News this Week

Science  23 Jan 2009:
Vol. 323, Issue 5913, pp. 446

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    Acquittals in CJD Trial Divide French Scientists

    1. Barbara Casassus*
    1. Barbara Casassus is a writer in Paris

    PARIS—Few criminal investigations drag on so long that one of the accused dies, and fewer draw upon the opinions of someone soon to win a Nobel Prize. But a court case here in which both have happened finally reached a verdict last week. Three French judges acquitted six doctors and pharmacists of charges of involuntary homicide and aggravated fraud after a stunningly prolonged investigation centering on the distribution of human growth hormone contaminated with deadly prions in the 1980s. The nearly 2-decade-old saga may not be over, however, as prosecutors immediately appealed.

    Final verdict?

    Fernand Dray leaves the courtroom after his acquittal, but appeals loom.


    Around the world, human growth hormone (HGH) used to be isolated from the pituitary glands of cadavers before the recombinant product came on the market. And much of the French trial centered on whether the accused used appropriate purification standards, an issue that resulted in several prominent scientists being called to the witness stand. The Pasteur Institute, which was involved in purifying the hormone, had already been fined by a civil court, but whether someone had committed a crime remained an open matter.

    The defendants' 14 January acquittals come more than 25 years after high-risk batches of HGH were administered to 968 French children and 18 years after the criminal investigation began. So far, 116 of the youngsters have died from Creutzfeldt-Jakob disease (CJD), a human illness similar to mad cow disease, and three more have recently shown symptoms.

    The French scientific community remains split on the case. “No one committed a real fault or negligence,” says one witness, neurologist Yves Agid, who was formerly in charge of monitoring CJD cases in France and is scientific director at the Institute of Brain and Spinal Cord Disorders here. “At the time, no one could imagine that patients would contract CJD from human growth hormone.”

    But virologist Luc Montagnier, also a witness in the trial and a winner of this year's Nobel Prize in physiology or medicine, says the ruling arouses concern. “I fear we may have not learned any lessons from this case and will face other and bigger public health scandals in the absence of adequate scientific and medical caution over the effects of new treatments on young people and future generations,” he says.

    In 1980, Montagnier recommended a series of precautions to be taken in the gathering and processing of pituitary glands but says he was ignored. He argues that the authorities should have halted the use of cadaver-derived HGH when the first case of CJD was linked to the product in the United States. “This disaster could have been partly avoided,” Montagnier told Science. Montagnier adds that he was “surprised and saddened” by the court's failure to attribute responsibility, and he was also critical of the fact that since the scandal broke, there has been little research into technology that could detect early signs of CJD.

    The criminal case dragged on as the number of deaths grew over the years. They added to the prosecution's case, but each required an investigation, says Jean-François Funcke, one of the victims' lawyers. The defendants tried to persuade higher courts to throw the case out, the statistics matching infected batches of HGH to the patients were complicated, and charges of corruption involved inquiries abroad, he adds.

    The public prosecutor had demanded 4-year suspended sentences for the two main defendants, pediatrician-endocrinologist Jean-Claude Job, who headed the now-defunct association in charge of collecting the hormone-containing pituitary glands from cadavers and who died after the trial ended, and Fernand Dray, who was in charge of purifying the material at the Pasteur Institute. Dray was also accused of corruption over the foreign HGH purchases, but the charges were dropped because the statute of limitations had expired.

    The criminal court case had proceeded despite a dismissive 2005 report from the French National Institute for Health and Medical Research that concluded: “It is not reasonable to expect the players involved in the production of growth hormone to have guessed there was a possible risk of CJD from a treatment used since the 1960s” without a single incidence of disease. That report was prepared by an international group including Stanley Prusiner, who won the Nobel Prize for his discovery of prions, and prion expert Paul Brown, formerly of the U.S. National Institute of Neurological Disorders and Stroke in Bethesda, Maryland.

    Two years earlier, however, a French civil appeal court had upheld an earlier ruling that the Pasteur Institute was responsible for the 2001 death of 30-year-old Pascale Fachin from CJD contracted from contaminated HGH. The institute was fined €322,000. The criminal court last week did award civil damages to families who hadn't already accepted a compensation offer from the state. And the public prosecutor said he would appeal the acquittals of Dray, Marc Mollet, former chief of the Central Hospital Pharmacy in Paris, who faced a 2-year suspended sentence, and Elisabeth Mugnier, a pediatrician who faced a 1-year suspended sentence. The appeal hearing should be held in 2010.


    Western U.S. Forests Suffer Death by Degrees

    1. Elizabeth Pennisi

    An insidious problem has taken hold in the forests of the American West, quietly thinning their ranks. Mortality rates in seemingly healthy conifer stands have doubled in the past several decades. Often, new trees aren't replacing dying ones, setting the stage for a potentially dramatic change in forest structure, says Phillip J. van Mantgem, a forest ecologist at the U.S. Geological Survey (USGS) in Arcata, California. Warmer temperatures and subsequent water shortfalls are the likely cause of the trees' increased death rate, he and his colleagues report on page 521.

    “This is a stunningly important paper,” says David Breshears, an ecologist at the University of Arizona, Tucson. For years, he and others have lamented massive diebacks that occur when fungal and insect pests ravage stands of trees. “What's harder to detect,” he explains, is any subtle but significant shift in the trees' background death rate. “They have done a very thorough job” of documenting it.

    In 2005, mortality rates weren't even on van Mantgem's radar. But while he was evaluating long-term data about forests in California's Sierra Nevada mountains for changes in species composition and other forest characteristics, he noticed an upward trend in tree deaths. At first he thought it was an artifact. Once he and his colleagues became convinced that the trend was real, they looked to see how widespread it might be.

    Forest ecologist Nathan Stephenson of USGS in Three Rivers, California, combed the literature and canvassed his colleagues for long-term sites in the western United States where forest experts had tracked mortality and other parameters at regular intervals. They considered only old-growth forests, as these well-established communities would be less likely to undergo changes that could confound the analysis. “They were extremely rigorous in site selection,” says Nate McDowell, an ecologist at Los Alamos National Laboratory in New Mexico.

    Slow demise.

    A comprehensive study shows that forests are losing trees faster now than they were 40 years ago.


    All told, they wound up with 76 sites in the Pacific Northwest, California, Idaho, Colorado, and Arizona. They found that in the Pacific Northwest, mortality rates jumped to 1.3% today from 0.3% in the 1970s; in California, that percentage went to 1.7% from 1% in 1983; mortality in the interior forests climbed to 0.6% from 0.2% in roughly the same period. “It's not just one local spot,” says van Mantgem. In contrast, they detected no trends in recruitment, the number of seedlings that survive to become mature trees. New growth is often failing to replace dying trees, he notes. Oliver Phillips, a tropical ecologist at the University of Leeds in the United Kingdom, says mortality rates have similarly increased in the tropics, but forest growth rates have increased there, more than compensating for the loss.

    At first glance, a shift of a percent or less may seem insignificant. “The change in forests is subtle so far,” says Stephenson. But just as a small percent difference in interest rates can compound the cost of a loan, a small difference in mortality rates can have a big effect over time. As the forest thins, ever smaller trees become dominant, affecting the land's carbon storage capacity and ability to support wildlife.

    Next, the researchers evaluated the possible causes of the increased mortality rate. No matter how they sliced and analyzed the tree data—by size, type, elevation, and location—they still detected the increase in mortality. Air pollution couldn't be blamed because the increase occurred in pristine as well as polluted areas.

    Ultimately, “the finger seems to be pointed to warming.” says Breshears. Temperatures in the United States have risen about 0.4°C per decade in the past 40 years. Snowpack of the regions examined diminished over the time period they studied and is melting earlier, effectively lengthening the summer drought. Warmer air also leads to more evaporative loss, exacerbating the effect.

    Michael Goulden, an ecosystem ecologist at the University of California, Irvine, thinks the data fall short of pinning the problem on global warming, as regional warming related to natural climatic variation could be to blame. But Julio Betancourt of USGS in Tucson, Arizona, disagrees. “Models suggest that most of this change was due to the buildup of greenhouse gases,” he says. Moreover, local Pacific Northwest and Southwest climates tend to fluctuate in opposite directions.

