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September 15, 2014

Drugs May Rebuild Muscle in Frail Elderly



(p. B1) In 1997, scientist Se-Jin Lee genetically engineered "Mighty Mice" with twice as much muscle as regular rodents. Now, pharmaceutical companies are using his discovery to make drugs that could help elderly patients walk again and rebuild muscle in a range of diseases.


. . .


"I am very optimistic about these new drugs," says Dr. Lee, a professor of molecular biology at Johns Hopkins University in Baltimore, who isn't involved in any of the drug trials. "The fact that they're so far along means to me they must have seen effects."

Myostatin is a naturally occurring protein that curbs muscle growth. The drugs act by blocking it, or blocking the sites where it is detected in the body, potentially rebuilding muscle.



For the full story, see:

HESTER PLUMRIDGE and MARTA FALCONI. "Drugs Aim to Treat Frailty in Aging." The Wall Street Journal (Mon., April 28, 2014): B1-B2.

(Note: ellipsis added.)

(Note: the second paragraph quoted above is divided into two mini-paragraphs in the online, but not in the print, version.)

(Note: the online version of the story has the date April 27, 2014, and has the title "Drugs Aim to Help Elderly Rebuild Muscle.")






July 7, 2014

Proof-of-Concept: Life Can Be Very Long



Eucalyptus13000YearsOld2014-06-04.jpg "Rare Eucalyptus (species redacted for protection) (13,000 years old; New South Wales, Australia). This critically endangered eucalyptus is around 13,000 years old, and one of fewer than five individuals of its kind left on the planet. The species name might hint too heavily at its location, so it has been redacted." Source of caption and photo: online version of the WSJ article quoted and cited below.



(p. C12) Photographer Rachel Sussman has spent the past decade looking for the oldest things alive.   . . .    She documents 30 of those organisms in her new book, "The Oldest Living Things in the World" (University of Chicago Press, $45).


For the full, brief, review, see:

Alexandra Wolfe. "EXHIBIT; The 2,000-Year-Old Plant." The Wall Street Journal (Sat., April 26, 2014): C12.

(Note: ellipsis added.)

(Note: the online version of the review has the date April 25, 2014, and has the title "EXHIBIT; The 2,000-Year-Old Plant.")


The book under review is:

Sussman, Rachel. The Oldest Living Things in the World. Chicago: University of Chicago Press, 2014.



BristleconePineOldestUnitaryOrganismInWorld2014-06-04.jpg
"Bristlecone Pine (White Mountains, California). Bristlecone pines are the oldest unitary organisms in the world, known to surpass 5,000 years in age. In the 1960s, a then-grad student cut down what would have been the oldest known tree in the world while retrieving a lost coring bit. A cross section of that tree was placed in a Nevada casino." Source of caption and photo: online version of the WSJ review quoted and cited above.






May 23, 2014

30,000 Year Old Virus Revived from Permafrost



(p. D5) From Siberian permafrost more than 30,000 years old, [French and Russian researchers] have revived a virus that's new to science.

"To pull out a virus that's 30,000 years old and actually grow it, that's pretty impressive," said Scott O. Rogers of Bowling Green State University who was not involved in the research. "This goes well beyond what anyone else has done."


. . .


Measuring 1.5 micrometers long, the viruses are 25 percent bigger than any virus previously found.


. . .


"Sixty percent of its gene content doesn't resemble anything on earth," Dr. Abergel said. She and her colleagues suspect that pithoviruses may be parasitic survivors of life forms that were very common early in the history of life.


. . .


"Its potential implications for evolutionary theory and health are quite astonishing," said Eske Willerslev, an evolutionary biologist at the University of Copenhagen.



For the full story, see:

Carl Zimmer. "Out of Siberian Ice, a Virus Revived." The New York Times (Tues., MARCH 4, 2014): D5.

(Note: ellipses, and bracketed words, added.)

(Note: the online version of the story has the date MARCH 3, 2014.)







March 20, 2014

Aging Brains May Be Slower Because They Have More Data to Search Through



(p. D3) In a paper published in Topics in Cognitive Science, a team of linguistic researchers from the University of Tübingen in Germany used advanced learning models to search enormous databases of words and phrases.

