PloS Genetics has just published a new study identifying genes that could provide a partial explanation for why pygmies are so short. It’s a fascinating question: Haven’t we all been intrigued by pygmies since we first came across pictures of them in the National Geographic when we were kids?

The researchers used a gene chip to analyze the genes of three pygmy groups and three neighboring groups of Bantu-speaking people–who are taller, and with whom the pygmies have sometimes had children, leading to some mixing of genetic traits. They found regions in the genome that seemed related to the pygmies’ adaptation to their environments. Genes in these regions are related to insulin and insulin-like growth factor, and to immunity and reproduction and metabolism, according to the study’s abstract. The genetic analysis also revealed portions of the genome related to height and to “growth hormone-stimulated STAT5 signaling,” whatever that might be.

This is tough stuff. At one point in the introduction to the study, the authors say that their findings provide insights into the adaptations in the ancestors of West African pygmies and the genetic “architecture” of short stature. Further down in the study, the authors link the findings concerning height and adaptation. “Our results raise the possibility that the adaptive process that produced small body size in Pygmies may be the result of selection for traits other than stature, including early reproduction, metabolism, and immunity…”

The University of Pennsylvania press release is little help. The study, it says, identifies genes that might be associated with height. It goes on to say that the study “also provides evidence based on genetic signatures of natural selection to suggest why these groups evolved to be small, with signs pointing to hormonal pathways and immune system regulation as possible drivers.” What? A couple of quotes from the lead author of the study (Sarah Tishkoff, in the photo above) don’t help either.

But a few good reporters have helped to clear up the issues here.

At Scientific American, Gary Stix clearly draws a connection between adaptation and height. “It may be that genes that protect against microbes may also hinder growth. Diminished stature could  be a byproduct of bolstering immune and metabolic defenses and not a direct adaptation to a hunter-gatherer lifestyle,” he writes. Interesting, isn’t it? The short height itself is not an adaptation to the harsh living conditions faced by the pygmies–but merely a side-effect, so to speak, of the adaptations that actually do help them survive.

At the Chronicle of Higher Education, Josh Fischman also neatly draws the link. He writes that the researchers have “identified a ‘master gene’ for immune response that is much more common in Pygmies than in their taller neighbors, the Bantu.” And he reports that “this same gene can disrupt growth-hormone pathways.”

At Nature, Erika Check Hayden takes a very different approach. Rather than focusing on the evolutionary tradeoffs, she takes great care to note the limitations of the study. That’s never a bad thing, but I’m not sure she gives the researchers their due. Her lede is that the pygmy study “underscores how tricky it can be to find the genetic underpinnings of human characteristics.” That caution arrives before we know what the researchers are claiming. She then reports the identification of genes possibly linked to height, without discussing the immune factors, or insulin or metabolism. She continues with a discussion of the shortcomings of the study and the difficulty of doing such research in remote populations.

Elizabeth Norton at Science Now raises the natural-selection question: Is the short height a selective advantage in dense jungles, as some have speculated? This study, she notes, argues against that. She gets down to a bit more detail than some of the others, discussing the role of the CISH gene in the study. (I’ll refer you to Norton for more on that.)

Dr. Christopher Token, in a blog post at ABC News, notes speculation that the pygmies’ short stature was due to a lack of Vitamin D, because the deep shadows of the rainforest keep them out of sunlight. No, he writes: It’s genes!

So far, there has been less coverage of the story than I would have expected. We’ll likely see more in the coming days. And we should. It’s newsworthy, and it’s a good opportunity to enlighten readers to some of the complexities of genetic research–and its value.

- Paul Raeburn

Source: Grist, 4/23/2012

Last week, I wrote a piece here, On the Corn Syrup Theory of Autism, which took a critical look at a Grist story concerning a scientific paper proposing that high fructose corn syrup consumption was responsible for the rise in autism cases in the United States. My point was that the author, Tom Laskaway, was far too quick to embrace that conclusion, to cheer lead for a paper which was, at best, speculative, and, at worst, not credible.

And I wasn’t the only person to make that point. At his blog, Collide-A-Scape, environmental journalist and former Audubon magazine editor, Keith Kloor, called it “shoddy and irresponsible journalism.” And Grist’s readers were just as tough in their response. To partially quote one comment:  By writing an article about this terrible study and giving it such a misleading title you are revealing yourself as either a) too stupid to be trusted with the responsibility of writing about science or b) willing to knowingly mislead the public in the service of your irrational personal hatred of HFCS.

As Grist editor, Scott Rosenburg, wrote in the aftermath, a genuine furor arose. Some furors are healthy, he noted; they encourage people to consider new ideas, to challenge their own assumptions. But some furors are more like, “Guys, you messed up.” I’m afraid that from where I sit this was one of the latter kind.

