entail the compilation and analysis of an almost unthinkable mass of biotechnical data. Who has the big-data skillset and financial resources to back such an undertaking?

Silicon Valley.

But what about the economics, ethics and religious implications of an immortality united with youthful vigor? Should aging be viewed as a medical disease to be treated as any other or are we just asking for it with such hubristic thinking?

Ken Baker is a scientist and a retired biology professor. If you have a natural history topic youd like the author to consider for an upcoming column, email your idea to rweaver@advertiser-tribune.com.

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The human life span is the maximum number of years an individual from the human species can live based on observed examples. Though this definition of life span may seem simple enough, it is often confused for other common concepts in the study of the aging, life, and death of living organisms.

In order to better understand the human life span, let's dive a little deeper into the concept and its important distinctions from other commonly used terms.

The term life span is most commonly confused with another important concept: life expectancy. While both terms relate to the number of living years, they actually define very different concepts. While the term life span refers to the maximum number of years an individual can live, life expectancy refers to an estimate or an average number of years a person can expect to live. Most simply put, life expectancy can be attributed to and impacted by an individual and their personal health history, genetics, and lifestyle, whereas life span holds for all living humans.

For example, my life expectancy is affected by personal factors like my family history, my environment, my diet, and even my age and sex. My life expectancy might be different for your life expectancy and it may even change over time. Our life spans, however, are one in the same. We share it as members of the same species.

So what is the human life span?

Given that the human life span is defined by the longest observed human life from birth to death, it is a figure that has changed over the years. For humans, the current accepted maximum life span is 122 years. This age was achieved by Jeane Louise Calment of France.

Calment lived from February 21, 1875, to August 4, 1997, until she was exactly 122 years and 164 days old. Remarkably, Calment remained relatively healthy and mentally intact until her 122nd birthday.

Though there have certainly been claims of longer lives, none of the claims were acceptably documented and verified. Calment remains the first verified person to reach any age between 116 and 122 and the only verified person to reach the age of 122.

With the United State's average life expectancy currently hovering at around 78.88 years, the age to which most Americans can expect to live is still forty-four years younger than the human life span. So how do we close that gap and elongate our lives? There will always be factors that are out of our individual control like our inherited genes, but we shouldn't discount the impact of those that we can control. It is generally understood that closing the gap between life expectancy and life span can be done through healthier living, less exposure to toxins, the prevention of chronic illnesses, and a little bit of luck.

More here:
The Human Life Span Defined - Verywell

If you could use a molecular crystal ball and see which sets of genes and variants could predict how long youll live, would you want to know? Researchers at the Swiss Institute of Bioinformatics (SIB) are defiantly interested in that information. So much so that they have just released data from a comprehensive study that used an innovative computational approach to analyze a dataset of over 116,000 individuals and probe 2.3 million human single-nucleotide polymorphisms (SNPs).

Findings from the new studypublished recently in Nature Communications in an article entitled Bayesian Association Scan Reveals Loci Associated with Human Lifespan and Linked Biomarkersrevealed an unparalleled number of SNPs associated with lifespan (16), including 14 previously unknown variants. While the environment in which we live, including our socio-economic status and the food we eat, plays a considerable role in longevity, about 20% to 30% of the variation in human lifespan comes down to our genome. Changes in particular locations in our DNA sequence may hold some of the keys to human endurance.

In our approach, we prioritized changes in the DNA known to be linked to age-related diseases in order to scan the genome more efficiently," noted senior study investigator Zoltn Kutalik, Ph.D., group leader at SIB and assistant professor at the Institute of Social and Preventive Medicine (CHUV). This is the largest set of lifespan-associated genetic markers ever uncovered.

About 1 in 10 people carry some configurations of these markers that shorten their life by over a year compared with the population average. Moreover, the researchers found that a person inheriting a lifespan-shortening version of one of these SNPs may die up to seven months earlier.

