New Ways To Grow Old, Age

PART 1 : Japan, New Ways To Grow Old
http://www.bbc.co.uk/programmes/p05yq3lm?ns_mchannel=email&ns_source=worldservice_ps_newsletter&ns_campaign=worldservicenewsletter060318&ns_linkname=bbcrworldservice_documentary_japan1_link&ns_fee=0

Part 2:

http://www.bbc.co.uk/programmes/p05zfg1c

Japan: New Ways to Grow Old - Part One

The Documentary

Japan has the fastest ageing society in the world with more than a quarter of its population over the age of 65. It currently has 66,000 centenarians, more than any other country. Toshiko Katayose and AkiMaruyama Leggett explore some of the innovative ways in which Japanese people are adapting to living longer.

For over 20 years Toshiko Katayose edited Japan’s most popular magazine for senior readers. Now 67 and facing retirement, she reveals how her generation of baby-boomers born after World War Two, are overturning stereotypes about old age and how businesses are responding to these more demanding silver consumers. She visits Japan’s first supermarket built specifically to serve older shoppers which offers everything from crystal-studded walking sticks to try-before-you-buy coffin experiences.

(Photo: A cornucopia of stylish walking sticks at Japan’s first supermarket for older consumers. Credit: Mukti Jain Campion)

Show ,http://www.bbc.co.uk/programmes/p05zfg1c'

Japan: New Ways to Grow - Part Two

The Documentary

Could living in a home designed to deliberately demand more effort from you each day help you stay fitter and more alert in your later years? And could people living with dementia be better integrated in the community through work? Aki Maruyama Leggett examines some of the novel ideas for senior housing and social care emerging in Japan.

Harper's Bazaar, November 2017, 150th Anniversary Issue, P. 316 :

The Future of Anti-Aging

Experts believe that exciting new innovations in the longevity space may one day redefine the way we age—and help us look better as we do it.

By Anne-Marie Guarnieri

Oct 27, 2017

Fake fuller, younger-looking lips with Laura Mercier Lip Glacé in Poppy($26).

Kenneth Willardt

“Technology has reached a point where extending animal life span by 30 percent is routine,” says David Sinclair, a professor of genetics at Harvard Medical School and a renowned authority on longevity. “Dozens of companies are testing aging-reversal technologies in human clinical trials, and the combination of these could extend life span by decades.” Why is that a good thing? Because with science, those additional years could be happier, healthier ones. It does seem cruel, however, to have all that extra time if we’ll also look 150 years old. Fortunately, the most visionary anti-aging treatments on the horizon make pioneering plastic-surgery procedures seem run-of-the-mill. Read on to find out how a key supplement, DNA editing, and young blood could someday add years to your life, erase wrinkles, and potentially wipe out age-related diseases.

A molecule called NAD+ may hold the secret to boundless energy. The good news: Our cells already produce it, as it helps regulate our metabolism. The bad news: NAD+ declines as we age—by 50, levels are half of what they were at age 20. But scientists have discovered some powerful boosters that can help cells produce more NAD+. One of the most promising is NMN (nicotinamide mononucleotide), a form of vitamin B3 found in fruits and vegetables like avocado and broccoli. A 2013 study showed that older mice that were given an NAD+-boosting compound containing NMN had dramatically healthier cells and muscle tissue. “We took a mouse that was the human equivalent of a 65-year-old back to a 25-year-old—in a week,” says Sinclair, one of the study’s authors. What’s more, he says, the mice not only had more energy and could run farther but were resistant to diseases like cancer and diabetes. “If you reverse aging in one organ or tissue, usually the whole body is reversed, because all cells have the same underlying defects,” he explains.

Could NMN have the same effect on us? Sinclair, 48, has been taking his own custom NMN supplement (500 milligrams) for almost two years. Tests have revealed that his cells now behave like that of a 31-year-old. “I started taking it in my late 40s, and sometimes in your late 40s you feel tired during the day or you don’t feel like getting up early in the morning,” he says. “I don’t feel that way anymore. I feel upbeat mentally and physically, and I have the endurance of an athlete, but I don’t exercise.”

"You may one day be able to delete the negative signs of aging from your DNA for good, say scientists."

Another NAD+ booster, NR (nicotinamide riboside), found in ChromaDex’s Tru Niagen supplement (different in molecular structure from NMN, which Sinclair says is “better” and more stable than NR), can easily be purchased online, and has been shown to be safe in humans. “A single dose of 100 milligrams can raise NAD+ levels,” says Amy Boileau, director of scientific affairs for ChromaDex. Boileau believes that restoring depleted NAD+ levels could lead to fewer wrinkles but that additional testing is required. “It’s not hard to find a disease associated with NAD+ depletion that doesn’t also affect [visible aging],” she says. “I would like to see it work in skin because there’s so much promise there. It’s going to be an important question as to the role NAD+ can play.”

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In August, Sinclair and his team began human trials on a prescription-strength NMN NAD+ booster. “We’re trying to see if it’s safe, and what the best dosage would be before going into Phase II studies with a particular disease, like diabetes or obesity,” he explains. The idea that a simple molecule could restore lost energy and wipe out major diseases seems like a fantasy. But Sinclair is resolute. “Antibiotics are pretty simple too,” he says with a shrug. “We first showed that NAD+ extends the life span of cells back in 2003, but now it’s really taken off. It’s real.”

