Richard Conniff's Blog, page 50

Autism Link To Male Genital Malformations, Environmental Toxins

Male genital malformations have become so common that epidemiologists talk about Testicular Dygenesis Syndrome.  Now a Big Data examination of epidemiological records has turned up a strong link to autism, and that suggests both problems may be caused by some factor in the environment.

Here’s the press release from the University of Chicago:

An analysis of 100 million US medical records reveals that autism and intellectual disability (ID) rates are correlated at the county level with incidence of genital malformations in newborn males, an indicator of possible congenital exposure to harmful environmental factors such as pesticides.

Autism rates — after adjustment for gender, ethnic, socioeconomic and geopolitical factors — jump by 283 percent for every one percent increase in frequency of malformations in a county. Intellectual disability rates increase 94 percent. Slight increases in autism and ID rates are also seen in wealthier and more urban counties.

The study, published by scientists from the University of Chicago March 13 in PLOS Computational Biology, confirms the dramatic effect of diagnostic standards. Incidence rates for Autism and ID on a per-person basis decrease by roughly 99 percent in states with stronger regulations on diagnosis of these disorders.

“Autism appears to be strongly correlated with rate of congenital malformations of the genitals in males across the country,” said study author Andrey Rzhetsky, PhD, professor of genetic medicine and human genetics at the University of Chicago. “This gives an indicator of environmental load and the effect is surprisingly strong.”

Although autism and intellectual disability have genetic components, environmental causes are thought to play a role. To identify potential environmental links, Rzhetsky and his team analyzed an insurance claims dataset that covered nearly one third of the US population. They used congenital malformations of the reproductive system in males as an indicator of parental exposure to toxins.

Male fetuses are particularly sensitive to toxins such as environmental lead, sex hormone analogs, medications and other synthetic molecules. Parental exposure to these toxins is thought explain a large portion of congenital reproductive malformations, such as micropenis, hypospadias (urethra on underside of the penis), undescended testicles and others.

The researchers created a statistical baseline frequency of autism and ID across the country. They then looked at the actual rates of these disorders, county-by-county. Deviations from the baseline are interpreted as resulting from local causes. Factors such as age, ethnicity, socioeconomic groups and geopolitical statuses were analyzed and corrected for.

The team found that every one percent increase in malformations in a county was associated with a 283 percent increase in autism and 94 percent increase in ID in that same county. Almost all areas with higher rates of autism also had higher rates of ID, which the researchers believe corroborates the presence of environmental factors. In addition, they found that male children with autism are almost six times more likely to have congenital genital malformations. Female incidence was linked with increased malformation rates, but weakly so. A county-by-county map of autism and ID incidence above or below the predicted baseline for the entire US is included in the study.

Non-reproductive congenital malformations and viral infections in males were also associated with double digit increases in autism and ID rates. Additionally, income appeared to have a weak effect — every additional $1,000 of income above county average was correlated with around a three percent increase in autism and ID rates. An increased percentage of urban population in a county also showed a weak increase in rates.

The most striking negative effect was state regulation. State-mandated diagnosis of autism by a clinician for consideration in special education was linked with around a whopping 99 percent decrease in the rate of incidence for autism and ID. Certain ethnic backgrounds, such as pacific islanders had significantly lower risk for both diseases.

While the effect of vaccines was not analyzed as part of this study, Rzhetsky notes that the geographic clustering of autism and ID rates is evidence that if vaccines have a role, it’s a very weak one as vaccinations are given uniformly across the US.

Rzhetsky acknowledges there are potential confounders to the study, for example ease of access to data could differ between counties or uneven genetic distribution, beyond the factors they controlled for, could have an effect. The team anticipates future studies could leverage data from the Environmental Protection Agency and other sources to identify links between specific environmental causes and increased rates of autism and ID.

“We interpret the results of this study as a strong environmental signal,” Rzhetsky said. “For future genetic studies we may have to take into account where data were collected, because it’s possible that you can get two identical kids in two different counties and one would have autism and the other would not.”

Story Source:

The above story is based on materials provided by University of Chicago Medical Center. Note: Materials may be edited for content and length.

Journal Reference:

Andrey Rzhetsky, Steven C. Bagley, Kanix Wang, Christopher S. Lyttle, Edwin H. Cook, Russ B. Altman, Robert D. Gibbons. Environmental and State-Level Regulatory Factors Affect the Incidence of Autism and Intellectual Disability. PLoS Computational Biology, 2014; 10 (3): e1003518 DOI: 10.1371/journal.pcbi.1003518

Ocean Extremists and the Strange World of Bomb Dating

Billfish preparing to dice and slice (or rather gun and stun).

