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December 26, 2011

Bright Prospects for Longer Life



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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.






November 6, 2011

Of Mice and Men and Health and Longevity



MiceSenescentCells2011-11-04.jpg"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.





October 24, 2011

Reasons to Hope for 150 Year Life Span



100PlusBK2011-08-31.jpg













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."



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.)


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.





October 7, 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.





August 25, 2011

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



MiceLiveLonger2011-08-19.jpg"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.)







July 21, 2011

"People Condemned to Short Lives and Chronic Hardship Are Perhaps Unlikely to Worry Overmuch about Decor"




If "necessity is the mother of invention," then why did it take so long for someone to invent the louvered slats mentioned at the end of this passage?


(p. 55) In even the best homes comfort was in short supply. It really is extraordinary how long it took people to achieve even the most elemental levels of comfort. There was one good reason for it: life was tough. Throughout the Middle Ages, a good deal of every life was devoted simply to surviving. Famine was common. The medieval world was a world without reserves; when harvests were poor, as they were about one year in four on average, hunger was immediate. When crops failed altogether, starvation inevitably followed. England suffered especially catastrophic harvests in 1272, 1277, 1283, 1292, and 1311, and then an unrelievedly murderous stretch from 1315 to 1319. And this was of course on top of plagues and other illnesses that swept away millions. People condemned to short lives and chronic hardship are perhaps unlikely to worry overmuch about decor. But even allowing for all that, there was just a great, strange slowness to strive for even modest levels of comfort. Roof holes, for instance, let smoke escape, but they also let in rain and drafts until somebody finally, belatedly invented a lantern structure with louvered slats that allowed smoke to escape but kept out rain, birds, and wind. It was a marvelous invention, but by the time it (p. 56) was thought of, in the fourteenth century, chimneys were already coming in and louvered caps were not needed.



Source:

Bryson, Bill. At Home: A Short History of Private Life. New York: Doubleday, 2010.





June 30, 2011

Laron Syndrome Villagers Free of Cancer and Diabetes, Suggesting Longevity Breakthrough



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Source of graph: online version of the NYT article quoted and cited below.




(p. A6) People living in remote villages in Ecuador have a mutation that some biologists say may throw light on human longevity and ways to increase it.

The villagers are very small, generally less than three and a half feet tall, and have a rare condition known as Laron syndrome or Laron-type dwarfism. They are probably the descendants of conversos, Sephardic Jews from Spain and Portugal who were forced to convert to Christianity in the 1490s but were nonetheless persecuted in the Inquisition. They are also almost completely free of two age-related diseases, cancer and diabetes.

A group of 99 villagers with Laron syndrome has been studied for 24 years by Dr. Jaime Guevara-Aguirre, an Ecuadorean physician and diabetes specialist.


. . .


IGF-1 is part of an ancient signaling pathway that exists in the laboratory roundworm as well as in people. The gene that makes the receptor for IGF-1 in the roundworm is called DAF-2. And worms in which this gene is knocked out live twice as long as normal.

The Laron patients have the equivalent defect -- their cells make very little IGF-1, so very little IGF-1 signaling takes place, just as in the DAF-2-ablated worms. So the Laron patients might be expected to live much longer.

Because of their striking freedom from cancer and diabetes, they probably could live much longer if they did not have a much higher than usual death rate from causes unrelated to age, like alcoholism and accidents.


. . .


A strain of mice bred by John Kopchick of Ohio University has a defect in the growth hormone receptor gene, just as do the Laron patients, and lives 40 percent longer than usual.


. . .


The longest-lived mouse on record is one studied by Dr. Bartke. It had a defect in its growth hormone receptor gene, just as do the Laron patients. "It missed its fifth birthday by a week," he said. The mouse lived twice as long as usual and won Dr. Bartke a prize presented by the Methuselah Foundation (which rewards developments in life-extension therapies) in 2003.



For the full story, see:

NICHOLAS WADE. "Ecuadorean Villagers May Hold Secret to Longevity." The New York Times (Thurs., February 17, 2011): A6.

(Note: ellipses added.)

(Note: the online version of the story is dated February 16, 2011 and has the title "Ecuadorean Villagers May Hold Secret to Longevity.")



LoranSyndromeManAndChildren2011-06-05.jpg









"A 67-year-old man who has Laron-type dwarfism with his daughter, 5, and sons, 7 and 10." Source of caption and photo: online version of the NYT article quoted and cited below.






