Aging – Page 14 – artdiamondblog.com

Jobs’ Protest Against Mortality: Omit the On-Off Switches on Apple Devices

(p. 571) . . . [Jobs] admitted that, as he faced death, he might be overestimating the odds out of a desire to believe in an afterlife. “I like to think that something survives after you die,” he said. “It’s strange to think that you accumulate all this experience, and maybe a little wisdom, and it just goes away. So I really want to believe that something survives, that maybe your consciousness endures.”
He fell silent for a very long time. “But on the other hand, perhaps it’s like an on-off switch,” he said. “Click! And you’re gone.”
Then he paused again and smiled slightly. “Maybe that’s why I never liked to put on-off switches on Apple devices.”

Source:
Isaacson, Walter. Steve Jobs. New York: Simon & Schuster, 2011.
(Note: ellipsis and bracketed “Jobs” added; italics in original.)

Resveratrol Activates Sirtuins to Switch on Energy Producing Mitochondria

A new study, just published in the prestigious journal Science, appears to substantially vindicate the recently beleaguered resveratrol longevity research of David Sinclair:

. . . a new study led by David Sinclair of the Harvard Medical School, who in 2003 was a discoverer resveratrol’s role in activating sirtuins, found that resveratrol did indeed influence sirtuin directly, though in a more complicated way than previously thought. . . . . . . activated, the sirtuins do several things, one of which is to switch on a second protein that spurs production of the mitochondria, which provide the cell’s energy. This would explain why mice treated with resveratrol ran twice as far on a treadmill before collapsing from exhaustion as untreated mice.

For the full story, see:
NICHOLAS WADE. “New Optimism on Resveratrol.” New York Times “Well” Blog Posted on MARCH 11, 2013. URL: http://well.blogs.nytimes.com/2013/03/11/new-optimism-on-resveratrol/
(Note: ellipses added.)

The Sinclair article (see last-listed co-author) is:
Hubbard, Basil P., Ana P. Gomes, Han Dai, Jun Li, April W. Case, Thomas Considine, Thomas V. Riera, Jessica E. Lee, Sook Yen E (sic), Dudley W. Lamming, Bradley L. Pentelute, Eli R. Schuman, Linda A. Stevens, Alvin J. Y. Ling, Sean M. Armour, Shaday Michan, Huizhen Zhao, Yong Jiang, Sharon M. Sweitzer, Charles A. Blum, Jeremy S. Disch, Pui Yee Ng, Konrad T. Howitz, Anabela P. Rolo, Yoshitomo Hamuro, Joel Moss, Robert B. Perni, James L. Ellis, George P. Vlasuk, and David A. Sinclair. “Evidence for a Common Mechanism of Sirt1 Regulation by Allosteric Activators.” Science 339, no. 6124 (March 8, 2013): 1216-19.

Entrepreneur Kurzweil Says If He Gets Cancer, He Will Invent a Cure

“Ray Kurzweil.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. 12) As a futurist, you are famous for making predictions of when technological innovations will actually occur. Are you willing to predict the year you will die?
My plan is to stick around. We’ll get to a point about 15 years from now where we’re adding more than a year every year to your life expectancy.

To clarify, you’re predicting your immortality.
The problem is I can’t get on the phone with you in the future and say, “Well, I’ve done it, I have lived forever,” because it’s never forever.
. . .
You’ve said that if you woke up one day with a terminal disease, you’d be forced to invent a cure. Were you being serious?
I absolutely would try. I’m working now on a cancer project with some scientists at M.I.T., and if I develop cancer, I do have some ideas of what I would do.
I imagine a lot of people would hear that and say, Ray, if you think you’re capable of curing yourself, why don’t you go ahead and start curing others?
Well, I mean, I do have to pick my priorities. Nobody can do everything. What we spend our time on is probably the most important decision we make. I don’t know if you’re aware, but I’m joining Google as director of engineering.

For the full interview, see:
Andrew Goldman, Interviewer. “TALK; The Life Robotic; The Futurist Ray Kurzweil Says We’re Going to Live Forever. Really.” The New York Times Magazine (Sun., January 27, 2013): 12.
(Note: ellipsis added; bold in original, indicating interviewer questions.)
(Note: the online version of the interview has the date January 25, 2013, and has the title “TALK; Ray Kurzweil Says We’re Going to Live Forever.”)

Entrepreneur Peter Thiel Says We Should Fight for Longer Lives

Source of book image: http://si.wsj.net/public/resources/images/OB-PJ926_bkrv10_DV_20110829191924.jpg

(p. C13) Sonia Arrison’s “100 Plus” was first published in 2011, but its message is evergreen: how scientists are directly attacking the problem of aging and death and why we should fight for life instead of accepting decay as inevitable. The goal of longer life doesn’t just mean more years at the margin; it means a healthier old age. There is nothing to fear but our own complacency.