...we developed a Mendelian randomization-based method combining 58 disease-related GWA [genome-wide association] studies to derive longevity priors for all HapMap SNPs, the authors wrote. A Bayesian association scan, informed by these priors, for parental age of death in the UK Biobank study (n=116,279) revealed 16 independent SNPs with significant Bayes factor at a 5% false discovery rate (FDR). Eleven of them replicate (5% FDR) in five independent longevity studies combined; all but three are depleted of the life-shortening alleles in older Biobank participants.

The SIB team found that most SNPs influenced lifespan by impacting more than a single disease or risk factorfor example, through being more addicted to smoking as well as being predisposed to schizophrenia. The discovered SNPs, combined with gene expression data, allowed the researchers to identify that lower brain expression of three genes neighboring the SNPs (involved in nicotine dependence) was causally linked to increased lifespan.

Further analysis revealed that brain expression levels of nearby genes (RBM6, SULT1A1 and CHRNA5) might be causally implicated in longevity. Gene expression and caloric restriction experiments in model organisms confirm the conserved role for RBM6 and SULT1A1 in modulating lifespan," the authors concluded.

These three genes could, therefore, act as biomarkers of longevity, i.e., survival beyond 85 to 100 years, commented study co-author Johan Auwerx, Ph.D., a professor at the EPFL. To support this hypothesis, we have shown that mice with a lower brain expression level of RBM6 lived substantially longer.

Study co-author Marc Robinson-Rechavi, Ph.D., a SIB group leader, and professor at the University of Lausanne, concluded that interestingly, the gene expression impact of some of these SNPs in humans is analogous to the consequence of a low-calorie diet in mice, which is known to have positive effects on lifespan.

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16 Biomarkers May Predict Human Lifespan - Genetic Engineering & Biotechnology News

Why do some of us live longer than others? While the environment in which we live, including our socio-economic status or the food we eat, plays the biggest part, about 20 to 30% of the variation in human lifespan comes down to our genome. Changes in particular locations in our DNA sequence, such as single-nucleotide polymorphisms (SNPs), could therefore hold some of the keys to our longevity.

Until now, the most comprehensive studies had found only two hits in the genome, points out Prof. Zoltan Kutalik, Group Leader at SIB and assistant professor at the Institute of Social and Preventive Medicine (CHUV).

In a new study, a team of scientists, led by Kutalik, has used an innovative computational approach to analyse a dataset of 116,279 individuals and probe 2.3 million human SNPs.

An unparalleled number of SNPs associated with lifespan (16) were uncovered, including 14 new to science. In our approach, we prioritized changes in the DNA known to be linked to age-related diseases in order to scan the genome more efficiently, says Kutalik. This is the largest set of lifespan-associated genetic markers ever uncovered.

About 1 in 10 people carry some configurations of these markers that shorten their life by over a year compared with the population average. In addition, a person inheriting a lifespan-shortening version of one of these SNPs may die up to seven months earlier.

The approach also enabled the researchers to explore how the DNA changes affected lifespan in a holistic way. They found that most SNPs had an effect on lifespan by impacting more than a single disease or risk factor, for example through being more addicted to smoking as well as through being predisposed to schizophrenia.

The discovered SNPs, combined with gene expression data, allowed the researchers to identify that lower brain expression of three genes neighbouring the SNPs (RBM6, SULT1A1 and CHRNA5, involved in nicotine dependence) was causally linked to increased lifespan.

These three genes could therefore act as biomarkers of longevity, i.e. survival beyond 85-100 years. To support this hypothesis, we have shown that mice with a lower brain expression level of RBM6 lived substantially longer, comments Prof. Johan Auwerx, professor at the EPFL.

"Interestingly, the gene expression impact of some of these SNPs in humans is analogous to the consequence of a low-calorie diet in mice, which is known to have positive effects on lifespan, adds Prof. Marc Robinson-Rechavi, SIB Group Leader and professor at the University of Lausanne.

Our findings reveal shared molecular mechanisms between human and model organisms, which will be explored in more depth in the future, concludes Prof. Bart Deplancke, SIB Group Leader and professor at the EPFL.