One problem with a lot of writing about the natural world is that it’s all plotline, and the plotline is depressingly familiar: The world is a mess, it’s getting messier by the minute, and in the end, or probably sooner, everybody dies.

Oh, and it’s your fault.

“How can you care about the plot,” asks Stephen R. Palumbi, a biologist and director of the Hopkins Marine Station at Stanford University, “until you care about the characters?” That’s how he and his son Anthony R. Palumbi, a science writer, came up with the idea for their new book The Extreme Life of the Sea, a tour of “the fastest, the deepest, the coldest, and the hottest” creatures in the oceans, minus “the sensational fearmongering of ‘Shark Week.’ ”

The result is a giddy scientific tour of weird underwater life, or what the elder Palumbi calls “a collection of guiltless wonder about amazing things going on in the oceans, things that are mostly secrets, except to marine biologists.”

For instance, the authors point out that some Antarctic fish can die of heat stroke at 43 degrees Fahrenheit. Many corals, meanwhile, falter at 90 degrees. But hold that guilt! They mean this by way of introducing the Pompeii worm, Alvinella pompejana, which looks like a red-and-white feather boa and lives around deep-sea hydrothermal vents. These bizarre creatures, five inches in length, somehow live with their hind ends tucked into burrows where the temperature can surge to 200 degrees, while their heads “may as well be on another planet,” in icy 40 degree currents.

Seeing or reading about such creatures as they go about their natural lives has a way of eliciting strong feelings, bordering on awe. The Pompeii worm made me think of an old poem about the sinking of the Titanic and about the cold ocean currents flooding its fiery boilers: “Steel chambers late the pyres / Of her salamandrine fires / Cold currents thrid, and turn to rhythmic tidal lyres.” The author, Thomas Hardy, had no idea that hydrothermal vents could superheat the bottom of the ocean.  Or that a sea bottom creature could live simultaneously in the boiler and the icebox.  No one had any clue about such things until scientists began to describe the life around hydrothermal vents in 1979.

Researchers still can’t say how the Pompeii worms manage it. But billfish—including marlins, sailfish, and swordfish—employ a thermoregulatory mechanism that’s visible to anyone who has ever seen a swordfish steak: That dark-brown flesh on either side of the spinal cord is specialized muscle that cannot contract but instead converts calories directly to heat to keep the core of the body warm. The same sort of tissue turns up in the braincase and next to the eyes, giving billfish a kind of stop-motion ability to spot the flashing maneuvers of smaller fish. They pursue their prey at high speed and then—poetry again—“the vorpal blade” goes “snicker-snack,” that is, they slash with their long, sharp bills and gulp down the stunned victims with toothless mouths.

As plotlines go, this is juicy stuff. The authors also occasionally dabble in playful sensationalism. One way creatures in the deepest parts of the ocean endure the “enormous, crushing hydrostatic pressure from all the water above them,” says Tony Palumbi, is with gigantism, becoming “movie-monster variants” of familiar species. He describes the giant isopod, Bathynomus giganteus, as “a bloodcurdling beast from a sci-fi movie: a pill bug the size of a small dog, scuttling across the blackened sea floor devouring the dead.” This is, he admits, just another way of saying that it is a docile scavenger.

Sharks inevitably also turn up here and there in the book.  But the authors are more interested in talking about the biggest creatures in the history of the planet, blue whales, which still thunder thousands of miles down migratory corridors off California and other coastlines around the world. “The tail fluke delivers thrust at 90% efficiency—far higher than the best commercial ship propellers,” they report. Tony Palumbi adds that a blue whale can hold half its own 200-ton weight in its mouth but “cannot swallow anything bigger than a basketball.”

So beyond the colorful characters, what’s the point? Stephen Palumbi tells a story—OK, it is a disturbing kink in the plotline—about what marine biologists call “bomb dating,” which isn’t something fun to do on Saturday nights.

In March 1954—60 years ago this month—the United States dropped the largest nuclear bomb ever tested, with a yield of 15 megatons, more than twice what had been expected. Radioactive carbon-14, which had existed only in trace amounts until then, drifted far beyond the test site, and recently, it dawned on researchers that this carbon-14 is useful as a biological marker: If a fish was born before 1954, a bone in its ear called the otolith is free of carbon-14; if born after that date, carbon-14 is present.

Once they knew that, researchers were able to determine that fish commonly found in supermarkets labeled “Pacific red snapper” can be 100 years old. Likewise, discoveries beginning in the 1990s that freshly killed bowhead whales had 19th-century spear points made of ivory, slate, or jade embedded in their flesh led scientists to recognize that these animals may be as much as 200 years old.

