Aging – Page 14 – artdiamondblog.com

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.)

Adipotide Kills Fat Cells in Obese Mice and Monkeys

Source of graphic: online version of the WSJ article quoted and cited below.

(p. A6) A drug that kills a type of fat cell by choking off its blood supply caused significant weight loss in obese monkeys, potentially setting the stage for a new pharmaceutical approach to attacking obesity, according to a study released Wednesday.

After four weeks of treatment, obese monkeys given daily injections of the drug, called adipotide, lost an average of 11% of their body weight. They also had big reductions in waist circumference and body-mass index and, importantly, striking improvement in their ability to process insulin, researchers said. The drug had no effect on weight when given to lean monkeys.
Results of the study, performed at M.D. Anderson Cancer Center in Houston and published online by the journal Science Translational Medicine, confirmed a 2004 report from the same research team showing marked weight loss in mice treated with the agent.
. . .
The researchers’ 2004 paper showing a 30% weight loss in obese mice drew skepticism. Randy J. Seeley, director of the diabetes and obesity center at the University of Cincinnati, figured destroying white fat cells would make animals–and people–sick. But his own lab eventually replicated the mouse study, using rats instead, and now he is intrigued.
“This is really new stuff,” Dr. Seeley said of the latest results. “There’s no way to know if this will become a therapy or not, but at least it opens up a new way to think about therapies, and we have not had a lot of those.” He isn’t involved with the research.

For the full story, see:
RON WINSLOW. “Drug Offers Hope in Obesity Fight; Treatment Targeting Fat Cells Caused Significant Weight Loss in Monkeys; Human Trials to Begin Soon.” The Wall Street Journal (Thurs., November 10, 2011): A6.
(Note: ellipsis added.)
(Note: the last two sentences quoted above appeared in the online, but not the print, version of the article.)

“One of the monkeys used in the study. Obese monkeys lost an average of 11% of their body weight after four weeks of treatment.” Source of caption and photo: online version of the WSJ article quoted and cited above.

Jobless Rate Appears Lower as Aging Population Leaves Labor Force

(p. A4) As more baby boomers leave the job market, the participation rate should continue to decline–a group of economists at the Federal Reserve projected in 2006 that it would fall to 62.5% by 2015. While that suggests the economy won’t need to create as many jobs to bring down the unemployment rate, said Barclays Capital economist Dean Maki, the downside is that it won’t have as large a work force to power it along and pay for the needs of an aging population.
“If you have a greater fraction of the population not working, that will make it harder to pay for costs that will be ballooning,” he said.

For the full story, see:
JUSTIN LAHART. “Aging Population Eases Jobless Rate.” The Wall Street Journal (Sat., November 5, 2011): A4.

Bright Prospects for Longer Life

Source of book image: online version of the WSJ review quoted and cited below.

(p. A13) “We are at the cusp of a revolution in medicine and biotechnology,” Ms. Arrison announces, “that will radically increase not just our life spans but also, and more importantly, our health spans.”
. . .
She recounts advances in stem-cell research, pharmaceuticals and synthetic biology. And the tinkering with genes still goes on. We learn about Dr. Cynthia Kenyon at the University of California in San Francisco, who discovered that the life span of the tiny worm Caenorhabditis elegans could be doubled by partially disabling a single gene. Further improvements on the technique resulted in worms living six times longer than normal. “In human terms,” Ms. Arrison says, “they be the equivalent of healthy, active five-hundred-year-olds.” That may be a bit much to expect, but Ms. Arrison says she is confident that “human life expectancy will one day reach 150 years.”
. . .
What is more, technology heavyweights are paying attention, including Bill Gates (if he were a teenager today, Mr. Gates once said, he’d be “hacking biology”) and Jeff Bezos (“atom by atom we’ll assemble small machines that will enter cell walls and make repairs”). Larry Ellison, of Oracle, started a foundation more than a decade ago to support anti-aging research; the institution donates about $42 million a year.