Look Younger by Editing Your Genes

You may one day be able to delete the negative signs of aging from your DNA for good. In late summer, the news was ablaze with talk of a fascinating procedure. Scientists at Oregon Health & Science University successfully removed harmful gene mutations from human embryos. Specifically, they fixed a mutation behind a common heart condition. Using a gene-editing tool known as CRISPR, or “genetic scissors,” they cut out the mutation and inserted a reparative enzyme. “If you want to add functionality to a gene, knock it out altogether, or change it just a little bit— that’s what CRISPR gave us the ability to do,” says biologist Daisy Robinton, a postdoctoral scientist at Boston Children’s Hospital who has used it in her work on cancer cells to positive result.

Though there were related stories warning of more nefarious uses for gene editing—designer babies, for example—for now, the focus is on higher-stakes concerns. Many CRISPR human trials are currently being done in China on patients with HPV, HIV, and lung cancer. “At first it’s going to be used only on cases where it’s worth the risk,” Robinton says, “and on people who are willing to take the risk because they don’t have many options.” As to whether CRISPR will be used for vainer pursuits—think curing baldness, eliminating gray hair, erasing wrinkles—Robinton, 30, is optimistic. “This isn’t the first time that biotech has invaded the beauty space,” she says. “It’s not [yet] real, but it’s our hopeful reality.”

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Other forms of genetic rejuvenation are being pursued by BioViva, a Seattle biotech company led by Elizabeth Parrish, 46, a self-described humanitarian, entrepreneur, and innovator. Two years ago, Parrish traveled to Colombia to receive two experimental anti-aging gene therapies: one meant to decrease the depletion of lean muscle mass; the other to increase the length of her telomeres, the end segments of DNA that shorten each time a cell divides. When telomeres reach a certain length, cells no longer divide and eventually die. If they could be extended, the thinking goes, so would the life cycle of the cell, thus prolonging its—and, by extension, our—existence. BioViva wants to make gene therapies like these as common as preventative medicine, Parrish says, and is developing targeted treatments for aging-related degenerative conditions, such as Alzheimer’s, and cosmetic procedures, like skin rejuvenation. “If we can’t regenerate the skin, the largest organ, you’re going to die,” explains Parrish. “People need to understand that this is not aesthetics—this is survival.”

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And it’s also not a fantasy: The FDA recently approved a gene-altering leukemia treatment developed by the pharmaceutical giant Novartis. Yet some in the scientific community were rattled by Parrish’s self-experimentation. For her part, Parrish, who, it must be noted, is not a scientist, professes to be unconcerned, claiming that her biomarkers (such as triglycerides and inflammation—both down since her personal trial) are “fantastic,” and believes that her company’s therapies will be available to consumers within the next two decades. “This is proven science,” she says. “We just need to prove it in humans.”

Blood Transfusions to Turn Back the Clock

Another youth-focused start-up is the San Francisco–based Ambrosia, which specializes in infusing blood—specifically “young” blood, from teenage donors (ages 16 and up)—into older clients, in hopes of regaining stamina, improving cognition, and repairing muscles. Why teens? Because younger blood has far lower levels of the harmful proteins that build up with age, which may cause decreased production of brain cells and inflammation. (If it sounds ghoulish, keep in mind that platelet-rich plasma therapy, which uses vials of your own blood, has long been used to treat injuries, osteoarthritis, and hair loss.)

Still, the science behind young-blood transfusions, which has focused primarily on mice, is somewhat inconclusive. That hasn’t deterred Ambrosia founder Jesse Karmazin, M.D., from trying for a moon shot. Yet when word of Ambrosia’s efforts began to spread, it was met with some healthy skepticism and not a little ribbing: Recall the “blood boy” episode of Silicon Valley. The problem, according to Karmazin, 32, is that what he’s doing is still so new, it’s misunderstood. “People thought my idea was crazy. Until recently, anti-aging wasn’t really a field. But it’s amazing how quickly it’s exploded,” he says. “There’s all this research and decades of experiments in mice showing that it reverses aging, so I thought, ‘Why aren’t we doing this in people?’ ” Ambrosia is recruiting participants between the ages of 35 and 100 for a clinical trial to evaluate Karmazin’s theory, and expects to publish the findings within the next year. So far, Karmazin says, the results are “strong.” He has estimated that patients would need to have transfusions only twice a year to maintain the benefits. “People look younger when they leave the clinic. We’ve all been surprised at how well it seems to work,” he says. “A crucial part of the picture is that [blood transfusions are] an already proven medical treatment—we’re just purposefully using younger donors. If you get a transfusion, you’re likely going to get blood from someone who is older than you. But if we could encourage younger people to donate blood, it could help reverse aging.”

"Encouraging younger people to donate blood could help reverse aging," says Jesse Karmazin, M.D.

The Future Is Soon

Given how promising this sounds, it would be tempting to seek out a doctor who specializes in longevity and offer yourself up to science. Not so fast, says Sinclair. “Gene therapy is risky. Unlike a pill, if there’s a problem you can’t just stop taking it. It’s there forever.” And right now it’s also breathtakingly expensive: Novartis’s gene therapy costs $475,000. That makes the $45 price tag for a month’s supply of Tru Niagen feel like couch change. There is good news, however, and it’s not just for babies. With a wellspring of money into longevity research from tech companies like Google, experts feel confident that in the next five to 10 years, supercharged anti-aging treatments like these will begin to come to market. “I don’t want to get wrinkles or gray hair, and I want to be able to lift weights and run forever,” says Robinton. “It’s important to be grounded in reality, but I feel the science is closer than ever before.”