    However, Betancourt, who is not a co-author of the paper, stresses that forest researchers need to focus on seedlings, not mortality, in these threatened ecosystems. “If there is an affordable point of intervention, a way to adaptively manage for climate change,” he points out, “it may be in how we manage seedlings, not mature forests and adult trees.”


    Debate Continues Over Rainforest Fate--With a Climate Twist

    1. Erik Stokstad

    WASHINGTON, D.C.—Depending on whom you talk to, the future of tropical rainforest biodiversity is either “truly catastrophic” or not as bad as feared.

    The common wisdom tends toward the catastrophic, says tropical ecologist William Laurance of the Smithsonian Tropical Research Institute (STRI), who is based in Brazil. According to some estimates, he notes, tropical forests are vanishing at a rate of 13 million hectares per year. Two prominent conservation biologists have predicted that only 5% to 10% of tropical old-growth forests would survive in 2050, and they gloomily forecast extinctions of up to 75% of the species.

    But that view was challenged by two papers published in 2006, both by Joseph Wright of STRI and Helene Muller-Landau of the University of Minnesota, Twin Cities. They argued that a trend toward urbanism would mean fewer people living in forests and thus a slowing rate of deforestation. They predicted that more than a third of tropical forests overall would remain in 2030. Moreover, the regrowth of forests on abandoned farms would provide a refuge for tropical species. So in the end, 16% to 35% of species would be threatened with extinction, they estimated.

    The reaction was fierce. Many biologists felt Wright and Muller-Landau's conclusions would undermine attempts to preserve more rainforest. Laurance, who wrote a high-profile rebuttal in Trends in Ecology and Evolution, says one scientist commented: “Their argument is just plain dangerous. We should hit them hard—and with one voice.”

    As the public faces of the debate, Wright and Laurance decided to host two symposia, one at STRI in Panama last August and another here at the Smithsonian's National Museum of Natural History last week, to evaluate recent evidence on the threat to tropical biodiversity. Their talks, before an audience of 400 at the natural history museum, were illustrated with good-natured caricatures of each other as pro wrestlers, devils, and angels. The bout isn't over: Still unsettled are key points such as the amount of tropical forest that will remain in 2030, the biodiversity contained in degraded and recovering forests, and the effectiveness of nature reserves. But the speakers were united in their concerns that climate change may pose even greater risks of unprecedented disturbance to biodiversity than they realized 3 years ago.

    Speakers presented evidence that gave cause for both hope and concern. On the negative side, Gregory Asner of the Carnegie Institution of Washington's Department of Global Ecology in Stanford, California, noted that small-scale selective logging affects 28% of tropical forest worldwide. “The take-home message is that selective logging, compared to other forms, is massive globally,” Asner said. The figures will be reported in a special issue of Conservation Biology devoted to the symposium. Although selective logging itself is less destructive than clear-cutting, new roads lead to increased hunting, fires, and other disturbances, Asner noted. On the plus side, however, he reported that 1.7% of forests worldwide have been regrowing since the 1990s, and up to 2.4% in Central America.


    Tropical forests continue to be cut down and converted to agriculture, such as these soybean fields in Mato Grosso state in western Brazil.


    These regrowing forests can house a substantial amount of biodiversity (Science, 13 June 2008, p. 1436). Robin Chazdon of the University of Connecticut, Storrs, described her research on regrowing Central American forests, which are often planted with coffee under the canopy. In an unpublished study of northeast Costa Rica, her team found that 90% of old-growth tree species were present in secondary forests. “That's a pretty promising picture,” she said. Secondary forests can't substitute for old-growth reserves (the source of seeds, for example), she conceded, but a network of secondary forests could eventually reconstruct a landscape that would work for many species.

    That will be important, because the existing reserves are in trouble, said Laurance, who presented preliminary results of a survey of 60 tropical reserves worldwide. After interviewing several experts at each, he found that biodiversity appears to be declining while threats are on the rise. “Far more reserves are getting worse than [are] getting better,” he told the audience. “The overall trend is one of worsening conditions.” Wright says the parks aren't as remote as they used to be, but many tropical reserves are generally successful.

    Wright firmly agrees that the situation for tropical species could deteriorate as the region warms. That's already clear for highland species—some 165 frog species have gone extinct as warmer climates enable a deadly fungus to thrive. Wright noted that a temperature increase will likely be harmful to lowland tropical species as well. He showed a new analysis suggesting that species living near the equator will have to disperse much farther, up to 2000 kilometers or more, to find climates that match what they're used to. Some researchers have noted that species may be able to adapt (Science, 10 October 2008, p. 206). But not Nigel Stork of the University of Melbourne in Australia, who said that climate change “will tip the scales toward massive extinctions.”

    Whatever the extent of the threat, everyone agreed with Thomas Lovejoy of the Heinz Center here that preserving tropical forest would yield multiple benefits: storing more carbon, rather than releasing it from burning, and maintaining habitat. For that to happen, the wealthy countries will have to pitch in more than they are now, added Wright: “We're asking the poorest countries in the world to solve this biodiversity threat by themselves.”


    Confused Pelicans May Have Lingered Too Long Up North

    1. Greg Miller

    When pelicans start showing up in grocery store parking lots, backyards, and on roadways, something is seriously wrong. The large seabirds normally stay close to the shoreline and keep plenty of distance from humans. But in recent weeks, hundreds of disoriented and emaciated brown pelicans have turned up in strange places along the Pacific coast from the Baja peninsula to Washington state, prompting concern for this once-imperiled bird now on the verge of removal from the endangered species list.

    More than 460 sick and dead pelicans were reported between 10 December and 14 January, says Rebecca Dmytryk, a spokesperson for the International Bird Rescue Research Center (IBRRC), a nonprofit organization headquartered in Fairfield, California. Although young pelicans often succumb to harsh weather during their first winter, Dmytryk says many of the affected birds are adults.

    Brown pelicans have rebounded since the 1960s and '70s, when exposure to DDT and other environmental toxicants pushed some populations to the brink, says Daniel Anderson, an avian ecologist at the University of California, Davis. Both the federal government and the state of California are considering removing the birds from their respective endangered species lists as early as this spring. So far, the current outbreak doesn't seem dire enough to alter that decision, Anderson says, but federal and state agencies are keeping an eye on it.

    One early suspect has been domoic acid, a neurotoxin produced by algae that has caused previous outbreaks of neurological problems in birds and other marine animals. But the symptoms don't entirely fit, says Heather Nevill, a veterinarian working with IBRRC. Domoic acid can cause erratic behavior and disorientation, but it also typically causes seizures and a characteristic head-weaving motion—neither of which has been seen in the recent cases.

    The timing would also be unusual, because domoic acid toxicity is usually associated with algal blooms in springtime, says microbial ecologist David Caron of the University of Southern California in Los Angeles. Five of 14 water samples collected by Caron's lab in southern California in early January did test positive for the toxin but at very low concentrations. As Science went to press late last week, Caron's lab had tested blood and other samples from 18 afflicted pelicans. Four had detectable levels of domoic acid, but only two had levels comparable to those found previously in pelicans with classic symptoms of domoic acid toxicity, he says. These preliminary results suggest to Caron that domoic acid could be a contributing factor to the mysterious outbreak but not the primary cause.


    Earlier this month, a disoriented pelican ended up in a parking lot in Culver City, California.


    Another leading suspect is a sudden cold snap that caught thousands of pelicans that lingered longer than usual at the northern edge of their range. “Twenty years ago, you couldn't find pelicans north of California in November,” says Deborah Jaques, a wildlife biologist with Pacific Eco Logic, a consulting firm in Astoria, Oregon, near the Washington border. But the birds have been creeping northward recently, and a mild fall in 2008 may have enticed them to stay even longer before migrating south. Jaques says several thousand pelicans lingered near Astoria into mid-December, when the first big winter storm made its belated arrival. “This was unprecedented in terms of the numbers of pelicans that were here, how late they were here, and the severity of the storm,” Jaques says.

