Sharon Begley's "Science Journal"

Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 1:59 am

Sharon Begley's "Science Journal"
Wall Street Journal



A Spotless Mind May Ease Suffering, But Erase Identity
Are Tainted Vaccines Given to Baby Boomers Now Causing Cancer?
As the Stakes Increase, Prime-Number Theory Moves Closer to Proof
Chimeras Exist, What if Some Turn Out Too Human?
Definition of Infinity Expands for Scientists and Mathematicians
Early Cancer Detection Doesn't Always Give Patient an Advantage
Evolutionary Psych May Not Help Explain Our Behavior After All
Fluoridation, Cancer: Did Researchers Ask the Right Questions?
'Gene Pill' Offers Alternative to Shots
Grandma's Behavior While Pregnant Impacts Lineage
How Brief Drop in Cars Can Trigger Tie-Ups, And Other Traffic Tales
Hurricane Forecasters Try Model That Focuses on Chances of Landfall
Imprinted Genes Offer Key to Some Diseases
Improved Formula in England, Girls are Closing Gap with Boys in Math
Interrogation Methods Can Elicit Confessions From Innocent People
Religion and the Brain
How Do I Love Thee? Let Me Count the Ways--And Other Bad Ideas
Man-Made Mistakes Increase Devastation of 'Natural' Disasters
Mission on the Cheap Will Launch Spaceship That Uses Solar Sails
Scientists Research Questions Few Others Would Bother to Ask
Simulations of Attacks By Terrorists Illustrate Challenge Officials Face
So Much For Destiny: Even Thoughts Can Turn Genes 'On' and 'Off'
Study of the Cosmos Proceeds, But Will Take New Directions
Study Says Hurricanes Are Getting Stronger
Theory Men Are Wired To Kill Straying Mates is Offensive and Wrong
U.S. Science Research Is In Danger of Losing Place on Cutting Edge
Very Old Eggs Reveal A Fast, Changing Path Through Evolution
Water-Flea Case Shows That Ability to Adapt is What's Really Innate
Why Just Detecting Hidden Explosives May Not Cut Deaths
Why George Gershwin May Have Called It 'Rhapsody in Blue'
Yes, Evolution Still Has Unanswered Questions; That's How Science Is
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:01 am

A Spotless Mind May Ease Suffering, But Erase Identity
by Sharon Begley
August 19, 2005

As a teenager, the woman had suffered a horrific rape, the memory of which she carried into adulthood. The slightest mention, on television or in conversation, of a child being harmed left her short of breath and bathed in sweat. She regularly relived the trauma in nightmares and flashbacks. Once, when she was having her hair done, a radio show began to discuss sexual assaults of children; she sprang from her chair and fled the salon.

For her and for every other victim of post-traumatic stress disorder, or PTSD, bad memories are only the beginning. Recalling a traumatic memory, scientists now think, does something even worse than trigger the disabling physiological response the woman suffered: It "reconsolidates" the memory, wiring it more strongly into the mind.

Emerging evidence that remembering a trauma strengthens that memory is inspiring controversial studies in which people take a drug that may block memory reconsolidation, leaving the memory intact but weakened, and extinguishing the emotion associated with it. That raises a troubling question: Will the drug rob people of an essential, even defining, aspect of their selves?

It is no mystery why traumatic memories are so vivid. Compare your recollection of Sept. 11, 2001, with that of Sept. 10, 2001. "When we experience something traumatic, stress hormones such as noradrenalin are released from the brain stem and reach the amygdala," says Roger Pitman of Harvard Medical School, Boston. "The amygdala tells the [memory-processing] hippocampus to remember better, burning in the memory of that event."

Because memories run on chemicals, they can be altered by chemicals. Compounds called beta blockers, which treat hypertension, are the brain's version of pushy people who sneak into company parking spaces reserved for particular employees. The beta blockers occupy the beta receptors in the amygdala that noradrenalin ordinarily fits into. Just as an employee can't go to work if she can't park, noradrenalin can't burn memories into the brain if it can't get into the receptor.

In a 2002 pilot study, Dr. Pitman and colleagues gave a beta blocker, propranolol, to people arriving at an emergency room after accidents, and for 10 days after. Three months later, the patients had fewer PTSD symptoms, and weaker memories of their trauma, than ER patients given a placebo. When reminded of their accident, they recalled it with less suffering than the placebo group.

"We interpret that as saying that propranolol interferes with the consolidation of traumatic memories," Dr. Pitman says. "The result is that you don't remember a traumatic experience any better than an ordinary one." The memory loses its emotional sting.

Scientists also have seen hints that propranolol can intervene in memories long after they form. Given to lab rats that have learned to associate a tone with an electric shock, for instance, it erases the animals' fear of the impending shock enough that they no longer freeze in terror when the tone sounds.

"The theory is, when you reactivate a memory, it needs to be reconsolidated in order to be well retained," says Dr. Pitman. "In animals, propranolol interferes with this. If it does the same in people, you have another shot at helping them." Even though the original memory was consolidated, maybe drugs can weaken it and strip it of its emotion when it is recalled.

That is what psychiatrist Margaret Altemus of Weill Medical College of Cornell University, New York, and colleagues hope to find out. In their study, PTSD patients take a pill whenever they recall the trauma and succumb to panic, as the rape victim did in the salon. If the theory is right, propranolol should sever the link between memory and terror. The patients will recall the horror, but not be so crippled by it.

