gene expression
Devon Ryan: It’s in the genes – there may be hope for pikas hit by climate change, Stanford researchers find
As climate change drives mountain-dwelling pikas to higher altitudes, the animals can dial certain genes up or down to make the most of their cooler home's limited oxygen.
Boom and busted.
In trying to untangle a mysterious herring collapse from the aftermath of the Exxon Valdez oil spill, scientists in Prince William Sound are revealing just how resilient—and unpredictable—marine ecosystems can be.
On a cold day in June, Scott Pegau leans toward the passenger window of a Cessna floatplane and peers out at the teal waters of Prince William Sound. The glacier-rimmed pocket of seawater on the southern coast of Alaska is protected from the open ocean by a string of rugged islands. It is both moody and alluring. Clouds dally on the snowy peaks and fray against the forested hillsides. The sea is flat and frigid, except for a single row of waves lapping at the rocky shore.
Pegau aims his gaze at the shallow waters behind the breakers. After a few minutes of searching, above a deep bay on one of the outer islands, he finally spots what he’s looking for: a school of juvenile herring. Pegau can distinguish them from other schooling species by the unique way they sparkle—an effect produced by sunlight playing off their silver flanks as the fish bank and roll. Try as I might, I can’t make out any twinkling, just the inky splotch of a few tons of small fish swarming below the surface.
“Small H1,” Pegau says into the headset microphone, tucked snugly under his thick, grey mustache. That’s code for a small school of one-year-old herring. He enters the location on his computer; huddled in the back seat, I make a tick mark on the backup tally. It’s the first of dozens of schools we’ll see on our flight.
Pegau conducts these surveys every year in hopes of understanding what’s in store for the herring population in Prince William Sound. The fish mature and begin to join the spawning stock at the age of three, so the counts give scientists and managers a clue about how many adults may be coming up the pipeline. Researchers and fishers alike always hope the answer will be many. But every year for the past quarter century, they have been disappointed.
The herring population in Prince William Sound crashed in 1993, just 4 years after the Exxon Valdez oil spill released 11 million gallons of crude into these waters. The collapse put an end to an $8-million-dollar-a-year fishery, and left a hole in the middle of the marine food web. Scientists have spent years trying to understand if and how the spill played a role in the herring’s demise here, and the results have been hotly contested. All of the legal proceedings finally closed in 2015, with herring listed as an impacted species but with most herring fishers feeling poorly compensated.
Even more concerning is the fact that, unlike most species hit by the spill, the herring haven’t bounced back over the decades since. Populations of forage fish are known to boom and bust, so most scientists thought it was only a matter of time before they rebounded. But 25 years later, there’s still no sign of recovery on the horizon.
“There’s definitely a possibility that the ecosystem went through a tipping point,” says Pegau, who coordinates the herring program at the Prince William Sound Science Center, an independent research institute whose work is funded in part by money from the spill settlement. A host of factors, which scientists are still trying to untangle, could be to blame, from hungry whales to virulent disease. “There’s no one thing that’s keeping them down,” Pegau says. “I think pretty much everyone is convinced of that.”
The herring mystery is a maddeningly concrete example of the often-abstract interconnectedness of nature, which frequently gives ecosystems their resilience, but can sometimes make them rebellious. If jolted a particular way—for instance, by a human-caused disaster or an environmental shift—an ecosystem may not revert to its original state. Instead it may settle into a new normal, leaving both the organisms and economies that rely on it reeling.
But the herring in Prince William Sound may also hold clues to long-standing questions about why ecosystems change, and how they cause fish populations to flourish or founder. After 25 years of research, scientists have collected reams of data on the herring, and half a dozen hypotheses to explain their plight. The data have yet to reveal satisfying answers, but what researchers learn about ecological resilience—and the true value of a species—could have ramifications well beyond Alaska’s shores.
After a few hours of surveying, the floatplane splashes down in Eyak Lake, which fills the Y-shaped valley separating Cordova from the looming peaks of the Chugach Mountains. “We survived another one,” jokes the pilot, as we taxi to a floating dock and unload. Pegau makes plans to fly again the next day, and we climb into the well-worn seats of his white F-250 for the short drive back to town.
Cordova is a no-frills community on the far eastern edge of Prince William Sound that has weathered its share of ups and downs. It was established in 1906 as the seaport from which to ship vast quantities of copper mined in Kennecott, 200 miles inland. When the mine closed in 1938, Cordova fell back on its reputation as the self-proclaimed razor clam capital of the world. But that industry went belly up on March 27, 1964—Good Friday—after a magnitude 9.2 earthquake heaved the clam beds 2 meters (6 feet) above sea level.
That left fishing and canning as the main games in town. Both revolved around salmon and herring. While the much smaller herring rarely exceed 25 centimeters (10 inches) in length, they are prized for their roe, as well as for food and bait.
But in 1989, again on Good Friday, the Exxon Valdez oil spill cast the town’s future into question once again. Many residents considered it the worst blow yet. “There’s a natural disaster, and there’s a manmade disaster,” says Sylvia Lange, a Cordova native and longtime fisher who now runs a local hotel. She has experienced both kinds of catastrophes in her life, and the two, she says, feel completely different.
The ecological impacts of the spill, by now, are legend. Despite the efforts of thousands of response workers, wildlife including sea birds and otters perished in droves. The financial impacts followed swiftly too. The cleanup effort provided some business, but tourism lagged and managers closed fisheries until they knew how the spill had affected fish populations. Meanwhile, for unrelated reasons, the price of pink salmon tanked. “Cordova was in a deep, deep depression,” Lange says, “not only psychologically but economically.”
At first, it seemed like the herring made it out unscathed. The Alaska Department of Fish and Game reopened the fishery in 1990, and in the two years that followed, herring fishers had some of their best seasons on record. But when the spring of 1993 rolled around, the herring all but disappeared. The population dropped from more than 100,000 metric tons (110,000 U.S. tons) to less than 30,000 (33,000 U.S. tons).
The crash devastated a community still coping with disaster. John Renner, a long-time Cordova fisher and chairman of the herring division at Cordova District Fishermen United, says the spring herring roe harvest was a staple of Cordova’s economy. “The whole town depended on it for the first shot of revenue of the season,” Renner says “People paid their taxes, got out of debt, that type of stuff.” For many, it was a big part of their livelihood; Renner once made a quarter of his annual income off of herring roe, and just talking about the collapse still makes him angry. A draft report commissioned by the science center estimates that, in total, losing the herring has cost Cordova almost $200 million and the region nearly $1 billion.
The passage of time has done little to settle questions about what caused the herring crash. Initially, many scientists doubted whether the oil spill could have caused a decline four years later. Some early studies also suggested the impact of the oil was minimal, including those by Walt Pearson, then a fisheries biologist with Battelle Marine Sciences Laboratory whose work was funded by Exxon. Pearson’s research found that adult herring could only have been exposed to low levels of oil for a short window of time, and that there had been little overlap between oiled beaches and herring spawning grounds. “The effects were quite localized,” Pearson says. He concluded that the biggest factor contributing to the crash was that there were too many herring and not enough food, due to a natural shift in ocean conditions.
