Science Tuesday - Climate Change, Genetics, Ozone Hole, and "Tropical Diseases."
FINDINGS: Corporate Backing for Research? Get Over It
By JOHN TIERNEY, The New York Times, January 26, 2010
I find myself in the unfamiliar position of defending Al Gore and his fellow Nobel laureate, Rajendra K. Pachauri.
When they won the prize in 2007, they were hailed for their selfless efforts to protect the planet from the ravages of greedy fossil fuel industries. Since then, though, their selflessness has been questioned. Journalists started by looking at the money going to companies and nonprofit groups associated with Mr. Gore, and now they have turned their attention to Dr. Pauchauri, the chairman of the United Nations Intergovernmental Panel on Climate Change.
The I.P.C.C., which is supposed to be the gold standard of peer-reviewed climate science, in 2007 warned of a “very high” likelihood that global warming would cause the Himalayan glaciers to disappear by 2035. When the Indian government subsequently published a paper concluding there was no solid evidence of Himalayan glaciers shrinking because of global warming, Dr. Pachauri initially dismissed it as “voodoo science” beneath the I.P.C.C.’s standards.
But then it came out that the I.P.C.C.’s projection was based not on the latest peer-reviewed evidence, but on speculative comments made a decade ago in a magazine interview by Syed Hasnain, a glaciologist who now works in an Indian research group led by Dr. Pachauri.
Last week, the I.P.C.C apologized for the mistake, which was embarrassing enough for Dr. Pachauri. But he also had to contend with accusations of conflict of interest. The Telegraph of London reported that he had a “worldwide portfolio of business interests,” which included relationships with carbon-trading companies and his research group, the Energy and Resources Institute.
Dr. Pachauri responded with a defense of his ethics, saying that he had not profited personally and that he had directed all revenues to his nonprofit institute. He denounced his critics’ tactics: “You can’t attack the science, so attack the chair of the I.P.C.C.”
I can’t defend that entire sentiment, because you obviously can attack some of the science in the I.P.C.C. report, not to mention other dire warnings in Dr. Pachauri’s speeches.
But I do agree with his basic insight: Conflict-of-interest accusations have become the simplest strategy for avoiding a substantive debate. The growing obsession with following the money too often leads to nothing but cheap ad hominem attacks.
Sure, money matters to everyone; the more fears that Dr. Pachauri and Mr. Gore stoke about climate change, the more money is liable to flow to them and the companies and institutions they are affiliated with. Given all the accusations they have made about the financial motives of climate change “deniers,” there is a certain justice in having their own finances investigated.
But I don’t doubt that Mr. Gore and Dr. Pachauri would be preaching against fossil fuels even if there were no money in it for them, just as I don’t doubt that skeptics would be opposing them for no pay. Why are journalists and ethics boards so quick to assume that money, particularly corporate money, is the first factor to look at when evaluating someone’s work?
One reason is laziness. It is simpler to note a corporate connection than to analyze all the other factors that can bias researchers’ work: their background and ideology, their yearnings for publicity and prestige and power, the politics of their profession, the agendas of the public agencies and foundations and grant committees that finance so much scientific work.
Another reason is a snobbery akin to the old British aristocracy’s disdain for people “in trade.” Many scientists, journal editors and journalists see themselves as a sort of priestly class untainted by commerce, even when they work at institutions that regularly collect money from corporations in the form of research grants and advertising.
We trust our judgments to be uncorrupted by lucre - and we would be appalled if, say, a national commission to study the publishing industry were composed only of people who had never made any money in the business. (How dare those amateurs tell us how to run our profession!) But we insist that others avoid even “the appearance of impropriety.”
This snobbery was codified by The Journal of the American Medical Association in 2005, when it essentially required chaperones for any researchers receiving corporate money. Citing “concerns about misleading reporting of industry-sponsored research,” the journal refused to publish such work unless there was at least one author with no ties to the industry who would formally vouch for the data.
That policy was called “manifestly unfair” by BMJ (formerly The British Medical Journal), which criticized JAMA for creating a “hierarchy of purity among authors.” The hierarchy looked especially dubious after a team of academic researchers (not financed by industry) analyzed dozens of large-scale clinical trials in previous decades and reported that industry-sponsored ones met significantly higher standards than the nonindustry ones.