“The basic point,” says Stephen Palumbi, “is that there are all these amazing creatures out there, living their lives in amazing ways. A lot of people just think of them as seafood.”

The Extreme Life of the Seas argues that we should think about them instead almost as characters in a novel. The more we become invested in their lives, the more likely we are to find the plotline of environmental destruction unthinkable. And thus the more likely we are to push for a happier ending.

The Man Who Turned Antibiotics Into Animal Feed: Part 1

I did the research for this story with help from an Alicia Patterson Fellowship.  This version appears today in the Australian science magazine Cosmos:

On Christmas Day in 1948, a biochemist named Thomas H. Jukes slipped away from his family and made the short drive to his workplace at drug company Lederle Laboratories in Pearl River, New York. A small experiment with chickens was in progress, and the subordinate who would normally have weighed and fed the birds was home for the holiday.

As he made his rounds, Jukes noticed something peculiar. In one group of a dozen chicks, the feed was being supplemented with a pricey new liver extract, which was certain to make those birds gain weight much faster than normal. But Jukes was puzzled that birds in another group were growing even faster. The only thing added to their feed was a new antibiotic called Aureomycin. “The record shows,” Jukes later wrote, staking his claim to the discovery, “that I weighed the chicks on Christmas Day, 1948.”

No one understood how or why an inexpensive antibiotic could cause animals to put on meat more rapidly. (Even now, researchers talk only about “proposed possible mechanisms” to explain it.) But after some quick follow-up work in the field confirmed the finding, Lederle rolled out its product. It was the beginning of a vast uncontrolled experiment to transform the biology of the animals we eat – and perhaps also the biology of the humans who eat them. Antibiotics added to feed at very small, or subtherapeutic, levels would quickly become a standard tool for rearing food animals, so much so that, even now, about 80% of antibiotic sales in the US go to livestock production rather than to human health care.

The food industry has long argued that any limit on use of antibiotics in livestock feed would be an agricultural disaster, or at least the end of affordable meat. But critics are applying increasing pressure on the industry to address its share of the blame for an epidemic of antibiotic-resistant infections that kills hundreds of thousands of people worldwide each year.  So how did antibiotics get into our food supply in the first place? It was largely the work of one otherwise highly esteemed researcher, as well as a classic case of economic interests distorting scientific judgment.

The Man Who Turned Antibiotics Into Animal Feed–Part 2

Thomas H. Jukes (Photo: UC BERKELEY)

Thomas H. Jukes, the man who turned antibiotics into animal feed, was a remarkable biologist. Born in 1903, he was an old school environmentalist, a life member of the Sierra Club, an enthusiastic outdoorsman, and in later years when he was a professor at the University of California at Berkeley, a pioneer in the new science of molecular biology.

He was also an ardent defender of science, or at least his view of it. He wrote hundreds of opinion pieces, often polemical, on topics of the day, and, among other achievements, fought effectively to prevent the introduction of creationism into California schools. He also campaigned against quack cancer cures, and lambasted Nobel-winning chemist Linus Pauling for advocating massive vitamin doses as a panacea.

But Jukes formed his ideas in an age of medical miracles, and firmly believed in the power of science to conquer sickness and hunger. So he also defended the use of DDT against malaria, even calling attempts to ban the insecticide “unquestionably genocidal”. When the prescription drug DES, or diethylstilbestrol, became notorious in the 1970s for causing birth defects and cancers in young women, Jukes argued for its continued use as a growth promoter in cattle, saying the risk to consumers was minuscule. He took what he saw as a rigorous, evidence-based approach to such questions, in contrast to the supposedly “emotional” language of the emerging environmental movement. He often quoted Renaissance medical writer Paracelsus  who believed that everything and nothing is poisonous, or as Jukes noted: “The dose alone makes the poison.”

His fierce opposition to environmental critics undoubtedly reflected his own career history. Before moving to Berkeley in 1963, Jukes had spent his most productive years, from his mid-30s to his late 50s, in the pharmaceutical industry. He worked for Lederle, a division of American Cyanamid, at a facility just outside New York City that now belongs, by a series of mergers, to pharmaceutical giant Pfizer. There, his own writing indicates, he was considerably less rigorous about insisting on detailed experimental evidence.

In particular, his 1985 memoir of how antibiotics first came to be used in livestock feed is often startling to a modern reader because of the casual and freewheeling nature of the pharmaceutical business in the era before the thalidomide birth defect headlines of the 1960s launched strict modern regulation of drug safety. Jukes’ article made it clear that he regarded the unfettered environment in the industry in the mid-20th century as a key to that era’s genius for invention. He and other pioneers “retain a warm spot for those early days”, he wrote.