For the full review, see:
NICK SCHULZ. “BOOKSHELF; Bioengineering Methuselah; Human beings living to be 150? And you thought Social Security and Medicare were in trouble now.” The Wall Street Journal (Weds., AUGUST 31, 2011): A13.
(Note: ellipses added.)

The book under review 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.

Of Mice and Men and Health and Longevity

“Two 9-month-old mice from the study. The one on the right received the drug to eliminate senescent cells.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. A1) In a potentially fundamental advance, researchers have opened up a novel approach to combating the effects of aging with the discovery that a special category of cells, known as senescent cells, are bad actors that promote the aging of the tissues. Cleansing the body of the cells, they hope, could postpone many of the diseases of aging.

The findings raise the prospect that any therapy that rids the body of senescent cells would protect it from the ravages of aging. But many more tests will be needed before scientists know if drugs can be developed to help people live longer.
Senescent cells accumulate in aging tissues, like arthritic knees, cataracts and the plaque that may line elderly arteries. The cells secrete agents that stimulate the immune system and cause low-level inflammation. Until now, there has been no way to tell if the presence of the cells is good, bad or indifferent.
The answer turns out to be that (p. A4) the cells hasten aging in the tissues in which they accumulate. In a delicate feat of genetic engineering, a research team led by Darren J. Baker and Jan M. van Deursen at the Mayo Clinic in Rochester, Minn., has generated a strain of mouse in which all the senescent cells can be purged by giving the mice a drug that forces the cells to self-destruct.
Rid of the senescent cells, the Mayo Clinic researchers reported online Wednesday in the journal Nature, the mice’s tissues showed a major improvement in the usual burden of age-related disorders. They did not develop cataracts, avoided the usual wasting of muscle with age, and could exercise much longer on a mouse treadmill. They retained the fat layers in the skin that usually thin out with age and, in people, cause wrinkling.

For the full story, see:
NICHOLAS WADE. “Prospect of Delaying Aging Ills Is Raised in Cell Study of Mice.To Challenges For Obama, Add Another.” The New York Times (Thur., November 3, 2011): A1-A4.
(Note: the online version of the article is dated November 2, 2011 and has the title “Purging Cells in Mice Is Found to Combat Aging Ills.”)
(Note: thanks to Luis Locay for sending me the link to this.)

Another worthwhile article summarizing the same research, is:
SHIRLEY S. WANG. “Cell Study Finds a Way to Slow Ravages of Age.” The Wall Street Journal (Thur., November 3, 2011): A2.

Reasons to Hope for 150 Year Life Span

Source of book image: online version of the WSJ review quoted and cited below.

(p. A13) Ms. Arrison is in the hopeful camp. She recounts advances in stem-cell research, pharmaceuticals and synthetic biology. And the tinkering with genes still goes on. We learn about Dr. Cynthia Kenyon at the University of California in San Francisco, who discovered that the life span of the tiny worm Caenorhabditis elegans could be doubled by partially disabling a single gene. Further improvements on the technique resulted in worms living six times longer than normal. “In human terms,” Ms. Arrison says, “they be the equivalent of healthy, active five-hundred-year-olds.” That may be a bit much to expect, but Ms. Arrison says she is confident that “human life expectancy will one day reach 150 years.”
. . .
What is more, technology heavyweights are paying attention, including Bill Gates (if he were a teenager today, Mr. Gates once said, he’d be “hacking biology”) and Jeff Bezos (“atom by atom we’ll assemble small machines that will enter cell walls and make repairs”). Larry Ellison, of Oracle, started a foundation more than a decade ago to support anti-aging research; the institution donates about $42 million a year.
. . .
And if humans do begin living to 150, then what?
. . .
. . . , Ms. Arrison argues that apocalyptic prophecies are unlikely to be realized. Increasing wealth and mankind’s adaptability and ingenuity mean that as new problems emerge, new solutions will be forthcoming. “In looking at the trends of history,” she says, “we can see that even when there are downsides to a particular wealth- or health-enhancing technology, the problem is often fixed once the population reaches a point where it feels secure in spending the resources to do so.”

