Field of Science

Of lice and men: An itchy history

If you've read my About page, you're aware of my interest in lice. I got the chance to expand on my interest in a long-form blog post over at the Scientific American guest blog, and if you're looking for something that'll make you scratch your head, this one's the read you seek.

It begins:

Ponder the louse. Consider its plural, lice. Try now not to scratch the multiple itches that have just populated your head at the very thought of these near-microscopic insects crawling around in that forest of hair follicles, laying eggs, sucking blood, and generally creeping you out.

The thing is, your head may not be the likeliest place to feel the itch. After all, we’re home not only to the louse, but to lice, plural. As in two genera of lice, and three different kinds. One of those, the pubic louse, appears to trace back to contact between the Homo lineage and the gorilla, but more on that in a bit.

Interested? Hope so. Continue reading here.

Terbutaline and autism...or not

[Can being really freaking cold during pregnancy cause autism in your child? Dunno. Via Wikimedia Commons, of all places.]

Dr. Jay (a.k.a., um, "Dr. Jay") Gordon tweeted something this morning that gave me pause. His tweet read that "terbutaline for pre-term labor doesn't work" with a link provided and continued with "and might increase autism," with another link provided. Curious about this alleged association between autism and terbutaline (a beta2-adrenergic receptor agonist, used to open air passages on-label and to stop pre-term labor off-label), I went to that latter link provided. I was just oh-so-shattered only to find "autism" inserted out of the blue via a quote from one Richard Dodd, a senior partner with Cappolino Dodd Krebs LLP. A quick visit to Google U turned up the URL Yep. They turned to an attorney who specializes in malpractice suits for an extensive quote alleging a connection between autism and terbutaline. He and his firm are not alone in pushing the terbutaline-autism link.

I've got no dog in this hunt, as I never was exposed to terbutaline and neither were my children. I am also not in the pay of whoever it is who makes the stuff. But I'd never seen any final ruling substantiating this link, so I turned again to Google U, the post-grad version, Google Scholar. There, I happened to find this review-of-a-review by Rodier et al. in the American Journal of Obstetrics and Gynecology, entitled "Does treatment of premature labor with terbutaline increase the risk of autism spectrum disorders?" It's from the February 2011 issue. The answer, according to the authors who performed the review of another review by Witter et al., is as follows:

Beta-adrenergic agents have been used in pregnant women for the treatment of premature labor and for the treatment of asthma. Concerns have been expressed that exposure to terbutaline, which is a beta-2 adrenergic agonist, may increase the risk of autism spectrum disorders (ASDs) in the offspring. This hypothesis deserves critical review, given the number of patients who have been exposed to the drug in the last 2 decades. The results are important to both the obstetricians and patients who weigh the risks and benefits of interventions and to the pediatricians who counsel the families of affected children.

We conducted an examination of the human and animal studies that have been used to support this hypothesis in a recent review,1 and we have reached a different conclusion. We find no support for the hypothesis that the use of terbutaline as a tocolytic agent is associated with the subsequent development of ASDs.

They note that studies lack analysis of the role that prematurity itself may play in ASD and overlook the fact that premature labor itself may well be "evidence of injury."

The horrible piece that "Dr. Jay" linked to, in addition to turning to an injury lawyer for medical expertise, also contains the following completely unsubstantiated and somewhat oddly phrased statement:
Toxins and bad medical drugs, including vaccinations, are often the leading suspects of autism disorders.
That would be news to the people who are actually involved in autism research, say the ones who find evidence of a high level of genetic contribution to autism, those who engage in studies of copy number variation, and those who conducted studies of identical vs fraternal twins, finding concordance as high as 90%. But you'd better watch out for those "bad medical drugs."

It's beyond me why someone who is presumably trained in medicine would even have linked to an "article" like this. It goes off topic in describing the FDA's warning about the use of terbutaline in pre-term labor, which focuses on the potential harm to the pregnant woman and calls for doctors to stop this off-label use.

The "article" also refers to "recent" studies from a team at Duke University on the autism-terbutaline link. Those studies date to 2007 and 2005. I'm not saying that the Duke team is not onto something with the overall mechanism, but when their only reference to "these findings have been extended to include autism" is their own work, a study of dizygotic twins...that's not a case-closed argument, counselor.