Many fishers didn’t buy that. “Anyone with half a brain would figure out it was oil,” says Jerry McCune, president of Cordova District Fishermen United, a union-turned-non-profit advocacy organization. The herring spawn occurred just weeks after the spill, and McCune, Renner, and others think that the oil devastated the cohort of herring born in 1989. They say the failure of those fish to show up in 1993 accounted for the collapse.
But survey data collected during the crash suggest that it affected fish of all ages, says Pegau, not just the young ones. And a recent statistical analysis found little evidence for any direct impacts of the spill. Instead, Pegau and others think that if the oil did play a role in the collapse, it probably did so by weakening the herring, or the food sources upon which they depend, making it easier for something else to do them in.
The prime suspect, in Pegau’s estimation, is a disease called viral hemorrhagic septicemia (VHS). While there was no official monitoring program then, fishers and scientists saw signs of VHS in 1993. “It can take a population down in a real big hurry,” Pegau says. As the name implies, fish with VHS hemorrhage and can die from organ failure. The disease spreads quickly through herring’s dense schools or when fishers corral them into an enclosure to harvest their spawn, as local fishers were doing around the time of the spill. Some researchers think that this practice, called pounding, combined with the high herring numbers before the crash, contributed to a deadly outbreak of VHS.
But the risk of an outbreak could have been exacerbated by the spill, too. Fish embryos that don’t die when exposed to oil may carry genetic scars, particularly in something called the aryl hydrocarbon receptor gene. “It turns out that that gene gets completely knocked out among survivors,” says Paul Hershberger, a disease ecologist with the U.S. Geological Survey. And compromising that gene may weaken the immune system in fish, potentially making them more susceptible to disease. Hershberger’s colleagues have demonstrated this effect in Atlantic killifish, and now, his team is testing it in herring.
Exposing herring embryos to oil may also cause them to develop heart defects that put them at a general disadvantage. They can’t swim as fast or as long, which makes them more likely to get eaten, says John Incardona, a toxicologist at NOAA’s Northwest Fisheries Science Center and lead author of a study on this subject published in 2015. In lab experiments, Incardona has found that developmental effects occur even when herring embryos encounter levels of pollution far below what is generally considered harmful. “We think all of us are way underestimating what the initial injury was to herring,” he says.
Richard Thorne, a fisheries scientist who recently retired from the Prince William Sound Science Center, takes issue with the idea of a delayed collapse altogether. Evidence that the herring population remained high until the 1993 crash came from the Alaska Department of Fish and Game’s population estimates, which are based on the stock assessment models the state uses to manage its fisheries responsibly and set sustainable harvests. But in 1993, Thorne started conducting acoustic surveys of the herring population, and realized his numbers lined up best with a different set of data collected by Fish and Game: observations of how many miles of shoreline were covered in herring spawn. Looking back at this pre-crash spawning record, Thorne came up with an alternative population history, which suggested that herring numbers started falling immediately after the spill. He thinks the fish died from ingesting oil and that the collapse, if there was one, resulted from allowing fishers to harvest a herring stock in the early '90s that managers didn’t yet realize was already declining.
Pegau, for one, doesn’t think scientists will ever know what actually transpired. “We’ll never be able to say one way or the other because no one was collecting data when it happened,” Pegau says. And frankly, he doesn’t really care what caused the initial collapse. The more pressing question, Pegau says, is why the herring haven’t come back.
I meet John Platt on a floating dock in the old harbor, and the first thing he says as he shakes my hand is, “Why are we still talking about herring 25 years later?” Platt is a third-generation Cordova fisher with a leathery face and the gnarled physique of a former wrestler. And he’s being coy; we both know the answer to his question.
Platt used to fish for herring, collecting them using a type of net called a purse seine to harvest roe. He gamely drives me out to see the net, which he stores 10 minutes outside of town and which is—as far as I can tell—the only piece of herring gear left in all of Cordova. “I always thought they would come back,” he says. We pull up to a rusted white pickup truck overgrown by weeds and Platt gestures toward the sorry sight before us. “This basically sums up the herring fishery.” He gets out and starts to unwrap a battered blue tarp covering a lumpy mass on the truck’s flatbed, He finally tugs free a loop of black mesh for me to see. The net—which cost about $20,000 new—still looks good decades later. After all, it’s hardly been used.
Like many, Platt was nearly destroyed by the herring collapse. Commercial fishing permits in Alaska are traded like stocks; the state issues a limited number, and fishers buy and sell them at prices that generally reflect the value of the fishery. And the seine fishery was a high-stakes gamble. Herring roe was a hot commodity and fishers like Platt jockeyed for position near schools of herring so they could scoop them up when the fishery opened, sometimes only for an adrenaline-filled 15-minute window. Before the crash, when Platt bought his seine permit, the going price was nearly a quarter of a million dollars. Today, the same permit is worth just $31,000.
Some note that’s remarkably high, given that the roe market has deflated and there have only been two modest herring harvests in Prince William Sound since the crash, in 1997 and 1998, when managers thought the fish might be making a comeback. But the permit’s unsinkable value is of little use to people like Platt, who purchased his permit with a loan from the state, and struggled to make the payments—and pay taxes—without any fish to catch. In total, those who held permits for herring in Prince William Sound took a $50 to $60 million-dollar hit in lost permit values, according to a recent economic analysis.
Platt got paid by Exxon for working on the cleanup effort immediately after the spill, but that money went straight into paying off boats and gear. To settle his permit debt, Platt ultimately had to sell off his salmon boat and turn over the payout from a class-action lawsuit against the company, which, after going before the Supreme Court in 2008, came in at a fraction of the original award. For many, though, it was too little, too late; the loss of the herring had already taken its toll. “It caused divorces, ruin, a few people killed themselves,” Platt says.
Like many, Platt thought the failure of the herring to recover might be grounds for reopening the 1991 settlement between the government and Exxon, (now ExxonMobil), which closed before the herring crashed. The settlement included $900 million in payments, in addition to criminal fines, and a clause that would make an additional $100 million dollars available for long-term impacts that weren’t considered in the original agreement. “This is textbook what it was for,” Platt says.
In 2006, government lawyers did launch an effort to file a claim under the reopener, but it was later aborted. Moreover, the claim made no mention of herring. “It’s maddening,” Platt says. But Pegau thinks there was a simple reason: Linking the fish’s poor recovery to the spill would have been a hard case to make.
Traces of oil still remain in Prince William Sound, buried a few feet in the sediment among beach pebbles and sand, but most scientists say it has little ecological impact on herring today. Indeed, if the spill had any role in the fish’s demise, it was by helping to knock the population off a cliff in the first place. Other forces have now taken over and seem to be holding the herring down. And they don’t seem to be letting up. In 2015, after what seemed like a few promising years, the herring population dropped again to around 8,000 metric tons (8,800 U.S. tons)—less than half of what it was after the crash in 1993.
“I think the system reset itself,” says Ron Heintz, a nutritional ecologist in Juneau with NOAA’s Alaska Fisheries Science Center. “We ended up in a new state that apparently doesn’t include herring.”