Since educated older people generally know more words than younger people, simply by virtue of having been around longer, the experiment simulates what an older brain has to do to retrieve a word. And when the researchers incorporated that difference into the models, the aging "deficits" largely disappeared.

"What shocked me, to be honest, is that for the first half of the time we were doing this project, I totally bought into the idea of age-related cognitive decline in healthy adults," the lead author, Michael Ramscar, said by email. But the simulations, he added, "fit so well to human data that it slowly forced me to entertain this idea that I didn't need to invoke decline at all."


. . .


Scientists who study thinking and memory often make a broad distinction between "fluid" and "crystallized" intelligence. The former includes short-term memory, like holding a phone number in mind, analytical reasoning, and the ability to tune out distractions, like ambient conversation. The latter is accumulated knowledge, vocabulary and expertise.

"In essence, what Ramscar's group is arguing is that an increase in crystallized intelligence can account for a decrease in fluid intelligence," said Zach Hambrick, a psychologist at Michigan State University. In a variety of experiments, Dr. Hambrick and Timothy A. Salthouse of the University of Virginia have shown that crystallized knowledge (as measured by New York Times crosswords, for example) climbs sharply between ages 20 and 50 and then plateaus, even as the fluid kind (like analytical reasoning) is dropping steadily -- by more than 50 percent between ages 20 and 70 in some studies. "To know for sure whether the one affects the other, ideally we'd need to see it in human studies over time," Dr. Hambrick said.



For the full commentary, see:

BENEDICT CAREY. "MIND; Older Mind May Just Be a Fuller Mind." The New York Times (Tues., JANUARY 28, 2014): D3.

(Note: ellipsis added.)

(Note: the online version of the commentary has the date JANUARY 27, 2014, and has the title "MIND; The Older Mind May Just Be a Fuller Mind.")



The Ramscar article mentioned above is:

Ramscar, Michael, Peter Hendrix, Cyrus Shaoul, Petar Milin, and Harald Baayen. "The Myth of Cognitive Decline: Non-Linear Dynamics of Lifelong Learning." Topics in Cognitive Science 6, no. 1 (Jan. 2014): 5-42.


One of the papers by Hambrick and Salthouse that discusses crystallized knowledge is:

Hambrick, David Z., and Timothy A. Salthouse. "Predictors of Crossword Puzzle Proficiency and Moderators of Age-Cognition Relations." Journal of Experimental Psychology, General 128, no. 2 (June 1999): 131-64.






February 20, 2014

The Young, with Managerial Experience, Are Most Likely to Become Entrepreneurs



(p. A13) In a current study analyzing the most recent Global Entrepreneurship Monitor (GEM) survey, my colleagues James Liang, Jackie Wang and I found that there is a strong correlation between youth and entrepreneurship. The GEM survey is an annual assessment of the "entrepreneurial activity, aspirations and attitudes" of thousands of individuals across 65 countries.

In our study of GEM data, which will be issued early next year, we found that young societies tend to generate more new businesses than older societies. Young people are more energetic and have many innovative ideas. But starting a successful business requires more than ideas. Business acumen is essential to the entrepreneur. Previous positions of responsibility in companies provide the skills needed to successfully start businesses, and young workers often do not hold those positions in aging societies, where managerial slots are clogged with older workers.

In earlier work (published in the Journal of Labor Economics, 2005), I found that Stanford MBAs who became entrepreneurs typically worked for others for five to 10 years before starting their own businesses. The GEM data reveal that in the U.S. the entrepreneurship rate peaks for individuals in their late 20s and stays high throughout the 30s. Those in their early 20s have new business ownership rates that are only two-thirds of peak rates. Those in their 50s start businesses at about half the rate of 30-year-olds.

Silicon Valley provides a case in point. Especially during the dot-com era, the Valley was filled with young people who had senior positions in startups. Some of the firms succeeded, but even those that failed provided their managers with valuable business lessons.