The new fetish for disclosing “conflicts” has led some of the best medical researchers to shun drug company money altogether - not because they think it leads to bad research, but because they are tired of that fact being highlighted every time they are identified in a news story, as if that were the most important thing to know about their work.
There are, of course, notorious cases of corporate money buying predetermined conclusions, like the reports once put out by the Tobacco Institute to rebut concerns about smoking and cancer. But there has also been dubious work promoted by government agencies and foundations eager to generate publicity and advance their own agendas.
It’s naïve to caricature scientific disputes as battles between “industry” and the “public interest,” as if bureaucrats and activists didn’t have their own selfish interests (and wealthy, powerful allies like trial lawyers). Too often, corporate conflict-of-interest accusations have been used as smear tactics to silence scientists who ended up being correct. (Go to nytimes.com/tierneylab for examples.)
Instead of stigmatizing certain kinds of research grants, perhaps we should consider the bigger picture. If scientists listed all their public and private donors on their Web pages, journalists could simply link to that page and let readers decide which ones are potentially corrupting. Instead of following rigid rules to report “conflicts,” journalists could use their judgment and report only the ones that seem relevant.
Sometimes you can’t understand a debate or a controversy without knowing who is paying whom. But in general, I’m with Dr. Pachauri: follow the science, not the money.
A New Way to Look for Diseases’ Genetic Roots
By NICHOLAS WADE, January 26, 2010
The hunt for the genetic roots of common diseases has hit a blank wall.
The genetic variants found so far account in most cases for a small fraction of the genetic risk of the major killers. So where is the missing heritability and why has it not showed up?
A Duke geneticist now suggests that the standard method of gene hunting had a theoretical flaw and should proceed on a different basis. The purpose of the $3 billion project to decode the human genome, completed in 2003, was to discover the genetic roots of common diseases like diabetes, cancer and Alzheimer’s. The diseases are called complex, meaning that several mutated genes are probably implicated in each.
A principal theory has long been that these variant genes have become common in the population because the diseases strike late in life, after a person has had children. Bad genes would not be eliminated by natural selection at that age, as they would if the diseases struck before the child-bearing years.
So to find disease genes, the thinking went, do not decode the entire genome of every patient - just look at the few sites where genetic variations are common, defined as being present in at least 1 percent of the population.
These sites of common variation are called SNPs (pronounced “snips”), and biotech companies have developed ingenious devices to recognize up to 500,000 SNPs at a time. The SNP chips made possible genomewide association studies in which the genomes of many patients are compared with those of healthy people to see which SNPs are correlated with the disease.
The SNP chips worked well, the studies were well designed, though enormously expensive, and some 2,000 disease-associated SNPs have been identified by university consortiums in the United States and Europe.
But this mountainous labor produced something of a mouse.
In each disease, with few exceptions, the SNPs accounted for small percentage of the genetic risk. A second puzzling feature was that many of the disease-linked SNPs did not occur in the DNA that codes for genes, but rather in the so-called junk regions of the genome. Biologists speculated that these SNPs must play an as-yet-undefined role in deranging the regulation of nearby genes.
In an article this week in the journal PLoS Biology, the Duke geneticist David B. Goldsteinph.d and his colleagues propose an explanation for both findings.
They argue that the common disease-common variant idea is largely incorrect: natural selection has in fact done far better than expected in eliminating disease-causing variants from the population. It follows that the major burden of disease is carried by a multitude of rare variants - ones too rare to have been programmed into the SNP chips.
So why have the genomewide association studies linked some SNPs to disease, if in fact it is the rare variants that cause it?
In Dr. Goldstein’s view, the SNPs could simply be acting as surrogate markers for the rare variants. Until now, geneticists have assumed a disease-linked SNP was either itself a cause or was a marker for a disease variant nearby. But Dr. Goldstein’s team calculated that the rare variants associated with a SNP can occur up to two million units of DNA away from it. This means that the disease-associated SNPs do not necessarily point to anything useful and that it is dangerous to assume the nearest gene is the cause of the disease.
If SNPs are indeed rather indirect markers of disease, that would explain why many have turned up in junk DNA.
But why do the SNPs get implicated in the genomewide association studies if in fact it is the rare variants that cause disease? Most of the SNPs are ancient, which is how they got to be common, whereas the disease-causing rare variants are mostly recent, because natural selection is always sweeping them away. After a SNP is created, some of the population has it and the rest continue to carry the standard DNA unit at that site in their genome.