This study, which is a part of the AgingX Project supported by SystemsX.ch (the Swiss Initiative in Systems Biology), therefore brings us a step closer to grasping the mechanisms of human aging and longevity. It also proposes an innovative computational framework to improve the power of genomewide investigations of diseases more generally. As such, the framework could have promising applications in the field of personalized medicine.

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16 Genetic Markers Can Shorten Life Span - R & D Magazine

Pippa Malmgren: "Wherever you go in the world, everyone's totally obsessed with the rising cost of living."

To casual readers, the cover of the June 2009 edition of British Vogue, featuring supermodel Natalia Vodianova in the nude, was a little unusual and perhaps a bit daring.

To London-based economist and entrepreneur Pippa Malmgren, however, the magazine's departure from its usual celebration of haute couture was a sign that the fashion industry had lost a large slice of its consumer base.

These were "the young who were receiving unsolicited credit cards with large borrowing balances in the mail", writes Malmgren in the first chapter of her just-launched book, Signals.

The rest, as they say, is history. The shockwaves of a financial crisis that started in Wall Street rolled out across Main Street, taking with them businesses, jobs, confidence and spending power.

"Once the financial crisis hit, the fashion industry became aware that it had no idea who its new customers would be," says Malmgren.

In Sydney to promote Signals, the former adviser to Barack Obama and one-time deputy head of global strategy at UBS says the fiscal pump-priming and extreme monetary easing employed by governments and central banks to refloat the global economy seem to have worked.

And while growth remains sluggish and inflation slow to take hold, there are signs things are gradually returning to, if not a pre-GFC type of normal, a "new" normal with its own set of economic characteristics and signals.

One of those is disguised inflation.

"All the professional data everywhere you go says there's no inflation at all," says Malmgren.

"But wherever you go in the world, everyone's totally obsessed with the rising cost of living.

"Young people can't afford to buy a home anymore; people's rent is going up to the point where the kids boomerang back into the parental home; rail fares; grocery bills; the list goes on," she says.

Malmgren has identified "shrinkflation" where the price of an item remains the same but the weight or size is reduced as a type of disguised inflation that is straining household budgets.

Another statistical distortion can be found in hedonic pricing, where, for example, the computing power of a tablet can double over a couple of years, but the price rises only a little, if at all.

In the same way, chemically-treated fresh fruit can often have such a long shelf-life that external price pressures from rising energy and labour costs pass it by.

"Hedonics can make it look like prices are falling, but we often only include the items that are falling and we are ignoring the ones that go up," says Malmgren.

And while she concedes that fears in recent years of disinflation becoming deflation were well-founded, this also means that households have become ultra-sensitive to even the slightest rise in consumer prices. Heavy government and personal debt, added to greater human longevity, also means less relative spending on social services and tighter budgets in retirement.

All of this along with technological disruption to job markets helps explain the rise of populist politics across the West, she says.

The return of inflationary pressures also goes some way to explaining why China, the world's second largest economy and most populous, is stepping up its drive to secure food and energy sources across the globe, with the much-touted "One Belt, One Road" infrastructure push at the heart of this.

"The Chinese view is that the West is going to default on the debt owed to it, because don't forget that it financed our overspending," says Malmgren.

"Beijing says: 'You will default via inflation, which is why interest rates were lowered so much and cash was thrown at the economy'.

"It says: 'You will pay me back, but that money will buy me a smaller stake in that Beijing restaurant that I wanted to invest in than it would have a few years ago.'"

Indeed, Malmgren attributes much of China's modern expansion mainly the One Belt One Road program and island-building in the disputed South China Sea to Beijing's concerns about rising food and energy costs, and its determination to secure new export and import markets.

Surging wages and costs mean the country has also priced itself out of many of the manufacturing industries it dominated in the 1980s and 1990s, to the point where it is often now more economical with quality control and access to consumer markets taken into account to make electronic components in Mexico or the United States.