One factor at play is predation. Forage fish, by definition, get eaten, and herring are no exception. “It’s a critical food resource,” says Mary Anne Bishop, an ecologist at the Prince William Sound Science Center. She describes the spring spawn as a frenzied feast when the herring turn coastal waters white with eggs—each female releases about 20,000 of them each year. “It’s the whales, it’s the sea lions, the harbor seals, all the birds coming in,” she says. Predation doesn’t stop as herring age, either; dozens of species consume them throughout their life cycle.
While there may have been enough herring to fill bellies and nets when the fish were plentiful, they may now be trapped in what scientists call a “predator pit.” After everyone has had their fill, there simply aren’t enough fish left for the herring population to climb out of the hole. More young adults join the spawning stock each year, but not enough to outweigh the number being eaten.
There’s debate about which animals are doing the most damage, but humpback whales are a possible culprit. Their numbers have quintupled in Prince William Sound in recent decades as the gentle giants have recovered from whaling. Scientists say the whales here have learned to specialize in herring, sometimes banding together to trap the fish in “bubble nets” before taking turns gulping them down en masse. Studies suggest humpbacks may consume 20 to 75 percent of the spawning herring population each year—the equivalent of the fishers’ historic share and then some.
Other scientists, including Pearson, have suggested that salmon hatcheries may bear much of the blame. Starting in the late 1970s, managers began releasing hatchery-raised pink salmon into the sound, and in the 1980s, they began to ramp up the numbers. Researchers have hypothesized that young salmon may eat or compete with juvenile herring for food, while older salmon returning from the sea may eat herring of all ages.
It also appears that the herring in Prince William Sound continue to see diseases like VHS more than their neighbors. Hershberger developed a test to detect whether fish have recently encountered disease, and found consistently higher levels of exposure in Prince William Sound than in Sitka, 450 miles to the southeast. Some wonder whether, as Platt puts it, the herring here are “wimpy” because of some lingering epigenetic effect of the spill that has been passed down from generation to generation. Hershberger says no one has tested that yet. “At this point, all we can do is speculate.”
Factors like predation, competition, and disease can limit populations from the top down. But that’s only half of the story: There has also been a low supply of young herring. Researchers call this poor recruitment, and they suspect it’s the result of environmental factors limiting the population from the bottom up.
For the herring to recover, they need a few big years in close succession to overwhelm the demands of predation and escape the threat of disease. But that hasn’t happened in a long time, Pegau says. “It’s been 25 years of bad luck.” He points to sweeping natural changes in the North Pacific in 1989—the same year as the spill—as a potential turning point. The exact nature of the shift was complicated, with some parts of the ocean warming and others cooling, but the impact on marine organisms was pronounced. Across the Gulf of Alaska, animals toward the bottom of the food web, like shrimp, crab, and herring have fared poorly since, while larger fish like halibut and cod have multiplied. This apparent contradiction continues to stump Pegau. “I have yet to figure out what in the world supports them,” he says of the thriving predators.
Much of the science center’s research looks at how oceanographic conditions affect herring in hopes of understanding why the tide has turned against them in recent decades. Among other things, that involves tracking where currents carry larvae, determining which environments young fish inhabit, and studying what controls the quantity and quality of food available to them as they store up energy to survive the harsh winter.
New research also suggests that herring recruitment may be linked to the amount of freshwater that pours into the Gulf of Alaska. High discharge years correlate with recruitment failures, says Eric Ward, a statistician at the Northwest Fisheries Science Center who led the study, published earlier this year. The mechanism, though still unclear, may have to do with how freshwater from rainfall and melting ice affects the strength and timing of the spring plankton bloom—the flurry of photosynthesis that kickstarts the entire ecosystem every year. In recent decades, there have been fewer years with extremely low runoff, which correlate with upticks in herring recruitment—what Ward calls “herring baby booms.” And as climate change melts glaciers and messes with rainfall patterns, the trend may continue.
These oceanographic factors may help explain why herring recruitment has also been weak in other parts of Alaska since the early 1990s. The reason places like Sitka still have a healthy herring fishery despite these changes, Pegau says, may simply be that the population there never crashed in the first place.
Scientists hope that figuring out what’s going on with herring will shed light on bigger questions about what fish need for successful recruitment—a problem that has stumped researchers for decades. Trevor Branch, a fisheries scientist at the University of Washington who studies the herring, says it’s possible that a whole host of things have to line up for successful recruitment: the right water temperatures, the right salinity, and abundant food, among them.
If scientists are to have any shot at figuring out how these fit together, they need lots of data collected over many years. And the research sparked by the Exxon Valdez oil spill and the subsequent herring crash have furnished just that. “If ever we were able to pinpoint something, it would be with Prince William Sound herring,” Branch says.
The day of my second flight with Pegau, the weather is sublime. We head across Prince William Sound to survey its far southwestern corner. A cruise ship glides beneath us, then a cluster of salmon seiners. The small skiffs that accompany them trace lazy circles on the surface, like ripples from giant raindrops, as they loop their nets around unsuspecting fish.
We officially begin the survey in a milky, ice-flecked fjord with a reclusive glacier tucked away at its head, and follow the coastline in and out of emerald bays. In the narrow passages between Evans, Elrington, and Latouche Islands, we spot school after school of herring, clustered along the rugged shoreline. In the afternoon light, I finally see them sparkle.
Nearly a hundred years ago, these were prime fishing grounds for an earlier incarnation of the herring fishery. Fishers caught huge quantities of herring, which were reduced for oil. For five consecutive years, they brought in in an average of 40,000 tons a year, Pegau says, marveling at the scale. Catch records show that those big hauls likely drove the herring to collapse, but remarkably, they appear to have recovered in the span of just 3 or 4 years. Pegau takes this as evidence that the herring in Prince William Sound have rallied back from the brink before, like others around the world.
John Trochta, one of Trevor Branch’s graduate students at the University of Washington, has analyzed more than 50 historical herring populations across the globe, most of which have collapsed at some point. He found that the majority rebounded within a decade, but there were a few exceptions where herring numbers remained low for at least twenty years after a crash. One is in Prince William Sound; another is off the coast of Japan and southeastern Russia. There, fishers once harvested nearly a million metric tons of fish per year from the legendary Hokkaido-Sakhalin stock. But by the 1930s, perhaps due to intense fishing pressure and oceanographic changes, the stock began to decline sharply, until, by 1955, there were hardly any fish left. It’s the only herring stock yet to come back after more than 60 years. No one knows whether the same fate awaits the herring in Prince William Sound.
On my final day in Cordova, I stop by Pegau’s office at the science center—a converted icehouse perched on stilts just inside the entrance to Cordova’s harbor. From Pegau’s second-story window, he has a clear view of the bustling docks and the mountains that stand guard over town. With this year’s survey nearly complete, I ask him how it looks. “This is probably the best year we’ve seen,” he admits. He saw a lot of schools, and the schools held a lot of fish. Still, he’s reluctant to wager whether that bodes well for herring. “I’ve felt optimistic in the past; now I’m a lot more reserved.”