When the rare disease-causing variants build up much later, Dr. Goldstein suggests, some will be on stretches of DNA containing the SNP and others on stretches of DNA with the standard unit. Since the allocation is random, more rare variants will be sometimes lie on the DNA with the SNP, and the SNP will appear as statistically associated with the disease even if it is not.
The association is not exactly spurious - Dr. Goldstein calls it “synthetic” - but it is indirect, so much so as to make many SNPs useless for identifying the genes that cause disease.
Geneticists have long been aware of this possibility, but Dr. Goldstein’s team has shown theoretically that this could happen more often than expected. He has also examined the question in reverse by doing a genomewide association study of sickle cell anemia.
Though the disease is known to be caused by a variant in a single gene, the Duke geneticists found a statistically significant association with 179 SNPs, spread across a stretch of DNA two and a half million units in length and containing dozens of genes. Most of these SNPs were clearly pointing at the wrong thing.
Genomewide association studies, conducted with hundreds of patients, can each cost in the range of $10 million or more. Though the studies may have led researchers up a blind alley in many cases, they were not a mistake, Dr. Goldstein believes.
“I think most people now view genomewide association studies as something we absolutely had to do and have now done,” he said. “It’s fair to say that for many common diseases nothing of very great importance was discovered, but those studies have told us what to do next.”
That next step, in his view, is to sequence, or decode, patients’ entire genomes and then to look for likely mutations in the genes themselves. The cost of sequencing a human genome has been plummeting in recent years, and it may now be possible to sequence large numbers of patients.
Finding even a few of the rare variants that cause disease could point to genes that make suitable targets for drug makers. The SNPs statistically linked to disease have mostly failed to identify the right genes, but the rare variants may, Dr. Goldstein said.
The Icelandic gene-hunting firm deCODE genetics, which emerged last week from bankruptcy, has long led in detecting SNPs associated with common disease. Dr. Kari Stefansson, the company’s founder and research director, agreed that whole genome sequencing would “give us a lot of extremely exciting data.” But he disputed Dr. Goldstein’s view that rare variants carried most of the missing heritability. Both deCODE genetics and scientists at the Broad Institute in Cambridge, Mass., have sequenced regions of the genome surrounding SNPs in search of rare variants, but have found very few, Dr. Stefansson said.
“We can speculate till we are blue in our faces,” he said, “but the fact of the matter is that there is no substitute for data.”
The Ozone Hole Is Mending. Now for the ‘But.’
By SINDYA N. BHANOO, The New York Times, January 26, 2010
That the hole in Earth’s ozone layer is slowly mending is considered a big victory for environmental policy makers. But in a new report, scientists say there is a downside: its repair may contribute to global warming.
It turns out that the hole led to the formation of moist, brighter-than-usual clouds that shielded the Antarctic region from the warming induced by greenhouse gas emissions over the last two decades, scientists write in Wednesday’s issue of Geophysical Research Letters.
“The recovery of the hole will reverse that,” said Ken Carslaw, a professor of atmospheric science at the University of Leeds and a co-author of the paper. “Essentially, it will accelerate warming in certain parts of the Southern Hemisphere.”
The hole in the layer, discovered above Antarctica in the mid-1980s, caused wide alarm because ozone plays a crucial role in protecting life on Earth from harmful ultraviolet radiation.
The hole was largely attributed to the human use of chlorofluorocarbons, chemical compounds found in refrigerants and aerosol cans that dissipate ozone. Under an international protocol adopted in 1987, many countries phased out the compounds, helping the ozone to start reconstituting itself over the Antarctic.
For their research, the authors of the new study relied on meteorological data recorded between 1980 and 2000, including global wind speeds recorded by the European Center for Medium-Range Weather Forecasts.
The data show that the hole in the ozone layer generated high-speed winds that caused sea salt to be swept up into the atmosphere to form moist clouds. The clouds reflect more of the sun’s powerful rays and help fend off warming in the Antarctic atmosphere, the scientists write.
The sea spray influx resulted in an increase in cloud droplet concentration of about 46 percent in some regions of the Southern Hemisphere, Dr. Carslaw said.