The Duke research team further provides two citations to support the statement that " Indeed, a connection of organophosphate exposures to autism has been proposed." Unfortunately, the authors of one of the studies cited found a link in North America but not in Italy, and instead of concluding that perhaps there isn't a link, they determined that there was instead "regional specificity in gene-environment interactions." And it's not about terbutaline.

The second citation they provide, "Szpir M. New thinking on neurodevelopment. Environmental Health Perspectives 2006; 114:A101-A107," unfortunately devotes three paragraphs of serious consideration to the "thimerosal-autism" link--in 2005!--and mentions SafeMinds, of all things. In other words, it is a review/commentary, not a presentation of new data. These three citations are the only ones in the 2007 paper that the authors offer as support of a "terbutaline-autism" link. Only one is a study involving terbutaline, and it's their own work.

Of interest, this sort of sketchy citation history is one thing that the AJOG review-of-the-review focuses on. Indeed, Rodier et al. note the echo chamber effect. One of the human studies the Witter et al. review cited is really a case study with commentary by four pediatricians, none of whom offer support of a link between terbutaline exposure and the patient's symptoms. The citation simply doesn't support the assertion.

Of further interest, however, is that the next human study the Witter et al. review cites is...that same dizygotic twin study self-cited above, which happens to be the work of some of the authors on the Witter et al. review. In other words, they self-cited again. As Dory from Finding Nemo would say, "Echo! Echo! Echo!" Here's what Rodier et al. have to say about that study:

The second reference that is cited in the article is to a study that had been reported by several of the same authors of the review.13 The review states that the earlier paper demonstrated increased concordance for ASDs in dizygotic twins after terbutaline treatment in utero. However, a careful review of the data found no significant association of concordance with terbutaline exposure in the whole twin sample (36 cases). Only when the investigators divided the sample into smaller subgroups and focused on twin pairs who were both male and had no other cases of ASDs in their family were they able to find a significant association between drug exposure and outcome. This group of 16 twin pairs should have been at increased risk for ASDs because they were male and at decreased risk because of the absence of ASDs in their families. It is unclear why such a subgroup would ever be selected for study a priori. If it was selected a posteriori, then the results should be considered “hypothesis-generating” at best.

Rodier et al. effectively address the shortcomings of the three other human studies offered up--one doesn't draw a conclusion that's related to terbutaline use, another is a personal communication (unpublished information) that doesn't fit with what the abstract for the presentation says, and the third was, according to the authors, of a "peculiar" design involving eight autistic children from two families with completely uninformative results.

When Rodier et al. turn to the animal studies, they observe that
However, it is important to note that the studies that are cited come almost exclusively from 1 research group and use the same dose at the same stage of development for the same number of repeated doses. If there is any error in the dose or timing or duration of exposure that was chosen to mimic terbutaline as a tocolytic therapy, it is shared by all the articles that were cited.
Guess which "one research group" that is?

Somehow, this morning, thanks to "Dr. Jay," I've managed to uncover a self-echoing terbutaline-autism cottage industry involving lawyers and, separately, a Duke University research team. Unfortunately, it also happens to be the day that the review in AJOG came out directly addressing the data for the proposed link and finding it faulty. Sometimes, whether it's development or social media, it can be all about the timing.

Suzanne Humphries: I think the oath isn't "First, tell us your CV"

[Image: An evil practitioner of "allopathic" medicine tries to kill a little girl.]

I don't normally go all ad hominem on people, but in this case, I've clearly been invited. Suzanne Humphries would like us to know a little bit about her. In fact, she wants us to know so much about her and her glorious prowess that she devotes 598 words of a 976-word blog post allegedly about vaccines and how godawful they are to...Suzanne Humphries. Her main claim to knowing all things medical and scientific is that she is a "Medical Doctor" (sic). Never mind that she's abandoned her profession or any pretense at that profession and is now, according to a biography over at the laughable, working toward certification as a "homeopathic physician."

Alas, I fear that she will do far greater harm with her writing than she's ever going to do good with her watered-down "treatments."