"Curing" Aging ! Can Human Mortality Be Hacked ?!

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Can Human Mortality Really Be Hacked?

Backed by the digital fortunes of Silicon Valley, biotech companies are brazenly setting out to “cure” aging

Aubrey de Grey says, “There’s no such thing as aging gracefully.” (Timothy Archibald)

By Elmo Keep

Smithsonian Magazine | Subscribe
June 2017

It’s just after 10:30 a.m. on a pleasant weekday morning at SENS, a biotech lab in Mountain View, California. I’ve come to speak to its chief science officer, Aubrey de Grey. I find him sitting in his office, cracking open a bottle of Stone pale ale. “Would you like one?” he offers hospitably. De Grey drinks three or four pints of ale a day, and swears it hasn’t kept him from maintaining the same vigor he felt as a teenager in London.

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Now the 54-year-old’s long hair, tied back in a ponytail, is turning gray, a change that would be unremarkable if he weren’t one of the world’s most outspoken proponents of the idea that aging can be completely eradicated. De Grey first gained notoriety in 1999 for his book The Mitochondrial Free Radical Theory of Aging, in which he argued that immortality was theoretically possible. Since then, he’s been promoting his ideas from prominent platforms—the BBC, the pages of Wired, the TED stage. He delivers his message in seemingly unbroken paragraphs, stroking his dark brown wizard’s beard, which reaches below his navel. Unlike most scientists, he isn’t shy about making bold speculations. He believes, for example, that the first person who will live to be 1,000 years old has most likely already been born.
In 2009, de Grey founded the nonprofit SENS, the world’s first organization dedicated to “curing” human aging, not just age-related diseases. The organization, which conducts its own research and funds studies by other scientists, occupies an unassuming space in a small industrial park. Its walls are affixed with large, colorful posters illustrating human anatomy and the inner workings of cells.
The basic vision behind SENS is that aging isn’t an inevitable process by which your body just happens to wear out over time. Rather, it’s the result of specific biological mechanisms that damage molecules or cells. Some elements of this idea date back to 1972, when the biogerontologist Denham Harman noted that free radicals (atoms or molecules with a single unpaired electron) cause chemical reactions, and that these reactions can damage the mitochondria, the powerhouses within cells. Since then, studies have linked free radicals to all sorts of age-related ailments, from heart disease to Alzheimer’s.

De Grey takes this concept further than most scientists are willing to go. His 1999 book argued that there could be a way to obviate mitochondrial damage, slowing the process of aging itself. Now SENS is working to prove this. Its scientists are also studying other potential aging culprits, such as the cross-links that form between proteins and cause problems like arteriosclerosis. They’re looking at damage to chromosomal DNA, and at “junk” materials that accumulate inside and outside cells (such as the plaques found in the brains of Alzheimer’s patients).
The area of research that gives the organization its name has to do with senescent cells. (SENS stands for Strategies for Engineered Negligible Senescence.) These are cells that stop dividing but accumulate inside us, secreting proteins that contribute to inflammation. It’s widely accepted that inflammation is involved in arthritis, heart disease, cancer, dementia and any number of other conditions that define old age. As de Grey’s thinking goes, if we could figure out how to remove senescent cells using approaches like drugs or gene therapy, along with other types of repair, we could potentially keep our bodies vital forever.
This desire to eradicate aging has, in the last decade, inspired a mini-boom of private investment in Silicon Valley, where a handful of labs have sprung up in SENS’ shadow, funded most notably by tech magnates. The secretive Calico was established by Google, in collaboration with Apple chairman Arthur Levinson, to tackle the problem of aging. Facebook’s Mark Zuckerberg and his wife, Priscilla Chan, have invested $3 billion in the attempt to “cure all disease.” Amazon’s Jeff Bezos invested some of his fortune in South San Francisco–based Unity Biotechnology, which has been targeting cell senescence in animal trials and hopes to begin human drug trials next year.
It’s this influx of wealth that has brought novel anti-aging theories out of the scientific fringes and into gleaming Silicon Valley labs. De Grey notes that developing the means to make everyone live forever is not cheap. “This foundation has a budget of somewhere around $4 million a year, not $4 billion, which is what it should be,” de Grey says. He invested $13 million of his own money in SENS, the lion’s share of the $16.5 million he inherited when his mother died. (He says she earned her wealth through property investments.) SENS has also been the beneficiary of PayPal co-founder Peter Thiel, perhaps Silicon Valley’s best-known advocate for curing death. As Thiel told the Washington Post in 2015, “I’ve always had this really strong sense that death was a terrible, terrible thing....I prefer to fight it.”