Rosenburg’s post-mortem is both thoughtful and, I think, wonderfully non-defensive.  He zeroes in on the essential fault in Laskaway’s piece – that it was a superficial response to a flawed paper about a complicated issue. And he details Grist’s rapid response to that realization.

First, editors changed the original headline from a statement “New Study Links Autism to High Fructose Corn Syrup” to a question: “Paper Asks: Does High Fructose Corn Syrup Contribute to A Rise Autism?”

And second, Rosenburg asked science blogger and writer Emily Willingham to take a more thorough look at the paper itself.  Before I tell you what she wrote, let me take a minute here to say that I think tagging Willingham – who is one of the best science writers working today – was a brilliantly right move.  She’s one of those writers – as evidenced,  for instance, in this January piece for Slate about GMO food alarmist – who always leaves the reader feeling  smarter.

Actually, I think I usually am smarter after reading her work. Willingham’s piece for Grist, which ran Tuesday, is titled Why That Corn Syrup and Autism Study Leaves Such A Sour Taste. And I’ve rarely read a better deconstruction – or maybe evisceration is a better word – of a deeply flawed scientific paper. There’s history here, there’s original statistical analysis, and there’s deep understanding of what science is, how it works, and when it doesn’t.

As Willingham notes, the autism paper  (technically a review, rather than a study) waves “several red flags of pseudoscience”.

For instance, the authors’ theory of autism is based on the idea that high-fructose corn syrup is contaminated with mercury which they link to developmental disorders. They base this on a three-year old paper by the lead author, Renee Dufault, which claimed to find such contamination. As Willingham points out, studies attempting to confirm that finding were unable to do so. And she points out, the whole mercury question is dismaying vague.  The authors randomly rule out any other sources of mercury (including emissions from coal-fired plants) and they fail to even analyze for or distinguish between different types of mercury exposure. Pure elemental mercury, for instance, is far less of a health risk than such mercury compounds as methylmercury (the type that tends to bioaccumulate in fish) or salts of mercury, such as mercury bichloride).

But my favorite part of Willingham’s debunking of the Dufault paper is a graph she produced, based on her careful analysis, showing that U.S. consumption of high fructose corn syrup doesn’t track actually with the increased rates of  autism diagnosis. As it shows (I’ve included it at the top of this story) those rates have clearly been rising even as HFCS consumption has been falling.

It’s such a good breakdown that I wish it could be required reading; certainly my science writing students are destined to study it. So I come here, at last, not to criticize Grist but to praise it. This is one of the best responses to a bad article I’ve ever seen. Absolute redemption, Scott Rosenburg!

— Deborah Blum

All this time we’ve been looking in the wrong place! American women? Don’t waste your time. It’s been in Poland for decades, hiding inside the soft tissues of an 83-year-old Warsaw woman! Unfortunately, she’s now deceased, and her G-spot has been carved up by a “cosmetic gynecologist.”

No, you have not stumbled on to The Onion or The Daily Show. Here it is from Melissa Healy in the Los Angeles Times:

Like so many explorers before him, Dr. Adam Ostrzenski has long dreamed of finding a piece of elusive territory with a reputation for near-mythic powers. Ostrzenski’s quarry is the G spot, the long-conjectured trigger for enhancing female orgasm. And in an article published Wednesday by the Journal of Sexual Medicine, the semi-retired Florida gynecologist declared that he had found it.

This is Tina Hesman Saey in Science News:

Despite what’s written in sex advice books, the scientific search for the female erogenous zone known as the G-spot has proved surprisingly elusive. But now one physician claims to have found the first anatomical evidence of the fabled structure.

She gets to the skeptics in her third paragraph, which is roughly two paragraphs below where the skepticism should have been.

Helen Thomson at The New Scientist properly gets the skepticism into the first graf:

G marks the spot. Or does it? One researcher claims to have pinpointed and described the anatomy of the elusive G spot, an area of the vagina reputed to produce intense orgasms when stimulated. Many others are not so sure, saying that the G spot is unlikely to be a single structure.

If you want to know what the study claims, you can read the press release, or look at the study itself if you have access to The Journal of Sexual Medicine.

Science bloggers were clearly the rational voices in this story. The blogger Ed Yong (Not Exactly Rocket Science) alerted me to a post by a British blogger I didn’t know, Dr. Petra Boynton. Dr. Petra, as she calls herself on her blog, recounts the long, depressing history of news stories saying the G-spot does exist, or it doesn’t, or that it is the most important thing in sex research, or other silly things, most of which are described as coming from “groundbreaking studies.” An excerpt from her lengthy criticism of the coverage:

Each time studies on the g-spot have been published the media has reacted as though
- these are groundbreaking studies
- the do they/don’t they have g-spots issue is the most pressing topic in sex research
- these studies require no critical attention

And in all these cases journalists – including health and science correspondents – have responded to these studies in one simple way. To frame their stories with the question ‘does the g-spot exist?’