Speaking of watered down, in the 378 words that she manages to devote to something other than herself, she makes the following claims:
"Vaccines did not save humanity and never will."
I'm not going to argue with that. I don't know anyone who's ever said that vaccines "saved humanity." They've saved millions of lives, but we're so hell bent on harming ourselves in other ways, I'm pretty sure no vaccine could ever be invented that could stop us.
"Vaccines have never been proven truly safe except for perhaps the parameters of immediate death or some specific adverse events within up to 4 weeks."
Translation, please? No one who understands vaccines has ever claimed that they are "truly" safe. They are relatively quite safe. They are among the safest medical interventions and among the most successful and effective, yea verily, among the "greatest practical advances" in medicine. A hell of a lot safer than, say, meningitis. And unlike Dr. Humphries, I'm going to go ahead and link you to references for the assertions I make. Vaccines' general effectiveness and safety have demonstrably gone well beyond only considerations of immediate death or a brief month from vaccination. To avoid making this a novel-length blog post, I'll just link you to two of many possible appropriate Google searches. That way, you can also earn hours towards your degree from Google U, like Jenny McCarthy did.

Next, I bring you a series of completely unreferenced statements that demand referencing:
"Smallpox was not eradicated by vaccines as many doctors readily say it was. They say this out of conditioning rather than out of understanding the history or science."
This statement is counter to the information you can find referenced here, here, and here (heavily referenced, so see also the reference lists). A full-court-press effort from WHO made this happen.

"Polio virus was not responsible for the paralysis in the first part of the 20th century. Polio vaccine research, development, testing and distribution has committed atrocities upon primates and humanity. Bill Gates is not a humanitarian."
These statements are simply false. Regarding polio, the assertion that it didn't cause paralysis in (or before) the first part of the 20th century would have shocked, say, the subject of the 3000-year-old ancient Egyptian stele indicating a case of paralyzing poliomyelitis or the people living during the Great Depression when paralytic poliomyelitis was "one of the most feared diseases known." Indeed, President Franklin D. Roosevelt who contracted, um, paralytic poliomyelitis in 1921 (you know, in the early 20th century), was apparently so pissed off about it that he declared war on polio during his administration. Again, the writing is confusing, so perhaps she means that whatever people blamed on polio as the paralytic agent in the early 20th century was, in fact, caused by some other agent. Odd how the polio vaccine made that go away, anyway.

I can't exactly see how research, development, testing, or distribution of anything could commit an atrocity. Perhaps it's the wording that's throwing me off, again. You know, that degree from Rutgers wasn't in English, after all. As for Bill Gates, I simply link you to this. Sure, Bill could be sittin' around, eating bon-bons and thinking about a world takeover, but instead, he's spending time on, oh, polio eradication. Asshole.

Humphries coughs up more unsubstantiated statements, all of them opinion anyway. I know this because I homeschool my 9-year-old, and we just did a little unit on detecting the difference between fact and opinion.
"Vaccines are dangerous and should never be injected into anyone for any reason. They are not the answer to infectious diseases. There are many more sustainable and benevolent solutions than vaccines."
But this one really pisses me off, too, all jocularity aside. You tell the millions of children who die from vaccine-preventable diseases every year about those "benevolent" solutions to keep them from the grave. You tell their mothers about how your watered-down, homeopathic shit is somehow going to prevent their child from dying from encephalitis, meningitis, diarrhea, or malaria. Vaccines are not the answer to infectious diseases: They are the easy, accessible, effective, walloping kick in the ass against infectious diseases, and the best one we've got. Are they risk free? No. But neither is being alive. Every move we make carries risk. Vaccines carry a very limited risk relative to their enormous benefits (sorry about the paywall). But nothing angers me quite as much as this insouciant attitude from a first-world crackpot with too much time on her hands about diseases that kill children every single day because they don't have vaccines available.
"Medical authorities should not have the final word on how doctors treat individual patients in the privacy of their own offices and should not be able to dictate injections into our private hospital patients."
I love this one because it raises the specter of "authorities" hell bent on invading everyone's privacy and interfering with how doctors interact with their patients. All part of that big Pharma-Industrio-Medico-Governmento-Bill-Gateso conspiracy. Just a little appeal to the libertarian woo-ville out there. As though the AAP had a rep in every pediatrician's office, standing there with a little checklist and interrupting whenever the pediatrician goes off script. I'm not sure why her statement involves "private hospital patients," as most vaccines are not administered in a hospital. From my experience working with pediatricians and having them as my children's doctors, their decisions about vaccines are pretty much theirs to make. To take an example from Woo-Ville itself, Dr. Jay Gordon and Dr. Robert Sears, Woolebrities of the first order, feel free not only to ignore the gold standards of their guiding professional body but write and tweet about it quite a bit.