June 16, 2011

The Secret to a Long Life Is Conscientiousness



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






(p. D3) Cheerfulness, optimism, extroversion and sociability may make life more enjoyable, but they won't necessarily extend it, Howard S. Friedman and Leslie R. Martin found in a study that covered eight decades. The key traits are prudence and persistence. "The findings clearly revealed that the best childhood personality predictor of longevity was conscientiousness," they write, "the qualities of a prudent, persistent, well-organized person, like a scientist-professor -- somewhat obsessive and not at all carefree."


. . .


There are three explanations for the dominant role of conscientiousness. The first and most obvious is that conscientious people are more likely to live healthy lifestyles, to not smoke or drink to excess, wear seat belts, follow doctors' orders and take medication as prescribed. Second, conscientious people tend to find themselves not only in healthier situations but also in healthier relationships: happier marriages, better friendships, healthier work situations.

The third explanation for the link between conscientiousness and longevity is the most intriguing. "We thought it must be something biological," Dr. Friedman said. "We ruled out every other factor." He and other researchers found that some people are biologically predisposed to be not only more conscientiousness but also healthier. "Not only do they tend to avoid violent deaths and illnesses linked to smoking and drinking," they write, "but conscientious individuals are less prone to a whole host of diseases, not just those caused by dangerous habits." The precise physiological explanation is unknown but seems to have to do with levels of chemicals like serotonin in the brain.

As for optimism, it has its downside. "If you're cheerful, very optimistic, especially in the face of illness and recovery, if you don't consider the possibility that you might have setbacks, then those setbacks are harder to deal with," Dr. Martin said. "If you're one of those people who think everything's fine -- 'no need to back up those computer files' -- the stress of failure, because you haven't been more careful, is harmful. You almost set yourself up for more problems."



For the full review, see:

KATHERINE BOUTO. "BOOKS ON SCIENCE; Eighty Years Along, a Longevity Study Still Has Ground to Cover." The New York Times (Tues., April 19, 2011): D3.

(Note: ellipsis added.)

(Note: the online version of the article is dated April 18, 2011.)


The book under review is:

Friedman, Howard S., and Leslie R. Martin. The Longevity Project: Surprising Discoveries for Health and Long Life from the Landmark Eight-Decade Study. New York: Hudson Street Press, 2011.






February 4, 2011

Healthy Longevity Can Mean You "Get a Do-Over in Life"



PoolGidComic2011-02-02.jpg "Gid Pool performing at the Buford Variety Theater . . . " Source of caption and photo: online version of the WSJ article quoted and cited below.


(p. R1) It's easy, these days, to think about later life and retirement as limiting. And with good reason: The economy remains fragile; nest eggs are smaller than they should be; and Social Security and Medicare are looking pale. Millions of people are delaying retirement and scaling back plans for the future.

And then there's Gid Pool.

Almost five years ago, on something of a lark, he enrolled in a class near his home in North Port, Fla., that taught stand-up comedy. He was 61 years old. Today, he performs in clubs, theaters, colleges and corporate settings throughout much of the South, playing at times to hundreds of people and clearing as much as $1,000 an evening. For good measure, he spends, on average, a week each month on cruise ships, where he teaches comedy classes.


. . .


"I was thinking last night about how lucky I am, at this stage in my life, to have something that really gets me up in the morning," he says. "I saw my grandfather, an engineer on the Illinois Central Railroad, turn my age with a body beaten down by his daily job. My father was a pilot in World War II and suffered all his adult life from an injury in a plane crash.

"Today I'm part of a generation that has literally been given a second chance to live a first life. People say you don't get a do-over in life. I beg to differ."



For the full story, see:

GLENN RUFFENACH. "Did You Hear the One About the Retired Real-Estate Agent? He became a stand-up comedian. And he has never been happier." The Wall Street Journal (Mon., December 20, 2010): R1 & R9.

(Note: ellipsis added.)





December 8, 2010

After Being "Nasty and Unruly for Decades" Henry Becomes a Father at Age 111



TuataraLivingFossil2010-12-06.jpg












"TUATARA. The tuatara, scientists have learned, is in some ways a so-called living fossil." Source of caption and photo: online version of the NYT article quoted and cited below.




