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.”)

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.

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.)

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.)

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.)

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

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

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

Resveratrol Activates Sirtuins to Switch on Energy Producing Mitochondria

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

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

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

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

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

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.”)

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.

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.