This, too, is weighing on China's strategic, long-term thinking.

Malmgren goes further to suggest that the resurgence of old geopolitical tensions, and emergence of new ones, is behind a revival in defence spending, particularly by global powers such as the US, China and Russia. She calls this "the new quantitative easing".

"The new way governments are pumping money into the economy is via defence spending," she says.

"This is why the weakness of the world economy actually converted the peace dividend [from the end of the Cold War] into a conflict premium," she says.

"It's a grab for resources that's all it is.

"This grab always existed, but it has intensified because of the debt problem and the return of inflation.

"What is in the South China Sea? Ten per cent of the world's fish supplies," she says.

So faced with rising inflation, renewed geopolitical unease, the spread of populism and massive disruption to traditional labour markets, what is today's fashion telling us about the future?

"Transparent jeans," says Malmgren, "I think are a cry for transparency, a reminder that the emperor is not wearing clothes.

"In fact, it's all a bit like that cover of Vogue."

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Economist Pippa Malmgren identifies signals of disguised inflation - The Australian Financial Review

As far as brain regions go, the hypothalamus is something of a multi-tasker: it helps control our temperature, hunger, sleep, emotions, and sex drive.

But that's not all. A new study suggests it's also responsible for keeping us young, thanks to a supply of neural stem cells that regulate our ageing.

Sadly, these disappear with time which could be why we get old but tests with mice show that implanting new cells to replace them can actually extend lifespan.

"Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates ageing," says molecular pharmacologist Dongsheng Cai from the Albert Einstein College of Medicine in the Bronx.

"But we also found that the effects of this loss are not irreversible. By replenishing these stem cells or the molecules they produce, it's possible to slow and even reverse various aspects of ageing throughout the body."

Cai and his team discovered back in 2013 that the hypothalamus plays a role in ageing, and that by reducing inflammation in the brains of mice, the animals were able to live longer lives.

Now, in a follow-up study, the researchers think they've pinpointed the particular cells in the hypothalamus that matter here: neural stem cells, which serve to generate replacements for dead and damaged cells.

In mice, these cells start to disappear when the animals are about 10 months old (mice middle age), and are largely gone by the time they turn two (elderly).

To figure out if this reduction is what helps cause ageing as opposed to just a correlation the researchers disrupted the neural stem cells in a group of mice, using a toxin to destroy around 70 percent of the cells.

Doing so not only caused the mice to live a few months less than naturally ageing control animals, but it also increased the effects of ageing while they still lived.

"There was a decline in learning and memory, coordination, muscle mass, endurance, and skin thickness," Cai explained to Jessica Hamzelou at New Scientist.

To see if an opposite effect was also possible in other words, whether stocking up on neural stem cells could produce youthful vigour and longevity the team injected hypothalamic stem cells taken from newborn mice into the brains of two groups of mice.

One of these groups was made up of normal old mice; the other consisted of animals that had had their hypothalamus disrupted by the toxin.The treated animals lived significantly longer than untreated animals, enjoying a lifespan up to 15 percent longer than the controls.

The team thinks that the longevity provided by these neural stem cells comes down to molecular secretions called microRNAs (miRNAs), which help to regulate gene expression.

Scientists uninvolved with the research have described this ageing mechanism as "totally novel and quite unexpected", although there's no guarantee the same physiological function is at work in people.

Finding out whether it is will be on the horizon for the researchers, who now want to launch clinical trials to see if neural stem cells implanted into human volunteers acts like some kind of elixir of youth.

"Of course humans are more complex," Cai explained to Ian Sample at The Guardian.

"However, if the mechanism is fundamental, you might expect to see effects when an intervention is based on it."

The findings are reported in Nature.