There’s nothing Pegau can do to help the herring. There’s no fishery to manage or acute environmental stress to relieve. That’s not the way he sees his job anyway. His goal is to understand the vulnerability and value of the fish so that other scientists and managers around the world can be better equipped to do the same. Increasingly, he and others think that the answer lies in studying an ecosystem as a whole, and how an individual species like the herring fits in. And in that regard, he is more hopeful than ever. “It’s a great puzzle,” Pegau says, his dark eyes twinkling with excitement. “One of the real joys is to see how all those pieces fit together.”
ABOUT THE AUTHOR
Julia Rosen is a freelance journalist based in Portland, Oregon. She writes about science and the environment for publications including Science, Nature, Orion, and High Country News, as well as many others. Follow her on Twitter @sciencejulia, and find more of her writing at www.julia-rosen.com.
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Can shellfish adapt to ocean acidification?
Scientists explore the genomes of oysters and clams to help the shellfish industry survive changes in the ocean’s chemistry.
Scientists explore the genomes of oysters and clams to help the shellfish industry survive changes in the ocean’s chemistry
By Deirdre Lockwood
A shellfish farmer at Hama Hama Oyster Co. harvests Pacific oysters from Hood Canal in Washington.
Credit: Hama Hama Oyster Co.
If you’re an oyster aficionado living in the Pacific Northwest, you’ve likely tasted Chris Langdon’s scientific handiwork. Since 1996, his Molluscan Broodstock Program at Oregon State University has been breeding plump, fast-growing, and hardy oysters as stock for the $250 million West Coast oyster industry. But in the past several years, the program has taken on an additional goal: identifying and studying oysters that may be better prepared to thrive in an increasingly acidified ocean.
In 2007, oyster hatcheries in Oregon and Washington began experiencing massive die-offs of their larvae that continued for several years. Eventually, managers and scientists realized that the larvae were dying during periods of strong upwelling, when deep waters rich in CO2—and low in pH—come to the surface. These deep waters were even more acidified than in the past because of the oceans’ increasing uptake of CO2 from an atmosphere where levels of the greenhouse gas have been growing. When CO2 dissolves in water, carbonic acid forms, releasing hydrogen ions that lower pH. These ions convert carbonate ions already in the seawater to bicarbonate.
The corrosive upwelling in 2007 dropped carbonate levels in the seawater enough that aragonite, the main form of calcium carbonate that bivalves use to build shells, became undersaturated. Langdon and his colleagues showed that aragonite undersaturation ultimately drives oyster larvae to make smaller shells than usual or to not develop them at all (Nat. Clim. Change 2015, DOI: 10.1038/nclimate2479). Both outcomes can spell death.
Scientists, including Langdon’s colleague Burke Hales, quickly began working with oyster growers to monitor carbonate chemistry in hatcheries and to buffer the water with sodium carbonate when aragonite became undersaturated during upwelling episodes. In 2010, the National Oceanic & Atmospheric Administration sponsored a $500,000 network of six monitoring systems at West Coast hatcheries.
Since 2011, this intervention has helped avert major larval die-offs, Langdon says. But the experience made it clear that ongoing ocean acidification, which threatens marine organisms ranging from certain plankton at the base of the food chain to shellfish and corals, could endanger the shellfish industry worldwide.
Fortunately, evidence exists that some shellfish may be able to acclimate or adapt to these changes, thanks to the variable conditions these creatures experience and the wide genetic variation among individuals in a given species. Because oysters reside in intertidal zones, where they’re submerged at high tide and exposed at low tide, they see a lot of environmental change even daily, says Steven Roberts, a fisheries scientist at the University of Washington.
Scientists would like to know how shellfish such as oysters (top) and geoducks (bottom) respond to acidified waters.
Credit: Shutterstock
In an effort to identify hardier shellfish stocks, Langdon, Roberts, and many other researchers are exploring the genetic and metabolic underpinnings of how these creatures might be adapting to ocean acidification. The scientists are on the hunt for biomarkers that could eventually help shellfish growers select more resilient stock or adjust hatchery conditions for improved survival and growth.
Langdon was inspired by University of Sydney researcher Laura Parker’s work showing that in acidified conditions, stocks of the Sydney rock oyster bred for aquaculture grew shells better than did wild oysters, suggesting that the species has the genetic potential to adapt to ocean acidification and that selective breeding for good hatchery performance could be a key to this. But Langdon’s first attempt to repeat this experiment with his stock of Pacific oysters from the Molluscan Broodstock Program did not show the same advantage: The bred oysters fared about the same as their wild counterparts.
So he and his colleagues are now testing the survival of a variety of farmed oyster stocks in acidified conditions similar to those found during upwelling and comparing them with stocks grown in ambient seawater conditions. The team is sequencing the oysters’ DNA and tracking gene expression to identify genes and metabolic pathways associated with better survival and growth in acidified conditions.
The sequencing of the Pacific oyster genome, achieved in 2012, has made this effort much easier, revealing the function of thousands of oyster genes. But many details are still unclear, including the exact cellular machinery oysters use to form their shells and how it becomes dysfunctional when the chemical environment around the oysters changes, says Pierre De Wit, an evolutionary biologist at the University of Gothenburg who is collaborating with Langdon. Before oysters’ resilience can be understood, these questions will need answers.
For oysters, the first 24 hours of development are critical: They have to deposit a lot of shell quickly. In one of the earliest steps, certain proteins produced inside larval tissue are transported to an extracellular compartment surrounding the larva. There, the proteins form a scaffold on which calcium carbonate crystals precipitate. Meanwhile, protease inhibitors prevent the breakdown of these proteins. De Wit has found that acidified conditions seem to affect expression of both the scaffolding proteins and the inhibitors. “In stressed larvae, this protein matrix could get disorganized and prevent larvae from forming proper shells,” he says.
But this is only one of many factors that are involved in oysters’ response to ocean acidification. So far, De Wit and Langdon have found about 50 genes whose expression is delayed in oyster larvae during the first 18 hours of development while exposed to lower pH. These genes are involved in shell matrix formation, transport of cellular cargo inside larval cells, and transport of ions across cell membranes. Based on these studies, “it may be possible down the road to develop genetic markers that will allow us to identify stocks that are more resistant to ocean acidification,” Langdon says.
Other researchers are looking beyond aquaculture to wild shellfish for hallmarks of adaptation that growers might eventually exploit. Studies of sea urchins and rock oysters show that some organisms exposed to lower pH have offspring that are more resilient to these conditions, indicating some capacity for adaptation to acidification.
In Long Island Sound, south of Connecticut’s shores, where pH varies widely because of the effects of nutrient pollution, Bassem Allam of Stony Brook University is trying to detect how wild samples of eastern oysters and hard clams may adapt to acidification. In previous studies on the clams, he and his team identified gene variants called single-nucleotide polymorphisms (SNPs) that are linked with resistance to the parasitic disease QPX. He’s now using a similar approach to identify potential SNPs that confer tolerance to ocean acidification.
In addition to DNA sequence variations such as SNPs, epigenetic changes may also help shellfish tolerate stress. These are chemical modifications to DNA, or to proteins associated with the DNA, that influence gene expression. They can be heritable—passed over generations—and may preserve a “memory,” or history, of environmental conditions the organisms encountered. To investigate this, the University of Washington’s Roberts and Hollie Putnam of the University of Rhode Island are working to jog the memory of giant clams of the Pacific Northwest called geoducks, which represent a $74 million industry in the U.S.