This hides a whole heap of bad science and poor journalism and misinformation on sex, arousal and orgasm.

Bora Zivkovic, editor of the blog network at Scientific American, alerted the Tracker to other blog posts critiquing the coverage, including one by Debby Herbenick (of the Kinsey Institute) at The Daily Beast, another by Ricki Lewis at Scientific American, and a few others.

My criticism of the study is simpler and lazier. Did we ever learn much of anything from a study with a sample size of one? Yes, there are exceptions, I know. But an autopsy of one subject should never lead to broad conclusions about women everywhere, especially when we’re dealing with something as prone to misinformation as the G-spot.

It’s probably the case that the traditional requirements of objectivity in the legacy media prevented reporters from saying what the bloggers said–that the emperor has no clothes. It’s another example of how we benefit from the diverse menu of journalistic offerings we have at our fingertips. Science blogs, as we’ve known for a long time now, are clearly enriching our world.

In the interests of decorum, I’ve decided not to add a picture to this post.

- Paul Raeburn

Once, while striding across Harvard Yard with the biologist and Harvard professor E.O. Wilson, I said something about the history of the place, which bears the memory of the footprints of hundreds of thousands of Harvard students, including some who later became presidents or great scholars and thinkers. (Or had less exalted careers; let’s be honest.) Wilson raised an arm, swept it across the landscape before us and said the yard’s dank, black soil, even after centuries of human habitation, almost certainly harbored species unknown to science.

I thought of that while reading Carol Kaesuk Yoon‘s lead piece in today’s Science Times, “So Much Life on a Little Patch of Earth.” Yoon lives on a street in Bellingham, Wash. that “is crowded enough that when someone sneezes in a backyard, the person next door is likely to say ‘gesundheit.’” Yet she spotted, on her window (the one that looks on to her neighbor’s bathroom window), a species of moth never before seen alive in North America. Yoon didn’t know that, but her husband, an entomologist at the local university, did–or at least he determined that after collecting the moth in his net and corresponding with colleagues.

They later found, in their backyard, a species of sawfly never before seen on the West Coast. The lesson Yoon draws from this is not that their home is ecologically unique, but that, echoing Wilson, “Any patch of earth, large or small, turns out to be a mad surprise party of species.” Her backyard is no more or less ecologically diverse than that hallowed ground at Harvard.

She goes on to recount a project that she and her family undertook to identify every species they could find in and around their home. Of course, such a task is impossible. But it can lead us to a greater appreciation of what’s around us. “For those, like children, with eyes open wide,” she writes, “rarities can abound.”

Former Vice President Dick Cheney’s heart transplant a month ago sprung former Times writer Lawrence K. Altman, M.D. from his retirement to note that Cheney’s medical history could almost be “a history of medical progress against heart disease.” Altman draws on his medical training and decades of experience analyzing and writing about the medical records of presidents and kings to trace Cheney’s heart ailments and treatments. It’s the kind of story that became Altman’s signature at the Times, and he still does it well.

Natalie Angier is here with what might be called a signature story for her–using animals to say something about human behavior. Here it’s the “spirit of sisterhood” among “animals as diverse as African elephants and barnyard mice, blue monkeys of Kenya and feral horses of New Zealand.” It is told with Angier’s typical wit and literary flair. ”A familiar friend calms and equilibrates, mops up the cortisol spills that can weaken the immune system, and in so doing may help lengthen life — in baboons, humans and other group-minded kinds,” she writes. Or, as the scientist she’s interviewing puts it,  “having coffee with friends is good for you.” The story is pegged to the new HBO series, “Girls.”

For more, including briefs on raven friendships, lingering regret, and optimism and heart disease, turn to: the whole section.

- Paul Raeburn

Warren Buffett is a smart guy, and he’s done reasonably well for himself. But he made a mistake when he crossed Laura Newman. (I probably shouldn’t be giving stock tips, but–psssst–sell Berkshire Hathaway now!) Newman, on her Patient POV blog, lets the billionaire have it. In her view, and in the view of some other smart people, Buffett’s stock-market wisdom doesn’t make him any smarter than the rest of us with regard to health care. “He’s an icon who other men will follow,” she writes–but they shouldn’t. For reasons that Newman explains, Buffett probably should not have been screened for prostate cancer and, at the age of 81, probably should not be treated. But he’s not taking her advice. Newman makes her 10 points cleverly and convincingly. Read them here. And–spoiler alert–the No. 1 reason why Buffett bugs Newman?

If he wants to be a role model, maybe he should get castrated with an orchiectomy. It’s a low-tech option that few men choose. I wonder why.

Take that, Buffett.