(p. D1) . . . the animal that may well be New Zealand's most bizarrely instructive species at first glance looks surprisingly humdrum: the tuatara. A reptile about 16 inches long with bumpy, khaki-colored skin and a lizardly profile, the tuatara could easily be mistaken for an iguana. Appearances in this case are wildly deceptive. The tuatara -- whose name comes from the Maori language and means "peaks on the back" -- is not an iguana, is not a lizard, is not like any other reptile alive today.

In fact, as a series of recent studies suggest, it is not like any other vertebrate alive today. The tuatara, scientists have learned, is in some ways a so-called living fossil, its basic skeletal layout and skull shape almost identical to that of tuatara fossils dating back hundreds of millions of years, to before the rise of the dinosaurs. Cer-(p. D2)tain tuatara organs and traits also display the hallmarks of being, if not quite primitive, at least closer to evolutionary baseline than comparable structures in other animals.


. . .


Tuataras are living fossils in more than one sense of the term. Through long-term capture, tag and recapture studies that were begun right after World War II, researchers have found that tuataras match and possibly exceed in attainable life span that other Methuselah of the animal kingdom, the giant tortoise. "Tuataras routinely live to 100, and I couldn't tell you they don't live to 150, 200 years or even more," said Dr. Daugherty.

They live, and live it up. "We know there are females that are still reproducing in their 80s," said Dr. Daugherty. At the Southland Museum and Art Gallery in Invercargill, New Zealand, a captive male tuatara named Henry, a local celebrity that had been nasty and unruly for decades until a malignancy was removed from his genitals, mated with an 80-year-old female named Mildred, and last year became a first-time father -- at the age of 111.



For the full story, see:

NATALIE ANGIER. "Basics; Reptile's Pet-Store Looks Belie Its Triassic Appeal." The New York Times (Tues., November 23, 2010): D1 & D2.

(Note: ellipses added.)

(Note: the online version of the article is dated November 22, 2010.)





December 6, 2010

Telomerase Can Reverse Aging Ills in Mice



MiceInTelomeraseExperiment2010-12-05.jpg"Two mice involved in an experiment on age-related degeneration. Mice whose telomerase gene was activated, left, showed notable improvements." Source of caption: print version of the WSJ article quoted and cited below. Source of photo: online version of the WSJ article quoted and cited below.


(p. A3) Scientists have partially reversed age-related degeneration in mice, an achievement that suggests a new approach for tackling similar disorders in people.

By tweaking a gene, the researchers reversed brain disease and restored the sense of smell and fertility in prematurely aged mice. Previous experiments with calorie restriction and other methods have shown that aspects of aging can be slowed. This appears to be the first time that some age-related problems in animals have actually been reversed.

The study was published online Sunday in the peer-reviewed journal Nature.

"These mice were equivalent to 80-year-old humans and were about to pass away," says Ronald DePinho, co-author of the paper and a scientist at Dana-Farber Cancer Institute in Boston. After the experiment, "they were the physiological equivalent of young adults."



For the full story, see:

GAUTAM NAIK. "Aging Ills Reversed in Mice; Scientists Tweak a Gene and Rejuvenate Cells, Raising Hopes for Uses in Humans." The Wall Street Journal (Mon., NOVEMBER 29, 2010): A3.

(Note: online version of the article is dated NOVEMBER 28, 2010.)



TelomeraseGraphic2010-12-05.gif







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






November 8, 2010

Being Bilingual Increases "Cognitive Reserve"



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



At first glance the graph and the text quoted below seem inconsistent on whether bilingualism delays the onset of dementia. The text says no, the graph says yes. On closer reading, the text is referring to the "physical signs of deterioration" while the graph is referring to "visible symptoms."


(p. D1) A lifetime of speaking two or more languages appears to pay off in old age, with recent research showing the symptoms of dementia can be delayed by an average of four years in bilingual people.

Multilingualism doesn't delay the onset of dementia--the brains of people who speak multiple languages still show physical signs of deterioration--but the process of speaking two or more languages appears to enable people to develop skills to better cope with the early symptoms of memory-robbing diseases, including Alzheimer's.

Scientists for years studied children and found that fluently speaking more than one language takes a lot of mental work. Compared with people who speak only one language, bilingual children and young adults have slightly smaller vocabularies and are slower performing certain verbal tasks, such as naming lists of animals or fruits.

But over time, regularly speaking more than one language appears to strengthen skills that boost the brain's so-called cognitive reserve, a capacity to work even when stressed or damaged. This build-up of cognitive reserve appears to help bilingual people as they age.