In one experiment, Putnam exposed juvenile geoducks to ambient and acidified treatments for about three weeks. Then she returned both groups to ambient conditions and tracked their growth for several months before exposing them both to acidified conditions. “They do seem to have a memory of what they experienced early on,” she says. Geoducks exposed to lower pH initially grew more slowly than control clams but then made up for this by growing faster when switched to ambient conditions. They also grew faster than control clams when re-exposed to lower pH. “It suggests environmental history is important in how they respond to future stressors,” Putnam says. Eventually, hatcheries might carry out similar treatments to bolster the tolerance of their stocks, she says.
But it’s early days for such solutions. In the short term, NOAA expanded carbonate chemistry monitoring in shellfish hatcheries and coastal waters along the West Coast, including Alaska, with a three-year, $1.5 million grant in 2015. And although the West Coast has been a sentinel for ocean acidification because of its upwelling, shellfish growers elsewhere are also facing change. Parts of New England, the Chesapeake Bay, the Gulf of Mexico, the East China Sea, the Baltic Sea, and more are considered ocean acidification hot spots for various reasons, including coastal pollution and river input, which can dilute carbonate concentrations.
In 2013, Maine oyster grower Bill Mook installed a monitoring system similar to those on the West Coast after larvae die-offs at his Mook Sea Farm. Developed by the University of New Hampshire’s Joe Salisbury with NOAA support, it’s nicknamed the “black box”; more such systems may be needed in these hot spots before long.
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VIDEO: Were humans to go extinct, should the species be revived?
It's a tough call, but maybe not, according to a panel of five experts who debated "de-extinction" during the annual Isaac Asimov Memorial Debate at the American Museum of Natural History in New York City.
NEW YORK — If humans were to go extinct, would it be ethical to revive the species, to allow us to live once more on this blue planet?
It's a tough call, but maybe not, according to a panel of five experts who debated "de-extinction" during the annual Isaac Asimov Memorial Debate at the American Museum of Natural History (AMNH) in New York City on Wednesday (March 29). Astrophysicist Neil deGrasse Tyson, director of the AMNH Hayden Planetarium, moderated the debate, which honors Isaac Asimov (1920-1992), a biochemist and science-fiction writer who famously wrote the "three laws of robotics."
Were another intelligent life to de-extinctify humans, would they put us in a zoo-like environment? For a sentient being, that would be "extremely frightening and scary," said panelist Greg Kaebnick, a research scholar at the Hastings Center, an independent bioethics research institute in Garrison, New York. "The animal welfare concerns just get overwhelming." [6 Extinct Animals That Could Be Brought Back to Life]
Then, to further muddy the waters, Kaebnick asked, "Do we deserve to be brought back?"
Yes, we do, said panelist George Church, a professor at Harvard University and the Massachusetts Institute of Technology, who is working on reviving bits and pieces of the woolly mammoth. But then again, Church, a geneticist, molecular engineer and chemist, has often opined that the science of de-extinction is already here or within reach, and should be pursued.
The panel grappled with the issues of de-extinction for more than 2 hours, discussing not only logistics but also ethical quandaries. Logistically, scientists need an animal's entire genetic code to bring it back. But this can be a challenging task: The oldest authenticated DNA is from the bone of a 700,000-year-old horse found in Yukon, Canada, said panelist Beth Shapiro, who co-wrote a 2013 study about the horse in the journal Nature.
It's difficult to get authenticated DNA from extinct animals, even those younger than that horse, including the mammoth, thylacine (a marsupial from Tasmania that's also called the Tasmanian tiger), dodo and passenger pigeon, Shapiro said. But Church disagreed, saying that there are ways to move forward.
Researchers could either find DNA in these animals' frozen nuclei, or re-create "a successful approximation" of the genome through DNA modification, Church said at a roundtable discussion later that evening.
"These are exponential technologies that improve very, very quickly and have many biomedical uses, like transplants," Church said. "I have no particular reason to doubt that we could make all of the genetic and epigenetic changes we will want to if we wanted to bring back an entire genome."
However, Church's comments were met with disbelief from some of the other panelists. Epigenetic changes are external influences on the genome that can change how much or little a gene is turned on or off, and could be difficult to modulate in a de-extinctified animal.
Lawful look
Even if the science will one day be possible, the legal framework addressing de-extinction is murky at best. If the "resurrected" animal is not a perfect copy, would it be considered the same species? Would it immediately be classified as an endangered species?
Moreover, what if its environment, microbiota (bodily bacteria) and food sources no longer exist? How many animals of a species should be brought back, so that they can have genetic diversity and mate on their own? When does human responsibility toward these revived animals end? [WipeOut: History'sMostMysteriousExtinctions]
"I think one of the toughest moral issues about de-extinction is animal welfare. How many maimed, deformed, stillborn, quasi-mammoths, quasi-elephants is it worth to bring back a sort of mammoth?" asked panelist Henry (Hank) Greely, a professor of law at Stanford University. "There are actually laws in this country, the Animal Welfare Act, that deal with some of those issues."
In addition, why not spend that money for de-extinction efforts instead on saving still-living animals, the panel asked.
De-extinction is a dangerous road, said panelist Ross MacPhee, the curator of mammalogy and vertebrate zoology at the AMNH. For instance, it's hard to know what ramifications an extinct animal will have on modern ecosystems, he said.
Rather than use science to bring back extinct animals, perhaps researchers could use these technologies to design bacteria that would help humans, for instance, by producing fuel or meat alternatives, MacPhee said. Or maybe this science could be used to insert or activate genes in plants and animals that could help them survive in an era of climate change, he added.
Some of this work is already a reality, said Church, who pointed out that scientists have made some plants more resistant to drought and pests.
Also, there have been other successful de-extinction efforts, albeit for local, not worldwide extinctions. For instance, horses used to live in North America, but went extinct at the end of the last ice age. When European explorers arrived in the New World, they inadvertently re-introduced horses to the continent, where they have since flourished.
Likewise, a fungus has rendered the American chestnut functionally extinct, meaning the species is still around (at least in lab-monitored spaces), but not in its natural environment; but scientists have tweaked the chestnut's genome to make it fungus-resistant, Greely said.
The experts agreed that this technology could also be used for evil — for instance, to bring back an extinct virus or to alter an existing virus to make it more contagious.
As this science moves forward, it's crucial to educate and involve the public, the panel said.
"We actually have to have that [discussion] to some degree, case by case, because each effort at de-extinction raises its own unique considerations," Kaebnick said.
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Gene-silencing spray lets us modify plants without changing DNA.
A single application keeps working for nearly a month, which could allow us to modify plants without actually altering their DNA.
By Michael Le Page
Don’t like the look of those roses in your garden? One day you might be able to buy a spray that changes the colour of their flowers by silencing certain genes.
Farmers may use similar gene-silencing sprays to boost yields, make their crops more nutritious, protect them from droughts and trigger ripening. The technique could let us change plant traits without altering their DNA.