Book under review:
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.

Another Nod to Planck’s “Cynical View of Science”

The Max Planck view expressed in the quote below, has been called “Planck’s Principle” and has been empirically tested in three papers cited at the end of the entry.

(p. 12) How’s this for a cynical view of science? “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”

Scientific truth, according to this view, is established less by the noble use of reason than by the stubborn exertion of will. One hopes that the Nobel Prize-winning physicist Max Planck, the author of the quotation above, was writing in an unusually dark moment.
And yet a large body of psychological data supports Planck’s view: we humans quickly develop an irrational loyalty to our beliefs, and work hard to find evidence that supports those opinions and to discredit, discount or avoid information that does not.

For the full commentary, see:
CORDELIA FINE. “GRAY MATTER; Biased but Brilliant.” The New York Times, SundayReview Section (Sun., July 31, 2011): 12.
(Note: ellipses added.)
(Note: the online version of the article is dated July 30, 2011.)

Three of my papers that present evidence on Planck’s Principle, are:
“Age and the Acceptance of Cliometrics.” The Journal of Economic History 40, no. 4 (December 1980): 838-841.
“Planck’s Principle: Do Younger Scientists Accept New Scientific Ideas with Greater Alacrity than Older Scientists?” Science 202 (November 17, 1978): 717-723 (with David L. Hull and Peter D. Tessner).
“The Polywater Episode and the Appraisal of Theories.” In A. Donovan, L. Laudan and R. Laudan, eds., Scrutinizing Science: Empirical Studies of Scientific Change. Dordrecht, Holland: Kluwer Academic Publishers, 1988, 181-198.

Drug from David Sinclair’s Sirtris Start-Up Lengthens Life of Obese Mice

“An obese mouse given the drug SRT-1720, center, and one not given the drug, right.” Source of caption and photo: online version of the NYT article quoted and cited below.

(p. A1) Sustaining the flickering hope that human aging might somehow be decelerated, researchers have found they can substantially extend the average life span of obese mice with a specially designed drug.

The drug, SRT-1720, protects the mice from the usual diseases of obesity by reducing the amount of fat in the liver and increasing sensitivity to insulin. These and other positive health effects enable the obese mice to live 44 percent longer, on average, than obese mice that did not receive the drug, according to a team of researchers led by Rafael de Cabo, a gerontologist at the National Institute on Aging.
Drugs closely related to SRT-1720 are now undergoing clinical trials in humans.
The findings “demonstrate for the first time the feasibility of designing novel molecules that are safe and effective in promoting longevity and preventing multiple age-related diseases in mammals,” Dr. de Cabo and colleagues write in Thursday’s issue of the new journal Scientific Reports. Their conclusion supports claims that had been thrown in doubt by an earlier study that was critical of SRT-1720.
A drug that makes it cost-free to be obese may seem more a moral hazard than an incentive to good health. But the rationale behind the research is somewhat different: the researchers are trying to capture the benefits that allow mice on very low-calorie diets to live longer. It just so happens that such benefits are much easier to demonstrate in mice under physiological stress like obesity than in normal mice.
. . .
. . . , a small pharmaceutical concern in Cambridge, Mass., designed SRT-1720 and a set of similar drugs to mimic resveratrol — the trace ingredient of red wine that is thought to activate protective proteins called sirtuins.
The sirtuins help bring about the 30 percent extension of life span enjoyed by mice and rats that are kept on very low-calorie diets.

For the full story, see:
NICHOLAS WADE. “Longer Lives for Obese Mice, With Hope for Humans of All Sizes.” The New York Times (Fri., August 19, 2011): A1 & A3.
(Note: ellipses added.)
(Note: the online version of the story was dated August 18, 2011.)