Proponents of the therapy take offense at those who caution against yet another drug that tinkers with the mind and the brain. At a time when we seem to drug every mental quirk from shyness to fidgetyness, it seems cruel and hypocritical to draw a line at alleviating the suffering of people with PTSD. Also, lifting the paralyzing emotion of traumatic memories could enable victims to use their experiences to alleviate the suffering of others.

Critics see the prospect of white-washing memories differently. Some worry that propranolol could be abused, perhaps desensitizing soldiers, or even terrorists, so that they could commit atrocities, unconstrained by bad memories.

Others who don't go quite that far still have concerns. "We are, in essence, the sum of our memories," says Andrew Solomon, author of the 2002 best-seller "The Noonday Demon," about his battle with depression. "To work through the trauma of a memory is important and valid; to eliminate that memory and its essential affect is to rob us of some of our deep humanity."

He also worries about the slippery slope. "PTSD is an acute illness that should be treated, but the temptation to start knocking out painful day-to-day memories could become irresistible," he says. "Obliterating something that makes us human is, to me, a terrifying prospect."
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:02 am

Are Tainted Vaccines Given to Baby Boomers Now Causing Cancer?
by Sharon Begley
Wall Street Journal, Science Journal
July, 2002

Snapshots of your government at work:

1961. The U.S. Public Health Service, having learned in 1960 that millions of batches of polio vaccine were accidentally laced with a simian virus (vaccine was grown on minced monkey kidneys), quietly orders manufacturers to rid the vaccine of the contaminant, called SV40. PHS issues neither recall nor public announcement. Contaminated stocks already distributed are used until 1963.

1999. H.M. Ratner, a former public-health official in Oak Park, Ill., invites Michele Carbone of nearby Loyola University School of Medicine over for coffee. In 1955, Dr. Ratner says, he had refused to administer the Salk polio vaccine. He felt it might not be safe. But he kept seven vials in his basement refrigerator for 44 years, hoping that, one day, someone would be interested in them. Someone is. Dr. Carbone is investigating the possibility that SV40-contaminated polio vaccine made by several manufacturers was, decades after being given to about 98 million baby boomers, increasing the risk of three rare cancers.

2000. Last week, the Immunization Safety Review Committee of the Institute of Medicine (IOM) meets to consider evidence for and against that unthinkable hypothesis.

Amid dueling data, some facts are uncontested. An estimated two-thirds of the polio vaccines--the oral Sabin and the injected Salk--administered from 1955 to 1963 contained SV40, including the vials Dr. Ratner saved. Contaminated vaccine was also given to children and some adults in Australia, Canada, Denmark and Germany, and possibly Russia, Mexico, and other countries.

SV40 is a known carcinogen. It targets the lung's mesothelial cells, brain cells, bone cells and blood cells, producing a protein that knocks out two human tumor-suppressor genes, p53 and Rb. There is no reliable blood test for SV40 exposure.

Government data shows the incidence of SV40-linked cancers has risen. A brain cancer called ependymoma is up 25%. Bone malignancies are up 23%. Mesothelioma (infamous for being triggered by asbestos) is up 90%. All are extremely rare: Ependymoma, for example, strikes one in a million.

Are the rising cancer rates coincidence? In 1994, Loyola's Dr. Carbone and colleagues examined human mesotheliomas. He found SV40 genetic sequences in 29 of 48 studied. SV40 has now been found in up to 80% of mesotheliomas in the U.S. and Europe. Dozens of labs have found SV40 in bone and brain cancers. Those, as I said, are rare. Epidemiologist Howard Strickler of Albert Einstein College of Medicine in New York, a leading skeptic of the vaccine-cancer link, notes that many studies fail to find SV40 in human tumors.

In March, however, researchers led by Janet Butel of Baylor College of Medicine, Houston, reported that 42% of the non-Hodgkin lymphomas they analyzed contained genetic sequences from SV40. And not just any SV40: In several tumors, it was precisely the genome of the SV40 in the vials of the 1955 polio vaccine that Dr. Ratner had held onto, waiting for someone to care. Lab-grown SV40 harbors a variant genome. There might be other sources, in addition to vaccine, of this strain of SV40, but to more and more scientists Dr. Butel's findings were the smoking gun.

With non-Hodgkin lymphoma, we're no longer talking about rare malignancies. This cancer has spiked 82% in the U.S. since 1973, epidemiologist Susan Fisher of the University of Rochester, New York, told the IOM panel, with 56,200 new cases in 2001 and 24,000 deaths.

An analysis of Dr. Strickler shows no extra cancers among people thought to have been exposed to SV40-lacked polio vaccine--or, no extra increase that can't be explained by chance. Trouble is, with no test for SV40 exposure, it's impossible to be sure you're comparing an exposed to an unexposed group. You might be comparing populations exposed to SV40 with populations also exposed. Of course there'd be no difference.

What are the ramifications of this? Today's children are at no risk from polio vaccine; it's now grown in SV40-free cells.

The public-health risk from SV40-laced polio vaccine is...well, one scientist told me it's "minimal." Another says "unknown" Tumors linked to SV40 are, except for lymphomas, so rare that even a doubling of risk due to SV40 still leaves you with good odds of never developing these cancers.