The Man Who Turned Antibiotics Into Animal Feed–Part 3

Benjamin Duggar (Photo: : BETTMANN/CORBIS)

The introduction of penicillin during World War II was the great world-changing product of that genius, and it prevented tens of thousands of deaths from infected wounds among Allied troops. After the war, the astonishing promise of the antibiotic era set off a scramble for other bacteria-killing drugs. Benjamin Duggar, a botanist who worked mainly on plant diseases caused by fungi, had joined Lederle as a full-time consultant after reaching mandatory retirement age at the University of Wisconsin. Duggar was soon assigned to the search for new antibiotics, which were now making their mark as wonder drugs in civilian health care, too. Duggar’s long interest in fungi soon paid off. “It was a few months later,” Jukes recalled, “that he wrote me that they were having good results, so much so that his assistants and others were ‘stealing’ portions of the crude extracts to cure their colds.” (The idea then was that antibiotics could cure anything, even perhaps cancer.)

Duggar was working with a fungus he had collected from the soil at an experimental agronomy plot belonging to the University of Missouri in Columbus. In culture, the fungus not only demonstrated powerful antibiotic effects, but also produced a yellow pigment for which Duggar named it Streptomyces auriofaciens, or “the gold-bearing streptomyces.”

The name had an apt double meaning. When the president of the company showed off a vial of the stuff to his research committee, he boasted that it “would make a million dollars for Lederle.” This would turn out to be a wild underestimate. By the end of 1948, the antibiotic was being marketed as Aureomycin. It was the first of the tetracycline antibiotics, a genuine miracle drug, effective against a much broader spectrum of disease-causing microbes than the other leading antibiotics, penicillin and streptomycin. Doctors found it particularly useful, The New York Times soon reported, against whooping cough, Rocky Mountain spotted fever, eye infections, typhus, amoebic dysentery, and both streptococcus and staphylococcus infections.

That December, Jukes received a sample to test on chickens. The poultry industry had lately begun to feed its birds soybean meal as a cheaper substitute for fishmeal. But the chickens weren’t thriving. Soybeans lacked an essential ingredient, the elusive “animal protein factor” or “anti-pernicious anemia factor” that we now know to be the essential vitamin B12. In humans, pernicious anemia had until recently been routinely fatal; it had killed Alexander Graham Bell, Annie Oakley, and Madame Curie, among many others. Then, in the 1920s, researchers found a lifesaving cure in the form of raw liver. But eating a half-pound of raw liver daily was almost worse than the disease.

A concentrated liver extract became available in the 1940s. Soon after, competing researchers at Glaxo in England and Merck in Rahway, New Jersey, finally identified the life-saving ingredient. The animal protein factor thereafter became known as vitamin B12. Merck didn’t say so at the time, but it had managed to extract B12 from the fungus Streptomyces griseus, meaning that it could now mass-produce the precious “animal protein factor” in huge fermentation vats.

Lederle must have felt the competitive pressure. It was also searching for a microbial source of animal protein factor, Jukes later wrote, because researchers there had independently concluded that it was a product not just of animal meat, as the name suggested, but also of microorganisms in an animal’s gut, since it was present in their manure. Jukes and a colleague, Robert Stokstad, were experimenting with hens given just enough feed to allow their eggs to hatch. The resulting “depleted” chicks were generally doomed to die within two weeks unless they got more of the critical animal protein factor.

Some of the chicks received diets supplemented with animal protein factor, in the form of liver extract, and some received an Aureomycin supplement, on a hunch that the fungus it came from might also produce the animal protein factor. Soon after their experiments began, though, the researchers realised that they had stumbled upon something unexpected. The chicks being fed the Aureomycin brew were growing even faster than chicks supplemented with animal protein factor alone. It seemed to supply the animal protein factor, plus something extra: “an unidentified growth factor that made the chicks grow more rapidly than did a complete diet”. (University of Wisconsin researchers had in fact demonstrated a similar effect with other antibiotics several years earlier, but without any commercial consequence.)

Looking back almost 35 years later, Jukes wrote, “If such a discovery were made … in 1985, there would be round after round of committee meetings, and plans would be made to cope with various US Food and Drug Administration (FDA) roadblocks. Long-term and short-term toxicity tests would be started. Metabolites and residues would be isolated and identified. Above all, the product would be tested for carcinogenicity. Finally, the FDA would refuse permission to market it.

“None of these things took place in 1949.” Instead, the company informed Jukes that his animal feed lab “could have no more of the product because it was needed for the extraction of the antibiotic for use in human medicine”. It was just about the last time for many decades that human medical need for antibiotics would take priority over livestock and drug industry profits.