For the full review essay, see:
Peter Thiel (author of passage quoted above, one of 50 contributors to whole article). “Twelve Months of Reading; We asked 50 of our friends to tell us what books they enjoyed in 2012–from Judd Apatow’s big plans to Bruce Wagner’s addictions. See pages C10 and C11 for the Journal’s own Top Ten lists.” The Wall Street Journal (Sat., December 15, 2012): passim (Thiel’s contribution is on p. C13).
(Note: the online version of the review essay has the date December 14, 2012.)

The book Thiel endorses is:
Arrison, Sonia. 100 Plus: How the Coming Age of Longevity Will Change Everything, from Careers and Relationships to Family and Faith. New York: Basic Books, 2011.

Lichen Fungi May Never Age

“ANNUAL VISITOR; For the last eight years, Anne Pringle of Harvard has been collecting data about the lichens on the gravestones at a cemetary in Petersham, Mass.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. D3) PETERSHAM, Mass. — On a sparkling New England afternoon, as hawks coasted overhead and yellow leaves drifted to the ground, Anne Pringle stood before a large granite obelisk that marked the graves of a family called French.
. . .
For eight years, Dr. Pringle, 42, has been returning to this cemetery each fall, to measure, sketch and scrutinize the lichens, which belong to the genus Xanthoparmelia. She wants to know whether they deteriorate with the passage of time, leaving them more susceptible to death.
. . .
Lichens are not individuals but tiny ecosystems, composed of one main fungus, a group of algae and an assortment of smaller fungi and bacteria.
. . .
While lichens are communities, Dr. Pringle is largely interested in the fungi. Mycologists, the scientists who study fungi — not the most glamorous corridor of biology — have long assumed that many of these organisms don’t age.
. . .
“What you know is based on the organisms you study,” she said. “What would you say about the evolution of senescence if instead of working with insects, you worked with modular organisms, which is what lichen are?”
Daniel Doak, a University of Colorado ecologist, agrees that the question is worth asking. Research like Dr. Pringle’s — along with other studies of species including the bristlecone pine tree and the wandering albatross, a bird, both of which may avoid senescence — suggests another possible path.
“It’s saying something fundamental,” Dr. Doak said, “that senescence is not an inevitable part of life. Which means there might be ways to prevent it.” That idea could eventually have implications for human medicine.
. . .
Dr. Pringle’s preliminary results show that as a lichen grows older and larger, it is less likely to die. “If you made me answer the question now,” she said, “I’d say there can be senescence of parts of an individual. But I don’t think an individual ever senesces.”

For the full story, see:
HILLARY ROSNER. “In a Place for the Dead, Studying a Seemingly Immortal Species.” The New York Times (Tues., January 1, 2013): D3.
(note: ellipses added.)
(Note: the online version of the story has the date December 31, 2012.)

“THRIVING; Dr. Pringle’s initial results show that as a lichen grows older and larger, it is less likely to die.” Source of caption and photo: online version of the NYT article quoted and cited above.

Early Retirement Reduces Cognitive Ability

(p. 136) Early retirement appears to have a significant negative impact on the cognitive ability of people in their early 60s that is both quantitatively important and causal. We obtain this finding using cross-nationally comparable survey data from the United States, England, and Europe that allow us to relate cognition and labor force status. We argue that the effect is causal by making use of a substantial body of research showing that variation in pension, tax, and disability policies explain most variation across countries in average retirement rates.

Further exploration of existing data and new data being collected would allow a considerably deeper exploration of the roles of work and leisure in determining the pace of cognitive aging. For example, the HRS contains considerable information on how respondents use their leisure time that would allow both cross-sectional and longitudinal analysis of changes in cognitive exercise that are associated with (p. 137) retirement. In addition, detailed occupation and industry data could be used to understand differences in the pace of technical change to which workers must adjust during the latter part of their careers. Also, in the 2010 wave, the HRS will be adding measures of other components of fluid intelligence. Future work in this area should be able to separate the effects of the “unengaged lifestyle hypothesis” (that early retirees suffer cognitive declines because the work environment they have left is more cognitively stimulating than the full-time leisure environment they have entered) from the “on-the-job retirement hypothesis” (which holds that incentives to invest among older workers are significantly reduced when they expect to retire at an early age).

During the past decade, older Americans seem to have reversed a century-long trend toward early retirement and have been increasing their labor force participation rates, especially beyond age 65. This is good news for the standard of living of elderly Americans, as well as for the fiscal balance of the Social Security and Medicare systems. Our paper suggests that it may also be good news for the cognitive capacities of our aging nation.