But Judith Perlwitz, a University of Colorado professor and a research scientist at the National Oceanic and Atmospheric Administration, said that although the paper’s data were sound, she questioned the conclusions.
Even as the ozone layer recovers, greenhouse gas emissions are expected to expand, she said. She predicted that the rise in temperatures would cause wind speeds to increase over time and have the same cloud-forming effect that the ozone hole now has.
“The question is whether the wind is really going to slow down, and that I doubt,” she said.
“The future is not just determined by the recovery of the ozone hole,” she said. “We’re also increasing our use of greenhouse gases, which increases the speed of the winds all year long.”
Dr. Perlwitz also pointed out that the ozone hole was not expected to fully recover to pre-1980 levels until at least 2060, according to the World Meteorological Organization’s most recent report on the issue.
GLOBAL UPDATE: Parasites: ‘Tropical’ Diseases Are Common in Arctic Dwellers, a Survey Finds
By DONALD G. McNEIL Jr., The New York Times, January 26, 2010
The kind of worm and protozoan infections that are often called neglected “tropical” diseases are also common among aboriginal peoples living in the Arctic, according to a recent survey.
Outbreaks of trichinosis, a larval-worm disease commonly associated with eating undercooked pork and carnivorous wild game, also occur among people who eat infected polar bear and walrus meat, and the Arctic harbors a unique species of the worm that can survive subzero temperatures. Mild infestations cause nausea and stomach pain; severe ones can kill.
In Alaska, there are sporadic human cases of a fish tapeworm known as diphyllobothriasis. Echinococcosis, a tapeworm disease that fills human lungs or livers with cysts that can crush blood vessels or kill if they rupture, needs both canines and hoofed animals in its life cycle. In New Zealand, it once thrived in sheep and working dogs; in the Arctic, it cycles between reindeer and elk and both wolves and domesticated dogs. It is declining in Alaska and Canada, where snowmobiles are replacing sled dogs, but is still common in Siberia and northern Russia.
Toxoplasmosis, a particular threat to pregnant women, also occurs in the Arctic, though its origins are mysterious. With domestic cats uncommon, it may be linked to wild lynx, but it seems to be picked up from eating caribou and seal.
The survey was published in PLoS Neglected Tropical Diseases by Dr. Peter J. Hotez, who edits the online journal.
By JOHN TIERNEY, The New York Times, January 26, 2010
I find myself in the unfamiliar position of defending Al Gore and his fellow Nobel laureate, Rajendra K. Pachauri.
When they won the prize in 2007, they were hailed for their selfless efforts to protect the planet from the ravages of greedy fossil fuel industries. Since then, though, their selflessness has been questioned. Journalists started by looking at the money going to companies and nonprofit groups associated with Mr. Gore, and now they have turned their attention to Dr. Pauchauri, the chairman of the United Nations Intergovernmental Panel on Climate Change.
The I.P.C.C., which is supposed to be the gold standard of peer-reviewed climate science, in 2007 warned of a “very high” likelihood that global warming would cause the Himalayan glaciers to disappear by 2035. When the Indian government subsequently published a paper concluding there was no solid evidence of Himalayan glaciers shrinking because of global warming, Dr. Pachauri initially dismissed it as “voodoo science” beneath the I.P.C.C.’s standards.
But then it came out that the I.P.C.C.’s projection was based not on the latest peer-reviewed evidence, but on speculative comments made a decade ago in a magazine interview by Syed Hasnain, a glaciologist who now works in an Indian research group led by Dr. Pachauri.
Last week, the I.P.C.C apologized for the mistake, which was embarrassing enough for Dr. Pachauri. But he also had to contend with accusations of conflict of interest. The Telegraph of London reported that he had a “worldwide portfolio of business interests,” which included relationships with carbon-trading companies and his research group, the Energy and Resources Institute.
Dr. Pachauri responded with a defense of his ethics, saying that he had not profited personally and that he had directed all revenues to his nonprofit institute. He denounced his critics’ tactics: “You can’t attack the science, so attack the chair of the I.P.C.C.”
I can’t defend that entire sentiment, because you obviously can attack some of the science in the I.P.C.C. report, not to mention other dire warnings in Dr. Pachauri’s speeches.
But I do agree with his basic insight: Conflict-of-interest accusations have become the simplest strategy for avoiding a substantive debate. The growing obsession with following the money too often leads to nothing but cheap ad hominem attacks.