    Pelicans fare poorly in subfreezing weather, in part because their feathers aren't completely water-repellent and they need to dry off on land after diving for fish. Temperatures below freezing would have made it harder for the birds to dry off, increasing their risk of hypothermia. The cold could also explain other symptoms Nevill and colleagues have seen in rescued pelicans: lesions on the feet and splotches of discoloration on the neck pouches that look suspiciously like frostbite. She and others think it's possible that the blast of cold may have weakened the pelicans, perhaps impairing their ability to hunt as they made their way south and perhaps making them more susceptible to domoic acid or other hazards they encountered along the way.

    Still, the case is far from closed. Necropsies being carried out by the California Department of Fish and Game and the National Wildlife Health Center in Madison, Wisconsin, should provide valuable clues in the coming weeks. “We're keeping our minds open,” Nevill says. “We want to make sure we've covered all the bases.”


    Two Americans Win Japan Prize

    1. Yudhijit Bhattacharjee

    This year's Japan Prize goes to two U.S. academics, one a longtime advocate for sustainability and the other a radiologist who pioneered a standard tool for medical imaging.


    Dennis Meadows, a professor emeritus at the University of New Hampshire, Durham, fueled the burgeoning environmental movement with a 1972 paper, The Limits to Growth, that highlighted the impact of pollution and the depletion of natural resources on the planet. Meadows, 66, has expanded on that work to advocate for a sustainable society.

    David Kuhl, 79, a professor at the University of Michigan, Ann Arbor, developed a method in the 1950s to image organs and tissues by injecting radioactive isotopes into the body. It became the foundation for positron emission tomography, which has become a standard tool for evaluating tumors and tissue damage inside the brain.

    Each year, the Science and Technology Foundation of Japan chooses two fields. This year's categories were for “contributions toward a sustainable society in harmony with nature” and “technological integration of medical science and engineering.”


    European Pesticide Rules Promote Resistance, Researchers Warn

    1. Sara Coelho
    Fungal infection.

    Septoria kills tissue on wheat leaves, hindering the plant's growth.


    Despite intense opposition from farmer groups and scientists, the European Parliament voted last week to approve new regulations that could ultimately outlaw up to one-quarter of the pesticides on the European market. The legislation mandates a new licensing strategy inspired by the so-called precautionary principle, which calls for substances to be considered potentially harmful until proven safe for human health and the environment.

    Concerned that pesticides would be immediately banned, farmers had warned of devastated crop yields: “EU pesticides ban will ‘wipe out’ carrot crop,” declared one British newspaper. Although not endorsing such dire forecasts, some agricultural scientists opposed the regulations for other reasons: They say that any reduction in available pesticides will accelerate the development of plant pests' and pathogens' resistance to the remaining agents. They also question the scientific grounding of the hazard criterion.

    “The portfolio [of pesticides] that we have is already compromised in some cases by resistance,” says John Lucas of the U.K. agricultural institute Rothamsted Research in Harpenden, a vocal opponent of the new licensing rules. He and his colleagues fear that pesticide resistance could become as problematic as the multiresistant bacteria strains causing havoc in hospitals.

    Over the years, agricultural scientists have fought a cat-and-mouse game with insects and plant pathogens, developing new substances as the pests become more resistant to the older ones. Because novel pesticides can take a decade or more to develop, the scientists are concerned that they won't be able to keep up, as permits for existing ones expire and aren't renewed. Some worry especially about losing the azoles, a group of compounds used to manage plant diseases, including septoria leaf blotch, caused by the fungus Mycosphaerella graminicola. The most important wheat crop disease in northwestern Europe, septoria was originally controlled by several types of fungicides. But since the 1980s, M. graminicola has developed widespread resistance to two pesticide classes, leaving the azoles as the last line of defense.

    The rules approved by the European Parliament on 13 January were watered down compared with the first proposal, which would have outlawed about 85% of pesticides currently in use, according to an assessment by the U.K. Pesticide Safety Directorate (PSD). The approved regulations could still lead to the ban of 14% to 23% of pesticides, the PSD estimates.

    According to the European Parliament, the new legislation will be applied gradually, with “no sudden or large-scale withdrawal of products from the market,” and there should “be ample time for farmers to adapt by using alternatives or non-chemical methods, or for the pesticides industry to devise replacements.” The rules also include 5-year permit exceptions for substances deemed hazardous but needed to control serious dangers to plant health, including the development of resistance.

    The 5-year rule will “give us some breathing space,” says Lucas, who is nevertheless skeptical about its implementation. Time for research is also essential for developing an alternative to pesticide usage: disease-resistant crops. James Brown, who researches ways to make wheat varieties both septoria-resistant and high-yielding at the John Innes Centre in Norwich, U.K., says, “This is a gradual process.” He warns that “diseases don't stay the same.” For instance, breeding barley that resists ramularia, a disease that emerged in 1998, “will take at least 10 years.” In the meantime, he says, “fungicides are necessary to back up varieties' resistance” to disease.

    The pesticide regulations' dependence on the precautionary principle riles many. “This hazard-assessment argument is really where the big problem lies,” says Lucas. “As scientists, we find it very worrying that things go through that don't really stack up in terms of scientific evidence.”

    Alan Boobis, who studies toxic mechanisms of drugs and environmental chemicals at Imperial College London, agrees. “I feel that action is being taken on the basis of a policy position that doesn't reflect the state of the science,” Boobis says, arguing that pesticides are one of the most thoroughly evaluated types of products on the market.

    Last month, Lucas delivered to a member of the European Parliament a petition he and 71 other European scientists signed against the ruling. “We would be the first to say that we are not encouraging a solely chemical approach to the control of disease,” notes Lucas. But he wonders if even common toothpaste would be approved if everyday life were governed by the same precautionary principle now applied to pesticides.

    Emma Hockridge, a campaigner for the Soil Association, which supports the new rules, says she recognizes that narrowing down pesticide diversity can lead to increased resistance of certain pests. “But this highlights the fact that any agricultural system which is heavily reliant on pesticides for crop management is inherently unsustainable in the long term,” says Hockridge, adding that natural management methods promote healthier and more robust crops.

    For Mark Whalon, director of the Pesticides Alternatives Laboratory at Michigan State University in East Lansing, the issue has implications beyond European boundaries. In an age of globalization, if unwanted pest resistance arises in Europe, it will likely make its way to the United States, Whalon says. An organic farmer, Whalon understands the calls for a greener and safer environment. But as editor of the Arthropods Resistant to Pesticides Database, he also takes the resistance issue very seriously. He notes that eliminating pesticides primarily based on human health concerns could leave farmers with ones that are more dangerous to the ecosystems around crops. “Just because it is safer for humans doesn't make a pesticide safer for the environment,” he warns.


    Scientists Puzzle Over Ebola-Reston Virus in Pigs

    1. Dennis Normile

    An international team of human- and animal-health experts is in the Philippines this month, studying the first known outbreak of Ebola-Reston virus in pigs. The virus, which is related to the Ebola virus that causes the highly fatal Ebola hemorrhagic fever, had previously been found only in monkeys and a few humans who had been in contact with the sick animals. It has not caused any known incidents of serious illness or death in humans. But experts are concerned “because this is new, because it is unexpected, because the virus is slightly different [from previous isolates], and because it is in pigs,” which live in close proximity to humans, says Julie Hall, an infectious disease expert for the World Health Organization (WHO) and a member of the investigative team.

    “The finding is cause for further study but not further alarm,” says Stuart Nichol, a virologist at the U.S. Centers for Disease Control and Prevention in Atlanta. He says ongoing investigations may lead to a better understanding of Ebola viruses.

    Ebola viruses belong to the Filoviridae family and come in five strains: Zaïre, Sudan, Côte d'Ivoire, Bundibugyo, and Reston. The Zaïre, Sudan, and Bundibugyo strains have caused outbreaks of Ebola hemorrhagic fever among humans in Africa, killing up to 90% of those infected. Ebola- Reston was first isolated in 1989 from cynomolgus macaques imported from the Philippines for medical research in the United States. Unusual numbers of the monkeys started dying while in a quarantine facility in Reston, Virginia. About 1000 monkeys died or were euthanized. Subsequently, 21 animal handlers at the Philippine exporter and four employees of the quarantine facility were found to have antibodies to the virus, indicating that they had been infected, but just one reported flulike symptoms. Further outbreaks in monkeys in the Philippines were reported in 1992 and 1996.