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This mouse at the Buck Institute was engineered to accumulate senescent cells at an accelerated rate, making it age more rapidly. (Timothy Archibald)

Immortality, it turns out, is not such an easy sell: Most people don’t like the idea of living forever. In legends of old as well as in recent popular culture, eluding death typically comes at a terrible cost; like zombies or vampires, immortal beings must feast on the living. Besides, a large percentage of today’s population also subscribes to religious beliefs in which the afterlife is something to be welcomed. When the Pew Research Center asked Americans in 2013 whether they would use technologies that allowed them to live to 120 or beyond, 56 percent said no. Two-thirds of respondents believed that radically longer life spans would strain natural resources, and that these treatments would only ever be available to the wealthy.
I ask de Grey about how the world would change—socioeconomically especially—if no one ever died. Would people still have children? If they did, how long would the planet be able to sustain billions of immortals? Wouldn’t every norm predicated on our inevitable deaths break down, including all the world’s religions? What would replace them? At what point might you decide that, actually, this is enough life? After decades? Centuries? And once you made that decision, how would you make your exit?
“I find it frustrating that people are so fixated on the longevity side effects,” de Grey says, clearly irritated. “And they’re constantly thinking about how society would change in the context of everyone being 1,000 years old or whatever. The single thing that makes people’s lives most miserable is chronic disease, staying sick and being sick. And I’m about alleviating suffering.”
To explain his vision, de Grey uses the analogy of a car that has its parts continually repaired. People receiving cell regeneration therapies would be able to constantly add more time to their lives whenever their bodies began to break down. “We have a warranty period, it’s true,” he allows. “But cars also have warranty periods, and yet we still have vintage cars—because we know how to do comprehensive, regular, preventative maintenance.”
De Grey spent several years after college working as a computer scientist in the field of artificial intelligence, which might explain why he likes to compare human bodies to machines. He has a PhD in biology from Cambridge, but he received it for theoretical work rather than lab-based research. He often refers to himself as an engineer or a “technologically focused biologist.”
I ask de Grey how a planet full of immortals would support itself. Would people want to work for eternity? He answers that automation will take over most jobs. “We will be able to spend our lives doing things that we find fulfilling and we won’t have to worry about remuneration,” he says. De Grey has been closely associated with transhumanism, a movement that believes technology will help the human race evolve far beyond its current limitations, but he dislikes the term, noting that it “just scares people.”
De Grey has robust faith that humans will come up with “some new way to distribute wealth that doesn’t depend on being paid to do things we wouldn’t otherwise do.” The first step, he believes, is issuing a universal basic income. It’s an idea that’s shared by other Bay Area entrepreneurs, many of whom are in the business of developing automation technologies. Last year, Y Combinator, a highly successful start-up incubator, gave 100 Oakland families between $1,000 and $2,000 a month in unconditional free income to find out how they’d spend it. The city of San Francisco recently announced plans to launch a similar pilot program. But these are small-scale experiments, and if robots do take over more jobs, it isn’t clear whether our economic and political systems would reconfigure to support all unemployed people in time, least of all forever.
And that 1,000-year-old person: He or she has already been born?
“Oh absolutely, yeah,” de Grey assures me. “It’s highly likely.”

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In fact, the human body is not at all like a car, in the same way that the human brain is not like a computer. Such comparisons oversimplify the staggeringly complicated organic systems that researchers are only beginning to glimpse. The chaotic interactions between our trillions of cells and their enzymes are still poorly understood. We know almost nothing about why some people hit the genetic jackpot and live much longer and with much more vigor than others who have similar life circumstances. The question is all the more vexing because elderly humans are themselves an extremely recent phenomenon.
Judy Campisi is saying all this to me over coffee near her home in Berkeley. She works 45 minutes north in Novato at the Buck Institute for Research on Aging, a gleaming non-profit research institution. “For 99.9 percent of our human history as a species, there was no aging,” she says. Humans were very likely to die by our 30s from predation, starvation, disease, childbirth or any number of violent events.

Judy Campisi sits in the atrium at the Buck Institute. The campus was designed by I.M. Pei, the architect of the Louvre pyramid. (Timothy Archibald)

Life spans in the developed world have more than doubled over the past century or so, but this hasn’t happened through any interventions against aging itself. Rather, it’s a byproduct of innovations such as clean water, medication, vaccinations, surgery, dentistry, sanitation, shelter, a regular food supply and methods of defending against predators.
A biochemist and professor of biogerontology, Campisi has spent her career studying aging and cancer, and the role senescent cells play in both. She has researched these cells in her lab and published widely on the possible evolutionary reasons they remain in our bodies. She posits that for most of human history, natural selection didn’t favor living to old age. Evolution protected younger people so they could pass along their genes, and senescent cells play a very important role.
“One thing evolution had to select for was protection from cancer,” she says. “Because we are complex organisms, we have lots of cells in our body that divide, and cell division is a very risky time for a cell because it’s easy to pick up a mutation when you are replicating three billion base pairs of DNA.” If a cell doesn’t divide, there are fewer chances for such a mutation to creep in. “So evolution put into place these very powerful tumor suppressant mechanisms—senescent cells—but they only had to last for 40 years at the most.”
What serves as a preventive mechanism in early life later can become a cancer-causing agent of its own, Campisi says. Senescent cells contribute to inflammation, and “inflammation is the number one risk factor for all diseases of aging, including cancer.” Eliminating these cells might cut down on various ailments, but no one is yet sure what the side effects would be.
The idea that senescent cells contribute to aging was first postulated in the 1960s. Yet 50 years later, scientists still don’t entirely understand the role they play. All Campisi can say definitively is that, for most of human history, there was “no evolutionary pressure to make that system better because everybody died young.”
When I ask Campisi why some scientists talk about “curing” aging, she says it comes down to getting interventions approved. “There are people who want to consider aging a disease for the purposes of going to regulatory agencies and having a specific drug able to treat a specific symptom, which you can only do if it’s recognized as a disease.” But Campisi stresses that living forever is not the goal of most research on aging. Instead, she says it’s primarily aimed not at life span but “health span”—increasing the number of years that people can remain physically and mentally agile.
Campisi has known de Grey for years, collaborates with SENS and even serves on the organization’s advisory board. I ask what she makes of his assertion that someone alive today will reach the age of 1,000.
“I have to tell you Aubrey has two hats,” she says, smiling. “One he wears for the public when he’s raising funds. The other hat is when he talks to a scientist like me, where he doesn’t really believe that anyone will live to 1,000 years old. No.”