 - Paul Raeburn

I’m in the airport, on my way home from the annual meeting in Atlanta of the Association of Health Care Journalists. I saw a lot of old friends, met new friends, and established in-person friendships with many Twitter and Facebook friends. (Most overheard line at meetings: “It’s so nice to meet you in person!”) As usual, some of the best discussions occurred over a drink or at dinner, when we compared notes about stories, editors, the financial health of old and new media, and making a living as a freelancer. More than 600 of AHCJ’s members turned out for the meeting.

Former President Jimmy Carter and First Lady Rosalynn Carter kicked things off with a report on the health-care work the Carter Center is doing in Africa, including the near eradication of the guinea worm, a Carter Center signature project. Dr. Otis Brawley, chief medical officer of the American Cancer Society, gave a luncheon talk that managed to be both entertaining and frightening (not an easy rhetorical trick) about the need for reforms in cancer screening and treatment. I didn’t take notes so I can’t give you the exact quote, but after talking about a drug that did more harm than good and about the wide overuse of MRI and CT scanners, he said, in words to this effect, The treatment is going to give the patient a 5% increased risk of death, but we can take awfully good pictures of her as she dies. (Book plug: More of the same, along with a dark view of the future of American health care, appears in Brawley’s new book How we do Harm: A Doctor Breaks Ranks About Being Sick in America.)

Many AHCJ members spoke about their experiences freelancing (including this member, at a panel Sunday morning), and about covering health care and medicine. It is a very friendly and helpful group. I can’t prove it, but I strongly suspect the organization and its annual meeting do a lot to improve health and medical coverage in the U.S.

One of the highlights of the meeting, for me, was the announcement of the association’s Awards for Excellence in Health Care Journalism. (You can find the winners’ list here.) It’s inspiring to be reminded that reporters and editors are still putting out good stories, very good stories, at a time when journalism is in such turmoil.

Here’s an excerpt from one award-winning story in the “consumer and feature” category. It’s entitled “The Woman Who Fell to Earth.” Deborah Shurson was on a skidiving trip with her husband, Randy. He jumped first and landed with…

a thud when he heard screams, and turned to see Deborah, her partially opened white chute wrapped around her like a shroud as she streaked toward the ground. Her main chute had never opened, and she was frantically clawing her way to her reserve chute.

Deborah’s parents, who had brought a picnic lunch, stood paralyzed as they watched her in freefall at 125 miles per hour, then saw her disappear behind a hill in a little mushroom cloud — her reserve chute opening too late.

That was in 1982. You’ll have to follow the link if you want to know what happened, because you’re not going to get any spoilers from me.

That gripping story, written by Ruthann Richter for Stanford Medicine Magazine, was the second place winner in the category. The winner was written by Tahlia Honea of the Skagit Valley (Wash.) Herald. It was about a man suffering from throat cancer, who was told by his doctor that as the tumor in his throat grew, it would eventually block his airway, leading to “a horrible death” by asphyxiation. The patient’s choice: Should he use the lethal pills his doctor gave him, or not?

The Milwaukee Journal Sentinel won top honors in the categories of health policy reporting and investigative reporting in large publications. The top three awards for beat reporting went to David Armstrong of Bloomberg News (first place), Trine Tsouderos of the Chicago Tribune (second), and Jordan Rau of Kaiser Health News (third).

I counted 35 awards. There are familiar names among the winners, and unfamiliar names–a good sign that good journalism in thriving at more than a few outlets.

Now is the time for reporters who cover health care to decide whether they want to attempt a story that might be worthy of an award next year. Stories shouldn’t be written to win awards, but stories that win awards generally prove to have been worth the time and effort put into them.

- Paul Raeburn

Yesterday, John Timmer, the amazingly smart science editor at Ars Technica, posted this comment on Twitter:

@j_timmer Ugh. @grist, if your author doesn’t understand a science paper, maybe he shouldn’t make wild accusations based on it? http://t.co/4p5ezqsN

I don’t what it says about me but I immediately clicked on the link to discover this story about a study proposing that rising autism rates could be linked to consumption of high fructose corn syrup. And, again, I don’t what it says about me but my first reaction was not to check my pantry for such products but to think ‘Darn it (or words to that effect) didn’t I just write last week about studies linking autism to obesity during pregnancy?” Yes, and not in an entirely enthusiastic way.

Timmer then added this note:

@j_timmer That @grist article shows no indication of critical thinking skills whatsoever. Paper appealed to author’s biases, so he ran with it.

At this point, I took a more serious look at Tom Laskaway‘s Grist story, which states:

“The blaring headline version of the new study’s conclusion would read: “High-Fructose Corn Syrup Causes Autism. And while that may be a bit of an overstatement, it’s not off by much.”

Honestly, readers, I had to get up and kick a piece of furniture. Of course, some may feel that a better response would be to alert the Nobel committee that we are close (“not off by much”) to discovering the cause of autism and it appears to be something akin to a Theory of Corn Consumption. Or possibly obesity in pregnancy. Or could it be both, as Kristina Chew wondered over at the website Care2: “High Fructose Corn Syrup and Maternal Obesity: Autism Causes?”  Or could it be…well, I’ll get to that later.