The Man Who Turned Antibiotics Into Animal Feed–Part 4

Testing an aureomycin batch at Lederle (Photo: : SUPERSTOCK/GETTY)

Jukes and his staff soon figured out that the “unidentified growth factor” miraculously spurring chick growth was the antibiotic itself. They also found they could get the same growth-promoting effect by feeding chicks on the waste products from the fermentation vats in which Streptomyces auriofaciens was grown, no doubt because some residue inevitably was left behind.

Lederle allowed Jukes to send out Aureomycin samples for testing at universities and agricultural experimental stations. A University of Florida researcher got “the most spectacular results”, a reported tripling of the growth rate in young pigs. Others reported gains that were far smaller but still significant. The company quickly began selling the product, not waiting to complete toxicity testing or routine assays on animals. It sold by the tanker, and demand was intense, particularly in the Midwestern states, where Aureomycin also cured an epidemic of bloody diarrhoea in pigs. A US Senator from Nebraska was soon complaining that his state wasn’t getting its fair share of this miraculous product. A Minnesota pharmacist is said to have bought it in bulk, repackaged it, and sold it at such a high mark-up that he retired to Florida on the profits.

Misleadingly, Lederle marketed the product at first as a source of vitamin B12, Jukes wrote, and was thus “able to avoid any registration problems”. When the FDA finally found out a year later that American livestock were being fed large quantities of antibiotics, an official there merely asked “what level of Aureomycin should be authorised for use as an animal feed supplement?”, and the company told him.

The New York Times broke the news on its front page on April 10, 1950, under the headline, “’Wonder Drug’ Aureomycin Found to Spur Growth 50%”. Science writer William L. Laurence quoted a Lederle report saying that this “spectacular” discovery held “enormous long-range significance for the survival of the human race in a world of dwindling resources and expanding populations”. The article concluded, “No undesirable side effects have been observed.”

Other studies in that era suggested that adding antibiotics to animal feed could produce a gain in the four to 12% range (and much less in more recent studies, see box), not 50%. But that still represented a significant advantage in the business of getting more meat to market less expensively. By eliminating certain chronic diseases, the daily antibiotic regimen also made it possible to raise animals in highly concentrated facilities. It would become the central feature of modern industrial agriculture. The innovation by Jukes and his colleagues soon spread worldwide, and the era of antibiotics devoted primarily to meat production, rather than to human health, had begun.

The Man Who Turned Antibiotics Into Animal Feed–Part 5

Twelve years later, in June of 1962, Rachel Carson’s Silent Spring began to appear in weekly instalments inThe New Yorker, attacking the uncontrolled use of DDT and other pesticides, and raising broader questions about blind reliance on technological solutions. Jukes promptly responded in Chemical Week with a portrait of a more natural world, in which women had no time to be “writers of science fiction horror stories” because they were too busy “squashing black beetles; beating the clothes moths out of the winter woollens; scraping the mould from the fatback pork; and wondering if they could afford the luxury of a chicken for their Sunday dinner”.

That last line hints that he foresaw the eventual attack on the use of antibiotics as growth promoters in livestock. It came just three years later, when a salmonella strain that was resistant to multiple antibiotics killed six people in the UK. The British government’s “Swann Report” subsequently concluded that the disease organisms “acquired their resistance through the use of antibiotics in animals”. Jukes responded that this remained to be proven. He seemed worried mainly that the press would now “threaten us with the propaganda device of a new Silent Spring”.

When Jukes died in 1999, his friends and colleagues remembered him as a brilliant scientist and polemicist (“cantankerous” but “usually right and always honest”). They also celebrated a decent, well-rounded man, who loved to take his family on hikes into the mountains, was a careful reader of the novels of Aldous Huxley, listened to Bach and Beethoven, could quote Shakespeare at will, held season tickets to Berkeley’s “Cal Bear” football games, and, although he had grown up in England, enjoyed few things more than watching Oakland A’s pitcher Dennis Eckersley strike out the other side in the ninth inning of a close game.

An obituary described Jukes as “one of the giants of 20th century biological science”. He may also have been one of its greatest failures. During the long fight over antibiotics in livestock feed, he always focused on the benefits and minimised the risks. When another deadly outbreak of antibiotic resistant salmonella occurred in 1983, for instance, he noted in Science that “feeding antibiotics to animals has increased meat production by millions of pounds annually for 30 years”. That was what mattered — feeding a hungry world.