“A spray can be used immediately without having to go through the years involved in development of a GM or conventionally bred crop,” says David Baulcombe at the University of Cambridge, who studies gene silencing in plants. One spray can also be used on many different varieties, he points out.
Companies like Monsanto are already developing gene-silencing sprays that get inside bugs and kill them by disabling vital genes.
Long-lasting action
Now a team at the University of Queensland in Australia has managed to achieve long-lasting gene silencing inside plant cells. They have protected tobacco plants from a virus for 20 days with a single application of a gene-silencing spray.
“We believe it offers a step change in environmentally sustainable crop protection,” says team member Neena Mitter.
The technique should allow plant traits to be altered, too, but the team has not tried this as they are focusing on crop protection.
Many other teams around the world are trying to achieve such long-lasting effects in plants. Mitter’s is the first to publish such results.
It is a very exciting result, says John Killmer of biotech startup Apse. “This could open up all kinds of plant ‘modification’ unrelated to insect and disease control.”
Gene silencing exploits a natural defence system. When viruses invade cells, the cells cut up some of the viral RNAs to make short pieces of double-stranded RNAs, which they use to recognise and destroy any RNAs with matching sequences. Without viral RNA, no viral proteins are made, so viruses cannot replicate.
RNA interference, as this often called, can be used to block production of any protein. Efforts to produce RNAi-based drugs for people have not got far because even when injected into the blood RNAs are rapidly broken down.
Next-generation defence
But many genetically modified plants work by producing gene-silencing RNAs. What is more, it has been discovered that specific genes can be shut down in some – although not all – bugs and plants simply by spraying them with small double-stranded RNAs with sequences matching the genes.
Monsanto, for instance, is developing RNAi sprays that kill pests. Its spray targeting the varroa mites contributing to the woes of bees is now entering the final stages of development, the company revealed on 5 January.
One challenge with the spray approach is that the effects on plants last only a few days because unprotected RNAs soon break down. Farmers will not want to apply expensive sprays this often.
In experiments with tobacco plants, Mitter’s team has now shown it can make the protective effect last at least 20 days. This was achieved by combining the RNAs with clay nanoparticles developed by her colleague Gordon Xu.
The positively charged clay nanoparticles, made of stacked sheets of common minerals such as magnesium chloride, bind and protect the negatively charged RNAs. Over time, the clay particles react with carbon dioxide and break down, slowly releasing the RNAs.
Lack of options
Plant viruses are a huge problem for farmers around the world, and no existing treatments target them directly. Farmers must either grow resistant varieties, if they exist, or try to kill the organisms that spread plant viruses, such as aphids.
So if the antiviral spray works as well in field tests on crop plants, there could be huge demand. “We do believe it will be commercially viable,” Mitter says.
The biggest obstacle is cost – while clay nanoparticles are cheap to make, making RNA is expensive. A few years ago, it would have cost over $100,000 to make the gram or so needed to treat a small field. But this is changing fast. Killmer’s company Apse aims to mass-produce RNAs for under $2 per gram.
Gene-silencing sprays should be far safer than ordinary pesticides. RNAs cannot pass through human skin and are rapidly broken down in the body.
While one 2012 study claimed some of the plant RNAs present in the food we eat already could affect human genes, several follow-up studies have found no evidence of any such effect.
Flexible and safe?
Combining RNAs with clay nanoparticles should not make them any less safe, Baulcombe says. “I would not have any concerns about that at all.”
There is a risk that RNAi sprays could affect non-target organisms – such as worms or fungi in soil – if their DNA contains matching sequences. In theory, target organisms could also evolve resistance by changing their DNA.
The great advantage of gene silencing is that by altering the sequence of the RNAs it should be possible to avoid non-target effects and overcome most forms of resistance.
The technology looks set to divide those who oppose genetically modified crops, with at least a few in the anti-GM camp welcoming the new approach. “I have had organic growers call me up and tell me to hurry up with the technology,” says Killmer.
Gene-silencing sprays are not the only new kid on the block. Other biologists are developing trait-altering sprays based on plant signalling molecules.
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Sex lives of reptiles could leave them vulnerable to climate change.
Environmental factors such as temperature can trigger sex reversal in reptiles.
We are only just starting to appreciate the full sexual diversity of animals. What we are learning is helping us understand evolution and how animals will cope with a changing world.
In humans and other mammals, sex chromosomes (the Xs and Ys) determine physical sex. But in reptiles, sometimes sex chromosomes do not match physical sex. We call this “sex reversal”.
Environmental factors such as temperature can trigger sex reversal in reptiles. In our recent study, we investigated how common sex reversal is in reptiles. We concluded that it is widespread and a powerful evolutionary force.
This raises important questions about how reptiles will survive in a warming world.
Xs and Ys, Ws and Zs
In humans, sex chromosomes determine if an embryo’s physical sex is either male (XY) or female (XX).
Reptile sex determination is more complicated. Some species, including snakes, use sex chromosomes like humans do. But in other species, such as crocodiles and marine turtles, sex is determined by the temperature the eggs are raised in.
We’ve recently come to realise that many species use a combination of both. When the temperature sends opposite signals to the embryo’s sex chromosomes, sex reversal is the result. For these lizards, the sex chromosomes don’t match their physical appearance and reproductive function.
The central bearded dragon (Pogona vitticeps) is probably the best-known example of reptile sex reversal. Its sex chromosomes are named Z and W.
Male dragons have two Z chromosomes and females have a Z and W. Female dragons normally produce roughly equal numbers of male (ZZ) and female (ZW) offspring. But when the eggs are incubated in a hot environment (greater than 32℃), more females than males hatch. Some of these females from hot nests are sex-reversed.
Sex-reversed females are fully functional. In fact they produce twice as many eggs as females with female sex chromosomes. This suggests that sex reversal might actually be an advantage in this species.
Another fairly well-understood example from Australia is the eastern three-lined skink (Bassiana duperreyi).
In this species males are XY and females are XX. Although these chromosomes share the same name, they aren’t the same as those found in humans. They have arisen independently and use different genes to trigger male and female development.
In this skink, females (XX) can reverse to males, but at cool incubation temperatures, a phenomenon we’ve observed both in the lab and in a wild alpine population.
In both species, the sex with matching sex chromosomes (ZZ males in the dragon and XX females in the skink) is the one that reverses. In dragons it happens at high temperatures, and in the skink at low temperatures.
Why reverse sex?
Sex reversal can have major effects on the behaviour of an individual. Male-to-female central bearded dragons are bolder than males and females with matching sex chromosomes. This may help them find food and mates, but at the same time exposes them to predators.
Not all lizards lay eggs. Sex reversal caused by temperature is also thought to occur in species that give birth to live young, such as Tasmania’s snow skink (Niveoscincus ocellatus). In live bearers, sex reversal is caused by the environmental temperatures that a mother experiences during pregnancy.
We believe that sex reversal is widespread in reptiles. Emerging evidence suggests that environmentally induced sex reversal may also be common in fish and amphibians, playing a role in evolution of new species and having serious implications in rapidly changing environments.