As I’ve already written about the obesity coverage, let me take a minute here to further discuss the realities of that corn syrup study.  The study was published April 10 in the online, peer-reviewed journal Clinical Epigenetics in what the journal describes as provisional form. The lead author is Renee Dufault, a former toxicologist for the U.S. Food and Drug Administration (FDA) who is these days described as a government whistle blower.

According to the Government Accountability Project, she was forced out of the agency after discovering low-levels of mercury contamination in High Fructose Corn Syrup and refusing to follow an agency directive to conceal that.  Her findings were included in a 2009 paper, published in the journal Behavioral and Brain Functions, titled “Mercury Exposure, Nutritional Deficiencies, and Metabolic Disruptions May Affect Learning in Children.” (It’s important to note here that Dufault does not include vaccines in this equation and does not consider them a contributor to autism.)

Her latest paper continues to focus on the possible link between trace mineral deficiencies and developmental disorders, in which high fructose corn syrup may play a role. The basic idea is this: a diet high in mercury-contaminated corn syrup tends to interfere with the way we metabolize trace nutrients, lowering zinc levels in the body and allowing a higher load of other heavy metals. This nutrient imbalance also interferes with production of enzymes that work to break down dangerous substances – from metals to pesticides – as they enter the body. Without this protection, these contaminants are allowed to wreak greater havoc, in particular, in pregnant women,  they may affect the developing nervous system of an unborn child and – if all of this occurs as proposed – could possibly be a contributing factor in the Autism Spectrum Disorder.

Or as the authors put it in their 20-page paper (which is available for free download from the journal), this cascade of events, if occurring as described,  can “lead to oxidative stress in the brain reducing neuronal plasticity.”  In fact, this is, at least, an interesting idea and, I think, fits into our growing appreciation of the intricate dance between environment, biology, and behavior. Could it lead to a better understanding of such effects on developmental neurobiology? Yes. Eventually. Does it definitively establish corn syrup as a “cause” at this moment. No.

For one thing, other literature contradicts the idea that high fructose corn syrup always has a dramatic effect on mineral uptake, as, for instance, in this 1992 paper. For another, the authors point out in the paper that there are other dietary reasons that people may be low in certain minerals, such as “insufficient dietary intake of Ca (calcium), Mg (magnesium), and Zn (zinc.) The study compares populations in the US and Italy, where far less corn sweetener is used, but it’s fair to wonder about other dietary differences between these two cultures.

To be fair,  there’s been a fair amount of cautionary health studies concerning  an over-reliance on high fructose corn syrup as a sweetener. And to be fair again, Grist wasn’t the only publication to see the study as an opportunity to urge changes in the American diet. “Americans are screwed by the food we eat,” wrote Thom Hartman at The Talk Radio News Service.  “The typical American diet may be linked to the epidemic of autism in children in the U.S.,” noted the Public News Service. “The typical American diet may fuel autism,” agreed Deborah Mitchell at the EmaxHealth website.

Maybe but let’s hold off after all on that phone call to Stockholm. I tend to prefer the analysis over at he lifestyle blog Bliss Tree, where Hanna Brooks-Olsen called the study disturbing but noted a number of research challenges to be overcome, including the fact that “it’s difficult to truly study something that most of the population is consistently being exposed to at low levels.”

And at the Autism Key blog, writer Gary Porter called it more of a food safety concern than necessarily an autism finding. “With autism rates now at a mind-blowing 1 in 88,” he added, “there are many who are desperately looking for a definitive cause and a silver bullet theory.

And this, I think may be the most important point here, a legitimate connection between last week’s obesity analysis and this week’s targeting of high fructose corn syrup.  As Liz Szabo at USA Today noted in a savvy story earlier this month, the rising autism numbers are driving a new sense of urgency in understanding the causes of the disorder. In addition to long-standing genetic theories, she points out,  researchers are now looking at everything from the risk of living too close to a highway to the risk of maternal use of antidepressants to the risk of aging parents.

I’m in favor of the big picture here, the one that puts all this research together and suggests that autism is a complicated story and that we’re likely to find an intricate web of influences that lead to it. I hope, in fact, that such awareness will result in a lessening of the anti-vaccine misinformation related to this disease. But if we jump on the bandwagon of every one of these alternative theories and ideas, we do neither our readers or the science itself much service.  Instead, we may only add to misinformation. And that, readers, is why I chose to kick the furniture instead of making that long-awaited call to Stockholm.

— Deborah Blum

For many years dentists’ offices have displayed posters claiming that gum disease can lead to cardiovascular disease. Periodontists have even led patients to believe that treating gum inflammations and infections can help prevent heart attacks. The connection looked fishy when a supposed link first arose, a former staffer at the National Institute of Dental and Craniofacial Research told the Tracker, but that didn’t stop the institute from pushing the idea until it became widely accepted.