Elsewhere, Jukes often stated that he and his fellow researchers at Lederle had always foreseen the danger that feeding antibiotics to livestock would make bacterial strains resistant to antibiotics. But he also discounted the idea that antibiotic resistance would spill over to affect human health. Resistance would occur within the guts of animals receiving the antibiotics, and that mattered to him, he suggested around the time of the Swann Report, mainly on the narrow, practical grounds of “whether the effect of antibiotics on improving growth … in farm animals would disappear in a year or two because of the emergence of resistance. If this were the case, we would indeed be doing more harm than good by temporarily alleviating a problem only to replace it with a more intractable one”. Then he added this chilling sentence: “The experiment to provide the answer was under way on a gigantic scale by 1951 and is still in progress.”

Researchers continue to argue today about the consequences of this willy-nilly global experiment, particularly as the medical world’s “wonder drug” antibiotics become ineffective against an array of virulent pathogens, notably including salmonella, E. coli, MRSA (methicillin-resistantStaphylococcus aureus) and a totally drug-resistant variety of tuberculosis. Margaret Chan, director general of the World Health Organization, warned in 2012 that we stand on the brink of a “post-antibiotic era”. That could mean “an end to modern medicine as we know it. Things as common as strep throat or a child’s scratched knee could once again kill”. Infections caused by resistant strains of E. coli already kill more than 800,000 people each year worldwide. In response to this development, the EU, for example, has banned antibiotic-laced animal feed for boosting growth.

The livestock industry continues to deny that antibiotics in animal feed bear much blame for the growing threat from drug-resistant pathogens. But evidence increasingly indicates that resistance routinely spills over from food animals to people, in ways we are only beginning to recognise. In one revealing study published in 2010, for instance, Public Health Agency of Canada researcher Lucie Dutil and her colleagues monitored the effects when the poultry industry in Quebec briefly suspended use of a standard antibiotic. Levels of resistant salmonella and E. coli on supermarket chicken promptly dropped, as did resistant salmonella infections in humans. When use of the antibiotic resumed, resistant bacteria soon reappeared in both meat products and in human consumers.

Other studies have also found strong circumstantial evidence of a link to antibiotic resistance in humans. If he were alive today, Jukes might still deny that turning antibiotics into animal feed had anything to do with this problem. But given his public record, the remarkable thing is that he encouraged the pharmaceutical industry’s “gigantic” experiment to go forward in the first place. In arguing with his critics, he always insisted that they back up their words with hard scientific evidence. But in his own work at Lederle, with his tantalising new discovery ready to go to market la rgely untested, Jukes had behaved as if all the rules of basic science somehow did not apply. It was an extraordinary act of hubris. And, if those who oppose the practice of feeding antibiotics to livestock are correct, the terrible consequence is that vast numbers of people now pay for it every year with their lives.

The Man Who Turned Antibiotics Into Animal Feed–Post Script

Neither industry nor regulators ever conducted a proper large-scale long-term study to test whether the growth promotion Thomas H. Jukes reported was a lasting effect. Even 60 years later, researchers are only beginning to make up for this remarkable omission.

In 2007, researchers at Johns Hopkins University analyzed industry data and found that, while antibiotics produced a slight weight gain in chickens, the cost exceeded the resulting commercial benefit. A 2010 study by the US Department of Agriculture likewise found “no statistically significant impact on production” in broiler chickens, and another USDA study in 2011 found significant gains in nursery pigs, but none in animals close to market size.

Data from Denmark and Sweden, where the use of antibiotics in food animals is restricted, clearly show that tight control of the practice “does not lead to long-term negative effects on industry”, says Tyler Smith, a researcher at The Johns Hopkins Center for a Livable Future. “We are squandering a medical miracle on the basis of very limited evidence that it is necessary to produce animals,” he says.

If antibiotics do boost weight gain, even temporarily, how might it happen? Do they inhibit “bad” bacteria that would otherwise impair growth? Do they slow microbial metabolism, freeing up more nutrients for the host animal? Do they thin the intestinal walls or otherwise make it easier for the animal to absorb nutrients? Nobody knows for sure.

One promising development for livestock producers and health advocates alike is that new genetic insights into an animal’s “microbiome” – the microbes that colonize its gut and other niches – may provide far more exact answers to these questions. Livestock producers are already testing beneficial bacteria and other mechanisms to tweak the bacterial processes in an animal’s gut. In one case, using “good” bacteria to crowd out “bad” ones, a strategy called competitive exclusion, reduced the salmonella load in factory-reared turkeys by 90%. That kind of precise control could soon render subtherapeutic antibiotics in animal feed irrelevant.

Maybe Wolves Don’t Change Rivers, After All

The story of how wolves transformed the Yellowstone National Park landscape, beginning in the 1990s, has become a favorite lesson about the natural world.  A video recounting (above) has gone viral lately, with British writer George Monbiot re-telling the story in his best breathy David Attenborough.