    An increase in pig mortality on several farms in central Luzon, the Philippines' largest island, in 2007 and 2008 prompted an investigation by Philippine agencies. Last October, international reference laboratories studying samples supplied by the Philippines confirmed that the pigs were infected with a highly virulent strain of porcine reproductive and respiratory syndrome as well as the Ebola-Reston virus. Which virus is responsible for the increased mortality is not yet clear.

    The presence of Ebola-Reston virus on pig farms increases the odds of human exposure and infection. Previous human infections occurred in young men, who happened to be employees at both the Philippine exporter and the Reston lab animal supplier, Hall says. “We now have that virus in pigs that live in very close contact not just with fit, healthy, young men, but with pregnant women, children, and people with underlying medical conditions,” Hall says. Initial laboratory tests on animal handlers and slaughterhouse workers who might have been exposed were negative, the Philippine Department of Health has reported.


    A Philippines outbreak shows that pigs may host Ebola viruses.


    At the request of the Philippine government, WHO, the United Nations Food and Agriculture Organization, and the Paris-based World Organisation for Animal Health assembled an 18-member team that began its 10-day investigation on 6 January. So far, they have more questions than answers. It is not clear whether the virus alone causes clinical illness in pigs, how easily it spreads among the animals, or how it invaded the separate farms. The implications of the slight genetic differences in this strain are also not known.

    Answers to some of these questions should trickle in over the next several weeks. The international agencies and their local counterparts are planning further studies to determine, among other issues, whether the virus is in wider circulation in pigs and what its natural habitat might be. Meanwhile, the government is being cautious, quarantining the affected farms, even though there are no longer signs of illness among their pigs, and suspending all pork exports.

    Gary Kobinger, a virologist at Canada's National Microbiology Laboratory in Winnipeg, says there have long been rumors of unusual die-offs of pigs before Ebola outbreaks among humans in Africa. “The question is: Is it possible that pigs are hosts that amplify and transmit the virus to other animals and humans?” he asks.


    Educators Decry New Louisiana Policy

    1. Yudhijit Bhattacharjee

    Science teachers in Louisiana have been given permission to use supplementary material in the classroom in a move that many scientists and educators regard as a backdoor attempt to allow creationism and its variants into the classroom.

    Last year, as part of a wave of so-called academic freedom bills, Louisiana legislators passed a law covering the teaching of “controversial” scientific theories that include evolution, origins of life, and global warming (Science, 20 June 2008, p. 1572). State education officials initially drafted policy language explicitly prohibiting teachers from teaching intelligent design. But that language was dropped before last week's unanimous vote by the Louisiana State Board of Elementary and Secondary Education, along with a disclaimer saying that religion should not be taught under the guise of critical thinking.

    Supporters, including the Seattle, Washington-based Discovery Institute and the Louisiana Family Forum, say the policy will foster critical thinking in students. But opponents say that more is at stake. “We fully expect to see the Discovery Institute's book, Explore Evolution, popping up in school districts across the state,” says Barbara Forrest, a philosopher at Southeastern Louisiana University in Hammond. Patsye Peebles, a retired science teacher who helped the education department draft the earlier policy language, says there's no mistaking the meaning of the last-minute change in the board's policy: “The creationists got what they wanted.”


    Proposed Regulatory Czar Has Long and Perplexing Track Record

    1. Dan Charles*
    1. Dan Charles is a freelance writer in Washington, D.C.

    President-elect Barack Obama's choice to manage the regulatory policies of his new Administration has triggered a mixture of consternation and delight among conservatives and liberals. Cass Sunstein, who teaches law at Harvard University and the University of Chicago in Illinois, has written two dozen books and hundreds of articles on topics as diverse as animal rights and cost-benefit analysis. Despite that prodigious scholarly record, there's a surprising lack of consensus about his likely impact on the Office of Information and Regulatory Affairs (OIRA), a White House office that wields broad power over every federal regulatory agency and that sparked controversy under President George W. Bush.

    Sunstein has long kept a foot in opposing regulatory camps. He's a contributing editor for the liberal magazine The American Prospect and wrote an entire book praising the “second Bill of Rights” proposed by President Franklin D. Roosevelt that would have guaranteed every American a job, a home, and medical care. Yet Sunstein is also co-chair of the staunchly free-enterprise Center for Regulatory and Market Studies at the American Enterprise Institute in Washington, D.C. And he sounds like his two predecessors at OIRA—John Graham and Susan Dudley (Science, 21 March 2003, p. 1836; 18 May 2007, p. 973)—when he criticizes the public's tendency to get worked up over risks that appear, in the cold light of cost-benefit analysis, to be relatively small: abandoned toxic waste dumps, genetically engineered crops, or mad cow disease. “Unjustified fear is one of the most serious problems facing modern societies,” he wrote in 2002.

    Initial reaction to his pending nomination focused on his likely use of cost-benefit analysis in formulating regulations. An editorial in The Wall Street Journal called it “a promising sign,” whereas Rena Steinzor, an advocate of tighter regulation who teaches environmental law at the University of Maryland School of Law in Baltimore, sees Sunstein as “a strange, disconcerting choice.”

    Ruler of the rules.

    Cass Sunstein has been tabbed to oversee Obama's regulatory policies.


    Sunstein's detractors say he sometimes exhibits a naïve trust in scientists' ability to provide precise and objective answers. “Sunstein will take quantitative risk assessments from people who have a clear ax to grind and treat them as gospel,” says Thomas McGarity of the University of Texas, Austin, law school. Another critic, David Driesen of the Syracuse University College of Law in New York, says that efforts to regulate arsenic in drinking water demonstrate the shortcomings of cost-benefit analysis. The scientific committees have proposed a range of estimates for the number of people likely to get cancer because of exposure to the chemical. Plug those numbers into a cost-benefit calculation, says Driesen, and “the range turns out to be so large, it's not useful.”

    Some of Sunstein's colleagues say that his views on risk analysis are more subtle than either critics or supporters give him credit for. “I think both sides will be surprised,” says Richard Revesz, dean of the law school at New York University. The tools of cost-benefit analysis in the past “were captured by antiregulatory academic and interest groups” and misused, says Revesz. He predicts that Sunstein will deploy those same tools in support of novel regulatory initiatives.

    All sides expect Sunstein to play a formidable role within the new Administration, not least because he has the ear of the president. Sunstein, who has known Obama for 15 years and advised him during the campaign, recently married Samantha Power, a professor at Harvard's Kennedy School of Government. Part of the campaign's inner circle, Power resigned after calling Obama's then-rival, Senator Hillary Clinton (D-NY), a “monster” but later joined the transition team.


    U.S. Appellate Court Weighs 'Obvious' Patents

    1. Eli Kintisch

    These days, any competent graduate student can take a known protein and come up with the nucleotide sequence that encodes it. Does that mean the gene's code is obvious, in a legal sense, and therefore cannot be patented?

    A federal court is mulling that question after hearing oral arguments earlier this month in a case, in re Kubin, that involves a 2000 patent application that was rejected by the U.S. Patent and Trademark Office (PTO). Academic and industry scientists hope the answer, expected by early spring, is no. A yes answer would make it harder for researchers to patent discoveries, say biotech lawyers, stymieing innovation and investment.

    Scientists at Immunex, a Seattle, Washington-based company later acquired by Amgen, sought a patent on a gene that encodes a protein, called NAIL, found on certain white blood cells that protect the body from disease. In 2007, a PTO adjudicating board rejected the application, saying that obtaining the gene required little more than “routine skill” in biotechnology. Other scientists had previously isolated NAIL, PTO pointed out, and the steps subsequently needed to obtain the genetic sequence were “conventional methods” described in a laboratory manual. The Washington, D.C.-based U.S. Court of Appeals for the Federal Circuit took the case after Amgen appealed.

    By law, patents can be granted for discoveries found to be new, useful, and not obvious. But a string of recent court decisions have tossed out inventions in various fields after finding them obvious. Law professor Mark Lemley of Stanford University in Palo Alto, California, calls those decisions, which include a 2007 Supreme Court ruling in a case involving brake pedals, a “significant change” in a system that has historically been friendly to biotechnology patenting. After analyzing the questions raised by the three-judge panel at the 8 January hearing, law professor Chris Holman of the University of Missouri, Kansas City, says that the biotech community “might lose on the issue of obviousness.”