In 2005, for example, a research paper, promoted with a dental institute news release was headlined, “Study finds direct association between cardiovascular disease and periodontal bacteria.”

Now comes the American Heart Association, issuing what Sharon Begley of Reuters called “a rare ‘scientific statement’ ” saying that gum disease is not even a risk factor for cardiovascular problems. Its meta-analysis of 600 papers shows that a high percentage of studies finding a link were seriously flawed or used inappropriate methods. Begley’s story cites several recent studies, including from such prestigious institutions as the Harvard School of Public Health, supporting the alleged link.

Begley’s kicker illustrates how ingrained belief in the link is. She notes that the American Academy of Periodontology promotes the association on its Web site and that the academy’s president told Begley that she “did not see a need to revise the Web site.”

At the Los Angeles Times, Rosie Mestel ledes with “Gum disease–it raises the risk of heart disease and stroke, doesn’t it?” She then quotes a long, refutation from the heart association report and says, “Knock me down with a feather.”

The Telegraph of the U.K. uses a blunt hed: “Myth that gum disease causes heart attacks debunked.”

-Boyce Rensberger

Courtesy: Wikimedia Commons

If you go to the website of the journal, Pediatrics, you will find a section labeled eFirst pages. These are articles published online in advance of the print publication. This Monday, there were 15 such early releases, ranging from a look at codeine fatalities in children after tonsillectomy surgery to a Danish analysis of the impact on marriage of having a child with cancer.

But the study that got all the attention is titled “Maternal Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders.” (If you follow the link, you can download the entire study for free and I’d like to take a moment here to applaud the journal for making that possible.)

So, what made it the report of the week? Well, autism, of course, is an attention grabber.  Added to that, the phrase “metabolic conditions” in this case meant diabetes, obesity and hypertension. And it was the obesity connection – the idea that being obese while pregnant could increase the risk of a developmental disorder – that really made the story take off.

If you doubt that, you need only take a stroll through the 800-plus stories that resulted, with headlines that ranged from “Autism linked to obesity in pregnancy” at Science News to “Mom’s Pregnancy Weight May Increase Risk of Autism, Developmental Disorders” at Fox News to “Obese Mums Could Increase Autism Risk: Study” in the New Zealand Herald.

And this was despite the fact that the study’s primary focus was on Type 2 diabetes during pregnancy; “other conditions of interest were hypertension and obesity,” the authors note. They used the standard reference for obese of a Body Mass Index (a proportionate measure of fat in the body) of 30 or more.

BMI was actually self-reported, although checked against medical records for about a third of the women in the study. The study itself focused on 1004 children (517 diagnosed with autism, 172 with developmental delays, and 315 with no neurological diagnosis as a control). The children, aged two to five, were enrolled in the Childhood Autism Risks from Genetics and Environment (CHARGE) study. The researchers, from the University of California-Davis, then looked at the health of their mothers during pregnancy through a combination of questionnaires and medical records (available for about 58 percent of the participants).

The results are more complicated – and more interesting – then the simple obesity connection suggests. The analysis showed the autism diagnosis to be unaffected by race/ethnicity, education or whether families were covered by government or private health insurance. But children with other developmental delays were more likely to have mothers who were poorly educated Hispanics with only government health support.

Mothers of children with autism or other developmental disorders were more likely to suffer from hypertension during pregnancy but not with any statistical significance. Mothers with diabetes were 2.3 times more likely than those in the control group to have a child with a developmental delay. Within the autism group, children of diabetic mothers did by far the worst when tested on their ability to convey emotion.

And is she ever going to get to the obesity question, you may wonder?

Well, the researchers also found that women who were obese during pregnancy (either already overweight or showing dramatic weight gain during gestation) were at a higher risk of having  a child with Autism Spectrum Disorder.  Or, as the very carefully written press release from UC-Davis puts it:

The study found that mothers who were obese were 1-2/3 times more likely to have a child with autism as normal-weight mothers without diabetes or hypertension, and were more than twice as likely to have a child with another developmental disorder.

What does this mean? Hard to say because, of course, the study did not look at paternal influences or examine other possible maternal influences, from specific diet to medications to family health history. Further, it’s not as though only the mothers of autistic children were overweight. For the record, 20 percent of the mothers who had children with development disorders were classified as obese during pregnancy. But so were 14 percent of mothers of normally developing children. So, yes, a statistically significant difference but not an overwhelming, let-me-sit-down, knock-your-socks off one.