My co-author on the GEM study, James Liang, is an example. After spending his early years as a manager at the young and rapidly growing Oracle, he moved back to China to start Ctrip, one of the country's largest Internet travel sites.



For the full commentary, see:

EDWARD P. LAZEAR. "The Young, the Restless and Economic Growth; Countries with a younger population have far higher rates of entrepreneurship." The Wall Street Journal (Mon., Dec. 23, 2013): A13.

(Note: the online version of the commentary has the date Dec. 22, 2013.)


The Lazear paper mentioned above, is:

Lazear, Edward P. "Entrepreneurship." Journal of Labor Economics 23, no. 4 (October 2005): 649-80.






December 17, 2013

Stem Cells Used to Create Tiny, Simple Human Livers



LiverBudsMadeFromStemCells2013-10-27.jpg "Researchers from Japan used human stem cells to create "liver buds," rudimentary livers that, when transplanted into mice, grew and functioned." Source of caption and photo: online version of the NYT article quoted and cited below.


(p. A3) Researchers in Japan have used human stem cells to create tiny human livers like those that arise early in fetal life. When the scientists transplanted the rudimentary livers into mice, the little organs grew, made human liver proteins, and metabolized drugs as human livers do.

They and others caution that these are early days and this is still very much basic research. The liver buds, as they are called, did not turn into complete livers, and the method would have to be scaled up enormously to make enough replacement liver buds to treat a patient. Even then, the investigators say, they expect to replace only 30 percent of a patient's liver. What they are making is more like a patch than a full liver.

But the promise, in a field that has seen a great deal of dashed hopes, is immense, medical experts said.

"This is a major breakthrough of monumental significance," said Dr. Hillel Tobias, director of transplantation at the New York University School of Medicine. Dr. Tobias is chairman of the American Liver Foundation's national medical advisory committee.



For the full story, see:

GINA KOLATA. "Scientists Fabricate Rudimentary Human Livers." The New York Times (Thurs., July 4, 2013): A3.

(Note: the online version of the story has the date July 3, 2013.)


The research article is:

Takebe, Takanori, Keisuke Sekine, Masahiro Enomura, Hiroyuki Koike, Masaki Kimura, Takunori Ogaeri, Ran-Ran Zhang, Yasuharu Ueno, Yun-Wen Zheng, Naoto Koike, Shinsuke Aoyama, Yasuhisa Adachi, and Hideki Taniguchi. "Vascularized and Functional Human Liver from an iPSC-Derived Organ Bud Transplant." Nature (July 3, 2013) DOI: 10.1038/nature12271.






November 17, 2013

Foreign Aid Frees Despots from Having to Seek the Consent of the Governed



TheGreatEscapeBK2013-10-24.jpg











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






(p. 4) IN his new book, Angus Deaton, an expert's expert on global poverty and foreign aid, puts his considerable reputation on the line and declares that foreign aid does more harm than good. It corrupts governments and rarely reaches the poor, he argues, and it is high time for the paternalistic West to step away and allow the developing world to solve its own problems.

It is a provocative and cogently argued claim. The only odd part is how it is made. It is tacked on as the concluding section of "The Great Escape: Health, Wealth, and the Origins of Inequality" (Princeton University Press, 360 pages), an illuminating and inspiring history of how mankind's longevity and prosperity have soared to breathtaking heights in modern times.


. . .


THE author has found no credible evidence that foreign aid promotes economic growth; indeed, he says, signs show that the relationship is negative. Regretfully, he identifies a "central dilemma": When the conditions for development are present, aid is not required. When they do not exist, aid is not useful and probably damaging.

Professor Deaton makes the case that foreign aid is antidemocratic because it frees local leaders from having to obtain the consent of the governed. "Western-led population control, often with the assistance of nondemocratic or well-rewarded recipient governments, is the most egregious example of antidemocratic and oppressive aid," he writes. In its day, it seemed like a no-brainer. Yet the global population grew by four billion in half a century, and the vast majority of the seven billion people now on the planet live longer and more prosperous lives than their parents did.