Sure, money matters to everyone; the more fears that Dr. Pachauri and Mr. Gore stoke about climate change, the more money is liable to flow to them and the companies and institutions they are affiliated with. Given all the accusations they have made about the financial motives of climate change “deniers,” there is a certain justice in having their own finances investigated.
But I don’t doubt that Mr. Gore and Dr. Pachauri would be preaching against fossil fuels even if there were no money in it for them, just as I don’t doubt that skeptics would be opposing them for no pay. Why are journalists and ethics boards so quick to assume that money, particularly corporate money, is the first factor to look at when evaluating someone’s work?
One reason is laziness. It is simpler to note a corporate connection than to analyze all the other factors that can bias researchers’ work: their background and ideology, their yearnings for publicity and prestige and power, the politics of their profession, the agendas of the public agencies and foundations and grant committees that finance so much scientific work.
Another reason is a snobbery akin to the old British aristocracy’s disdain for people “in trade.” Many scientists, journal editors and journalists see themselves as a sort of priestly class untainted by commerce, even when they work at institutions that regularly collect money from corporations in the form of research grants and advertising.
We trust our judgments to be uncorrupted by lucre - and we would be appalled if, say, a national commission to study the publishing industry were composed only of people who had never made any money in the business. (How dare those amateurs tell us how to run our profession!) But we insist that others avoid even “the appearance of impropriety.”
This snobbery was codified by The Journal of the American Medical Association in 2005, when it essentially required chaperones for any researchers receiving corporate money. Citing “concerns about misleading reporting of industry-sponsored research,” the journal refused to publish such work unless there was at least one author with no ties to the industry who would formally vouch for the data.
That policy was called “manifestly unfair” by BMJ (formerly The British Medical Journal), which criticized JAMA for creating a “hierarchy of purity among authors.” The hierarchy looked especially dubious after a team of academic researchers (not financed by industry) analyzed dozens of large-scale clinical trials in previous decades and reported that industry-sponsored ones met significantly higher standards than the nonindustry ones.
The new fetish for disclosing “conflicts” has led some of the best medical researchers to shun drug company money altogether - not because they think it leads to bad research, but because they are tired of that fact being highlighted every time they are identified in a news story, as if that were the most important thing to know about their work.
There are, of course, notorious cases of corporate money buying predetermined conclusions, like the reports once put out by the Tobacco Institute to rebut concerns about smoking and cancer. But there has also been dubious work promoted by government agencies and foundations eager to generate publicity and advance their own agendas.
It’s naïve to caricature scientific disputes as battles between “industry” and the “public interest,” as if bureaucrats and activists didn’t have their own selfish interests (and wealthy, powerful allies like trial lawyers). Too often, corporate conflict-of-interest accusations have been used as smear tactics to silence scientists who ended up being correct. (Go to nytimes.com/tierneylab for examples.)
Instead of stigmatizing certain kinds of research grants, perhaps we should consider the bigger picture. If scientists listed all their public and private donors on their Web pages, journalists could simply link to that page and let readers decide which ones are potentially corrupting. Instead of following rigid rules to report “conflicts,” journalists could use their judgment and report only the ones that seem relevant.
Sometimes you can’t understand a debate or a controversy without knowing who is paying whom. But in general, I’m with Dr. Pachauri: follow the science, not the money.
A New Way to Look for Diseases’ Genetic Roots
By NICHOLAS WADE, January 26, 2010
The hunt for the genetic roots of common diseases has hit a blank wall.
The genetic variants found so far account in most cases for a small fraction of the genetic risk of the major killers. So where is the missing heritability and why has it not showed up?
A Duke geneticist now suggests that the standard method of gene hunting had a theoretical flaw and should proceed on a different basis. The purpose of the $3 billion project to decode the human genome, completed in 2003, was to discover the genetic roots of common diseases like diabetes, cancer and Alzheimer’s. The diseases are called complex, meaning that several mutated genes are probably implicated in each.
A principal theory has long been that these variant genes have become common in the population because the diseases strike late in life, after a person has had children. Bad genes would not be eliminated by natural selection at that age, as they would if the diseases struck before the child-bearing years.
So to find disease genes, the thinking went, do not decode the entire genome of every patient - just look at the few sites where genetic variations are common, defined as being present in at least 1 percent of the population.