We suspect the reason no one has yet fully appreciated the role of sex reversal in reptiles is because much research has focused on mammals and birds, where sex reversal is usually caused by mutations that affect gene expression during embryonic development. This has created the false impression that sex reversal is harmful to an individual.
Another reason is that many reptile species have sex chromosomes that are very difficult to tell apart. That makes instances of sex reversal very difficult to spot.
An obvious question of deep concern is whether climate change could cause extinction by reversing the sex of entire populations. For temperature-sensitive species like the bearded dragon, crocodiles and marine turtles, is the future a warmer world without males?
The answer will be different for each species. Reptile survival under climate change depends on the answer to several questions.
Can the species control when and where they nest? How quickly are environmental conditions changing? Can the temperature at which sex reversal occurs change?
Each species will face a unique path as we experience an uncertain and changing environment. Some paths will undoubtedly lead to extinction, but others may utilise flexibility in sex-determination strategies to survive.
This research was conducted at the Australian National Wildlife Collection CSIRO, in partnership with the Institute for Applied Ecology at the University of Canberra and the University of the Sunshine Coast.
Clare Holleley
Senior Research Scientist, Australian National Wildlife Collection, CSIRO
Disclosure statement
Clare Holleley receives funding from the Australian Research Council and the Commonwealth Scientific and Industrial Research Organisation (CSIRO).
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The new Secretary of Health and Human Services is a member of a fringe medical organization. Here’s what that means.
Yesterday, I woke up to the news that President-Elect Donald Trump had chosen Rep. Tom Price (R-GA) as his new Secretary of Health and Human Services.
The new Secretary of Health and Human Services is a member of a fringe medical organization. Here’s what that means.
Posted by Orac on November 30, 2016
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I’m always hesitant to write about matters that are more political than scientific or medical, although sometimes the sorts of topics that I blog about inevitably require it (e.g., the 21st Century Cures Act, an act that buys into the myth that to bring “cures” to patients faster we have to neuter the FDA and a retooled version of which is still being considered). This is one of those times. Yesterday, I woke up to the news that President-Elect Donald Trump had chosen Rep. Tom Price (R-GA) as his new Secretary of Health and Human Services. The Department of Health and Human Services (DHHS), of course, figures fairly prominently in a some regular topics discussed on this blog because major federal agencies that I write about are within the DHHS, including the CDC (vaccine issues, Zika virus, etc.), the FDA (drug approval and drug safety), and, of course, the National Institutes of Health (billions of dollars worth of medical research). So the HHS Secretary matters, at least for purposes of discussing science-based medicine. Then there’s also the issue of Donald Trump’s long history of rabid antivaccine views, coupled with the other issue of his having met secretly with Andrew Wakefield in August in Florida and, after the election, antivaccine activists seeking to influence him based on that meeting. Heck, as I’ve noted before, Vice President Mike Pence apparently doesn’t believe that smoking causes cancer and premature death. So I was looking for a signal in whomever Trump picked regarding whether he would actually do anything about vaccine policy potentially harmful to public health.
So why did Tom Price catch my attention more than other Trump cabinet picks? Yes, he detests Obamacare and is likely to be fully enthusiastic about gutting it, but pretty much anyone Trump picked would have been expected to hold that view. It’s pretty much par for the course for the Republican Party these days. I would have been more surprised if Trump had picked someone who was was relatively neutral on the Affordable Care Act. No, what caught my eye was that I learned that Tom Price is a member of the Association of American Physicians and Surgeons (AAPS), and that told me a lot about him, none of it good. For instance, in 2015 Charles Pierce referred to Price as “one of Georgia’s wingnut sawbones” (Price is an orthopedic surgeon), and noted an article by Stephanie Mencimer, The Tea Party’s Favorite Doctors, which included this description of the AAPS:
Yet despite the lab coats and the official-sounding name, the docs of the AAPS are hardly part of mainstream medical society. Think Glenn Beck with an MD. The group (which did not return calls for comment for this story) has been around since 1943. Some of its former leaders were John Birchers, and its political philosophy comes straight out of Ayn Rand. Its general counsel is Andrew Schlafly, son of the legendary conservative activist Phyllis. The AAPS statement of principles declares that it is “evil” and “immoral” for physicians to participate in Medicare and Medicaid, and its journal is a repository for quackery. Its website features claims that tobacco taxes harm public health and electronic medical records are a form of “data control” like that employed by the East German secret police. An article on the AAPS website speculated that Barack Obama may have won the presidency by hypnotizing voters, especially cohorts known to be susceptible to “neurolinguistic programming”—that is, according to the writer, young people, educated people, and possibly Jews.
I realize that just because Tom Price is a member of the AAPS doesn’t necessarily mean that he subscribes to all its views—or even most of them. Maybe he’s like the Trump voters who were attracted by other things about him or hated Hillary Clinton more than they were disturbed by his racism, embrace of the alt right white supremacist movement, misogyny, and conspiracy mongering. Maybe Price was attracted by the AAPS world view that rejects nearly all restrictions on physicians’ practice of medicine, purportedly for the good of the patient; its support of private practice and dislike of government involvement in medicine, either financially or regulatory; and its embrace of an Ayn Rand-style view of doctors as supermen and women whose unfettered judgment results in what’s best for patients and medicine. Perhaps he was so attracted to the AAPS vision of doctors as special and “outside of the herd” to the point that he ignored its simultaneous promotion of dangerous medical quackery, such as antivaccine pseudoscience blaming vaccines for autism, including a view that is extreme even among antivaccine activists, namely that the “shaken baby syndrome” is a “misdiagnosis” for vaccine injury; its HIV/AIDS denialism; its blaming immigrants for crime and disease; its promotion of the pseudoscience claiming that abortion causes breast cancer using some of the most execrable “science” ever; its rejection of evidence-based guidelines as an unacceptable affront on the godlike autonomy of physicians; or the way the AAPS rejects even the concept of a scientific consensus about anything. Let’s just put it this way. The AAPS has featured publications by antivaccine mercury militia “scientists” Mark and David Geier. Even so, the very fact that Price was attracted enough to this organization and liked it enough to actually join it should raise a number of red flags. It certainly did with me, because I know the AAPS all too well.
I haven’t written much about the AAPS, but the first time I ever encountered the group was over a decade ago. Given that Tom Price is now in the news as Trump’s selection for DHHS, now appears to be a good time to revisit the AAPS, although I have already briefly done so because, not surprisingly, the AAPS has been a huge foe of Obamacare. Consistent with the conspiratorial bent of many AAPS leaders, AAPS CEO Dr. Jane Orient peddled medical conspiracy theories that Hillary Clinton was “medically unfit to serve.”
Since it’s been a long time, I decided to peruse the most recent episodes of the Journal of American Physicians and Surgeons (JPANDS), to see what the group has been up to, “scientifically” speaking. Not surprisingly, the Fall 2016 issue contained the usual rants against Medicare and taxes and complaints about the “end of fee-for-service medicine” (perhaps the “threat” that animates the AAPS perhaps more than anything else), but it also contained other typical AAPS bugaboos. For instance, there is this article decrying mandatory influenza vaccination for health care professionals, in which a fictional nurse named Rebecca is demonized by her coworkers for refusing the flu vaccine, along with some familiar anti-flu vaccine tropes.