    High barrier.

    Scientists failed to win a patent on a gene encoding a protein found on certain immune system cells.


    Holman found special significance in an observation by one judge that the patent office made a “factual finding” that obtaining a gene sequence from a known protein was “routine.” “The court tends to defer to the patent office on such findings,” he says. Another judge called a 1997 patent in which researchers isolated the NAIL protein on a gel called a Western blot “of some consequence” because the scientists suggested subsequent steps that might yield the gene.

    The 2007 Supreme Court case, KSR v. Teleflex, made it easier to reject patent claims on the grounds that the discovery is obvious. The court ruled that an inventor could not claim a patent after following steps PTO found “obvious to try.” But attorney Hans Sauer of the Biotechnology Industry Organization (BIO) in Washington, D.C., finds the “obvious to try” standard misleading in this case and for gene-hunting in general. Scientists “have a reasonably good chance to get from the blot to the gene,” he says. “But that doesn't mean the sequence of the gene itself would be obvious to them.”

    Having PTO disqualify applications for DNA patents as it did in the Kubin case would “threaten the development of new drugs, diagnostic tests, and other biotechnology-derived products,” BIO argued in its brief. An adverse ruling could put into doubt the validity of tens of thousands of biotech patents, others say. Even so, attorney Kevin Noonan of the popular Patent Docs blog sees a silver lining. He thinks the court might rule favorably on a secondary issue in Kubin that would allow scientists to receive patents after filing slightly less detailed applications that make broader claims, covering more technology.


    Photon Sieve Lights a Smooth Path to Entangled Quantum Weirdness

    1. Adrian Cho

    Entanglement, a seemingly impossible link between distant particles, is key to physicists' plans for revolutionary quantum computers and uncrackable quantum communications systems. Creating entangled pairs of light particles, or photons, is a delicate business. Now, physicists from Japan and the United Kingdom have found a way to do it by simply passing ordinary photons through a novel optical filter.

    “This is pretty cool,” says Alan Migdall of the National Institute of Standards and Technology in Gaithersburg, Maryland. “I haven't seen an approach like this before.” Still, he and others say it's too soon to tell whether the new method, described on page 483, will outshine techniques that generate pairs of photons entangled from “birth.”

    Entanglement connects quantum particles no matter how far apart they are. Imagine two photons speeding away from each other. Each can be polarized horizontally, vertically, or—under the weird laws of quantum mechanics—both horizontally and vertically at the same time. Such a “diagonally” polarized photon can maintain its both-ways state until someone measures its polarization; then it will “collapse” into either the horizontal or vertical state.

    Physicists can entangle two diagonally polarized photons so that both must collapse into the same state. So if an experimenter measures one photon and it collapses into horizontal polarization, then the other photon will instantly do the same, no matter the distance. In quantum communications schemes, entangled photons can convey secret messages because an eavesdropper will spoil the entanglement and reveal his or her presence. They might someday ferry information within quantum computers able to tackle problems that stymie conventional machines.

    To generate entangled pairs, physicists have relied on “nonlinear” materials that cause photons to multiply or change frequencies. For example, in a technique called parametric down-conversion, a crystal converts one high-frequency photon into two identical lower-frequency photons. In the new approach, by contrast, Shigeki Takeuchi of Hokkaido University in Sapporo, Japan, and colleagues use conventional “linear” optical elements—mirrors and partially reflective “beam splitters”—to make an entanglement filter. The device “acts not just on one photon but on the combination of the polarizations of two photons,” Takeuchi says.

    The mazelike filter takes two unentangled, diagonally polarized photons as input. Because each is polarized both horizontally and vertically, the quantum state describing the pair has a part in which both are horizontal, a part in which both are vertical, and parts in which the first is horizontal and the second is vertical and vice versa. The filter lets through only the vertical-vertical and horizontal-horizontal parts—the ones involved in entanglement.

    Light maze.

    Two vertically or horizontally polarized photons can bounce through as only detectors 1 and 2 fire. A mixed pair won't make it through.


    As the photons bounce and split their way through the maze, they encounter two additional “ancilla” photons. A phenomenon called quantum interference affects the photons' tendency to stick together or separate as they pass through the beam splitters. Two of the four photons must trigger certain detectors in the maze to signal that the other two have been entangled, which happens 1/16 of the time.

    At the moment, the experiment produces only a few entangled pairs a minute. Nonlinear methods churn out millions per second, notes Paul Kwiat of the University of Illinois, Urbana-Champaign. But with the linear optics, he says, “you can ratchet up” to bigger circuits and more entangled photons much more easily. With improvement, the entanglement filter might light the way toward more ambitious devices.


    Friendship as a Health Factor

    1. Jennifer Couzin

    In a string of hot articles, two social scientists report that obesity, smoking, and other behaviors "spread" in networks. As the two friends expand their theory, doubters sharpen their questions.

    In a string of hot articles, two social scientists report that obesity, smoking, and other facets of health “spread” in networks. As the two friends expand their theory, doubters sharpen their questions


    BOSTON—On the first snowy day in December, Nicholas Christakis and James Fowler are ensconced in Christakis's rambling home in Concord, Massachusetts, plotting their next conquest. Christakis, at his desk, is nearly hidden behind two enormous Apple computer screens that beam dizzying network patterns of lines and circles representing community ties. Fowler sits cross-legged and barefoot on the couch, a laptop balanced on his knees. The pair are deep at work on their upcoming book, Connected: The Surprising Power of Social Networks and How They Shape Our Lives. On a mock cover taped to the wall, an orange goldfish leaps from one bowl of fish into another. The two men haven't left the house in 48 hours, and Christakis's watch stopped some time ago.

    Christakis, a social scientist and hospice physician—cheerful, given his line of work—and Fowler, an easygoing political scientist, hatched a plan about 6 years ago to study how social relations influence health. Their initial scheme required a massive number of volunteers and $25 million. It didn't take off, as funders balked at the price tag. But soon after, they stumbled upon something even better that would catapult their careers: a collection of loose-leaf papers locked in a record room in Framingham, Massachusetts, home to patient files of the nearly 15,000 participants in the Framingham Heart Study, begun in 1948.

    Christakis, who has joint appointments at Harvard Medical School and in Harvard University's sociology department, recalls as “delicious” the moment when a woman overseeing data collection for the Framingham study mentioned a critical detail. Christakis was wondering aloud how Framingham had kept its hold on so many people for so long. “‘Well, we have these tracking sheets,’” Christakis recalls her explaining, as she pulled a green sheaf from a cabinet nearby. For each participant, the forms requested home address, family physician—and at the bottom asked, Name a close friend who can find you in case we can't. Instantly, Christakis saw that a social network spanning 30 years was buried in that chart room. “Exactly the data that we were planning to spend millions of dollars to collect going forward had already been collected,” says Fowler.

    Dynamic duo.

    Nicholas Christakis (left) and James Fowler are dissecting social networks, gaining fans and foes in the process.


    Since then, Christakis and Fowler, from his perch at the University of California, San Diego, have pieced together and computerized the Framingham network, matching it with health over time. In a provocative set of papers, they've documented that every facet of health examined so far appears to “spread” from person to person. Obesity spreads. Happiness and unhappiness spread. Smoking habits spread. The work has landed the two everywhere from the front page of The New York Times (which wrote that obesity can spread “like a virus”) to the TV news parody The Colbert Report. With the fame have come skeptics, who suggest that Christakis and Fowler are drawing conclusions that go beyond their data.

    The work has also propelled the field of social networks and health into the spotlight—and, potentially, into medical care, for which findings could be used to modify behaviors that affect health. But the few efforts to apply network insights to patients have been mixed, in part because determining what causes network effects can be enormously difficult, and modifying them is even tougher (see sidebar, p. 456). Even if social interactions influence everything from heart disease to weight to mental health, intervening is far more daunting than proffering up a drug, says sociologist James Moody of Duke University in Durham, North Carolina, who has studied social networks among adolescents: “I can't write a prescription script for getting new friends.”