A wild card, though, is the World Trade Center collapse, which released asbestos into the air. Although SV40 alone rarely causes mesothelioma, when you add asbestos to the mix, all bets are off. The IOM committee's conclusions on SV40, polio vaccine and cancer are due out by the end of summer.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:02 am

As The Stakes Increase, Prime-Number Theory Moves Closer to Proof
by Sharon Begley
8 April 2005

THE ENGLISH mathematician G.H. Hardy (1877-1947) was an avowed atheist, but not above hedging his bets. Whenever he had to cross the Channel, he mailed postcards to friends saying he had proved the "Riemann hypothesis," an intriguing mathematical conjecture about prime numbers that had been proposed (but not proved) by Bernhard Riemann in 1859. By the early 20th century the Riemann hypothesis had become a Holy Grail for mathematicians. Hardy was therefore sure that if, on the off chance, God did exist, He would never let Hardy take the proof, unpublished, to a watery grave (Hardy also was apparently sure God would fall for the empty boast on the postcard).

In the decades since, the legend of the Riemann hypothesis has only grown, becoming "the most important unsolved problem in mathematics," says mathematician Dan of Dartmouth College, author of a nifty new book, "Stalking the Riemann Hypothesis: The Quest to Find the Hidden Law of Prime Numbers." Since 2000, the problem also has had a bounty on its head. The Clay Mathematics Institute, a private group in Cambridge, Mass., is offering $1 million to the first person who can prove it.

The prize sits unclaimed. But after a century of progress that can charitably be described as fitful, "frustration has begun to give way to excitement, for the pursuit of the Riemann hypothesis has begun to reveal astounding connections among nuclear physics, chaos and number theory," Prof. Rockmore says.

WHAT THESE appear to have in common is prime numbers, because deep down the Riemann hypothesis describes in detail how prime numbers are sprinkled along the number line. Primes are numbers that can be evenly divided only by themselves and 1. So 3, 5, 7, 11 and 13 are prime, as are 199, 409, 619, 829, 1039, 1249, 1459, 1669, 1879, 2089.

This last string is curious because the primes in it all are separated by 210. Last spring, two mathematicians proved that there exist strings (separated not by 210 but by other intervals) that contain an arbitrarily-long run of primes. That is, you can find a number, keep adding another number to it and get a run of primes as long as you like. Because prime numbers underlie digital cryptography and Internet security, such deep truths have become more than mere oddities.

An early discovery about the primes was that there is an infinite number of them, sprinkled "like indivisible stars scattered without end throughout a boundless numerical universe," Prof. writes. But how infinite? Although most of us think of infinity as one big number, some infinities are bigger than others. The number of numbers divisible by 2 is infinite, and so is the number divisible by 9. But the first infinity is bigger. There also is an infinite number of squares (4, 9, 16 . . .) and cubes (8, 27, 64 . . .), but more primes than either.

In 1859, Riemann got an inkling of how the primes thin out as you go along the number line. The number of primes around a particular number, he knew, equals the reciprocal of (that is, 1 divided by) the natural logarithm of that number. The natural logarithm of a number equals how many times you have to multiply a number called e (about 2.718) by itself to get that number. At around one million, whose logarithm is about 13, every 13th number or so is prime. At one billion, whose log is about 21, about every 21st number is prime.

RIEMANN WANTED to fathom why the heck primes were related to logarithms. He suspected he might find a clue in a formula that adds up 1 + 1/2 + 1/3 + 1/4 + 1-over-every-other-counting-number, but with the twist that each fraction is raised to an exponent (multiplied by itself some number of times). For bizarre exponents -- those that use the imaginary number the square root of -1 -- this sum equals zero. Riemann guessed at the general form of these "magical exponents." If his hypothesis is right, then mathematicians will know how primes thin out along the number line.

Proving the hypothesis means proving that every exponent of the form Riemann described makes the sum of the fractions zero. For more than a century mathematicians have been testing the magical exponents. In 1903 a researcher checked the first 15. By the 1930s, others had verified the first 1,000. By 1968, they had 3.5 million. Two years ago an IBM researcher using 500 computers verified the first 50 billion.

But that doesn't count as proving all of Riemann's exponents work. What if the 50-billionth-and-1st doesn't? The $1 million still is up for grabs.

The stakes are actually higher. The Riemann hypothesis now has been shown to underlie a plethora of puzzles in physics and math. The pattern of his magical exponents is related to the energies of particles in atomic nuclei, the energies of waves that fit precisely on geometric surfaces that describe space in Einstein's general theory of relativity, waiting times on bank lines and even how many cards you have to move to order the hand you're dealt in bridge. Why that should be so is -- depending how you look at it -- a coincidence, a profound truth of nature, or proof that God has a sense of humor. Maybe Hardy had the right idea with those postcards.

You can e-mail me at


Librarian's Comment:

The Sutra of the Cup

Polonius: What think you, Verbonious, is a cup a cup?

Verbonius: Like that one you hold, made of clay?

P: Yes, like this one.

V: No, it is not.

P: Why is that, Verbonious?

V: Lend it me.

P: You have it.

V: (Placing cup inside a cloth, he breaks it, then opens the cloth to show his friend.) Where is your cup?

P: You've broken it.

V: So it's not a cup.

P: Yes, it is, it's just that you've broken it.

V: (Shaking the cloth holding the shards.) There now, it's merely shards of clay.

P: Shards of the cup. (Turning to a friend, Neutronious) What think you, N?

N: I think Polonious makes the shards real to prove the cup unreal.