Then we get to a chunk. In this chunk, Humphries appeals to, yea verily, she challenges healthcare practitioners to, on their own (no receptionists do this, please) read books and "alternative literature sources." She asks them for a lot more that she seems to assume they have not done or don't understand, carefully explaining the huge conspiracy that peer review is. Then, she asks that they "place their egos beside them."

Please take a moment to cover your ears to protect against the deafening noise of all those irony meters exploding. Yes, the woman who just devoted 598 of 976 words to telling you that as a credentialed healthcare practitioner, she has a right to expect your unquestioning attention, is stating that other healthcare practitioners, presumably with the same credentials, just aren't capable of what she is. And then, Dr. 598 Words drags in Ego. But of course, that's how she began, isn't it?

ETA: This post from Orac over at Respectful Insolence goes into even more depth.

Slow down there, diet soda study

Recent news has a lot of women I know clasping their heads in horror, guilting over diet soda consumption, or swearing off the sweet, calorie-free little buggers forever.

I'd say to them and to anyone else horrified by the news that diet sodas "cause" "vascular events" to slow down, hoss. Before you trash all those full Coke Zero cans, send them my wa...I mean, note the following:

The study in question has not been peer reviewed. That's right. It was presented at a conference. That does not mean it's invalid or worthless; it just means that what they've said and what they've concluded has yet to undergo the standard processes of scientific evaluation.

So where do we find irresponsible representation of this study? Let's start with the news release from the American Heart Association, at whose conference (correction: release is from AHA; conference is American STROKE association, natch) these data were presented. It begins,
Even if you drink diet soda — instead of the sugar variety — you could still have a much higher risk of vascular events compared to those who don’t drink soda, according to research presented at the American Stroke Association’s International Stroke Conference 2011.
Their findings are summarized as follows:
During an average follow-up of 9.3 years, 559 vascular events occurred (including ischemic and hemorrhagic stroke, which is caused by rupture of a weakened blood vessel). Researchers accounted for participants’ age, sex, race or ethnicity, smoking status, exercise, alcohol consumption and daily caloric intake. And even after researchers also accounted for patients’ metabolic syndrome, peripheral vascular disease and heart disease history, the increased risk persisted at a rate 48 percent higher.
Way down in the news release, after it deals with a second aspect of the team's work (salt), the news release notes the obvious caveats: The researchers did not control for type of diet soda--there are a variety of non-calorie sweeteners and diet sodas out there--and the study relied on self-reported dietary behavior. And while there is mention of controlling for "daily caloric intake," there is not mention of controlling for other relevant dietary factors that might be associated with (a) diet soda consumption or (b) risk for stroke and other vascular events.

I see the absence of peer review as something that requires acknowledgment in any news story covering these findings. I see the above-noted weaknesses also as requiring acknowledgment...preferably early any story covering these findings.

Let's see if the news media agree with me.

From MSNBC, "Daily diet soda tied to higher risk for stroke, heart attack." There is no mention of the weaknesses noted above, although some of the quoted experts discuss the potential role of diet in the findings. And there's a strange wandering off task by one researcher who brings up "caramel coloring" as a potential explanation. It seems that it has "been linked to vascular issues." But it also happens to be present in dark-colored sodas, diet or otherwise.

WebMD teases us with, "Is diet soda linked to heart, stroke risk?" Is it? In this piece, an outside expert brings up two other potentially missing variables from the study: family history and weight gain. Good point, outside expert! This piece also notes the caveats already described. Another expert slams the questionnaire the researchers used. And at the end of the piece, after the jump to the second page, WebMD provides this statement:
These findings were presented at a medical conference. They should be considered preliminary as they have not yet undergone the "peer review" process, in which outside experts scrutinize the data prior to publication in a medical journal.