For the full story, see:

SHIRLEY S. WANG. "Building a More Resilient Brain." The Wall Street Journal (Tues., OCTOBER 12, 2010): D1 & D2.





October 1, 2010

Japanese "Longevity" Due Partly to Government Over-Counting Centenarians



WataseMitsueJapanCentenerian2010-09-10.jpg"A Kobe city official, left, visited Mitsue Watase, 100, at her home last week as Japanese officials started a survey on the whereabouts of centenarians." Source of caption and photo: online version of the NYT article quoted and cited below. Source of caption and photo: online version of the NYT article quoted and cited below.


Oskar Morgenstern is mainly known as the co-author with John von Neumann of the book that started game theory. But it may be that his most important contribution to economics is a little known book called On the Accuracy of Economic Observations. In that book he gave examples of social scientists theorizing to explain 'facts' that turned out not to be true (such as the case of the 14 year-old male widowers).

The point is that truth would be served by economists spending a higher percent of their time in improving the quality of data.

One can imagine Morgenstern sadly smiling at the case of the missing Japanese centenarians:


(p. 1) TOKYO -- Japan has long boasted of having many of the world's oldest people -- testament, many here say, to a society with a superior diet and a commitment to its elderly that is unrivaled in the West.

That was before the police found the body of a man thought to be one of Japan's oldest, at 111 years, mummified in his bed, dead for more than three decades. His daughter, now 81, hid his death to continue collecting his monthly pension payments, the police said.

Alarmed, local governments began sending teams to check on other elderly residents. What they found so far has been anything but encouraging.

A woman thought to be Tokyo's oldest, who would be 113, was last seen in the 1980s. Another woman, who would be the oldest in the world at 125, is also missing, and probably has been for a long time. When city officials tried to visit her at her registered address, they discovered that the site had been turned into a city park, in 1981.

To date, the authorities have been unable to find more than 281 Japanese who had been listed in records as 100 years old or older. Facing a growing public outcry, the (p. 6) country's health minister, Akira Nagatsuma, said officials would meet with every person listed as 110 or older to verify that they are alive; Tokyo officials made the same promise for the 3,000 or so residents listed as 100 and up.

The national hand-wringing over the revelations has reached such proportions that the rising toll of people missing has merited daily, and mournful, media coverage. "Is this the reality of a longevity nation?" lamented an editorial last week in The Mainichi newspaper, one of Japan's biggest dailies.


. . .


. . . officials admit that Japan may have far fewer centenarians than it thought.

"Living until 150 years old is impossible in the natural world," said Akira Nemoto, director of the elderly services section of the Adachi ward office. "But it is not impossible in the world of Japanese public administration."



For the full story, see:

MARTIN FACKLER. "Japan, Checking on Its Oldest People, Finds Many Gone, Some Long Gone." The New York Times, First Section (Sun., August 15, 2010): 1 & 6.

(Note: ellipses added.)

(Note: the online version of the article is dated August 14, 2010 and has the somewhat shorter title "Japan, Checking on Its Oldest, Finds Many Gone"; the words "To date" appear in the online, but not the print, version of the article.)


The Morgenstern book is:

Morgenstern, Oskar. On the Accuracy of Economic Observations. 2nd ed. Princeton: Princeton University Press, 1965.





July 22, 2010

"We're Spending at a Rate that's Just Unsustainable"



ShultzGeorgeVertical2010-07-5.jpg
George Shultz, former Dean of the University of Chicago Business School, former Secretary of the Treasury, and former Secretary of State. Source of photo: online version of the NYT article quoted and cited below.


(p. 12) What do you make of the direction the Republican Party has taken since you served in Washington? Isn't the Tea Party a corruption of the values you stood for?
From what I understand of it, it is a reaction, which I share, to the fact that our government seems to have gotten out of control. We're spending at a rate that's just unsustainable.

That's a legacy of the Bush era, I guess.
Everybody is conveniently blaming everything on Bush, but he's not responsible for what's happened in the last year.

You'll be 90 in December. How are you?
I'm terrific. Feeling great. I'm vertical, not horizontal. That's a big thing.



For the full interview, see:

DEBORAH SOLOMON. "Questions for George Shultz; The Statesman." The New York Times Magazine (Sun., July 4, 2010): 12.

(Note: bolding of interviewer questions was in original.)

(Note: the online version of the article is dated June 28, 2010.)