    Building blocks

    Christakis, 46, and Fowler, 8 years younger, came to social networks from different starting points. Christakis, while caring for the elderly in their last months, became fascinated by the widower's effect, a phenomenon first investigated in 1858 in which one spouse's death is often closely followed by the other's. Fowler, completing his dissertation at Harvard on voting patterns, was intrigued by how social interactions influence voter choice. One of Fowler's advisers introduced the unlikely pair. “It was thrilling to be taken so seriously,” says Fowler now. These days, the two have a video link set up between their homes in Massachusetts and California and chat at all hours of the day and night.

    Social networks have been studied for decades, but it's only recently that researchers have aggressively applied them to health-related questions. Early studies in this field focused on schools: whether, for example, a child in a school filled with smart children is more likely to excel than one in a school of underperformers. “Everyone thinks that, but it's darn hard to tell” if it's true, says Ethan Cohen-Cole, an economist at the Federal Reserve Bank of Boston, who studies social networks. Because so many factors feed into school performance, or weight, it's enormously difficult to separate out the effects of social interactions, says Cohen-Cole.

    One tack is to minimize confounding factors by searching for rare networks that form randomly. An economics professor at Dartmouth College took this approach, reporting in 2001 that freshmen who happened to be assigned roommates who were smarter than they were would perform better academically. Another method is to focus on individuals whose networks are unusually self-contained, such as teenagers, whose entire social scene tends to revolve around their high school.

    This was the strategy of the National Longitudinal Study of Adolescent Health, or Add Health. Begun in the 1990s, it surveyed 90,000 U.S. junior high and high schoolers. “We interviewed every kid at every school” and asked each to identify close male and female friends, says Peter Bearman, a sociologist at Columbia University who helped design Add Health. “You could characterize the social structure of every school” and identify where each student sat—at the center or around the less popular edges.


    Add Health, which is still following participants, has yielded hundreds of papers and many interesting observations about sexual health, drug use, isolation, and more. Bearman was struck by one in particular, that girls whose friends were not friends with each other—what he calls an “unbalanced network”—were much more likely to have suicidal thoughts than boys in the same situation. Bearman believes physicians ought to ask adolescents about the shape of their peer group—but like most people studying networks in academia, he has no idea whether the work has been applied.

    “For kids, their band, their friends, their work—it's all in the same physical space,” says Moody, who also participated in Add Health. “If you try to do this for adults, it's much more difficult.”


    Fowler speaks of his joint venture with Christakis in epic terms. “We have an opportunity to peer inside human society,” he says, “the same way Leeuwenhoek peered inside a cell” 3 centuries ago with the earliest microscopes.

    That opportunity stems directly from the Framingham network. One great advantage it offered over earlier social networks is that participants were monitored roughly every 3 years for a long period, and Christakis and Fowler could see changes in participants' weight as the years passed. This could include friends who gained weight at different times, making it easier to link one's weight gain to the other's.

    Christakis and Fowler chose to focus first on obesity, because weight is an objective measure that was recorded for many years. In the summer of 2007, they described in The New England Journal of Medicine (NEJM) their analysis of 12,000 people. About half were offspring of the original 1940s cohort, and the rest were parents and children who also participated in the study (and had named their own friends); the group was followed from 1971 to 2003. Christakis and Fowler found that an individual's chance of becoming obese increased 57% if someone named as a friend became obese in the same time interval. More surprisingly, the effect surfaced, but to a lesser degree, even when a direct friend wasn't involved: Obesity in a friend's friend (or any social contact) boosted the chance of obesity by 20%, and in a friend's friend's friend, by 10%. There was no effect beyond three degrees of separation—a pattern that the two have seen in subsequent studies of other health effects. The impact was also weaker among friends of the opposite sex, and there was no effect among neighbors.

    The two researchers followed up with a paper the next spring, in May 2008, on smoking. (While obesity increased in the United States during the Framingham years, smoking became less prevalent.) Again writing in NEJM, the two showed patterns similar to those for obesity—if a spouse quit smoking, an individual's chance of quitting increased 67%, and for a friend the figure was 36%. There were subtle distinctions, too. Those with more education were more influenced by others and had a greater influence themselves. The same “spread” pattern held, with friends of friends having an effect. Christakis and Fowler wrote in the British Medical Journal in December that happiness and unhappiness disperse in much the same fashion.


    They also have papers on alcoholism and depression in the works. Early this year, they expect to publish research on twins from the Add Health study, showing that the structure of one's social network, such as interconnections between friends, is partly inherited.

    The research has gotten a remarkable amount of attention. Top medical journals, which don't normally feature social-network research, have published all three of Christakis and Fowler's Framingham papers, in which they describe noninfectious disease with terms such as “person-to-person spread.” And the attention has transformed the authors' careers. Christakis and Fowler landed a 5-year, $11 million grant from the National Institute on Aging in April to study cardiovascular disease, cancer, obesity, violence, and substance use in networks. Their book, slated to appear in early 2010, is expected to be translated into more than a dozen languages. They've appeared 2 years running in Time Magazine's Year in Medicine. Even Fowler's high school in tiny Seminole, Oklahoma, in September inducted him into its hall of fame.


    Before the first Framingham paper appeared, Christakis's wife warned her husband that he'd be accused of wasting taxpayer money by looking at such a simple, obvious question, because of course friends influence one another. He and Fowler girded themselves for such an attack. Instead, people were incredulous, Christakis says. “We get, ‘Outrageous! How can you be claiming obesity spreads?’”

    That, say the doubters, is because identifying patterns among friends is not the same as proving that one friend causes another to do something. “They really have not shown adequately” that one person's obesity, or efforts to quit smoking, explain why another person gains weight or quits smoking, says Theodore Iwashyna, a critical-care specialist and social scientist at the University of Michigan, Ann Arbor, and one of Christakis's first graduate students. Iwashyna, who stresses that such challenges are faced in any social-network study, is enthusiastic about the “freaking cool” connections his mentor has demonstrated. But, he asks, what's behind them?

    Social scientists point to two other possible explanations for the clustering of friends with similar characteristics. The first, called “homophily,” is the tendency of individuals to associate with people similar to themselves. The second is shared environment. For example, a fast-food restaurant might pop up in a neighborhood, contributing to weight gain among people living nearby. In both cases, one person's weight gain is not the reason for another's.

    Christakis and Fowler acknowledge both pitfalls in their writings and emphasize that they've accounted for them. Indeed, says Fowler, “there's not a single argument a critic has made to us that we haven't thought of.” Homophily, they have determined, can't explain all the effects because of changes in the Framingham participants that show up over time. For example, two contacts might start off slender; over time, one gains weight, followed by the other. Shared environment has its own limitations. Some clustering, particularly for smoking and obesity, pops up across geographic distances (as when members of the Framingham study moved out of town) but doesn't appear among neighbors on the same block. Furthermore, Christakis and Fowler find that the strength of an effect depends on the strength of a friendship. The weight gain, for example, or boost in happiness, only occurs when one person named another as a friend; the effect did not run in the other direction if that person did not name the other. “It's really subtle,” says Christakis. And, Fowler chimes in, “completely ignored by all our critics.”

    Some of the most vocal detractors of Christakis and Fowler's work are economists who study social networks, in particular Cohen-Cole and his graduate school friend Jason Fletcher, a health economist at Yale University. Working with data from Add Health, the study of teens in high schools around the country, the two tried and failed to replicate the published obesity results. (Two other groups say they have replicated Christakis and Fowler's findings using Add Health, but one noted that evidence for obesity's contagion was “only suggestive at best.”) In December, Cohen-Cole and Fletcher published a damning paper in the British Medical Journal, applying Christakis and Fowler's methodology to three traits they did not consider transmissible: acne, height, and headaches. Again turning to the Add Health school networks, in which students were surveyed three times over the years, they reported that all three “spread,” although in some cases the effects were weak.

    Differences with critics run deep. Whereas Cohen-Cole and Fletcher express disbelief that acne or height could appear to spread, Christakis and Fowler think it's quite plausible, especially because Add Health relied on teenagers to report their own health habits. They say that a teen whose friends have acne, for example, may be more aware of his own and more likely to mention it—or the group might share a similar diet that leaves them prone to, or protected from, bad skin. Those with tall friends might be more likely to exaggerate their height. But they also might be more likely to exercise together, which has been shown to boost height slightly in growing adolescents, says Christakis.