V: There, well spoken, you make one thing real to make another unreal.

N: Further, he makes the shards equal to the cup, but the cup and the shards have never been in the same place together. How then can they be equal?

V: Well, I'm vexed.

P: Makes two of us.

V: Things can only be themselves, for once they become something else, they cannot be equal to another thing. These seeming "transformations" of things are apropos of nothing, for a thing can only be equal to itself, and what it becomes when broken tells us only the nature of a new thing, which has always been broken, never otherwise.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:06 am

Chimeras Exist, What if Some Turn Out Too Human?
by Sharon Begley
Science Journal
Friday, May 06, 2005

If you had just created a mouse with human brain cells, one thing you wouldn't want to hear the little guy say is, "Hi there, I'm Mickey." Even worse, of course, would be something like, "Get me out of this & percentGBP !! body!"

It's been several millennia since Greek mythology dreamed up the chimera, a creature with the head of a lion, the body of a goat and the tail of a serpent. Research on the chimera front was pretty quiet for 2,500 years. But then in 1984 scientists announced that they had merged embryonic goat cells with embryonic sheep cells, producing a "geep." (It's part wooly, part hairy, with a face only a nanny goat could love.) A human-mouse chimera made its debut in 1988: "SCID-hu" is created when human fetal tissue -- spleen, liver, thymus, lymph node -- is transplanted into a mouse. These guys are clearly mice, but other chimeras are harder to peg. In the 1980s, scientists took brain-to-be tissue from quail embryos and transplanted it into chicken embryos. Once hatched, the chicks made sounds like baby quails.

More part-human chimeras are now in the works or already in lab cages. StemCells Inc., of Palo Alto, Calif., has given hundreds of mice human-brain stem cells, for instance. And before human stem cells are ever used to treat human patients, notes biologist Janet Rowley of the University of Chicago, they (or the cells they develop into) will be implanted into mice and other lab animals. "The centaur has left the barn more than people realize," says Stanford University law professor and bioethicist Henry Greely.

Part-human creatures raise enough ethical concerns that a National Academy of Sciences committee on stem cells veered off into chimeras. It recommended last week that some research be barred, to prevent some of the more monstrous possibilities -- such as a human-sperm-bearing mouse mating with a human-egg-bearing mouse and gestating a human baby. "We're not very concerned about a mouse with a human spleen," says Prof. Greely. "But we get really concerned about our brain and our gonads."

That's why his Stanford colleague, Irving Weissman, asked Prof. Greely to examine the ethical implications of a mouse-human chimera. StemCells, co-founded by Prof. Weissman, has already transplanted human-brain stem cells into the brains of mice that had no immune system (and hence couldn't attack the foreign cells). The stem cells develop into human neurons, migrate through the mouse brain and mingle with mouse cells. The human cells make up less than 1 percent of the mouse brain, and are being used by the company to study neurodegenerative diseases.

But Prof. Weissman had in mind a new sort of chimera. He would start with ill-fated mice whose neurons all die just before or soon after birth. He planned to transplant human-brain stem cells into their brains just before their own neurons died off. Would that lead the human cells to turn into neurons and replace the dead-or-dying mouse neurons, producing a mostly human brain in a mouse?

Such a chimera could bring important scientific benefits. The SCID-hu mouse, though it hasn't yielded a cure for AIDS, has been "a very valuable animal model," says Ramesh Akkina of Colorado State University, Fort Collins, who directs a lab that uses this part-human mouse. "It has human T cells circulating, which will allow us to test gene therapy for AIDS" in a way that will be more relevant to patients than all-animal models. The co-creator of SCID-hu, Michael McCune of the Gladstone Institute of Virology and Immunology, San Francisco, notes that because the human organs last for months in the mice (they would die in days in a lab dish), "it is possible to study the effects of HIV" in many kinds of human cells in a living system.

Similarly, studying living human neurons in a living mouse brain would likely yield more insights than studying human neurons in a lab dish or mouse neurons in a mouse brain. "You could see how pathogens damage human neurons, how experimental drugs act, what happens when you infect human neurons with prions (which cause mad-cow disease) or amyloid (associated with Alzheimer's)," says Prof. Greely. "The big concern is, could you give the mouse some sort of human consciousness or intelligence?"

"All of us are aware of the concern that we're going to have a human brain in a mouse with a person saying, 'Let me out,'" Prof. Rowley told the President's Council on Bioethics when it discussed chimeras in March.

To take no chances, scientists could kill the mice before birth to see if the brain is developing mouse-y structures such as "whisker barrels," which receive signals from the whiskers. If so, it's a mouse. If it is developing a large and complex visual cortex, it's too human. "If you saw something weird, you'd stop," says Prof. Greely. "If not, let the next ones be born, and examine them at different ages to be sure they're still fully mouse."

To reduce the chance that today's chimeras will be as monstrous as the Greeks' were, the U.S. patent office last year rejected an application to patent a human-chimp chimera, or "humanzee." But that, of course, just keeps someone from patenting one -- not making one.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:06 am

Definition of Infinity Expands for Scientists And Mathematicians
by Sharon Begley
July 29, 2005; Page B1

At the Hotel Infinity, managers never have a problem with overbooking. If you arrive with a reservation and find that the hotel's infinite number of rooms (named 1, 2, 3 and so on, forever) are all occupied, the manager simply moves the guest in Room 1 to Room 2, the guest in Room 2 to Room 3, and on and on until every guest has a room and you get Room 1. In an "infinite set" such as the rooms at the Hotel, whatever you thought was the highest-numbered member of that set isn't.