That's great, but I wish they'd put it as the dek. I wish every report stated that information right up front. Why? Because of reactions like this one from a woman on Twitter:
I learned on the Today Show today that hockey is going to kill Jack & diet soda is going to kill me. (Carbon monoxide & vascular events) FML

And this one, from a woman interviewed for the MSNBC piece:
“This is pretty scary,” said Denise Gainey, a 49-year-old administrative assistant from Amelia, Va. Worried that she might have inherited a higher risk of heart disease, Gainey wants to be careful. “I guess I’ll just be drinking a lot more water,” she said.
That takes me to my favorite find of all today, the LA Times. And I mean that sincerely. Here's the headline:

Diet soda and heart/stroke risk: a link doesn't prove cause and effect

Damn straight. Then the writer, Rosie Mestel, whom I suspect might be a consumer of diet sodas, goes on:
A study just presented at the American Stroke Assn.’s International Stroke Conference reported a link between the amount of diet soda someone drinks and the risk of having a stroke or heart attack.


Then she brings up all of the caveats. There is not, however, mention of the lack of peer review.

A headline roundup
  • Can diet soda boost your stroke risk? Researchers find a 61% increased risk among those who drink daily (US News and World Report). I note that the much ballyhooed 61% drops to 48% with controlling for factors like metabolic syndrome. There is no mention of the caveats or the lack of peer review.
  • Study: Diet soda drinkers at increased risk for stroke (Fox News). I am completely grossed out by the fact that if you hover over "school of medicine"in the piece (if you get that linked; it changes with each reload), you get an ad for a plastic surgeon. Eww. Anyway, the link is to a limited report highlighting only the screaming numbers with no context.
  • Diet soda: Fewer calories, greater stroke risk (From an ABC affiliate running the ABC version of the piece). I don't think they meant the headline to imply that the absence of calories in diet soda causes a greater stroke risk, do you? That said, early on the piece reads, "This study has major flaws and should not change anyone's diet soda consumption," said ABC News Chief Health and Medical Editor Dr. Richard Besser."
  • Study: Diet soda may increase the risk of stroke (From AOL Health). They blow the lede in this one, referring to keeping weight down. The study didn't control for that. Oops.
  • Diet soda tied to stroke risk but reasons unclear (Seattle Times). The piece starts with, "It's far from definitive proof." At least. My favorite from this piece is, "A simple solution, health experts say, is to drink water instead."
Sure, I'd do that. If it gave me that bit o' sweetness, carbonation, and caffeine that I'm getting from my diet soda.

Academia: Women helping women? Or not?

In her right-where-I-live piece about her fall from the academic ladder (also blogged here at The Curious Wavefunction), Kathy Weston makes an important point: Anyone in science needs a great mentor.

How about a woman in science? It's possible that she might need a mentor who's more than a scientist, a mentor who is also a woman, She Who Came Before and Succeeded. A woman new to the path might expect some enlightenment from such a mentor about how to deal with the sex-unique obstacles that women can encounter in academe and in science. Right? Mightn't she?

Yet, these kinds of role models were vanishingly rare when I was in my PhD program and beyond. In fact, at that time, only a handful of tenure-track faculty in our department were women, and they were just as rare in my tenure-track positions. I had only one woman who taught one of my many graduate classes.

Each of my dissertation committees (we had a committee for orals and one for defense) featured one female faculty member. You might think that we'd have had some camaraderie, what with having the same type of gonads and all, but we did not. There was such a paucity of tenured women at that time that a cursory glance at the faculty pictures in the building directory quickly told the entire story. So many dudes, so few dames. My choices were limited, and they weren't interested in me.

That was my experience with female faculty in graduate school. In my first tenure-track job, another female faculty member emerged as the only member of our animal care and use committee to throw up roadblocks in front of my approvals for using animals in research. Our various interactions all held this tone. There was no evidence of mutual support or bonding or a desire to help the women faculty, still woefully underrepresented in the department at the time.

Mentors are great to have. My postdoctoral PI was--and is--a great mentor. He fostered what I did well, supported my goals, allowed me a ton of leeway in getting things done, guided me through various paths to meeting other amazing scientists. He even took me to do a c-section on a hyena. Yes, I said, "hyena." This guy is truly a mentor, and his support was so helpful to me after years of not experiencing a mentoring relationship like that.