For the full review, see:

FRED ANDREWS. "OFF THE SHELF; A Surprising Case Against Foreign Aid." The New York Times, SundayBusiness Section (Sun., October 13, 2013): 4.

(Note: ellipsis added.)

(Note: the online version of the review has the date October 12, 2013.)



The book reviewed is:

Deaton, Angus. The Great Escape: Health, Wealth, and the Origins of Inequality. Princeton, N.J.: Princeton University Press, 2013.






October 10, 2013

Gene-Altered Mice Live 20% Longer



MouseGeneAltertedLivesLonger2013-09-27.jpg "NIH researchers found that lowering the expression of a single gene helped extend the life of mice by about 20%. A mouse with a manipulated gene on the right and an unchanged mouse on the left." Source of caption and photo: online version of the WSJ article quoted and cited below.



(p. A3) By reducing the activity of one type of gene, scientists said they increased the average life span of mice by about 20%, a feat that in human terms is akin to extending life by about 15 years.

Moreover, the researchers at the National Institutes of Health found that memory, cognition and some other important traits were better preserved in the mice as they aged, compared with a control group of mice that had normal levels of a protein put out by the gene.

The findings, published Thursday [August 29, 2013] in the journal Cell Reports, strengthen the case that the gene, called mTOR, is a major regulator of the aging process.


. . .


The results . . . build on a growing body of research challenging the belief that aging is an intractable biological process, prompting scientists to think of slowing aging as a possible way to prevent disease.

"What we need right now is for scientists and the public to wake up to the concept that you can slow aging," said Brian Kennedy, president of the Buck Institute for Aging Research in Novato, Calif., who wasn't involved in the new study. "If you do, you prevent many of the diseases that we're so scared of and that are associated with aging." They include cardiovascular disease, cancer and Alzheimer's disease.



For the full story, see:

RON WINSLOW. "Altered Gene Points Toward Longer Life Spans; Successful Experiment With Mice May One Day Play Role in Slowing Human Aging; Side Effects Could Be Problematic." The Wall Street Journal (Fri, August 30, 2013): A3.

(Note: ellipsis, and bracketed date, added.)

(Note: the online version of the story has the date August 29, 2013, and has the title "Genetic Manipulation Extends Life of Mice 20%; But Translating Findings to Humans Faces Many Hurdles.")


The scientific article being discussed above, is:

Wu, J.  Julie, Jie Liu, Edmund B Chen, Jennifer J Wang, Liu Cao, Nisha Narayan, Marie M Fergusson, Ilsa I Rovira, Michele Allen, Danielle A Springer, Cory U Lago, Shuling Zhang, Wendy DuBois, Theresa Ward, Rafael deCabo, Oksana Gavrilova, Beverly Mock, and Toren Finkel. "Increased Mammalian Lifespan and a Segmental and Tissue-Specific Slowing of Aging after Genetic Reduction of mTor Expression." Cell Reports 4, no. 5 (Aug. 29, 2013): 913-20.






October 7, 2013

Google's Calico Company Seeks to Expand the Human Life Span



(p. B4) Google Inc.is backing a new company to research aging, taking an unusual business swing at the burgeoning science of extending the human life span.

The venture, which is long on goals but short on specifics, is known as Calico, and will operate separately from Google, the online search giant said on Wednesday.

"We believe we can make good progress within reasonable time scales with the right goals and the right people," Google CEO Larry Page said in a blog post. "This is clearly a longer-term bet."


. . .


Google provided scant details about how Calico would operate or how it would tackle its ambitions of improving the health of "millions of lives." But Jay Olshansky, an expert on aging at the University of Illinois of Chicago, said one potentially promising path is to research therapies that target the aging process itself.

While medical research typically focuses on finding treatments and cures for individual ailments such as cardiovascular disease and cancer, "if you're going to have an impact on human health and longevity in the future, the way to go is to go after aging itself," Dr. Olshansky said.

A founder of a consortium called the Longevity Dividend Initiative, Dr. Olshansky said [he gave a talk at conference (sic) in 2010 in which he said that finding a cure for cancer would only extend human life span by about three and one-half years. The reason is, he said, is (sic) it would "expose people who were saved from dying of cancer to all the other diseases and disorders" that are the result of aging.]