The next time you're in town, you have an infinite number of friends in tow, and you try the Hotel Infinity again. The manager is happy to accommodate a party of infinity even though his infinite rooms are, again, full. Knowing that your friends have an odd aversion to even numbers, he moves the guest in Room 1 to Room 2, the guest in Room 2 to Room 4, the guest in Room 3 to Room 6, etc. You and your friends get the odd-numbered rooms, of which there are, conveniently, an infinite number.

If thinking of infinities makes your head spin, you're in good company. Georg Cantor, the early-20th-century mathematician who did more than anyone to explore infinities, suffered a nervous breakdown and repeated bouts of depression. In the 1930s, some fed-up mathematicians even argued that infinities should be banned from mathematics. Today, however, infinities aren't just a central part of mathematics. More surprising, says cosmologist John Barrow of the University of Cambridge, England, in his charming new tome, "The Infinite Book," scientists who study the real world are having to take infinities seriously, too.

Not long ago, if the solution to an equation included an infinity, alarms went off. In particle physics, for instance, "the appearance of an infinite answer was always taken as a warning that you had made a wrong turn," Prof. Barrow says. So physicists performed a sleight-of-hand, subtracting the infinite part of the answer and leaving the finite part. The finite part produced by this "renormalization" was always in "spectacularly good agreement with experiments," he says, but "there was always a deep uneasiness" over erasing infinities so blithely. Might physicists, blinded by their abhorrence of infinities, have been erasing a deep truth of nature?

Suspecting just that, some scientists now see infinities "as an essential part of the physical description of the universe," says Prof. Barrow. For instance, Einstein's equations say the universe began in, and will end with, an infinity of density and temperature, something long regarded as a sign that his theory breaks down at the beginning and end of time. But in a 2004 paper, Prof. Barrow calculated that Einstein's equations allow a point of infinite pressure to arise throughout the expanding universe at some time in the future.

In addition to coming around to the view that infinities might be real, rather than signs of a problem with Einstein's and other theories, some cosmologists suspect that infinities at the beginning and end of time "have quite different structures," Prof. Barrow writes. Just as at the hotel, not all infinities are equal. And that is making the weird math of different-size infinities suddenly relevant in the physical world, too.

To mathematicians, "equal" means you can match the elements in one set to the elements in another, one to one, with nothing left over. For instance, there is an infinite number of integers: 1, 2, 3, 4 . . . . There is also an infinite number of squares: 1, 4, 9, 16 . . . . You can match every integer with a square (1 with 1, 2 with 4, and so on), so the two sets are equal, as long as you never stop matching. But wait: Every square also belongs to the set of integers. That suggests that the set of integers is larger, since it contains all the squares and then some. Surely there are more integers than squares, right?

Actually, no. Before his breakdown, Cantor asserted that if the elements in one infinite set match up one to one with the counting numbers, then those infinities are of equal size. The infinity of squares and the infinity of integers (and the infinity of even numbers) are therefore equal, even though the infinity of integers is denser.

Decimals, however, are different, mathematicians say. There is an infinite number of them, too, but this infinity is larger than the infinity of integers or squares. Even in the tiny space between zero and 1, there's an infinite number of decimals with no certainty as to what comes next. What comes after .1, for example? Is it .11 or .2?

Just as mathematicians found a distinction among infinities, so scientists trying to fathom the physical world may need to distinguish among infinities.

In his study of infinities, Prof. Barrow noticed that a universe like ours that seems infinite in size, extending without bound, presents curious ethical dilemmas. An infinite universe must have infinite amounts of good and evil, he writes. Nothing we do, or fail to do, can change that, for adding a bit of good to an infinite amount of good still leaves infinite good, and subtracting a bit of evil from an infinite amount of evil still leaves infinite evil. "What is the status of good and evil," he wonders, "when all possible outcomes actually arise somewhere" ... or sometime? Small wonder infinity drove Cantor mad.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:07 am

Early Cancer Detection Doesn't Always Give Patient an Advantage
by Sharon Begley
August 26, 2005; Page B1

(See Corrections & Amplifications item below.)

When Richard Bloch, co-founder with his brother of H&R Block, died of heart failure in 2004 at age 78, he was a medical success story. In 1978, he was diagnosed with terminal lung cancer. A decade later, he had colon cancer. He beat both, and went on to found a cancer hotline, a survivors group and other services. He was counted as someone whose cancer was detected early enough to save his life.

Should he have been?

Nothing has greater intuitive appeal than the claim that cancer screening leads to early detection, which leads to longer survival. Whether it is the PSA test for prostate cancer, mammograms, endoscopy for colon cancer or -- in the wake of Peter Jennings' untimely death -- X-ray screening for lung cancer, intuition screams that the earlier a cancer is caught, the better the odds that you'll be alive in five years. Like Mr. Bloch.

Cancer researchers are now augmenting that intuition with data, and the result isn't pretty. The impact of cancer screening "on reducing cancer mortality," says Elaine Jaffe of the National Cancer Institute, "still isn't proven for a number of cancers."

How can that be?