These sites of common variation are called SNPs (pronounced “snips”), and biotech companies have developed ingenious devices to recognize up to 500,000 SNPs at a time. The SNP chips made possible genomewide association studies in which the genomes of many patients are compared with those of healthy people to see which SNPs are correlated with the disease.
The SNP chips worked well, the studies were well designed, though enormously expensive, and some 2,000 disease-associated SNPs have been identified by university consortiums in the United States and Europe.
But this mountainous labor produced something of a mouse.
In each disease, with few exceptions, the SNPs accounted for small percentage of the genetic risk. A second puzzling feature was that many of the disease-linked SNPs did not occur in the DNA that codes for genes, but rather in the so-called junk regions of the genome. Biologists speculated that these SNPs must play an as-yet-undefined role in deranging the regulation of nearby genes.
In an article this week in the journal PLoS Biology, the Duke geneticist David B. Goldsteinph.d and his colleagues propose an explanation for both findings.
They argue that the common disease-common variant idea is largely incorrect: natural selection has in fact done far better than expected in eliminating disease-causing variants from the population. It follows that the major burden of disease is carried by a multitude of rare variants - ones too rare to have been programmed into the SNP chips.
So why have the genomewide association studies linked some SNPs to disease, if in fact it is the rare variants that cause it?
In Dr. Goldstein’s view, the SNPs could simply be acting as surrogate markers for the rare variants. Until now, geneticists have assumed a disease-linked SNP was either itself a cause or was a marker for a disease variant nearby. But Dr. Goldstein’s team calculated that the rare variants associated with a SNP can occur up to two million units of DNA away from it. This means that the disease-associated SNPs do not necessarily point to anything useful and that it is dangerous to assume the nearest gene is the cause of the disease.
If SNPs are indeed rather indirect markers of disease, that would explain why many have turned up in junk DNA.
But why do the SNPs get implicated in the genomewide association studies if in fact it is the rare variants that cause disease? Most of the SNPs are ancient, which is how they got to be common, whereas the disease-causing rare variants are mostly recent, because natural selection is always sweeping them away. After a SNP is created, some of the population has it and the rest continue to carry the standard DNA unit at that site in their genome.
When the rare disease-causing variants build up much later, Dr. Goldstein suggests, some will be on stretches of DNA containing the SNP and others on stretches of DNA with the standard unit. Since the allocation is random, more rare variants will be sometimes lie on the DNA with the SNP, and the SNP will appear as statistically associated with the disease even if it is not.
The association is not exactly spurious - Dr. Goldstein calls it “synthetic” - but it is indirect, so much so as to make many SNPs useless for identifying the genes that cause disease.
Geneticists have long been aware of this possibility, but Dr. Goldstein’s team has shown theoretically that this could happen more often than expected. He has also examined the question in reverse by doing a genomewide association study of sickle cell anemia.
Though the disease is known to be caused by a variant in a single gene, the Duke geneticists found a statistically significant association with 179 SNPs, spread across a stretch of DNA two and a half million units in length and containing dozens of genes. Most of these SNPs were clearly pointing at the wrong thing.
Genomewide association studies, conducted with hundreds of patients, can each cost in the range of $10 million or more. Though the studies may have led researchers up a blind alley in many cases, they were not a mistake, Dr. Goldstein believes.
“I think most people now view genomewide association studies as something we absolutely had to do and have now done,” he said. “It’s fair to say that for many common diseases nothing of very great importance was discovered, but those studies have told us what to do next.”
That next step, in his view, is to sequence, or decode, patients’ entire genomes and then to look for likely mutations in the genes themselves. The cost of sequencing a human genome has been plummeting in recent years, and it may now be possible to sequence large numbers of patients.
Finding even a few of the rare variants that cause disease could point to genes that make suitable targets for drug makers. The SNPs statistically linked to disease have mostly failed to identify the right genes, but the rare variants may, Dr. Goldstein said.
The Icelandic gene-hunting firm deCODE genetics, which emerged last week from bankruptcy, has long led in detecting SNPs associated with common disease. Dr. Kari Stefansson, the company’s founder and research director, agreed that whole genome sequencing would “give us a lot of extremely exciting data.” But he disputed Dr. Goldstein’s view that rare variants carried most of the missing heritability. Both deCODE genetics and scientists at the Broad Institute in Cambridge, Mass., have sequenced regions of the genome surrounding SNPs in search of rare variants, but have found very few, Dr. Stefansson said.