Cell samples are stored in liquid nitrogen so SENS researchers can later study their metabolic processes for clues about aging. (Timothy Archibald)

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One thing we do know is that there are more elderly people alive now than there have ever been in the history of the planet. Even if today’s life-extension researchers made meaningful breakthroughs, the therapies wouldn’t be available for many years to come. That means we’re about to face a lot of death, says Rachel Maguire, a research director focusing on health care at the Institute for the Future, in Palo Alto. “By 2025 or 2030, there will be more of a culture of dying and lots of different ways of experiencing it. There are early signs of new types of funerals and spiritual formations around this.” Maguire foresees new end-of-life plans, including assisted dying. When it comes to aging, she points out that biological research is only one piece of a puzzle that must also include economics, politics and cultural change. “I don’t think we have answers yet for how we’d do the other pieces. And the financial piece alone is huge.”
There’s already a huge disparity between the life spans of rich and poor Americans, and critics of the new longevity research worry the gap may only grow wider. A 2016 report from the Brookings Institution found that, for men born in 1920, there was a six-year difference in life expectancy between men at the top 10 percent and bottom 10 percent of the earnings ladder. For men born in 1950, the difference was 14 years. For women, the gap grew from 4.7 to 13 years. In other words, advances in medicine haven’t helped low-income Americans nearly as much as their wealthier counterparts.
I had a glimpse of that discrepancy as I used ride-hail apps to get around the Bay Area. On my way to Mountain View, where the median household income is $103,488, my driver, a woman in her 50s, told me she had trouble paying for gas and was sleeping in the car between nights on relatives’ couches. Sometimes, she said, she was stricken by bouts of rheumatoid arthritis. If her joints seized up while she was driving, she had to pull over and wait until the episode passed, usually not working anymore that day. I did not want to ask how she would feel if she ended up living so long that her future included another two decades of driving.
Jake Dunagan, the director of design futures at the consulting firm Very Nice, studies the cognitive biases that make it difficult for people to plan ahead. “That’s one of the conundrums of futurist work: The future doesn’t exist,” Dunagan tells me. “It’s always a projection.” Our minds, he says, have not evolved to be very good at seeing our future as connected to our present, as we spent so much of our early existence concerned with outwitting immediate threats.
Dunagan has little patience for Silicon Valley’s longevity research; he says proponents are not sufficiently interested in the details. “The rich people are defining the terms of the longevity conversation and have enhanced access to these technologies,” he says. “Everyone wants to live longer, to some degree, but it’s also the sense of privilege, of selfishness to it that’s ‘I want mine. I always want mine.’ Well, what if everyone had this? What would be the long-term implications of that?”

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In 2006, the magazine MIT Technology Review published a paper called “Life Extension Pseudoscience and the SENS Plan.” The nine co-authors, all senior gerontologists, took stern issue with de Grey’s position. “He’s brilliant, but he had no experience in aging research,” says Heidi Tissenbaum, one of the paper’s signatories and a professor of molecular, cell and cancer biology at the University of Massachusetts Medical School. “We were alarmed, since he claimed to know how to prevent aging based on ideas, not on rigorous scientific experimental results.”
More than a decade later, Tissenbaum now sees SENS in a more positive light. “Kudos to Aubrey,” she says diplomatically. “The more people talking about aging research, the better. I give him a lot of credit for bringing attention and money to the field. When we wrote that paper, it was just him and his ideas, no research, nothing. But now they are doing a lot of basic, fundamental research, like any other lab.”
In marked contrast with de Grey, however, Tissenbaum doesn’t see aging itself as the problem. “I don’t think it’s a disease,” she says. “I think it’s a natural process. Life and death are a part of the same coin.”

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Rachel Maguire of the Institute for the Future chooses to live in Austin, Texas. She finds Silicon Valley “a little too Truman Show.” (Timothy Archibald)