    So what traits should not be altered by social networks? Well, says Christakis, eye color and birth order, and anything else that is wholly genetic. Everything else, they agree, is fair game.

    Network makeovers

    Those wishing to intervene in real-life social networks must first settle on what's behind the health changes documented. “If kids are getting fatter because their friends are getting fatter, what you need to do as a policy-maker is very different than if they're getting fatter because there's a McDonald's nearby,” says Cohen-Cole.

    Even though there's no unanimity yet, interest in applying network findings is keen. Christakis says that he and Fowler have been contacted by companies interested in smoking cessation, by the White House drug policy office, and by an eating-disorders clinic wondering whether to include girls with varying weights in group therapy sessions in hopes that those who are a bit heavier will help shift the lightest ones to a healthier weight.

    But few people have actually tried to modify networks to change health, and those who have have experienced mixed results. Psychologist Rena Wing of Brown University reported that when one spouse participated in a weight-loss program, the other lost nearly 5 pounds, compared with no weight loss for spouses of nonparticipants. Whether the effects spread beyond one person wasn't examined. Still, such ripple effects, which Fletcher is also studying in smoking cessation, have strong implications. “We know the costs of the pill,” he says, “but we're not counting all the benefits.”

    Physicians are still a long way from adopting any of this work. The implications “are often not translated into messages that resonate with people who are delivering medical care,” says Carol Ford, an adolescent medicine physician at the University of North Carolina, Chapel Hill. In efforts to prevent the spread of sexually transmitted diseases, she says, networks can reveal which partners are most important to focus on.

    “I do think people in medicine are paying attention,” says Duke's Moody, but “it's one thing to show something matters. It's another to show you can do something with it,” especially in a world where most doctors spend mere minutes with each patient.

    But he and some others see networks adding an entirely new dimension to considerations of health. “For so long, science, medicine, and lots of other fields have succeeded by cutting things into small pieces,” he says. “The way science works is isolating smaller and smaller microunits. What the network model does is say, that can only take you so far. There's an effect that occurs at the population level,” even if capturing it, understanding it, and making use of it still has a long way to go.


    With Isolation Comes Ill Health

    1. Jennifer Couzin

    Social isolation, the flip side of social networks, is believed to have dire consequences, increasing the risk of certain diseases and earlier death. But attempts to transform this knowledge into action have had discouraging results.

    BOSTON—Epidemiologist Lisa Berkman has been fascinated for years by social isolation, the flip side of social networks. It's a state she and others believe has dire consequences, increasing the risk of certain diseases and earlier death. Attempts to transform this knowledge into action have been discouraging, however: The first ambitious efforts to blunt the harmful effects of solitude have not worked, but Berkman is still seeking ways to mitigate them. She's just beginning a 2-year, $20 million intervention study funded by the U.S. National Institutes of Health (NIH).

    Berkman, of the Harvard School of Public Health located here, says she was drawn to study isolation back in the 1980s, when she traced social patterns among 7000 people in Alameda County, California. She found that those who scored low on a scale measuring social integration were 2.5 to 3 times more likely to die over the next 7 years than those who scored high. That in itself wasn't a shock, because it's reasonable to assume that isolation is associated with risky behaviors. But Berkman ruled out specific risks, such as drinking alcohol, one by one—and the risk of death stayed high, about 2 to 2.5 times the norm. “What social isolation was doing was making you more susceptible or less resilient to any disease you might get,” she says. The work has been replicated in more than a dozen studies around the world.

    But unlike her social science colleagues Nicholas Christakis of Harvard Medical School and James Fowler of the University of California, San Diego, who beam confidence that social effects are causing changes in health (see main text), Berkman is not certain that a cause-and-effect linkage has been proved, at least where social isolation is concerned. She concedes that isolation may be a result rather than a cause of disease.

    Adding to her mixed feelings is that she's had “some really spectacular failures.” In 1995, Berkman chaired a nearly $40 million NIH study designed to bolster social networks to prevent a second heart attack in those who'd had one before. The intervention did improve social support and reduced depression but had no effect on heart disease. A second network intervention to help stroke victims had equally dismal results. It's a “totally legitimate interpretation” that the studies failed because social isolation doesn't cause cardiovascular disease after all, says Berkman, but that is not what she believes. Her theory is that the “exposure”—isolation—had already done too much harm, so that late intervention accomplished little physiologically. She also says it's difficult to change a social network enough to make a difference.


    Lisa Berkman aims to blunt the negative health effects of social isolation.


    In the new NIH-funded study, Berkman and others are turning to workplace interventions, focusing on 3000 nursing home employees and information technologists. Half of the 60 sites will implement family-friendly policies and half will not. The idea is to see if giving employees more time to spend at home and with friends will bolster their social networks. Berkman acknowledges that the outcome seems obvious—presumably having an amiable boss and a flexible work environment is good for one's health.

    But “the truth is we don't know, and the truth is we've been lousy at producing change,” Berkman says. “In fact, I'm incredibly wary that we're going to show health effects.” Many more scientists believe “that we should be thinking of molecular biology to solve these problems than to think about how work is organized, or how our social world is organized.” She and her colleagues will be following workers, their spouses, and their children, examining everything from heart disease and cancer to biomarkers of health such as levels of cholesterol, blood pressure, and C-reactive protein. If changes in the workplace can modify these physiological effects, says Berkman, “that's huge. That's totally huge.”


    Galloping Glaciers of Greenland Have Reined Themselves In

    1. Richard A. Kerr

    Ice loss in Greenland has had some climatologists speculating that global warming might have brought on a scary new regime of wildly heightened ice loss and an ever-faster rise in sea level. But glaciologists reported at the American Geophysical Union meeting that Greenland ice's Armageddon has come to an end.


    Glacial two-step.

    Helheim Glacier's flow to the sea sped up in 2005, as evidenced by the 5-kilometer retreat of its leading edge (left panel to middle panel), but by 2006 it had slowed back down.


    Things were looking bad around southeast Greenland a few years ago. There, the streams of ice flowing from the great ice sheet into the sea had begun speeding up in the late 1990s. Then, two of the biggest Greenland outlet glaciers really took off, and losses from the ice to the sea eventually doubled. Some climatologists speculated that global warming might have pushed Greenland past a tipping point into a scary new regime of wildly heightened ice loss and an ever-faster rise in sea level.

    So much for Greenland ice's Armageddon. “It has come to an end,” glaciologist Tavi Murray of Swansea University in the United Kingdom said during a session at the meeting. “There seems to have been a synchronous switch-off” of the speed-up, she said. Nearly everywhere around southeast Greenland, outlet glacier flows have returned to the levels of 2000. An increasingly warmer climate will no doubt eat away at the Greenland ice sheet for centuries, glaciologists say, but no one should be extrapolating the ice's recent wild behavior into the future.

    News of a broad slowdown comes from a wide-ranging survey of glacier conditions across southeastern Greenland. Researchers reported in 2007 that two of the area's major outlet glaciers—Helheim and Kangerdlugssuaq—had slowed by the previous summer. But at the meeting, Murray and 10 of her Swansea colleagues reported results from their 2007 and 2008 surveys of the shape and appearance of the 14 largest outlet glaciers of southeast Greenland. When glaciers speed up, they thin, and their lower, leading edge that floats on the sea retreats. So the Swansea researchers flew laser altimeters over the glaciers to estimate their changing volumes and, indirectly, their changing velocities. They also studied satellite images and aerial photographs in order to track the movements of natural markings on the ice.

    Taken together, the data show “there's a pattern of speeding up to maximum velocity and then slowing down since 2005,” Murray said. “It's amazing; they sped up and slowed down together. They're not in runaway acceleration. Something happened that has switched off” the acceleration event of 2003 to 2005.