I suspect rather, that while the study’s finding is more speculative than conclusive, it got extra traction from our growing concern over obesity rates in general.  Certainly, that was the main message of some stories: “Pregnant women might now have one more good reason to watch their diet and exercise,” wrote Amina Khan in the Los Angeles Times. Certainly, the study authors played to this connection: “Maternal MCs [metabolic conditions] may be broadly associated with problems in children. With obesity rates rising steadily, these results appear to raise serious public health concerns.”

And I don’t want to downplay the health concerns related to obesity (which include the other metabolic conditions here,  Type 2 diabetes and hypertension). But I do want to raise a note of caution about making a study like this a standard bearer for better eating habits. One, this research only shows an association and not an entirely uncomplicated one. And two, while I do believe in responsible and healthy eating habits by pregnant women, there’s a long, unfortunate blame-the-mother history regarding autism (think Bruno Bettleheim and the refrigerator mother) that makes me want to tread warily here.

So it was gratifying to find some definitely smart reporting of this study along just those cautious lines:

In The Atlantic, Brian Fung‘s piece, “Should We Really Worry About Obesity’s Link to Autism”, does a great job of exploring other better defined risk factors.

“The finding adds to the increasingly complex picture of possible factors that contribute to the disorders,” wrote Shirley S. Wang in the Wall Street Journal.

Jon Hamilton‘s piece for NPR’s Salt blog contains not just one but two warnings against drawing any conclusions.  Both he and Wang interviewed the study’s lead author, Irva Hertz-Picciotto, who goes out of her way, especially in the Journal story, to emphasize that this is not a “blame the mom” result.

And I also found this very nice article at a smaller paper, the Vallejo (Ca.) Times Herald, in which reporters Sarah Rohrs and Lindsey Tanner interviewed local physicians and urged their readers not to panic based on preliminary research.

All of which should remind us that there’s a lot more work to be done here. And none of which should discourage us from pursuing about the basic good principles of a healthy lifestyle.

– Deborah Blum

Sandra G. Boodman at The Washington Post has disrupted my morning once again.

An aggregator that I follow just picked up a story of hers from last December. And while I have other things to do this morning, I couldn’t pass Boodman’s story by.

It begins with a woman, Silvia Bacot, walking down the hall at work, saying hello to everyone she passes because she can no longer see well enough to tell whom she knows and whom she doesn’t. This is what hooked me, a few grafs into the piece:

It wasn’t until the summer of 2010, while undergoing a work-up for laser eye surgery, that Bacot, now 38, learned that her visual problems were not caused by the normal progression of myopia, but in fact indicated something far more serious.

“I turned white as a sheet of paper,” Bacot recalled, after corneal specialist Roy Rubinfeld told her that lasik was out of the question. “I didn’t even know I had anything wrong with me.”

The piece then flashes back to when the woman first had problems seeing, at age six, and we’re on the track of–something!

You won’t find any spoilers here. If you want to know what’s going on, you’ll have to read the piece.

Boodman has made a practice of these kinds of stories, as I’ve noted on the Tracker before, here and here. I don’t know how many of these she’s written, but I’d like to catch up with the others. A collection might make a nice Kindle single.

I’d buy it.

- Paul Raeburn

On Monday, we learned that the use of genome scans to predict illness is going to be less valuable than we might have thought.

“If every aspect of a person’s DNA is known, would it be possible to predict the diseases in that person’s future? And could that knowledge be used to forestall the otherwise inevitable?” asked Gina Kolata in The New York Times. “The answer, according to a new study of twins, is, for the most part, “no.”

In Science News, Tina Hesman Saey wrote, in a clever lede, “The human genetic instruction book is as lousy at predicting disease as an almanac is at predicting the weather.” Here’s Lauran Neergaard of The Associated Press: “Gene scans for everyone? Not so fast.” Robert Bazell of NBC: “So what will this ‘genetic blueprint’ tell us of our future health?  Not much, according to an important study out Monday…”

And John Fauber at the Milwaukee Journal-Sentinel, who was at the Chicago cancer meeting where the results were presented: ”Researchers have found that the increasingly popular form of disease prediction testing known as whole genome sequencing fails to provide solid insight into whether someone will develop a variety of common diseases.”

This seemed to be big news. Haven’t we been promised that the sequencing of the human genome, and its eventual incorporation into medical practice, would revolutionize health care? The new study challenges that, which should indeed be big news. Yet it seems there are problems with this study.

The study has the right pedigree. It comes from Johns Hopkins and Harvard, and one of the authors is Bert Vogelstein, known to science writers and others as a distinguished researcher who, among many other achievements, decoded much of the genetics of colon cancer. And yet…

“The problem, geneticists say, is not that the study, published on 2 April in Science Translational Medicine, arrived at a false conclusion, but that it arrived at an old, familiar one via questionable methods and is now being portrayed by the media as a new discovery that undermines the value of genetics.” That comes from Erika Check Hayden writing in Nature‘s newsblog.