February 12, 2010

"The Bus -- La Guagua -- Always Comes for Those Who Wait"



HerreraCarmen2010-01-24.JPG "Carmen Herrera in her Manhattan loft, surrounded by her art. She sold her first work in 2004." Source of caption and photo: online version of the NYT article quoted and cited below.



(p. 1) Under a skylight in her tin-ceilinged loft near Union Square in Manhattan, the abstract painter Carmen Herrera, 94, nursed a flute of Champagne last week, sitting regally in the wheelchair she resents.

After six decades of very private painting, Ms. Herrera sold her first artwork five years ago, at 89. Now, at a small ceremony in her honor, she was basking in the realization that her career had finally, undeniably, taken off. As cameras flashed, she extended long, Giacomettiesque fingers to accept an art foundation's lifetime achievement award from the director of the Walker Art Center in Minneapolis.

Her good friend, the painter Tony Bechara, raised a glass. "We have a saying in Puerto Rico," he said. "The bus -- la guagua -- always comes for those who wait."

And the Cuban-born Ms. Herrera, laughing gustily, responded, "Well, Tony, I've been at the bus stop for 94 years!"

Since that first sale in 2004, collectors have avidly pursued Ms. Herrera, and her radiantly ascetic paintings have entered the permanent collections of institutions like the Museum of Modern Art, the Hirshhorn Museum and the Tate Modern. Last year, MoMA included her in a pantheon of Latin American artists on exhibition. And this summer, during a retro-(p. 29)spective show in England, The Observer of London called Ms. Herrera the discovery of the decade, asking, "How can we have missed these beautiful compositions?"

In a word, Ms. Herrera, a nonagenarian homebound painter with arthritis, is hot. In an era when the art world idolizes, and often richly rewards, the young and the new, she embodies a different, much rarer kind of success, that of the artist long overlooked by the market, and by history, who persevered because she had no choice.

"I do it because I have to do it; it's a compulsion that also gives me pleasure," she said of painting. "I never in my life had any idea of money and I thought fame was a very vulgar thing. So I just worked and waited. And at the end of my life, I'm getting a lot of recognition, to my amazement and my pleasure, actually."


. . .


But Ms. Herrera is less expansive about her own art, discussing it with a minimalism redolent of the work. "Paintings speak for themselves," she said. Geometry and color have been the head and the heart of her work, she added, describing a lifelong quest to pare down her paintings to their essence, like visual haiku.

Asked how she would describe to a student a painting like "Blanco y Verde" (1966) -- a canvas of white interrupted by an inverted green triangle -- she said, "I wouldn't have a student." To a sweet, inquiring child, then? "I'd give him some candy so he'd rot his teeth."

When pressed about what looks to some like a sensual female shape in the painting, she said: "Look, to me it was white, beautiful white, and then the white was shrieking for the green, and the little triangle created a force field. People see very sexy things -- dirty minds! -- but to me sex is sex, and triangles are triangles."


. . .


Ms. Herrera's late-in-life success has stunned her in many ways. Her larger works now sell for $30,000, and one painting commanded $44,000 -- sums unimaginable when she was, say, in her 80s. "I have more money now than I ever had in my life," she said.

Not that she is succumbing to a life of leisure. At a long table where she peers out over East 19th Street "like a French concierge," Ms. Herrera, because she must, continues to draw and paint. "Only my love of the straight line keeps me going," she said.




For the full story, see:

DEBORAH SONTAG. "At 94, She's the Hot New Thing in Painting, and Enjoying It." The New York Times, First Section (Sun., January 20, 2010): 1 & 29.

(Note: the online version of the article has the title "At 94, She's the Hot New Thing in Painting" and is dated January 19, 2010.)



HerreraCarmenBlancoYVerde2010-01-24.JPG
HerreraCarmenRedStar2010-01-24.JPG








Ms. Herrara's ""Blanco y Verde" (1966-7)."









"Ms. Herrera's "Red Star" from 1949."

Source of captions and photos: online version of the NYT article quoted and cited above.







November 8, 2009

New Scientific Optimism on Life Extension



HandsOldAndYoung2009-10-26.jpg Source of photo: online version of the NYT article quoted and cited below.


(p. D1) It may be the ultimate free lunch -- how to reap all the advantages of a calorically restricted diet, including freedom from disease and an extended healthy life span, without eating one fewer calorie. Just take a drug that tricks the body into thinking it's on such a diet.