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Implanting Stem Cells Into The Brain Might Extend Human Lifespan - ScienceAlert

TORTOLA, British Virgin Islands--(BUSINESS WIRE)--Juvenescence Limited (Juvenescence) is pleased to announce the launch of a joint venture with Insilico Medicine, Inc. (Insilico Medicine), a Baltimore-based company using artificial intelligence (AI) principally focusing on ageing and age-related diseases. The new joint venture, Juvenescence AI Limited (Juvenescence AI), will focus on developing a pipeline of new compounds licensed from Insilico Medicine and on building AI-driven tools for clinical development. This partnership will produce commercially attractive drugs for Juvenescence AI while validating Insilico Medicines innovative AI approach for drug discovery. Juvenescence made an undisclosed investment into Insilico Medicine simultaneously with the creation of the joint venture.

We are very pleased to partner with Alex Zhavoronkov and his team at Insilico Medicine. Artificial intelligence is set to increase efficiencies in many sectors, something sorely needed in drug development as evidenced by the prolonged decline in the sectors productivity. Insilico Medicines approach has massive potential to reduce the cost associated with the discovery of new drugs, said Juvenescences Chairman, Jim Mellon, adding, We are excited by the potential for AI to streamline the longest and most costly portions of the drug development cycle: clinical trials. With Insilico Medicines help, we hope Juvenescence AI will both develop therapeutics that treat the diseases that plague all of us as we age and eventually treat the ageing process itself.

The principals of Juvenescence, Jim Mellon, Dr. Greg Bailey and Dr. Declan Doogan, have extensive track records in drug development, company formation, and biotech investment. The Juvenescence executive and scientific team hopes to combine the classical drug development expertise earned through careers in the pharmaceutical industry and through their successful early investments in companies such as Medivation and Biohaven Pharmaceuticals (NYSE:BHVN), to bear on the new prospects presented by AI-assisted drug development. The team believes that advances in AI provide new avenues for clinical, regulatory and commercial success. Dr. Doogan, the former Senior VP of Clinical Development at Pfizer and current Chairman of Biohaven Pharmaceuticals (NYSE:BHVN), said:

The application of AI techniques to drug discovery has enormous potential and could dramatically alter the way that we discover new drugs and define existing diseases. AI could decrease the cost and increase the speed with which we can bring new medicines to patients."

Juvenescence AI has agreed to license selected novel and repurposed compound families from Insilico Medicine on an ongoing basis, with the aim of developing therapies for both ageing itself and the diseases of ageing, such as diabetes, dementia, cancer, respiratory disease and cardiovascular disease, that increasingly burden our health systems as the worlds population continues to age.

The team at Juvenescence AI has demonstrated extraordinary foresight in recognising that the anti-ageing sector is currently experiencing a period of rapid advance, with vast sums of capital set to flow into the sector in coming years. They have also recognised the potential of AI early and that it will play a key role in adding billions of healthy life years to the lives of people around the globe. We are eager to work with them to develop life-saving and life-extending drugs, said Alex Zhavoronkov, PhD, Founder and CEO of Insilico Medicine, Inc. and Chief of Artificial Intelligence of Juvenescence AI.

About Juvenescence Limited

Juvenescence Limited is an investment company focussed on therapies to increase human longevity and complementary investments in related sectors. It was founded in 2017 by Jim Mellon, Greg Bailey,Declan Doogan, Anthony Chow, and Alexander Pickett. The Juvenescence team are highly experienced entrepreneurs and investors with a significant focus on the life science and commercial drug development sectors. Juvenescence creates new ventures and invests directly in both startup and established longevity related companies while offering strategic advice and operational support.

Juvenescence believes that advances in science have made real the possibility of slowing, halting or potentially reversing some elements of ageing. Juvenescence believes that the resulting increase in life expectancy will have profound implications on all sectors and in particular healthcare, education, insurance and leisure.

http://www.juvenescence.life

About Juvenescence AI Limited

Juvenescence AI Limited is a drug development and artificial intelligence company focussed on ageing and age-related diseases. Juvenescence AI combines advances in artificial intelligence with classical development expertise in order to prioritise and develop compounds from Insilico Medicine, Incs end-to-end automated drug discovery pipeline through to clinical proof of concept.

http://www.juvenescence.ai

About Insilico Medicine, Inc.