The only problem,  according to field biologist Arthur Middleton, writing in today’s New York Times, is that it isn’t true.

I don’t like the NYT headline “Is the Wolf A Real American Hero?” which seems to fault the wolf for our myth making.  But otherwise, this op-ed is a good reminder that nature is almost always more complex than the stories we tell about it :

FOR a field biologist stuck in the city, the wildlife dioramas at the American Museum of Natural History are among New York’s best offerings. One recent Saturday, I paused by the display for elk, an animal I study. Like all the dioramas, this one is a great tribute. I have observed elk behavior until my face froze and stared at the data results until my eyes stung, but this scene brought back to me the graceful beauty of a tawny elk cow, grazing the autumn grasses.

As I lingered, I noticed a mother reading an interpretive panel to her daughter. It recounted how the reintroduction of wolves in the mid-1990s returned the Yellowstone ecosystem to health by limiting the grazing of elk, which are sometimes known as “wapiti” by Native Americans. “With wolves hunting and scaring wapiti from aspen groves, trees were able to grow tall enough to escape wapiti damage. And tree seedlings actually had a chance.” The songbirds came back, and so did the beavers. “Got it?” the mother asked. The enchanted little girl nodded, and they wandered on.

This story — that wolves fixed a broken Yellowstone by killing and frightening elk — is one of ecology’s most famous. It’s the classic example of what’s called a “trophic cascade,” and has appeared in textbooks, on National Geographic centerfolds and in this newspaper. Americans may know this story better than any other from ecology, and its grip on our imagination is one of the field’s proudest contributions to wildlife conservation. But there is a problem with the story: It’s not true.

We now know that elk are tougher, and Yellowstone more complex, than we gave them credit for. By retelling the same old story about Yellowstone wolves, we distract attention from bigger problems, mislead ourselves about the true challenges of managing ecosystems, and add to the mythology surrounding wolves at the expense of scientific understanding.

The idea that wolves were saving Yellowstone’s plants seemed, at first, to make good sense. Many small-scale studies in the 1990s had shown that predators (like spiders) could benefit grasses and other plants by killing and scaring their prey (like grasshoppers). When, soon after the reintroduction of wolves to Yellowstone, there were some hints of aspen and willow regrowth, ecologists were quick to see the developments through the lens of those earlier studies. Then the media caught on, and the story blew up.

However, like all big ideas in science, this one stimulated follow-up studies, and their results have been coming in. One study published in 2010 in the journal Ecology found that aspen trees hadn’t regrown despite a 60 percent decline in elk numbers. Even in areas where wolves killed the most elk, the elk weren’t scared enough to stop eating aspens. Other studies have agreed. In my own research at the University of Wyoming, my colleagues and I closely tracked wolves and elk east of Yellowstone from 2007 to 2010, and found that elk rarely changed their feeding behavior in response to wolves.

Why aren’t elk so afraid of the big, bad wolf? Compared with other well-studied prey animals — like those grasshoppers — adult elk can be hard for their predators to find and kill. This could be for a few reasons. On the immense Yellowstone landscape, wolf-elk encounters occur less frequently than we thought. Herd living helps elk detect and respond to incoming wolves. And elk are not only much bigger than wolves, but they also kick like hell.

The strongest explanation for why the wolves have made less of a difference than we expected comes from a long-term, experimental study by a research group at Colorado State University. This study, which focused on willows, showed that the decades without wolves changed Yellowstone too much to undo. After humans exterminated wolves nearly a century ago, elk grew so abundant that they all but eliminated willow shrubs. Without willows to eat, beavers declined. Without beaver dams, fast-flowing streams cut deeper into the terrain. The water table dropped below the reach of willow roots. Now it’s too late for even high levels of wolf predation to restore the willows.

A few small patches of Yellowstone’s trees do appear to have benefited from elk declines, but wolves are not the only cause of those declines. Human hunting, growing bear numbers and severe drought have also reduced elk populations. It even appears that the loss of cutthroat trout as a food source has driven grizzly bears to kill more elk calves. Amid this clutter of ecology, there is not a clear link from wolves to plants, songbirds and beavers.

Still, the story persists. Which brings up the question: Does it actually matter if it’s not true? After all, it has bolstered the case for conserving large carnivores in Yellowstone and elsewhere, which is important not just for ecological reasons, but for ethical ones, too. It has stimulated a flagging American interest in wildlife and ecosystem conservation. Next to these benefits, the story can seem only a fib. Besides, large carnivores clearly do cause trophic cascades in other places.