Part of the answer is that many tumors are so slow to progress -- indolent, scientists call them -- that they'll hang out in an organ for decades with no ill effects. "Early on, the idea of an indolent tumor was just a theoretical construct," says Barnett Kramer of the NCI. But indolence was found to characterize many neuroblastomas (a cancer of the nervous system), "and then it was found that tumors in the prostate, lung and now breast can also be indolent."

That doesn't mean cancer screening is useless. Without question, some of the tumors it finds would, if left untreated, have killed patients before their time, and some of the improvement in survival rates after breast cancer likely reflect earlier detection. But you can be misled into attributing the decades of life you enjoy after "beating" cancer to early detection and treatment rather than to the properties of the tumor itself.

Left to its own devices, the tumor might well have left you alone until you died of something else entirely. "Overdiagnosis of cancer as a result of screening is the rule rather than the exception," says Dr. Kramer.

This overdiagnosis isn't the false positives that tests such as mammograms can spit out. In that case, what is detected might look like cancer, but on further examination is not. False positives cause great anxiety and cost, as patients undergo more tests. But diagnosing an indolent cancer is arguably worse, as patients undergo treatments that often have debilitating, even dangerous, side effects.

Overdiagnosis has another effect: on perceptions of progress in the war on cancer. More-sensitive screening means tumors are detected at ever-earlier stages. Let's say that, as a result of such a screening, a patient begins treatment on Aug. 26, 2005. She does well, and celebrates her five-year survival on Aug. 26, 2010.

If she succumbs to a recurrence or a spread of her initial cancer in, say, 2015, she still counts as a five-year survivor. But if she had a slow-growing cancer she might have made it to 2015 anyway, without early diagnosis and treatment. She is scored as a victory for cancer warriors, but in fact they didn't buy her a single extra day of life. All she got was more years knowing she had a dreaded disease.

"The improvement in long-term mortality may be due to the higher proportion of small or slow-growing tumors being detected, which means you start counting earlier," says Dr. Jaffe. That's why longer survival, measured from the time of diagnosis, is a misleading measure of progress against cancer, and no substitute for reductions in mortality.

The more scientists study cancers, the more indolent ones they discover. Researchers in Japan, for instance, find that CT scans detect almost as many lung lesions in nonsmokers as in smokers. But since nonsmokers have a mortality rate from lung cancer less than 10% that of smokers, the vast majority of what CT scans picked up would never have progressed to anything life-threatening. And a Mayo Clinic study found that although X-rays detect lung cancers at earlier stages, and lead to more five-year survivors, early detection does not lower death rates.

For colon cancer, the fecal occult blood test "does decrease your risk of dying of this cancer," says Dr. Kramer. "But for colonoscopy and sigmoidoscopy, which appeal to our intuition [about early detection], the evidence is not great." They pick up polyps earlier, but not all polyps become cancers, "and we don't know what proportion would lead to death."

The Pap test for cervical cancer has saved lives, but many of the abnormal cells it finds wouldn't go on to become cancer. Most women with low-grade or even high-grade lesions would have been fine anyway. Similarly, the PSA test for prostate cancer picks up tumors that are biologically nonaggressive.

The discovery that many tumors are innocuous casts doubt on the value of new screening tests. "You may fool yourself into thinking a test is twice as sensitive," says Dr. Kramer, "but the only extra cancers it picks up are those that wouldn't have harmed the patient.

Corrections & Amplifications:

Barnett Kramer is associate director for Disease Prevention at the National Institutes of Health. This article incorrectly said Dr. Kramer is with the NIH's National Cancer Institute, which was his previous employer.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:11 am

Evolutionary Psych May Not Help Explain Our Behavior After All
by Sharon Begley
April 29, 2005; Page B1

Like almost everyone else, David J. Buller says he was "completely captivated" by evolutionary psychology, and no wonder. This field claims to explain human behaviors that seem so widespread we must be wired for them: women preferring high-status men, and men falling for nubile babes; stepfathers abusing stepchildren. Even the more troubling claims, such as one saying rape gave our male ancestors a reproductive edge, have caught on, as laypeople and scientists alike say, yeah, that makes sense. In a nutshell, evo psych argues that Pleistocene humans who engaged in certain behaviors left more descendants than did contemporaries who did not engage in those behaviors. As a result, we, their descendants, are wired for the behaviors.

But as Prof. Buller, a professor of philosophy at Northern Illinois University, dug deeper, he concluded that the claims of evo psych are "wrong in almost every detail" because the data underlying them are deeply flawed. His book "Adapting Minds," from MIT Press, is the most persuasive critique of evo psych I have encountered.

Take the stepfather claim. The evolutionary reasoning is this: A Stone Age man who focused his care and support on his biological children, rather than kids his mate had from an earlier liaison, would do better by evolution's scorecard (how many descendants he left) than a man who cared for his stepchildren. With this mindset, a stepfather is far more likely to abuse his stepchildren. One textbook asserts that kids living with a parent and a stepparent are some 40 times as likely to be abused as those living with biological parents.

But that's not what the data say, Prof. Buller finds. First, reports that a child living in a family with a stepfather was abused rarely say who the abuser was. Some children are abused by their biological mother, so blaming all stepchild abuse on the stepfather distorts reality. Also, a child's bruises or broken bones are more likely to be called abuse when a stepfather is in the home, and more likely to be called accidental when a biological father is, so data showing a higher incidence of abuse in homes with a stepfather are again biased. "There is no substantial difference between the rates of severe violence committed by genetic parents and by stepparents," Prof. Buller concludes.