Insilico Medicine, Inc. is an artificial intelligence company located at the Emerging Technology Centers at the Johns Hopkins University Eastern campus in Baltimore, with R&D resources in Belgium, Russia, and the UK sourced through hackathons and competitions. The company utilises advances in genomics, big data analysis, and deep learning for in silico drug discovery and drug repurposing for ageing and age-related diseases. The company is pursuing internal drug discovery programs in cancer, Parkinson's Disease, Alzheimer's Disease, ALS, diabetes, sarcopenia, and ageing. Through its Pharma.AI division, Insilico provides advanced machine learning services to biotechnology, pharmaceutical, and skin care companies, foundations and national governments globally. In 2017, NVIDIA selected Insilico Medicine as one of its Top 5 AI companies in its potential for social impact.

Brief company video: https://www.youtube.com/watch?v=l62jlwgL3v8

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Juvenescence Limited - Artificial Intelligence to Discover Drugs in a Multi-Year Multimillion Dollar Deal - Business Wire (press release)

He also wrote a musical for children when he was 88 and a best-selling book when he was 101. He recently took up golf. Until a few months ago he was still treating patients and kept a date book with space for five more years of appointments.

In the early 1950s, Dr. Hinohara pioneered a system of complete annual physicals called human dry-dock that has been credited with helping to lengthen the average life span of Japanese people. Women born there today can expect to live to 87; men, to 80.

In the 1970s, he reclassified strokes and heart disorders commonly perceived as inevitable adult diseases that required treatment to lifestyle ailments that were often preventable.

Dr. Hinohara insisted that patients be treated as individuals that a doctor needed to understand the patient as a whole as thoroughly as the illness. He argued that palliative care should be a priority for the terminally ill.

He imposed few inviolable health rules, though he did recommend some basic guidelines: Avoid obesity, take the stairs (he did, two steps at a time) and carry your own packages and luggage. Remember that doctors cannot cure everything. Dont underestimate the beneficial effects of music and the company of animals; both can be therapeutic. Dont ever retire, but if you must, do so a lot later than age 65. And prevail over pain simply by enjoying yourself.

We all remember how as children, when we were having fun, we often forgot to eat or sleep, he often said. I believe we can keep that attitude as adults it is best not to tire the body with too many rules such as lunchtime and bedtime.

Dr. Hinohara maintained his weight at about 130 pounds. His diet was spartan: coffee, milk and orange juice with a tablespoon of olive oil for breakfast; milk and a few biscuits for lunch; vegetables with a small portion of fish and rice for dinner. (He would consume three and a half ounces of lean meat twice a week.)

Dr. Shigeaki Hinohara was born on Oct. 4, 1911, in Yamaguchi Prefecture, in western Japan. He decided to study medicine after his mothers life was saved by the familys doctor. His father was a Methodist pastor who had studied at Duke University.

Have big visions and put such visions into reality with courage, his father had advised him, Dr. Hinohara told the Asia Pacific Hospice Palliative Care Network. The visions may not be achieved while you are alive, but do not forget to be adventurous. Then you will be victorious.

Dr. Hinohara graduated in 1937 from Kyoto Imperial Universitys College of Medicine. (He later studied for a year at Emory University in Atlanta.) He began practicing at St. Lukes International Hospital in 1941. (It was founded by a missionary at the beginning of the 20th century.) He became its director in 1992.

In 1970, he was flying to a medical conference in Japan when his plane was hijacked by radical Communists armed with swords and pipe bombs. He was among 130 hostages who spent four days trapped in 100-degree heat until the hijackers released their captives and flew to North Korea, where they were offered asylum.

I believe that I was privileged to live, he later said, so my life must be dedicated to other people.

After spending his first six decades supporting his family, Dr. Hinohara devoted the remainder of his life largely to volunteer work.