. . .


{He said Mr. Brin attended the meeting and asked him questions about the talk. He hasn't discussed Calico with anyone at Google--the first he'd heard of the venture was Wednesday-- though he described the formation of Calico as "great news."}



For the full story, see:

GREG BENSINGER and RON WINSLOW. "Google Backs New Venture to Research Aging." The Wall Street Journal (Thurs., September 19, 2013): B4.

(Note: ellipsis added; square-bracketed words are in the print, but not the online, version of the article; curly-bracketed words are in the online, but not the print, version of the article.)

(Note: the online version of the story has the date September 18, 2013, and has the title "Google Backs Venture to Research Aging.")






August 4, 2013

Hunter-Gatherers Had High Child Mortality and Died Before Age 40



(p. 31) Child mortality in foraging tribes was severe. A survey of 25 hunter-gatherer tribes in historical times from various continents revealed that, on average, 25 percent of children died before they were 1, and 37 percent died before they were 15. In one traditional hunter-gatherer tribe, child mortality was found to be 60 percent. Most historical tribes had a population growth rate of approximately zero. This stagnation is evident, says Robert Kelly in his survey of hunting-gathering peoples, because "when formerly mobile people become sedentary, the rate of population growth increases." All things being equal, the constancy of farmed food breeds more people.

While many children died young, older hunter-gatherers did not have (p. 32) it much better. It was a tough life. Based on an analysis of bone stress and cuts, one archaeologist said the distribution of injuries on the bodies of Neanderthals was similar to that found on rodeo professionals--lots of head, trunk, and arm injuries like the ones you might get from close encounters with large, angry animals. There are no known remains of an early hominin who lived to be older than 40. Because extremely high child mortality rates depress average life expectancy, if the oldest outlier is only 40, the median age was almost certainly less than 20.



Source:

Kelly, Kevin. What Technology Wants. New York: Viking Adult, 2010.






May 10, 2013

Stem-Cell Researchers Developing Experimental Personalized Medicine



(p. C4) Last month a team at Johns Hopkins University and the Sloan-Kettering Institute for Cancer Research, using a version of Dr. Yamanaka's technique, successfully grew nerve cells from a patient suffering from a rare disease called Riley-Day syndrome, which is linked to early mortality, seizures and other symptoms and caused by a fault in one gene.

But the purpose was not to put these cells back into the patient. Instead the scientists tested 6,912 chemical compounds on the cells to see if they could find one that "rescued" the "expression" of the gene: that is to say, caused it to produce the protein it is supposed to produce. One of the compounds worked, inducing the gene to be actively transcribed by the cell.

In the not-very-distant future, when something is going wrong in one of your organs, one treatment may be to create some stem cells from your body in the laboratory, turn them into cells of that organ, or even rudimentary structures, and then subject them to experimental treatments to see if something cures the problem. The goal of personalized medicine, in other words, may be reached by stem-cell researchers before it's reached by geneticists.



For the full commentary, see:

MATT RIDLEY. "MIND & MATTER; Stem-Cell Cures Without the Controversy." The Wall Street Journal (Sat., December 8, 2012): C4.

(Note: the online version of the commentary has the date December 7, 2012.)





May 9, 2013

Sometimes There Are Second Acts in American Lives



LaughtonCharlesMutinyOnTheBounty2013-05-04.jpg "In the foreground, Ian Wolfe, Charles Laughton and Clark Gable in 1935's 'Mutiny on the Bounty.'" Source of caption and photo: online version of the WSJ article quoted and cited below.


(p. D10) In 1947 Charles Laughton's career, if not quite on the skids, was definitely in the doldrums. Long acclaimed as Hollywood's foremost character actor, he had made only one film of any artistic consequence, Jean Renoir's "This Land Is Mine," in the past seven years. The rest of the time he coasted, frequently indulging in self-parody--and nobody was easier to spoof than the man who played Captain Bligh in "Mutiny on the Bounty" and Quasimodo in "The Hunchback of Notre Dame." He wouldn't have been the first actor to sell his soul for a swimming pool (or, in his case, an art collection). But with Mr. Laughton the waste would have been unforgivable, since he was, in Laurence Olivier's words, "the only actor I ever knew who was a genius."