Instead of seeking out a universal cure for aging, Tissenbaum finds it more useful to look at the genes involved in specific factors, such as good metabolic function and resistance to stress. For her own research, she has artificially extended the lives of C. elegans roundworms and mice, but she’s found that the creatures are sluggish and frail during that extra period of life. In other words, extending life through lab-based means doesn’t necessarily lead to good health. “If applied to humans, this would likely lead to unsustainable healthcare costs,” she and her co-authors concluded in a 2015 study published in the Proceedings of the National Academy of Sciences.
There are all kinds of theories about how to close the gap between life span and health span, and not all of them focus on senescent cells. Some scientists think taking aspirin and vitamin D could reduce inflammation throughout the body and lower the incidences of all kinds of diseases. Others believe the key is to repair telomeres, the sequences at the ends of each chromosome that unravel with stress and age. Research is still very much in progress on all of these ideas.
Meanwhile, scientists are trying to understand why the brain deteriorates over time, losing mass and neural circuitry. Tissenbaum and others are trying to understand these mechanisms, hoping to find new treatments for neurodegenerative diseases. But she doesn’t expect any intervention to keep humans healthy forever. “It may be that the brain has a finite life span,” she says.
For now, Tissenbaum recommends the usual methods of fending off frailty. Studies have shown that regular physical exercise can stimulate neural networks and keep connections alive. So can challenging mental activities. “If you always do crossword puzzles, try Sudoku,” she says. “Where we have really progressed is in our understanding of how keeping your mind and body active is fundamental to healthy aging.”
Many of the world’s oldest stories are quests for eternal life, from Herodotus’ fountain of youth to the medieval Holy Grail. There’s a great deal of money and brainpower invested in the hope that science will finally deliver on this promise. The research in these labs might yield more incremental breakthroughs, revealing the mechanisms behind Alzheimer’s or certain types of cancer. But for some true believers, that won’t be enough. De Grey, for one, dislikes the idea of seeking cures for individual age-related diseases. “I believe that the term ‘disease’ has become one that does far more harm than good, as has ‘cure,’” he says, “such that some aspects of aging are inappropriately described as curable diseases and others as ‘aging itself.’”
I asked Judy Campisi if she thought there was an upper limit to the human life span. “I suspect there is,” she said. “Like you’d say there’s a limit to running a marathon. You aren’t going to ever run one in 30 seconds.” When it comes to extending life, she says, “we think the upper limit we could get to is around 115 to 120 years old—if we don’t blow ourselves up before then, or the planet doesn’t melt down.”
If Campisi and others are right, we may come to accept that we’re profoundly mortal creatures after all. Still, we seem to be driven, as a species, to overcome every adversity we encounter. We may not live forever, or even to 1,000, but a more vibrant old age could yet be on the horizon for all of us.
Editor’s Note, May 25, 2017: An earlier version of this article erroneously called the Buck Institute a “gleaming profit institution”, as opposed to a non-profit, and described its distance from Berkeley as two hours instead of 45 minutes.

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This article is a selection from the June issue of Smithsonian magazine

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About Elmo Keep

Originally from Australia, Elmo Keep is a freelance writer based in Brooklyn. Her work has appeared in Matter, The Awl, the International New York Times and other outlets.

U Will Live A Long Life IF.../Pig w/Apple in Mouth NEW YORKER CARTOONS

New Yorker Cartoons

Lianna Finck (pig)
Amy Hwang  (doctor) :

Perils of Aging-Financial Planning,Last Rites/Dead Husband=Dried Flower Arrangement COMICS

Pickles by Brian Crane

 


http://www.gocomics.com/pickles/2017/03/28


DeFlocked by Jeff Corriveau :

March 28, 2017

 

 

http://comicskingdom.com/deflocked

RIP Grandpa = Sleep Well !!!! COMIC

After Dying, He Stayed Put In His Easy Chair !! New Yorker Cartoon

 
“He just doesn’t know what to do with himself since he passed away.”


What will you do after you die ??!!

Bizarro Comic TIME passes quickly as you age !! AGING & Beetle Bailey Too old to grow up !!

Bizarro by Dan Piraro - Bizarro Comic Strip | Comics Kingdom



Aging !!  9/12/2015 Bizarro strip:

Too old to grow up !!, Beetle Bailey:

Machines to Make Us Happy/Robots=ElderCare New Era

Closing Thoughts: Machines to Make Us Happy | Dickinson College 

Please CLICK on hyperlink above (Closing . . . College) to access article.  Thank you.



Robots signal a new era of elder care !!!!

MAGAZINE

The Cheater's Guide to Living to 100 

APRIL 3, 2015 – 5:00 AM – 3 COMMENTS

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By PARADE @parademagazine

(Dollar Photo Club)

Four super-simple secrets to living longer, healthier and happier—from longevity expert Dan Buettner and centenarians around the world

By Ginny Graves

You turn 50 and suddenly you’re pegged as “middle-aged.” But what if it really was the middle, and you could expect to live to 100 or even 120? Don’t laugh. There are 53,364 centenarians in the U.S. today, according to the latest Census Bureau figures, and experts estimate that number could skyrocket to 600,000 by 2050. Better yet, many of these oldsters will defy the doddering stereotype. Take Jeralean Talley of Inkster, Michigan. She was still bowling at 104 and getting around with the help of a walker last May—when she celebrated her 115th birthday. Last year, UnitedHealthcare polled 104 people who’ve reached triple digits and found that not a single one felt sad or burdened, or even particularly old. On average, they said, they felt more like whippersnappers of 83.

Interested in joining this club? Enter journalist Dan Buettner. He has spent over a decade studying the healthiest, longest-living people around the world, from residents of the Japanese island of Okinawa to the Greek island of Ikaria—so-called “Blue Zones,” or longevity hotspots (Sardinia, Loma Linda, Calif. and Nicoya, Costa Rica are the others), where people live to 100 or older at much higher-than-average rates.

“These aren’t the frail elderly,” he says. “They’re still working, riding bikes, socializing, having sex and enjoying life.”

Since 2009, Buettner has taken the Blue Zones lessons to a few U.S. cities, transforming their residents’ health. Now, he’s letting the rest of us in on their secrets in his new book, The Blue Zones Solution: Eating and Living Like the World’s Healthiest People (National Geographic Books). Here are the most important longevity-boosting habits of centenarians around the globe. Adopt even a few, and you’ll stand a better chance of celebrating your 100^th birthday.