But by insisting that wolves fixed a broken Yellowstone, we distract attention from the area’s many other important conservation challenges. The warmest temperatures in 6,000 years are changing forests and grasslands. Fungus and beetle infestations are causing the decline of whitebark pine. Natural gas drilling is affecting the winter ranges of migratory wildlife. To protect cattle from disease, our government agencies still kill many bison that migrate out of the park in search of food. And invasive lake trout may be wreaking more havoc on the ecosystem than was ever caused by the loss of wolves.

When we tell the wolf story, we get the Yellowstone story wrong.

Perhaps the greatest risk of this story is a loss of credibility for the scientists and environmental groups who tell it. We need the confidence of the public if we are to provide trusted advice on policy issues. This is especially true in the rural West, where we have altered landscapes in ways we cannot expect large carnivores to fix, and where many people still resent the reintroduction of wolves near their ranchlands and communities.

This bitterness has led a vocal minority of Westerners to popularize their own myths about the reintroduced wolves: They are a voracious, nonnative strain. The government lies about their true numbers. They devastate elk herds, spread elk diseases, and harass elk relentlessly — often just for fun.

All this is, of course, nonsense. But the answer is not reciprocal myth making — what the biologist L. David Mech has likened to “sanctifying the wolf.” The energies of scientists and environmental groups would be better spent on pragmatic efforts that help people learn how to live with large carnivores. In the long run, we will conserve ecosystems not only with simple fixes, like reintroducing species, but by seeking ways to mitigate the conflicts that originally caused their loss.

I recognize that it is hard to see the wolf through clear eyes. For me, it has happened only once. It was a frigid, windless February morning, and I was tracking a big gray male wolf just east of Yellowstone. The snow was so soft and deep that it muffled my footsteps. I could hear only the occasional snap of a branch.

Then suddenly, a loud “yip!” I looked up to see five dark shapes in a clearing, less than a hundred feet ahead. Incredibly, the wolves hadn’t noticed me. Four of them milled about, wagging and playing. The big male stood watching, and snarled when they stumbled close. Soon, they wandered on, vanishing one by one into the falling snow.

That may have been the only time I truly saw the wolf, during three long winters of field work. Yet in that moment, it was clear that this animal doesn’t need our stories. It just needs us to see it, someday, for what it really is.

This Week’s Green News Roundup

Here’s the latest conservation news from The Nature Conservancy’s Cool Green Science blog.

Biodiversity

Tony Abbott, prime minister of Australia, declares the country will create no new parks under his administration. Scientists, not surprisingly, are outraged. (Conservation Bytes)

Stranger than fiction: Tiny pseudo-scorpions hitch a ride on beetles. (Mongabay)

Why being good for medicine is bad for the humble horseshoe crab…but being obsolete may be worse. (Atlantic)

Wildlife

The orange, cave-dwelling crocodiles of Gabon. (Abanda Expeditions)

The second edition of the Sibley Guide to Birds is here. Here are 10 things serious birders should know about the changes. (10,000 Birds)

Where do turtle toddlers disappear to? A mystery solved. (Discover)

Beavers back in the Bronx River. What will the zoopolitan future look like? (Strange Behaviors)

New Research

Meet the “information parasites” (they’re also birds). (The Loom)

Here’s an ecosystem engineering caterpillar that inadvertently builds nice homes for invasive weevils. (ESA Ecology)

How deep can fish swim? Even fish have their limits. (Science Magazine)

Climate Change

Climate risk to Indian cities is ‘huge,’ says Indian think tank TERI. (AlertNet, Reuters)

Nature News

Good news: the Javan rhino population is up 10 percent this year. Bad news: there are still only 58 Javan rhinos. (Mongabay)

One step closer to protection for Bristol Bay: the head of the EPA announces agency will begin process that could stop industrial mining in the region. (Trout Unlimited)

Conservation Tactics

A new use for invasive trees: feed them to zoo animals. (L.A. Times)

If there’s a good way to control pests without pesticides, why aren’t we using it more? (PNAS First Look Blog)

Science Communications

Social networking with a purpose: stemming brain drain and reconnecting communities. (PLoS Biology)

Miss ScienceOnline last week?

> Converge sessions (unconference talk for plenaries) are available online. (ScienceOnlineTogether)

> And a few bloggers shared their contributions directly: Social media is a scientific research tool. (Southern Fried Science)

> Meanwhile, Anton Zuiker (past defender of accused sexual harrasser and ScienceOnline cofounder @BoraZ) steps down as chairman of ScienceOnline. (Mister Sugar)

This & That

How much water do you use? If you’re like most people, your guess is way off. (Conservation Magazine)

Environmentalists often argue against economic growth. That’s just code for keeping poor people poor, argues Roger Pielke, Jr. (Earth Island Journal)