Instead, Mr. Laughton fooled everyone by returning to the stage for the first time since 1936. Nor did he choose a safe star vehicle for his return: He played the title role in the U.S. premiere of Bertolt Brecht's "Galileo," and he translated the play himself.


. . .


Except for "The Night of the Hunter," Mr. Laughton's post-"Galileo" career is no longer widely remembered save by scholars. But enough of it survives on sound recordings and kinescopes to prove that F. Scott Fitzgerald was all wet when he claimed that "there are no second acts in American lives." Charles Laughton, who moved from England to America to seek fame and fortune and came perilously close to losing his soul along the way, had a second act that redeemed all that came before it. No actor could ask for a better curtain.



For the full commentary, see:

TERRY TEACHOUT. "SIGHTINGS; Charles Laughton's Late Bounty." The Wall Street Journal (Fri., March 2, 2012): D10.

(Note: ellipsis added.)

(Note: the online version of the commentary has the date March 1, 2012.)






April 26, 2013

Longer Life Spans "Allowed More Time to Invent New Tools"



(p. 33) The primary long-term consequence of . . . slightly better nutrition was a steady increase in longevity. Anthropologist Rachel Caspari studied the dental fossils of 768 hominin individuals in Europe, Asia, and Africa, dated from 5 million years ago until the great leap. She determined that a "dramatic increase in longevity in the modern humans" began about 50,000 years ago. Increasing longevity allowed grandparenting, creating what is called the grandmother effect: In a virtuous circle, via the communication of grandparents, ever more powerful innovations carried forward were able to lengthen life spans further, which allowed more time to invent new tools, which increased population. Not only that: Increased longevity "provide[d] a selective advantage promoting further population increase," because a higher density of humans increased the rate and influence of innovations, which contributed to increased populations. Caspari claims that the most fundamental biological factor that underlies the behavioral innovations of modernity maybe the increase in adult survivorship. It is no coincidence that increased longevity is the most measurable consequence of the acquisition of technology. It is also the most consequential.


Source:

Kelly, Kevin. What Technology Wants. New York: Viking Adult, 2010.

(Note: ellipsis added; bracketed "d" in Kelly's original.)






March 27, 2013

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.)






March 12, 2013

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.






February 20, 2013

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



KurzweilRay2013-02-03.jpg











"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.")






February 18, 2013

Entrepreneur Peter Thiel Says We Should Fight for Longer Lives



100PlusBK2013-01-12.jpg











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.






February 8, 2013

Lichen Fungi May Never Age



PringleAnneLichenResearch2013-01-12.jpg "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.)



LichenCommunity2013-01-12.jpg"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.






December 7, 2012

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.






August 9, 2012

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.)





July 29, 2012

Neural Implants "Restored Their Human Functionality"



KurzweilRay2012-07-28.jpg




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.)






April 24, 2012

Campion Plant Sprouts from 32,000 Year-Old Seed



PlantGeneratedFromOldSeed2012-04-04.jpg

















"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.)





March 31, 2012

Quantum Computers May Revolutionize Nanotechnology and Drug Design



AaronsonScottMIT201-03-11.jpg










"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.)





March 25, 2012

Purging Senescent Cells Makes Mice More Youthful and Vigorous



SubdermalFatInMousePurgedOfSenescentCells2012-03-10.jpg




"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.)





February 22, 2012

Adipotide Kills Fat Cells in Obese Mice and Monkeys



AdipotideObesityGraphic2012-02-05.jpg











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.)




ObeseMonkeyLostWeight2012-02-06.jpg "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.






February 11, 2012

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.








December 26, 2011

Bright Prospects for Longer Life



100BK.jpg












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



LoranSyndromeCancerDiabetesGraphic2011-06-05.jpg











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



LongevityProjectBK.jpg











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"



BilingualDementia2010-10-23.gif













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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