1. Find Your Tribe
“Who you hang out with trumps just about everything else when it comes to your health,” says Buettner. He found that the people who live longest surround themselves with people who support healthy behaviors, and other research backs that up: When psychologists at Brigham Young University reviewed 148 studies on social relationships, they found that those with stronger connections were half as likely to die as those with weaker ties during the study periods. One explanation: “Health habits—both good and bad—can spread like a contagion,” says Noah Webster, Ph.D., an assistant research scientist at the University of Michigan’s Life Course Development Institute for Social Research.

Buettner uncovered especially strong evidence of the longevity-boosting effect of friends in ultra-old Okinawans, who form moais (rhymes with “doe eyes”)—groups of lifelong alliances. It’s a concept he has introduced in American cities, including Redondo Beach, Calif., where Joan Edelman lives. More than four years ago, Edelman and her husband met a handful of strangers at a Blue Zones get-together and formed a beach-walking moai; they’ve walked four miles four days a week ever since. “There are 13 of us, ranging from our 40s to 80s,” says Edelman, 67. “We’ve become very close. When someone has a crisis, we show up.”

Centenarians from Blue Zones also take advantage of the life-giving power of social connections in other ways: They belong to a faith-based community (attending services four times a month can add up to 14 years to your life, Buettner says) and have close-knit families.

“Extended families live near each other, if not together, and they invest time and energy not only in their children but in their parents, grandparents and life partners,” Buettner says. “Just committing to a life partner can add up to three years to your life, according to our research.”

2. Eat Smart
The world’s most robust 100-year-olds stick with diets that are 95 percent plant-based, says Buettner. “They eat a little meat, but mostly fish,” he says. British researchers tracked 65,000 people for 12 years and found that those who ate seven or more portions of vegetables and fruits every day lowered their risk of dying from the two leading causes of death—cancer and cardiovascular disease—by 25 percent and 31 percent.

“Protein, especially from animal sources, activates two sets of genes that accelerate aging,” says Valter Longo, Ph.D., director of the University of Southern California’s Longevity Institute, whose studies have shown that people with the highest protein intake have the highest risk of cancer and mortality compared with those who eat the least.

Never learned to love veggies? Take a page from David and Beverly Van Dillen, of Hermosa Beach, Calif., who formed a monthly potluck moai a couple of years ago. “We have a group of 12 people, and we support each other in healthy eating and share our favorite recipes,” says Beverly, 70. Since increasing their vegetable consumption, she’s been able to discontinue her cholesterol and blood pressure medications, and David, 69, has lost 40 pounds. “We feel better, we look better and we’re objectively healthier—and we have a great new group of friends we truly enjoy,” he says. (Go to Parade.com/LongevityStew for a longevity-boosting recipe.)

Blue Zones centenarians approach eating differently, too, says Buettner. Before every meal, Okinawans invoke a 2,500-year-old Confucian mantra, known as hara hachi bu, to remind themselves to stop eating when they’re 80 percent full. People in the Blue Zones also eat their largest meal in the morning and their smallest at night.

As for beverages, most Blue Zones centenarians have a glass of wine a day—a habit that research shows boosts longevity.

3. Seek a Purpose
Very old Blue Zoners share another trait: They have an activity, passion or career that motivates them and gives their lives meaning. “Okinawans call itikigai, and those who live in Nicoya, Costa Rica, call it plan de vida, both of which mean ‘Why I wake up in the morning,’” says Buettner. In one 14-year study, researchers found that the 569 participants who died had scored lower on ratings of life purpose and social relationships than those who survived. Their conclusion: Having a purpose in life provides a buffer against mortality, no matter your age.

Sense of purpose can come from a variety of sources, but volunteering is a common one. “There’s growing evidence that it not only keeps you healthier but might help you live longer,” says Webster. For some people, a sense of purpose evolves naturally—they discover they love singing in a choir, tutoring children or building model trains. For others, it’s less clear. “I looked into everything, from volunteering to a drum circle,” says Beverly Van Dillen. “Then I realized nothing gives me more satisfaction than helping our daughter with our grandchildren, who are 2 and 3.”

Having a sense of purpose might contribute to longevity by lowering the stress hormone cortisol. “Chronic stress leads to inflammation, which is associated with every age-related disease,” Buettner says.

Longevity-Boosting Tricks to Try Right Now

A Pill To Stave Off Diseases That Come With Age=Grow Old Without Disease, And Healthy

Wall Street Journal, Tuesday, March 17, 2015, PERSONAL JOURNAL section:

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YOUR HEALTH

Scientists’ New Goal: Growing Old Without Disease

Researchers plan to test a pill to prevent or delay Alzheimer’s, heart disease and other ailments that come with age

ENLARGE

BRIAN HARKIN FOR THE WALL STREET JOURNAL

By

SUMATHI REDDY

March 16, 2015 5:43 p.m. ET

41 COMMENTS

Some of the top researchers on aging in the country are trying to get an unusual clinical trial up and running.

They want to test a pill that could prevent or delay some of the most debilitating diseases of old age, including Alzheimer’s and cardiovascular disease. The focus of the project isn’t to prolong life, although that could occur, but to make the last years or decades of people’s lives more fulfilling by postponing the onset of many chronic diseases until closer to death.

The project aims to tap into the growing body of research targeting aging, which has revealed a half dozen or more drugs that appear to delay the aging process in laboratory experiments on animals and observational studies of people. Some of the drugs also have been found to reduce the incidence of chronic diseases associated with old age.