Source:
Rohwedder, Susann, and Robert J. Willis. “Mental Retirement.” Journal of Economic Perspectives 24, no. 1 (Winter 2010): 119-38.

In Cancer Treatment “a Breakthrough Moment”?

(p. A1) CHICAGO–Medical science efforts to harness the power of the immune system against cancer are beginning to bear fruit after decades of frustration, opening up a hopeful new front in the long battle against the disease.
In studies being presented Saturday, researchers said two experimental drugs by Bristol-Myers Squibb Co. . . . significantly shrank tumors in some patients with advanced skin, lung and kidney cancers.
Especially promising was that the drugs worked against several types of cancer, researchers said of the early findings. Most of the patients whose tumors responded significantly to the treatment saw long-term results.
. . .
(p. A2) Taken together, the findings are provoking excitement among researchers and the drug industry that immunotherapy has finally arrived as a viable cancer-fighting strategy.
“Those of us in the field really see this as a breakthrough moment,” said Suzanne Topalian, a researcher at Johns Hopkins School of Medicine and lead author of one of the studies. Both are being presented by Hopkins researchers at the annual meeting of the American Society of Clinical Oncology and published online by the New England Journal of Medicine.

For the full story, see:
RON WINSLOW. “New Cancer Drugs Use Body’s Own Defenses.” The Wall Street Journal (Sat., June 2, 2012): A1-A2.
(Note: ellipses added.)
(Note: the online version of the story has the date June 1, 2012.)

Neural Implants “Restored Their Human Functionality”

Ray Kurzweil. Source of photo: online version of the WSJ article quoted and cited below.

(p. C12) Inventor and entrepreneur Ray Kurzweil is a pioneer in artificial intelligence–the principal developer of the first print-to-speech reading machine for the blind, and the first text-to-speech synthesizer, among other breakthroughs. He is also a writer who explores the future of information technology and how it is changing our world.

In a wide-ranging interview, Mr. Kurzweil and The Wall Street Journal’s Alan Murray discussed advances in artificial intelligence, nanotechnology, and what it means to be human. Here are edited excerpts of their conversation:
. . .
MR. MURRAY: What about life expectancy? Is there a limit?
MR. KURZWEIL: No. We’re constantly pushing back life expectancy. Now it’s going to go into high gear because of the inherent exponential progression of information technology. According to my models, within 15 years we’ll be adding more than a year to your remaining life expectancy each year.
MR. MURRAY: So if you play the odds right, you never hit the endpoint.
MR. KURZWEIL: Right. If you can hang in there for another 15 years, we could get to that point.

What Is Human?
MR. MURRAY: What does it mean to be human in a post-2029 world?
MR. KURZWEIL: It’s a slippery slope. But we’ve already gone down that slope. I’ve talked to people who have neural implants in their brain, for Parkinson’s, and I’ve asked them, “Are you still human? Are you less human?”
Generally speaking, they say, “It’s part of me.” And they’re very proud of it, because it restored their human functionality.

For the full interview, see:
Alan Murray, interviewer. “Man or Machine? Ray Kurzweil on how long it will be before computers can do everything the brain can do.” The Wall Street Journal (Fri., June 29, 2012): C12.
(Note: ellipsis added; bold in original.)

Campion Plant Sprouts from 32,000 Year-Old Seed

“OLD DNA; A plant has been generated from the fruit of the narrow-leafed campion. It is the oldest plant by far to be grown from ancient tissue.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. D1) Living plants have been generated from the fruit of a little arctic flower, the narrow-leafed campion, that died 32,000 years ago, a team of Russian scientists reports. The fruit was stored by an arctic ground squirrel in its burrow on the tundra of northeastern Siberia and lay permanently frozen until excavated by scientists a few years ago.

This would be the oldest plant by far that has ever been grown from ancient tissue. The present record is held by a date palm grown from a seed some 2,000 years old that was recovered from the ancient fortress of Masada in Israel.
Seeds and certain cells can last a long term under the right conditions, but many claims of extreme longevity have failed on closer examination, and biologists are likely to greet this claim, too, with reserve until it can be independently confirmed. Tales of wheat grown from seeds in the tombs of the pharaohs have long been discredited. Lupines were germinated from seeds in a 10,000-year-old lemming burrow found by a gold miner in the Yukon. But the seeds, later dated by the radiocarbon method, turned out to be modern contaminants.
. . .
The new report is by a team led by Svetlana Yashina and David Gilichinsky of the Russian Academy of Sciences research center at Pushchino, near Moscow, and appears in Tuesday’s issue of The Proceedings of the National Academy of Sciences of the United States of America.
“This is an amazing breakthrough,” said Grant Zazula of the Yukon Paleontology Program at Whitehorse in Yukon Territory, Canada. “I have no (p. D4) doubt in my mind that this is a legitimate claim.” It was Dr. Zazula who showed that the apparently ancient lupine seeds found by the Yukon gold miner were in fact modern.