On a lighter note, evolutionary psychology claims that men prefer fertile, nubile young women because men wired for this preference came out ahead in the contest for survival of the fittest. The key study here asked 10,047 people in 33 countries what age mate they would prefer. The men's answer: a 25-year-old.

But the men were, on average, in their late 20s. One of the most robust findings about human behavior is that people prefer a mate who matches them in education, class and religious background, ethnicity -- and age. The rule that "likes attract" is enough to explain why young men prefer young women. Besides, if you scrutinize the data, you find that 50-ish men prefer 40- something women, not 25-year-olds, undermining a core claim of evo psych.

The argument that Stone Age women preferred good providers, and that today's women are therefore wired to see a big bankroll as the ultimate aphrodisiac, is also shaky. Among some hunter-gatherers today, young mothers receive more food from their mothers than from their husbands. That makes even the theoretical basis for the claim -- that women who sought good providers had an evolutionary edge -- problematic.

The empirical basis is no better. On average, 25-year-old women say they prefer 28-year-old men, even though 50-year-old men have much more of the high status and resources that evo psych says they are wired to lust after. Again, likes attract more than "good providers" do.

In defense of the "good provider" theory, evolutionary psychologists cite studies of female college students asked to choose their ideal mate. Shown photos of young men -- one in the uniform of a fast-food worker, one looking like a middle manager, the third like a CEO -- they indeed choose one of the latter two. But just as people prefer to marry someone near them in age, they prefer to marry someone like them socioeconomically. The fact that female college students, usually middle- or upper-class, prefer medium- or high-status men could simply reflect their preference for a man who looks as though he comes from the same socioeconomic background, Prof. Buller points out. Also, earning capacity is a sign of other traits, such as education level and socioeconomic background. So although it seems that the women are being asked how important their mate's income is, they are likely using income as a sign of the other things they care about. Evolutionary psychology has a more fundamental problem than the shakiness of its data and the fact that the data can be interpreted in more than one way. Why, if child abuse by stepfathers is such a great evolutionary strategy, do many more stepdads love and care for their stepchildren than abuse them? And why, if rape is "such an advantageous reproductive strategy, [is it that] there are so many more men who do not rape than who do," asks primatologist Frans de Waal of Emory University, Atlanta.

After "Adapting Minds," it is impossible to ever again think that human behavior is the Stone Age artifact that evolutionary psychology claims.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:11 am

Fluoridation, Cancer: Did Researchers Ask The Right Questions?
by Sharon Begley
July 22, 2005; Page B1

When health officials decided to add fluoride to the water supply of Grand Rapids, Mich., in 1945, they plunged ahead despite the lack of a rigorous, large-scale study of the risks and benefits. And for most of the next 60 years, fluoridation research has gone pretty much like that. It has not been science's finest hour.

Questions about fluoridation have returned with renewed vigor because of allegations of scientific misconduct against a prominent researcher at the Harvard School of Dental Medicine. The Environmental Working Group, an advocacy organization in Washington, charged last month that Chester Douglass misrepresented an unpublished study about bone cancer and fluoridated tap water. In written testimony to the National Research Council last year, Dr. Douglass said he had found no evidence that fluoridation increased risk of osteosarcoma, a rare bone cancer. But a 2001 study he cited, and oversaw, found that boys who drink fluoridated water have a greater risk of developing the disease. (Dr. Douglass did not respond to requests for comment.)

More interesting than what Dr. Douglass said or didn't say, however, is the study he swept under the rug. It was conducted by one of his doctoral students, Elise Bassin. She started with the same raw data as her mentor -- 139 people with osteosarcoma and 280 healthy "controls" -- but saw a way to improve on it. Since most of the 400 people diagnosed in the U.S. each year with osteosarcoma are kids, and since any ill effect of fluoride would likely come when bones are growing most quickly, she focused on the 91 patients who were under 20.

Her result: Among boys drinking water with 30% to 99% of the fluoride levels recommended by the U.S. Centers for Disease Control and Prevention, the risk of osteosarcoma was estimated to be five times as great as among boys drinking nonfluoridated water. At 100% or more, the risk was an estimated seven times as high. The association was greatest for boys six to eight.

To be sure, one study proves nothing. Moreover, Dr. Bassin hasn't published her core findings (though in 2004 she and colleagues published a description of their methodologies). As Boston University epidemiologist Richard Clapp says, "Peer review picks up things that even doctoral students at Harvard might miss."

So I asked scientists to read the study. BU's Kenneth Rothman, founding editor of the journal Epidemiology, called it "of publishable quality." Zeroing in on young patients, he said, was good science: "If there were an adverse effect of fluoride, it's possible an effect of early exposure would be manifest in the first 20 years of life -- but not after." Looking at all ages, in other words, could conceal any link between fluoridation and cancer.

Besides focusing on kids, Dr. Bassin and her colleagues found out where each cancer patient ever lived, and what kind of water they drank when. Other studies have just noted what water a patient was drinking at the time of diagnosis. The problem with that is, you risk classifying someone as drinking nonfluoridated water who in fact drank fluoridated water when it mattered -- in childhood. The result is that the osteosarcoma rates of people drinking fluoridated water might look no different from those of people drinking nonfluoridated. "She did great shoe-leather epidemiology," says William Maas, head of oral health at the CDC and a supporter of fluoridation.