“Aging is the major risk factor for all these diseases—heart disease, cancer, diabetes and Alzheimer’s,” said Nir Barzilai, director of the Institute for Aging Research at Albert Einstein College of Medicine in New York City who is leading the proposed study. “If you want to make a real impact you have to modulate the risk of aging and by that the risk for all those diseases of aging.”

ENLARGE

Dr. Barzilai expects to enroll more than 1,000 elderly participants in the randomized, controlled clinical trial to be conducted at multiple research centers and take five to seven years. The project is in the preliminary stages and permanent funding hasn’t yet been secured. Funding for the planning phase is coming from the American Federation for Aging Research, a nonprofit organization of which Dr. Barzilai is deputy scientific director.

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The trial aims to test the drug metformin, a common medication often used to treat Type 2 diabetes, and see if it can delay or prevent other chronic diseases. (The project is being called Targeting/Taming Aging With Metformin, or TAME.) Metformin isn’t necessarily more promising than other drugs that have shown signs of extending life and reducing age-related chronic diseases. But metformin has been widely and safely used for more than 60 years, has very few side effects and is inexpensive.

The scientists say that if TAME is a well-designed, large-scale study, the Food and Drug Administration might be persuaded to consider aging as an indication, or preventable condition, a move that could spur drug makers to target factors that contribute to aging.

A study that helped convince the gerontologists to pursue the TAME project was done in the U.K. and published last year in the journal Diabetes, Obesity and Metabolism. Researchers used data from a national registry of more than 180,000 people, comparing the treatment of metformin with that of sulfonylurea, another drug used for diabetes. They also created two control groups of nondiabetic people.

People who took metformin lived longer than those taking sulphonylurea, the study found. In addition, the people with diabetes who were 71-to-75-years-old at baseline and took metformin outlived their nondiabetic controls with a 15% greater survival rate.

“Observational studies like this are never definitive,” said Jill Crandall, director of the Diabetes Clinical Trials Unit at Albert Einstein College of Medicine and part of the TAME planning team. “But it is one of the observations that certainly supports our hypothesis—that certain pharmacological interventions, like metformin, may have broad effects in improving health and increasing health span.”

Dr. Crandall also participated in a federally funded study that found metformin and lifestyle changes were both effective in staving off diabetes in people at high risk for the disease for at least 10 years. Data from the study, which followed more than 3,000 adults for 15 years, are now being analyzed to see whether long-term use of metformin prevented the development of cardiovascular disease, cancer, cognitive decline and physical-function decline. The results could help in the planning of the TAME study, she said.

ENLARGE

Dr. Barzilai, who is leading the effort to test if the drug metformin can delay or prevent chronic diseases, also focuses in his work on the genetics of centenarians.PHOTO: BRIAN HARKIN FOR THE WALL STREET JOURNAL

Research has found that metformin targets the chemicals produced by age-related senescent cells—normal cells that stop dividing and produce toxic substances damaging to the cells around them, said James Kirkland, director of the Robert and Arlene Kogod Center on Aging at the Mayo Clinic in Rochester, Minn., and part of the TAME planning team. Senescent cells usually develop as people age or at sites of age-related chronic diseases, such as the brain in Alzheimer’s patients or around the plaques that lead to heart attacks and strokes, he said. It isn’t proven if senescent cells actually cause the disease.

Metformin appears also to slow the development of age-related symptoms by increasing the enzyme AMP kinase, which normally declines with age, and decreasing the protein mTOR, which helps to regulate cell growth.

Several other drugs also have shown life-extension properties in mice and in laboratory work, Dr. Kirkland said. His research group last week published a study on mice in the journal Aging Cell which showed that a combination of two drugs—dasatinib, a cancer drug, and quercetin, a supplement that can be found in health food stores—were potentially effective.

“There’s more and more evidence that by targeting aging itself we might be able to target these age-related chronic diseases that have been so intractable for us to try to come up with a cure for,” Dr. Kirkland said.

Fighting each major disease of old age separately isn’t winnable, saidS. Jay Olshansky, another TAME project planner and a professor at the school of public health at the University of Illinois at Chicago. “We lower the risk of heart disease, somebody lives long enough to get cancer. If we reduce the risk of cancer, somebody lives long enough to get Alzheimer’s disease.”

“We are suggesting that the time has arrived to attack them all by going after the biological process of aging,” Dr. Olshansky said.

Sandy Walsh, an FDA spokeswoman, said the agency’s perspective has long been that “aging” isn’t a disease. “We clearly have approved drugs that treat consequences of aging,” she said. Although the FDA currently is inclined to treat diseases prevalent in older people as separate medical conditions, “if someone in the drug-development industry found something that treated all of these, we might revisit our thinking.”

Other experts agree with the goal of delaying chronic disease for the elderly, but question whether medication is the best way to do that. “I can certainly see how medicine can play a role if it turns out this study shows some promising findings,” said Alicia Arbaje, a geriatrician and an assistant professor of medicine at Johns Hopkins School of Medicine. “But aging is very complex and it’s probably going to take a multifaceted approach to help people delay or ensure that they age in a healthy way,” said Dr. Arbaje, who isn’t affiliated with the TAME trial planning.

Effective interventions to delay aging already exist, Dr. Arbaje noted, such as exercise, nutrition, social engagement, stress reduction and getting adequate sleep. “These are reliable and effective ways to keep people healthy as they age,” she said. “The problem is they’re not as easy as taking a medication.”

Write to Sumathi Reddy at sumathi.reddy@wsj.com