“We can speculate till we are blue in our faces,” he said, “but the fact of the matter is that there is no substitute for data.”
The Ozone Hole Is Mending. Now for the ‘But.’
By SINDYA N. BHANOO, The New York Times, January 26, 2010
That the hole in Earth’s ozone layer is slowly mending is considered a big victory for environmental policy makers. But in a new report, scientists say there is a downside: its repair may contribute to global warming.
It turns out that the hole led to the formation of moist, brighter-than-usual clouds that shielded the Antarctic region from the warming induced by greenhouse gas emissions over the last two decades, scientists write in Wednesday’s issue of Geophysical Research Letters.
“The recovery of the hole will reverse that,” said Ken Carslaw, a professor of atmospheric science at the University of Leeds and a co-author of the paper. “Essentially, it will accelerate warming in certain parts of the Southern Hemisphere.”
The hole in the layer, discovered above Antarctica in the mid-1980s, caused wide alarm because ozone plays a crucial role in protecting life on Earth from harmful ultraviolet radiation.
The hole was largely attributed to the human use of chlorofluorocarbons, chemical compounds found in refrigerants and aerosol cans that dissipate ozone. Under an international protocol adopted in 1987, many countries phased out the compounds, helping the ozone to start reconstituting itself over the Antarctic.
For their research, the authors of the new study relied on meteorological data recorded between 1980 and 2000, including global wind speeds recorded by the European Center for Medium-Range Weather Forecasts.
The data show that the hole in the ozone layer generated high-speed winds that caused sea salt to be swept up into the atmosphere to form moist clouds. The clouds reflect more of the sun’s powerful rays and help fend off warming in the Antarctic atmosphere, the scientists write.
The sea spray influx resulted in an increase in cloud droplet concentration of about 46 percent in some regions of the Southern Hemisphere, Dr. Carslaw said.
But Judith Perlwitz, a University of Colorado professor and a research scientist at the National Oceanic and Atmospheric Administration, said that although the paper’s data were sound, she questioned the conclusions.
Even as the ozone layer recovers, greenhouse gas emissions are expected to expand, she said. She predicted that the rise in temperatures would cause wind speeds to increase over time and have the same cloud-forming effect that the ozone hole now has.
“The question is whether the wind is really going to slow down, and that I doubt,” she said.
“The future is not just determined by the recovery of the ozone hole,” she said. “We’re also increasing our use of greenhouse gases, which increases the speed of the winds all year long.”
Dr. Perlwitz also pointed out that the ozone hole was not expected to fully recover to pre-1980 levels until at least 2060, according to the World Meteorological Organization’s most recent report on the issue.
GLOBAL UPDATE: Parasites: ‘Tropical’ Diseases Are Common in Arctic Dwellers, a Survey Finds
By DONALD G. McNEIL Jr., The New York Times, January 26, 2010
The kind of worm and protozoan infections that are often called neglected “tropical” diseases are also common among aboriginal peoples living in the Arctic, according to a recent survey.
Outbreaks of trichinosis, a larval-worm disease commonly associated with eating undercooked pork and carnivorous wild game, also occur among people who eat infected polar bear and walrus meat, and the Arctic harbors a unique species of the worm that can survive subzero temperatures. Mild infestations cause nausea and stomach pain; severe ones can kill.
In Alaska, there are sporadic human cases of a fish tapeworm known as diphyllobothriasis. Echinococcosis, a tapeworm disease that fills human lungs or livers with cysts that can crush blood vessels or kill if they rupture, needs both canines and hoofed animals in its life cycle. In New Zealand, it once thrived in sheep and working dogs; in the Arctic, it cycles between reindeer and elk and both wolves and domesticated dogs. It is declining in Alaska and Canada, where snowmobiles are replacing sled dogs, but is still common in Siberia and northern Russia.
Toxoplasmosis, a particular threat to pregnant women, also occurs in the Arctic, though its origins are mysterious. With domestic cats uncommon, it may be linked to wild lynx, but it seems to be picked up from eating caribou and seal.
The survey was published in PLoS Neglected Tropical Diseases by Dr. Peter J. Hotez, who edits the online journal.