It sounds too good to be true, and maybe it is. Yet such drugs are now in clinical trials. Even if they should fail, as most candidate drugs do, their development represents a new optimism among research biologists that aging is not immutable, that the body has resources that can be mobilized into resisting disease and averting the adversities of old age.

This optimism, however, is not fully shared. Evolutionary biologists, the experts on the theory of aging, have strong reasons to suppose that human life span cannot be altered in any quick and easy way. But they have been confounded by experiments with small laboratory animals, like roundworms, fruit flies and mice. In all these species, the change of single genes has brought noticeable increases in life span.

With theorists' and their gloomy predictions cast in the shade, at least for the time being, experimental biologists are pushing confidently into the tangle of linkages that evolution has woven among food intake, fertility and life span. "My rule of thumb is to ignore the evolutionary biologists -- they're constantly telling you what you can't think," Gary Ruvkun of the Massachusetts General Hospital remarked this June after making an unusual discovery about longevity.

Excitement among researchers on aging has picked up in the last few years with the apparent convergence of two lines of inquiry: single gene changes and the diet known as caloric restriction.


. . .


In the view of evolutionary biologists, the life span of each species is adapted to the nature of its environment. Mice live at most a year in the wild because owls, cats and freezing to death are such frequent hazards. Mice with genes that allow longer life can rarely be favored by natural selection. Rather, the mice that leave the most progeny are those that devote resources to breeding at as early an age as possible.

According to this theory, if mice had wings and could escape their usual predators, natural selection ought to favor longer life. And indeed the maximum life span of bats is 3.5 times greater than flightless mammals of the same size, according to research by Gerald S. Wilkinson of the University of Maryland.

In this view, cells are so robust that they do not limit life span. Instead the problem, especially for longer-lived species, is to keep them under control lest they cause cancer. Cells have not blocked the evolution of extremely long life spans, like that of the bristlecone pine, which lives 5,000 years, or certain deep sea corals, whose age has been found to exceed 4,000 years.

Some species seem to be imperishable. A tiny freshwater animal known as a hydra can regenerate itself from almost any part of its body, apparently because it makes no distinction between its germ cells and its ordinary body cells. In people the germ cells, the egg and sperm, do not age; babies are born equally young, whatever the age of their parents. The genesis of aging was the division of labor in the first multicellular animals between the germ cells and the body cells.

That division put the role of maintaining the species on the germ cells and left the body cells free to become specialized, like neurons or skin cells. But in doing so the body cells made themselves disposable. The reason we die, in the view of Thomas Kirkwood, an expert on the theory of aging, is that constant effort is required to keep the body cells going. "This, in the long run, is unwarranted -- in terms of natural selection, there are more important things to do," he writes.

All that seems clear about life span is that it is not fixed. And if it is not fixed, there may indeed be ways to extend it.



For the full story, see:

NICHOLAS WADE. "Tests Begin on Drugs That May Slow Aging." The New York Times (Tues., August 18, 2009): D1 & D?.

(Note: ellipsis added.)

(Note: thanks to Luis Locay for calling my attention to the article quoted above.)





October 28, 2009

"A Man of Science Past Sixty Does More Harm than Good" (Unless His Name is "Avery")



(p. 421) . . . , in 1928, Fred Griffith in Britain published a striking and puzzling finding. Earlier Griffith had discovered that all known types of pneumococci could exist with or without capsules. Virulent pneumococci had capsules; pneumococci without capsules could be easily destroyed by the immune system. Now he found something much stranger. He killed virulent pneumococci, ones surrounded by capsules, and injected them into mice. Since the bacteria were dead, all the mice survived. He also injected living pneumococci that had no capsules, that were not virulent. Again the mice lived. Their immune systems devoured the unencapsulated pneumococci. But then he injected dead pneumococci surrounded by capsules and living pneumococci without capsules.

The mice died. Somehow the living pneumococci had acquired cap-(p. 422)sules. Somehow they had changed. And, when isolated from the mice, they continued to grow with the capsule--as if they had inherited it.

Griffith's report seemed to make meaningless years of Avery's work-- and life. The immune system was based on specificity. Avery believed that the capsule was key to that specificity. But if the pneumococcus could change, that seemed to undermine everything Avery believed and thought he had proved. For months he dismissed Griffith's work as unsound. But Avery's despair seemed overwhelming. He left the laboratory for six months, suffering from Graves' disease, a disease likely related to stress. By the time he returned, Michael Dawson, a junior colleague he had asked to check Griffith's results, had confirmed them. Avery had to accept them.