In 2000, he conceived a musical version of Leo Buscaglias book The Fall of Freddie the Leaf, which was performed in Japan and played Off Off Broadway in New York. He wrote scores of books in Japanese, including Living Long, Living Good (2001), which sold more than a million copies.

Until the last few months, he would work up to 18 hours a day. Using a cane, he would exercise by taking 2,000 or more steps a day. In March, unable to eat, he was hospitalized. But he refused a feeding tube and was discharged. Months later, he died at home.

Dr. Hinohara said his outlook toward life had been inspired by Robert Brownings poem Abt Vogler, especially these lines:

There shall never be one lost good! What was, shall live as before; The evil is null, is nought, is silence implying sound; What was good shall be good, with, for evil, so much good more; On the earth the broken arcs; in the heaven a perfect round.

What the poem evoked for him, he once explained, was a circle drawn so big that only the arch was visible. Seeing it in full, he said, could never be realized in his lifetime.

Makiko Inoue contributed reporting.

A version of this article appears in print on July 26, 2017, on Page A21 of the New York edition with the headline: Dr. Shigeaki Hinohara, Who Taught Japan How to Live Long, Dies at 105.

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Dr. Shigeaki Hinohara, Longevity Expert, Dies at (or Lives to) 105 - New York Times

Just as smaller animals of a given species generally live longer than their larger cousins, one might expect that taller humans are genetically programmed to sacrifice longevity for height.

But its not that simple.

A major multinational study of 841 men and women from across four populations found lower levels of insulin-like growth factor 1 (IGF-1) in men living to age 100 and yet most of them were taller than men in the younger control group.

The apparent explanation for this head-scratcher is that some long-lived men and only men have a genetic mutation that makes their growth hormone receptors more sensitive to the effects of the hormone. The cells absorb less growth hormone, yet protein expression is increased by several times.

This mutation seems to be responsible for their ability to live about 10 years longer than the control group of 70-year-old men without the mutation, even though they have a lower amount of growth hormone and are about 3 centimeters (1.18 inches) taller.

The lead author of the study is Prof. Gil Atzmon of Albert Einstein College of Medicine in New York and head of the Laboratory of Genetics and Epigenetics of Aging and Longevity at the University of Haifa. Since 2001, Atzmon has been studying the human genome and its impact on aging and longevity.

Longevity genes

The researchers working with Atzmon looked at four elderly populations: 567 Ashkenazi Jews in the Longevity Genes Project at Einstein, 152 from a study of Amish centenarians, and the rest from an American cardiovascular health study and a French longevity study.

In 2008, the Longevity Genes Project found a genetic mutation in the IGF-1 receptor of some women, though its not the same as the one affecting mens lifespan.

We knew in the past that genetic pathways associated with growth hormone were also associated with longevity and now we have found a specific mutation whose presence or absence is directly related to it, said Atzmon.

This study makes it an established fact that there is a relationship between the function of the growth hormone and longevity. Our current goal is to fully understand the mechanism of the mutation we found to express it, so that we can allow longevity while maintaining quality of life, he added.

The 16 researchers involved the study, published June 16 in Science Advances, are associated with institutions in Israel and France as well as the US states of New York, Maryland, California, Vermont, Massachusetts and Washington.

Clue to longer life

While more research is needed to understand why the receptor mutation affects longevity and why it happens only in men, the study suggests that making a slight change in this specific piece of DNA could possibly make people live longer.

Although the presence of the mutation almost certainly ensured longevity, Atzmon stressed that many other factors affect longevity and that many men without the mutation also live to 100 and older.

Atzmon is one of the principal researchers in the Longevity Genes Project at Einstein along with Israeli endocrinology specialist Dr. Nir Barzilai.

Their groundbreaking 10-year study of healthy Ashkenazi Jews between the ages of 95 and 112 and their children attempted to understand why humans dont all age at the same rate, and why only one in 10,000 individuals lives to 100.

The centenarians were found to have genetic protective factors (longevity genes) that overcame factors such as diet and lifestyle.

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Mutation explains why some men live to 100 - ISRAEL21c