    A short-lived speed-up makes sense if something had given the glaciers some sort of jolt at their lower ends, says glaciologist Richard Alley of Pennsylvania State University in State College. Two possibilities for a disturbance are the warmer air over southern Greenland in recent years and warmer coastal seawater. Either could have eaten away, weakened, and begun to break up the floating seaward ends of outlet glaciers, he says. That would have weakened the glacier's grip on its bounding rock and sent a wave of glacier thinning and acceleration inland. But given time, a glacier would regain its footing—like a fighter rolling with a punch—thicken again, and slow down to its original speed, he says.

    That's just what glacial modeler Faezeh Nick of Durham University in the United Kingdom and her colleagues found when they modeled the flow of Helheim Glacier, as they report this week in Nature Geoscience. In their model, Helheim, and presumably similar outlet glaciers, is extremely sensitive to disturbances at its margin but can adjust rapidly even as the disturbance continues. “Our results imply that the recent rates of mass loss in Greenland's outlet glaciers are transient,” the group writes, “and should not be extrapolated into the future.”

    Not that Greenland's ice is safe, says Alley. “If you turn the thermostat too high, it will melt,” he notes. And the glaciers of the West Antarctic Ice Sheet (WAIS), some of which have already picked up speed, don't have the shallow rocky underpinnings that allow Greenland's glaciers to regain their equilibrium. “With nothing to hold on to,” he says, “we think [WAIS] will run away.”


    Tang Hints of a Watery Interior for Enceladus

    1. Richard A. Kerr

    At the American Geophysical Union meeting, planetary scientists reported that Saturn's E ring, formed from icy particles spewed out of the planet's moon Enceladus, contains the chemicals they would see if a salty ocean lurks beneath the moon's surface.


    The search for habitable environs off-Earth is all about liquid water, and Saturn's icy moon Enceladus is looking more and more as though it has the precious substance. The latest evidence comes from Saturn's faint E ring, formed from icy particles spewed out of the moon. At the meeting, planetary scientists reported that the ring particles include the chemicals they would see if a salty ocean lurks beneath the moon's surface.

    The key to “tasting” the salty ring grains was the Cosmic Dust Analyzer (CDA) on board the Cassini spacecraft orbiting Saturn. Its mass spectrometer identifies the ions created when hypervelocity particles hit the CDA and explode. At the meeting, planetary scientist Frank Postberg of the Max Planck Institute for Nuclear Physics in Heidelberg, Germany—where the CDA was developed and is operated—and seven colleagues reported the clear detection of sodium in the E ring's ice particles. Six percent of the particles are rich in sodium and contain salts such as sodium chloride and sodium bicarbonate, along with smaller amounts of potassium. Cassini has traced the ice grains to a towering plume rising from Enceladus's south pole.

    The CDA results are what would be expected if water from a deep ocean makes it to the surface and blasts from the fissures of the south pole, the group says. The salts—resembling terrestrial sea salt—are just the ones that liquid water would extract from rock thought to lie deep within the moon. In a poster presentation, CDA team members headed by dynamicist Jürgen Schmidt of the University of Potsdam in Germany argued that the Enceladus plumes must blast out tiny water droplets, not just water vapor. Only liquid could carry off the salts, they say.

    Taken together, the salty ice grains appear to counter earlier arguments that Enceladus's plumes arise from frozen, not liquid, water. Geophysicist Susan Kieffer of the University of Illinois, Urbana-Champaign, had pointed out that liquid water could not possibly hold as much gas as Cassini has found in the plumes, but gasentrapping water ice called clathrate could. Planetary scientist Andrew Ingersoll of the California Institute of Technology in Pasadena and the Cassini camera team agrees. “She's right,” he says, but “it seems to me, Postberg holds the key to having it both ways.” The low-sodium particles could have condensed from vapor coming off clathrates, he says, and the high-sodium grains could come from liquid water. Time will tell whether such a compromise will fly.


    The Many Dangers of Greenhouse Acid

    1. Richard A. Kerr

    Geochemists reported at the American Geophysical Union meeting that most sorts of calcifying organisms--creatures that grow calcium carbonate skeletons or shells--suffered when pH sank much below the 8.2 of surface ocean seawater, not just the iconic coral reefs.


    If global warming has its hungry polar bears, ocean acidification by greenhouse carbon dioxide has its declining coral reefs. But poster children can be misleading. “It is not good to think about coral reefs as epitomizing all issues of acidification,” marine biologist Donald Potts of the University of California, Santa Cruz, warned during a session at the meeting. Other speakers showed that marine life is in peril almost across the board.


    Extreme carbon dioxide levels led to dissolution (bottom) of normal sea urchin spines (top). Scale bars = 1 cm.


    Geochemist Justin Ries of the University of North Carolina, Chapel Hill, and colleagues reported that most sorts of calcifying organisms—creatures that grow calcium carbonate skeletons or shells—suffered when pH sank much below the 8.2 of surface ocean seawater. They grew 18 species from eight major calcifying groups in the laboratory for 6 months under a range of carbon dioxide concentrations, including levels expected in the next decade, by the end of the century, and beyond.

    Although some species actually increased calcification with modest increases in carbon dioxide, most species—including periwinkles, oysters, urchins, and calcareous green algae—eventually formed less calcium carbonate under greater acidification. There were exceptions. One species of mussel showed no ill effects, and surprisingly, the crustaceans—an edible shrimp, an American lobster, and a blue crab—actually grew thicker shells under even the most severe acidification. But looking at the types of carbonate formed, the group found that only a tube-building worm could protect itself by producing a greater proportion of a more acid-resistant carbonate mineral.

    For “higher” marine animals such as squids and fishes, the problems center on respiration—and both carbon dioxide and oxygen come into play. Marine geochemists Peter Brewer and Edward Peltzer of the Monterey Bay Aquarium Research Institute in Moss Landing, California, pointed out that the higher the ratio of carbon dioxide to oxygen dissolved in seawater, the harder it is for the animals to gather oxygen. Seawater carbon dioxide is going up with rising atmospheric levels, they noted, and dissolved oxygen is decreasing in deeper waters as the warming of surface waters slows ocean circulation.

    To demonstrate why that's a risky combination, Brewer showed a video of a remotely operated vehicle they used to trap a small squid at a depth of 700 meters and immerse it in a higher-carbon dioxide, lower-oxygen brew. The squid dropped motionless to the bottom of the test vessel. “We can expect multiple impacts as we go forward into this strange CO2 world,” Brewer observed.


    Snapshots From the Meeting

    1. Richard A. Kerr

    Snapshots from the American Geophysical Union meeting include mostly upbeat news in the search for martian water and an ice core suggesting that changes in the far south of the Southern Ocean helped drive greenhouse warming at the end of the last ice age, 18,000 years ago.


    Following martian water. The news from Mars scientists in search of water was mostly upbeat. Radar probing from orbit shows that the Frozen Sea—supposedly dirt-covered ice—“is not ice,” but lava, said planetary geophysicist Roger Phillips of Southwest Research Institute in Boulder, Colorado. That's the bad news. More encouragingly, spectroscopist Bethany Ehlmann of Brown University reported spectroscopic signs that something had long ago altered minerals in and around impact craters. That alteration looks typical of hot groundwater. And Alfred McEwen of the University of Arizona, Tucson, showed orbital images of what may be the oldest rock now on the surface. Large impacts probably lifted the so-called megabreccia from deep in the crust. It consists of great boulders embedded in a fine matrix containing water-altered minerals. McEwen's bottom line: “These may be the best places in the solar system to study clues to the origin(s) of life.”


    Jumbled, deep-crustal rock exposed by impacts was once wet and possibly habitable.


    Some thermometer. Paleoceanographers analyze microscopic plankton remains from a few square centimeters of sea floor to gauge past ocean temperature at that one spot. But paleoclimatologist Melissa Headley of Scripps Institution of Oceanography in San Diego, California, and her colleagues wanted to read the average temperature at one geologic moment of the whole ocean—top to bottom globally—so they took a 1-kilogram chunk of old glacial ice and measured its krypton and xenon gas content. Because the total amount of the noble gases in the atmosphere and ocean remains constant over time and their solubility in water depends on temperature, the changing amount down an ice core provides a whole-ocean temperature history. Their record suggests that changes in the far south of the Southern Ocean helped drive greenhouse warming at the end of the last ice age, 18,000 years ago.