His work now turned in a different direction. He had to understand how one kind of pneumococcus was transformed into another. He was now almost sixty years old. Thomas Huxley said, "A man of science past sixty does more harm than good." But now, more than ever, Avery focused on his task.




Source:

Barry, John M. The Great Influenza: The Story of the Deadliest Pandemic in History. Revised ed. New York: Penguin Books, 2005.

(Note: ellipsis added.)

(Note: italics in original.)





August 10, 2009

Success Came Late to Author of Wizard of Oz



FindingOzBK.jpg















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



I remember a conversation with the late labor economist Sherwin Rosen on the substantial decline in research productivity of economists as they age. My memory is that he said the decline usually wasn't because of inability, but because, at some point, the older economists stop trying.

I think there's some truth to that. The belief that it is too late to succeed, can lead people to stop trying, and thereby make the prediction self-fulfilling.

Fortunately, L. Frank Baum kept trying:


(p. A15) If L. Frank Baum had been listed on the stock exchange in 1900, his shares would have been trading near historic lows. The soon-to-be famous author of "The Wonderful Wizard of Oz" had at that point failed at a long series of energetic attempts to find a career. At 44, Baum had already been a chicken farmer, an actor, a seller of machinery lubricants, a purveyor of novelty goods and a newspaper publisher. All his life he'd written lively prose -- plays, ads, columns -- but most of it seemed to go nowhere.

Then, suddenly, it did. The story of a girl named Dorothy who with her little dog, Toto, travels to the wondrous land of Oz burst from Baum's pencil, almost taking him by surprise. "The story really seemed to write itself," he told his publisher. "Then, I couldn't find any regular paper, so I took anything at all, including a bunch of old envelopes." Turned into a proper book with defining illustrations by W.W. Denslow, the story most of us know as "The Wizard of Oz" was an immediate sensation in 1900. In a review, the New York Times commended it, saying that it was "ingeniously woven out of commonplace material." Baum would produce 13 sequels, though none had quite the sparkle of the first.



For the full review, see:

JOHN STEELE GORDON. "Books; Inventing a New World; The men who engineered the astonishing emergence of the modern age." Wall Street Journal (Sat., April 11, 2009): W8.


The book being reviewed, is:

Schwartz, Evan I. Finding Oz: How L. Frank Baum Discovered the Great American Story. Boston, MA: Houghton Mifflin Harcourt, 2009.





August 8, 2009

Experiments Suggest We Can Live Longer



RhesusMonkeysLongevity2009_07_11.jpg"Rhesus monkeys, 27-year-old Canto, left, and Owen, 29, are among the oldest surviving subjects in a study of the links between diet and aging." Source of photo and caption: online version of the WSJ article quoted and cited below.


(p. A3) A study published Wednesday found that rapamycin, a drug used in organ transplants, increased the life span of mice by 9% to 14%, the first definitive case in which a chemical has been shown to extend the life span of normal mammals.

Anti-aging researchers also expect a second study, to be released this week, will show that sharply cutting the calorie intake of monkeys extends their lives substantially. The experiment is said to be the first technique shown to retard aging in primates.

The prospect of a reliable human longevity pill is still distant. A commentary released with the rapamycin study strongly cautioned against taking the drug to prolong life because of potentially deadly side effects. Rapamycin suppresses the immune system and carries strong warnings about the resulting risk of infections and death.

But the mouse and monkey findings appear to mark the most substantial scientific progress yet in the search for ways to extend human life spans -- once viewed as a fringe area of study.

"It's time to break out of our denial about aging," said Aubrey de Grey, a British gerontologist who has drawn controversy for his suggestions on how to forestall death. "Aging is, unequivocally, the major cause of death in the industrialized world and a perfectly legitimate target of medical intervention."



For the full story, see:

KEITH J. WINSTEIN. ""Two Mammals' Longevity Boosted; Transplant Drug Lengthens Lives of Mice, and Fewer Calories Benefit Monkeys." The Wall Street Journal (Thurs., JULY 10, 2009): A3.



LongerLivesBarChart2009_07_11.gif

















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





April 6, 2009

Experiments on Animal Genes Enthuses Longevity Researchers


YogiCharles.jpg










"Charles Yogi, 89, a track & field athlete, is part of the Hawaii Lifespan Study." Source of caption and photo: online version of the WSJ story quoted and cited below.