Previous studies have been contradictory. A 1991 animal study by the National Toxicology Program concluded that fluoride might raise the risk of osteosarcoma, but only in male rats, not female. Also in 1991, a scientist at the National Cancer Institute found an "unexplained increase" in osteosarcoma in men under 20 in fluoridated communities. Most human studies, though, provide "no credible evidence for an association between fluoride in drinking water and the risk of cancer," said a 1993 NRC report.

But when you look carefully at the negative studies, you have to wonder. Some investigated a link to all cancers; because osteosarcoma is rare, an increase would be unlikely to show up in that vast sea. Other studies were tiny, or included adults as old as 84, which would wash out effects that target kids. Most categorized osteosarcoma patients as drinking fluoridated or nonfluoridated water based on where they lived at diagnosis, not as kids. Concerned about such lapses, the NRC report called the studies "of limited sensitivity."

Even if fluoridation causes just a few hundred cases of osteosarcoma every year, does the public health benefit justify that risk? "When we started fluoridating water, we thought to get the benefits it would have to get incorporated into the enamel before the tooth erupted," which happens only if you swallow it, says the CDC's Dr. Maas. But that turns out not to be so. Topical fluoride, as in gels and toothpaste, works at least as well.

Most proponents now say fluoridation cuts the rate of tooth decay 18% to 25%. How much is that? Less than one tooth surface. "The absolute impact of 18% or even 25% is low," says Steven Levy of the University of Iowa, who supports fluoridation.

The next authoritative report on fluoridation will be the NRC's. One scientist close to the committee thinks it may be released this fall, months later than expected. "We thought this was going to be routine," he says. "It wasn't." With fluoridation, it seldom is.
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Re: Sharon Begley's "Science Journal"

Postby admin » Tue Oct 29, 2019 2:12 am

'Gene Pill' Offers Alternative to Shots
by Sharon Begley
June 21, 2005; Page D8

For people who have to inject themselves regularly with insulin to treat diabetes, erythropoietin to treat anemia or other protein drugs for various diseases, there may be hope for an end one day to being a human pin cushion.

University scientists and a biotechnology company are developing an alternative to injecting the drugs. Inspired by gene therapy, it is called a "gene pill" and contains the gene for a disease-treating protein rather than the protein itself.

Many helpful drugs are actually proteins. But proteins make poor pills, because they are broken down in the gut or poorly absorbed, with the result that they don't deliver the intended benefit. The only choice is to inject them.

However, the body itself makes proteins all the time in cells, following the instructions of genes in the cells. Now researchers are working on delivering genes for medicinal proteins to the body through a pill. A study in lab animals showed that, not only do the genes survive their digestive trip intact, they also get incorporated into cells of the gut -- which then produce the helpful proteins for the body to use.

Although the research is preliminary, with studies in humans still on the drawing boards, outside experts agree it shows promise. The gene pill "could provide an effective alternative method for delivering protein drugs currently administered only through injection," said David Klonoff, clinical professor at the University of California, San Francisco, and editor in chief of the journal Diabetes Technology & Therapeutics, which published the study in its June issue.

Today's protein drugs, such as growth hormone to treat dwarfism and blood factors to treat hemophilia, have several drawbacks. Patients often skip doses because the drugs have to be injected, rather than swallowed. Also, these proteins are either extracted from human cadavers or animal tissue, which is slow and inefficient, or -- more common -- produced through recombinant DNA, which is expensive. Moreover, injectable drugs are difficult and expensive to store, limiting their use in developing countries.

The gene pill is designed to avoid these problems. The cells lining the intestine are the only ones that take up the DNA for the therapeutic protein, which the cells release into the bloodstream.

The gene itself stays out of the bloodstream, with the result that it can't reach tissues where it might pose a risk. In some trials of traditional gene therapy, in which a virus ferries a therapeutic gene into a patient's cells, the virus has caused dangerous inflammation or disrupted cancer-suppressing genes, causing two deaths and leading the Food and Drug Administration to suspend some gene-therapy trials in the U.S.

Because cells of the intestine are sloughed off, excreted and replaced every few days, there is little danger that the inserted gene will go astray or deliver too high a dose of the therapeutic protein, says Stephen Rothman, professor emeritus at UCSF and a developer of the gene pill. The pill would be taken every two days or so.

In 1997, Dr. Rothman and three UC colleagues founded Genteric Inc., of Alameda, Calif., which is developing the gene pill commercially. UCSF holds four patents on the gene pill, for which it has granted an exclusive license to Genteric. Dr. Rothman has a financial stake in the closely held company.

In the new study, he and his colleagues gave lab rats and mice several different genes, through a tube. They found that the intestine cells do take up the gene and make the protein, and that they secrete the protein into the blood. When they used the gene for insulin, they showed that the insulin not only gets into the blood but also produces a therapeutic response, in this case lowering levels of blood sugar in rats with diabetes.

"Our approach seeks to avoid many of the problems with current approaches to gene therapy," Dr. Rothman says. In current approaches, once the gene is given to a patient it can't be undone even if it causes harm, as in the patients who developed cancer. In contrast, the effects of the gene pill last only a day or two, until the patient takes another pill.

Experts in gene therapy say they welcome variations on the standard approach. "For relatively small molecules like insulin, this should perhaps work," says Katherine High, a gene-therapy pioneer and professor of pediatrics at the Children's Hospital of Philadelphia.
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