Then, consistent with the hostility of the AAPS towards evidence-based medicine, there is this “gem” of an article, The Evidence-Based Transformation of American Medicine by Hermann W. Børg, MD. Let’s just say that Dr. Børg writes about evidence-based medicine as though it were a bad thing. If there’s another thing (besides Medicare or any hint of federal “control” of medicine) that the AAPS hates with a passion, it’s evidence-based medicine. It’s an article that combines the reasonable, such as questions about pharmaceutical influence in generating EBM guidelines and the contention that for preventative interventions we should pay attention to the number needed to treat and to absolute risk reductions more than relative risk reduction, and real howlers, like this paean to anecdotal evidence:
The very low level of quality assigned to anecdotal evidence in this system requires a brief comment. In keeping with the mantra that “the plural of anecdote is not evidence,” any usefulness of “anecdotes” in clinical practice is dismissed outright by EBM. However, as one wise professor observed, “Every epidemic starts with a single case report” (R.L. Kimber, personal communication, 2000). Serendipitous breakthroughs are made by individuals who make careful observations of patients from close range, seldom or never by a team encumbered by a rigid experimental protocol and the huge number of subjects needed to reach statistical signicance. Single observations may be extremely important, even if not statistically significant in the context of a large trial. Say, for example, a rare, otherwise unexplained event follows a medical intervention: a patient takes a drug and inexplicably goes blind. It might be a coincidence, or it might be a side effect of the drug. One cannot rule out a causal relationship based on lack of a statistically significant difference in this occurrence between the drug and placebo groups in a trial of insufficient power to detect a rare event. One is obligated to investigate further.
This is, of course, a straw man so massive that, were it real, the astronauts living on the International Space Station could see it from orbit. EBM (and science-based medicine) recognize the importance of anecdotes, but as hypothesis-generating observations, not hypothesis-confirming observations. Moreover, serious adverse events, such as blindness, are not dismissed as “correlation not equaling causation” without investigation. Certainly the FDA would not dismiss multiple reports of blindness after a drug dose as “the plural of anecdotes not being data.” While I will concede that sometimes skeptics use that quip about anecdotes a bit too freely, but in actual practice clinical observations of a reaction as serious as the example given by Dr. Børg are not dismissed as coincidence without investigation, consistent with the role of anecdotes as hypothesis-generating. Basically, Dr. Børg, again consistent with the AAPS view of the physician as supreme, wants the freedom to be able to use clinical observation in any way he wants without restriction by those pesky EBM guidelines and to interpret medical evidence any way he wants, even if it conflicts with how the vast majority of the field interprets it.
If you want a distillation of how the AAPS views EBM guidelines, Dr. Børg gives it:
Strict application of EBM implies a mechanistic algorithm- driven approach, similar to primitive pre-artificial-intelligence computer programs of the past. In such an approach, the doctor sees the patient as a statistic rather than an individual. This sort of medicine could be practiced by administrators. In the real world, however, clinical trials may tell which treatments are e ective, but not necessarily which patients should receive them.
Modern studies of the human genome and proteome have deepened our understanding of the importance and vast extent of biochemical individuality. The patient could be in a subset of patients whose excellent response to an intervention was diluted out in the large number of randomized subjects. It is recognized, for example, that two genes affect how patients process 25 percent of drugs now on the market. In fact, advances in pharmacogenetics may render the EBM model obsolete and replace it with “Genomic Medicine.” One of the major promises of pharmacogenomics is the ability to precisely predict the individual patient’s response to medical intervention, without the need to indirectly draw such conclusion from the large epidemiology-based studies.
Bloody hell. This is exactly the same sort of rationale that functional medicine quacks use to justify in essence, doing anything they believe in to treat patients, all in the name of respecting the patient’s “biochemical individuality” and as an excuse to make it up as one goes along. (Heck, he even uses the same term!) As I like to point out, there is already room in EBM guidelines for the physician’s clinical judgment. However, if a physician deviates from EBM guidelines significantly, it is expected that he or she should have a damned good reason for doing so.
Also, where nowhere near this precision medicine utopia yet, mainly because we lack understanding of the significance of various mutations and differences in gene expression when measured on a whole genome basis. Clinical trials are still necessary. They are also evolving in order to incorporate genomic data and biomarkers in treating patients. One form these new trials take is the so-called “adaptive trial,” which uses patient outcomes and biomarkers to immediately inform further treatment decisions. So, though, results from these trials have been disappointing. Again, Dr. Børg seems to be invoking genomics more as an excuse to dismiss EBM guidelines than anything else.
Now, one might say that Price might not know anything about articles like this, and that’s certainly possible. On the other hand, the reason I cited Dr. Børg is because his article represents what is perhaps the overarching view that is the cornerstone of the AAPS: The fetishization above all else of the individual doctor’s judgment and hostility to any restriction on physician autonomy, or, as I like to characterize it, anything that smacks of “telling doctors what to do.” Truly AAPS worships “brave maverick doctors” and castigates doctors following EBM as going with the herd. Basically, as I described the first time I discussed the AAPS, the leadership of the AAPS and apparently many who publish in JPANDS seem to be a bit too enamored of their self-proclaimed “maverick” status and give the appearance of thinking that, like Ayn Rand’s hero, they’re “supermen” whose egoism and genius will inevitably prevail over timid traditionalism and social conformism. Reigning them in with evidence only interferes with their autonomy and prevents them from exercising their genius for the good of their patients. If only the “herd” could appreciate that!
Oh, and as recently as the Summer 2016 issue of JPANDS, the AAPS was still publishing risible antivaccine pseudoscience in the form of an article by Neil Z. Miller entitled Combining Childhood Vaccines at One Visit Is Not Safe. Let’s just say that it lived down to the usual very low scientific standards of JPANDS, as I described in detail in June.
Tom Price probably doesn’t buy into all the quackery of the AAPS, but my reading thus far leads me to believe that he fully embraces the and Ayn Rand-worshiping wingnuttery the organization. I do feel obligated to state here, though, that, although I do believe he’s a very bad choice for DHHS, fortunately thus far I have found no evidence that he is antivaccine and have even heard rumblings that antivaccinationists are not happy with this choice for DHHS. I do know that the One Crank To Rule Them All, über-quack Mike Adams, is practically twisting himself into a pretzel justifying a “wait and see” attitude even though he is clearly very upset over this choice because Price voted against GMO labeling. (No, I’m not going to link to Adams.) However, you can learn a lot about a person by the people with whom he associates and the groups he joins and supports. By joining the AAPS, Price has shown that he is clearly attracted to a pre-Medicare vision of a golden era of absolute physician autonomy with minimal or no government interference or programs like Medicare, as well as a hostility towards evidence that conflicts with that vision. There is no arguing this, as these are beliefs that are baked into the DNA of the AAPS; they are central to the organization. Attraction to such beliefs is not a good trait for a Secretary of HHS to be attracted to, and I haven’t even really gotten into Price’s fundamentalist antiabortion beliefs, and his implacable opposition to gun control. It’s going to be a long four years when it comes to health policy.
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