For the full story, see:

NICHOLAS WADE. “Dead for 32,000 Years, an Arctic Plant Is Revived.” The New York Times (Tues., February 21, 2012): D1 & D4.
(Note: ellipsis added.)
(Note: the online version of the review is dated February 20, 2012.)

Quantum Computers May Revolutionize Nanotechnology and Drug Design

“Scott Aaronson.” Source of caption and photo: online version of the NYT commentary quoted and cited below.

(p. D5) When people hear that I work on quantum computing — one of the most radical proposals for the future of computation — their first question is usually, “So when can I expect a working quantum computer on my desk?” Often they bring up breathless news reports about commercial quantum computers right around the corner. After I explain the strained relationship between those reports and reality, they ask: “Then when? In 10 years? Twenty?”

Unfortunately, this is sort of like asking Charles Babbage, who drew up the first blueprints for a general-purpose computer in the 1830s, whether his contraption would be hitting store shelves by the 1840s or the 1850s. Could Babbage have foreseen the specific technologies — the vacuum tube and transistor — that would make his vision a reality more than a century later? Today’s quantum computing researchers are in a similar bind. They have a compelling blueprint for a new type of computer, one that could, in seconds, solve certain problems that would probably take eons for today’s fastest supercomputers. But some of the required construction materials don’t yet exist.
. . .
While code-breaking understandably grabs the headlines, it’s the more humdrum application of quantum computers — simulating quantum physics and chemistry — that has the potential to revolutionize fields from nanotechnology to drug design.
. . .
Like fusion power, practical quantum computers are a tantalizing possibility that the 21st century may or may not bring — depending on the jagged course not only of science and technology, but of politics and economics.

For the full commentary, see:
SCOTT AARONSON. “ESSAY; Quantum Computing Promises New Insights, Not Just Supermachines.” The New York Times (Tues., December 6, 2011): D5.
(Note: ellipses added.)
(Note: the online version of the commentary is dated December 5, 2011.)

Purging Senescent Cells Makes Mice More Youthful and Vigorous

“CELL SUICIDE. A subdermal fat layer, middle, in a mouse purged of senescent cells. These mice can run much longer and have larger fat deposits.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. D3) Until recently, few people gave much thought to senescent cells. They are cells that linger in the body even after they have lost the ability to divide.

But on Nov. 2, in what could be a landmark experiment in the study of aging, researchers at the Mayo Clinic reported that if you purge the body of its senescent cells, the tissues remain youthful and vigorous.
. . .
. . . the startling result is plausible because it ties together an emerging body of knowledge about senescent cells. And it raises the possibility that attacks on the cells might postpone the diseases of aging and let people live out more of their life span in good health.
. . .
The finding was made in a strain of mice that age fast and usually die of heart arrhythmia. So despite their healthier tissues, the mice purged of senescent cells died at the usual age of heart problems. Dr. van Deursen’s team is now testing to see whether normal mice will live longer when purged of senescent cells.
The treatment was started when the normal mice were a year old, and they have now been treated for five months. Next month they will run treadmill tests to see if they are in better shape than a comparison group of untreated mice, Dr. van Deursen said.
The genetic method used to purge mice of senescent cells cannot be used in people. Instead of trying to remove senescent cells from elderly people, Dr. Peeper believes, it may be more effective to identify which of the factors that the senescent cells secrete are the source of their ill effects and to develop drugs that block these factors.
But Dr. van Deursen thinks it would be better to go after the senescent cells themselves. In his view it should be easy enough by trial and error to find chemicals that selectively destroy senescent cells, just like the targeted chemicals now used to treat certain kinds of cancer. And unlike the cancer cells, which proliferate so fast that they soon develop resistance, the senescent cells cannot replicate, so they should be easy targets.
Several companies and individuals have already approached the Mayo Clinic to explore developing such drugs. “They think it’s possible, and they are very enthusiastic,” Dr. van Deursen said. “So I can guarantee that there will be initiatives to find drugs that kill senescent cells and mimic the system that we have developed in the mouse.”
. . .
“If you remove the senescent cells you improve things considerably, but you can’t reverse the process or completely stop the aging because it has other causes,” Dr. van Deursen said. “Personally I think we can slow aging down, and over time we will become more and more successful.

For the full story, see:

NICHOLAS WADE. “In Body’s Shield Against Cancer, a Culprit in Aging May Lurk.” The New York Times (Tues., November 22, 2011): D3.
(Note: ellipses added.)
(Note: the online version of the story is dated November 21, 2011.)