(p. A18) Based on animal experiments, gerontologists believe that one key to a healthy, longer lifespan may be found in a few master genes that affect cellular responses to famine, drought and other survival stresses. The more active these genes are, the longer an organism seems to survive -- at least in the laboratory. Moreover, researchers are convinced that some genes may protect us against the risks of heart disease, diabetes, cancer and dementia.

. . .

Recent insights into the genetics of aging among simple organisms are stoking their enthusiasm. In January, for example, gerontologist Valter Longo at the University of Southern California reported that by altering two genes he made yeast that lived 10 times longer than normal. "We can really reprogram the lifespan of these organisms," he said. In March, scientists at the University of Washington identified 15 genes regulating lifespan in yeast and worms that resemble genes found in humans. At least three companies are working independently on potential therapies based on the discovery that life span in mammals may be regulated partly by genetically controlled enzymes called sirtuins.



For the full story, see:

ROBERT LEE HOTZ. "Secrets of the 'Wellderly'; Scientists Hope to Crack the Genetic Code of Those Who Live the Longest." The Wall Street Journal (Fri., SEPTEMBER 19, 2008): A18.

(Note: ellipsis added.)




December 1, 2008

Age and Inventiveness


AgeProductivityGraph.gif Source of graph: online version of the WSJ article quoted and cited below.


(p. B5) A particularly stark view of age-related constraints on researchers' work comes from Benjamin Jones, an associate professor at Northwestern University's Kellogg School of Management. He examined biographical data over the past century for more than 700 Nobel laureates and renowned inventors.

His conclusion: "Innovators are productive over a narrowing span of their life cycle." In the early 20th century, he found, researchers at the times of their greatest contributions averaged slightly more than 36 years old. In recent decades, innovation before the age of 30 became increasing rare, with the peak age of contribution rising toward age 40. Meanwhile, the frequency of key contributions has consistently diminished by researchers in their early or mid-50s.

Occasionally, Mr. Jones says, booming new fields "permit easier access to the frontier, allowing people to make contributions at younger ages." That could account for the relative youth of Internet innovators, such as Netscape Communications Corp. founder Marc Andreessen and Messrs. Page and Brin. But "when the revolution is over," Mr. Jones finds, "ages rise."

Unwilling to see researchers at peak productivity for only a small part of their careers, tech companies are fighting back in a variety of ways. At microchip maker Texas Instruments Inc., in Dallas, executives are pairing up recent college graduates and other fresh research hires with experienced mentors, called "craftsmen," for intensive training and coaching.

This system means that new design engineers can become fully effective in three or four years, instead of five to seven, says Taylor Efland, chief technologist for TI's analog chip business. Analog chips are used in power management, data conversion and amplification.

At Sun Microsystems Inc., teams of younger and older researchers are common. That can help everyone's productivity, says Greg Papadopoulos, chief technology officer for the Santa Clara, Calif., computer maker. Younger team members provide energy and optimism; veterans provide a savvier sense of what problems to tackle.



For the full story, see:

GEORGE ANDERS. "THEORY & PRACTICE; Companies Try to Extend Researchers' Productivity; Teams of Various Ages, Newer Hires Combat Short Spans of Inventing." The Wall Street Journal (Mon., AUGUST 18, 2008): B5.


A large literature exists on the relationship between age and scientific productivity. I am particularly fond of the following examples:

Diamond, Arthur M., Jr. "Age and the Acceptance of Cliometrics." The Journal of Economic History 40, no. 4 (December 1980): 838-841.

Diamond, Arthur M., Jr. "An Economic Model of the Life-Cycle Research Productivity of Scientists." Scientometrics 6, no. 3 (1984): 189-196.

Diamond, Arthur M., Jr. "The Life-Cycle Research Productivity of Mathematicians and Scientists." The Journal of Gerontology 41, no. 4 (July 1986): 520-525.

Diamond, Arthur M., Jr. "An Optimal Control Model of the Life-Cycle Research Productivity of Scientists." Scientometrics 11, nos. 3-4 (1987): 247-249.

Diamond, Arthur M., Jr. "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.

Hull, David L., Peter D. Tessner and Arthur M. Diamond, Jr. "Planck's Principle: Do Younger Scientists Accept New Scientific Ideas with Greater Alacrity than Older Scientists?" Science 202 (November 17, 1978): 717-723.




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