Hayden wrote that scientists are “irked” over the paper, and she outlined their criticisms, which are worth reading in full in her post. But here are some of them–the things that everyone should know about genome screening.

–The study made claims about genetic prediction, but it included no genomic data. It was based on data on how often twins got the same illnesses, and assumptions about how their genetics affected their risk of disease. According to the people Hayden interviewed, those assumptions are not correct.

–Many other studies have concluded that genes alone don’t do a very good job of predicting a person’s risk of illness, and many stories have appeared criticizing the value of commercial genetic tests.

–Statisticians that Hayden talked to say the statistical model Vogelstein and colleagues used is not realistic.

–The study doesn’t correct for certain errors inherent in gene studies, such as considering that twins often grow up in the same environment.

–And the coverage of the story could weaken support for genetic research.

I’ll leave the last one aside; it’s not the concern of reporters how their stories affect support for research. But Hayden makes a powerful argument that the study had problems that should have been made clear in the reporting.

Luke Jostins at genomes unzipped dismisses some of the criticism by statistical geneticists as sour grapes, because they didn’t get the coverage Vogelstein did. But Jostins acknowledges the problem with the study and the coverage. “Identical twins, despite sharing the same DNA, the same socioeconomic background, the same childhood environment and (usually) the same bloody placenta, will usually not get the same disease. There is no health destiny,” he writes.

For a conversation about this among reporters on Twitter, see Hayden’s Storify.

The question here is how reporters might have suspected these criticisms and produced better stories–or how their reporting might have done a better job of uncovering the potential pitfalls of the study. Few reporters are qualified to assess the statistical soundness of the study. But why did they not find out more about this in their reporting? Perhaps some were so interested in the contrarian nature of the story–genomes aren’t all they’re cracked up to be–that they didn’t push hard enough to discover potential problems with the study.

One tip-off was the many stories that have been written questioning the value of commercial genome scans. Reporters should have asked whether the findings were new. That would not necessarily have uncovered the statistical issues, but it might have led reporters to scale back their coverage.

If I had covered this story, I fear I, too, would have missed the issues that Hayden presents so clearly. The main lesson I can draw from this is that reporters ought to be as skeptical and vigilant as they can be, especially when writing about subjects, such as this one, that they have written about many times before–enough to have formed opinions that might be getting in their way.

- Paul Raeburn

At his DotEarth perch former NYTimes science and environmental reporter (‘former’ by the gray lady’s official nomenclature) and now NYT opinion writer Andrew C. Revkin this week offered a breath of fresh air in describing what the recently visible third wing of the global warming debate is all about. At least, for me, it clarified things a bit.

This crowd has confused me recently. I won’t name them, but the general theme is that environmentalism (as it has been) is dead, that hectoring people to be green will never work, that we need to adapt to climate change while working on technologies that might someday avert or reverse it, and that not all the contrarians are lunatics and calling them that only makes things worse. I’ve felt the general tenor, which I won’t pin on anybody specific as this is just a hunch, is an argument that progressive people should stop talking truth to power. If one wants to get a climate, low-carbon policy in place, don’t say anything as scary as that the situation is desperate, or as insulting as that it is our own stupid fault, or generally to be hysterical and deluded, hypocritical ninnies. Rather, disguise it as a road to energy independence, as a route to prosperity via efficiency, whatever…

Back to Andy’s column. It offers a much-deserved salute to Paul Voosen at Greenwire (one of the E&E newsletters that mostly cost a bundle to read) , and links to ructions emanating from Peter Kereiva, the chief scientist at the Nature Conservancy. He lashes into the fantastic, almost magical thinking of many greens (think EarthFirst! etc.). It seems to me a desperate long shot to think a new, hard-headed and inclusive tone in climate change policy discussions will lead to faster progress than we’re getting now. But since the latter is measured in units of zilch, it’s worth talking about. And, it says here, it is gaining traction.

Here is the the direct link to Voosen’s recent story, a catalyst to Revkin’s column.

*UPDATE – While we’re on Andy Revkin, I nominate his April 1 column, which he stresses is no April Fools joke, as the most sensible reaction and put-down to all the hullabaloo and loud expressions of disgust and dismay about so-called pink slime. It’s an ingredient in beef that is taken out of dead animals. Just like all the rest of the ingredients including of course the antibiotics. Don’t worry about the ammonia used in its processing. The stuff is beef. If it’s disgusting, his column implies but these are my words, that’s because almost everything in a slaughterhouse would be disgusting if one stopped to ponder. What is done – my thoughts again, not Andy’s – to get the pink slime is little different from what you do with your own teeth when gnawing the last goodies from a barbecued rib. And the industry calls it LFBT, for lean, finely textured beef. Plus, as Revkin tells us, if the mad rush to remove this relatively healthful portion of a patty from the American food chain succeeds, that will impel a million+ extra steers and heifers to slaughter to make up the difference.

- Charlie Petit