Why is it that in my comparatively brief travels through academe--I figure I spent a total of 15 years in the gyre--I've encountered three women who could've been something to me, something important, yet none of them were? Why is it that my sole fantastic mentor is a man, one who investigates penile development, of all things?

I know I've made reference to my gender identity, which is complex, and maybe this interplay of gender identity has more to do with these instant attractions and repulsions than primary sex. But I also know that while that lack of attraction may have played out between women I met at the top of the ladder and me, it didn't work that way between me and the women I had in my own lab during my time on the tenure track. I mentored them. I guided them, fed them, had them over for holidays because they were far from home, encouraged them, networked for them, and Go-Girled them. So, I know it can be done. It just wasn't ever done for me.

If you're a woman in academe...has it been done for you?

The "working mom = fat children" study: How the news media say it

A new study is out linking longer working hours for mothers with a one- to two-pound increase in weight for their children, especially in the 11 to 12 age range (or a gain of 1 lb every 5 months beyond the typical expectations for age for every 5.3 months mom is employed). The PDF for the full paper is available here. Note that there a few points to embed in your brain before we move to what the news media have done with this one.

1. The role of fathers' employment was not investigated here.

2. There already have been studies linking weight and maternal employment. Can we get some studies that look at the role of fathers in mediating these factors, say, fathers who do more of the domestic work? Or even better as a sex-control, mom-mom households? At any rate, this study isn't exactly "news."

3. One fifth of the sample of 990 children was overweight. Note that this does not say "obese." In fact, nowhere in the paper does it say "obese" in reference to the findings. The authors note the "increasing rate of obesity" in general, but nowhere do they describe the children in this cohort as being obese. Remember that as you read what the news reports say.

4. They did not find evidence that "nonstandard" work--nights, evenings, weekends--was associated with greater weight gain in children, and they seem to be rather bothered by this finding. I can see why...and I refer you to (5) below.

5. The authors of the study speculate that the peak weight-gain risk they identified in children of working mothers might be explained as follows:

It is possible that because fifth and sixth graders generally have more independence and less adult supervision over their time use and food choices than third graders, maternal employment precipitates poorer food choices and more sedentary activity. Children’s lesser supervision at older ages may be related to the diminished likelihood of being in an after-school program and a greater likelihood of being in self-care (Johnson, 2005). The ways in which the link between maternal employment and child health may be moderated by child age warrants more research attention.

This speculation is less likely to make sense if you don't find greater evidence of weight gain among children whose mothers work "non-standard" hours--when children are even more likely to be left unsupervised, especially in single-parent homes.

6. Finally, I refer you to these findings from the paper:
Results from the RE models, which compare outcomes across different children, did not reveal any significant associations between mothers’ employment, or nonstandard employment, and their children’s BMI. Looking at the within-child FE regression models (our preferred models), which related within-child changes in mothers’ employment experiences to changes in that child’s BMI over time, we see in Model 1 that an additional period of maternal employment over the child’s lifetime was associated with a 10% of a standard deviation increase in children’s BMI (d = 0.10; 0.02/0.204). The fact that such an association was found in the FE models, but not the RE models, may be due to the different nature of such models; specifically, RE models compared across different children whose mothers had different employment experiences, while the FE models related an individual child’s accumulation of maternal employment to changes in that same child’s BMI. There were no significant associations between maternal employment status at a given time point (Model 2) and BMI, and also no associations (at conventional levels of significance) between maternal nonstandard work and child BMI (Models 3 and 4).
That strikes me as equivocal, but dammit, Jim, I'm a biologist, not a statistician.

The news reports make many references to "latchkey" kids gorging themselves on after-school garbage while Mom is not around. Not one single writeup I've read so far mentions that the children in this study, in large part, each had another parent. Rarely does a report include discussion of the possibility that two parents might be involved in the health of their child, might have a role in a child's weight gain.

Many, many of these reports bring up, yet again, the "childhood obesity epidemic" and either directly or obliquely blame working mothers for having a role in it. Some even mention how working moms don't "cook from scratch." (For the record, this working mom does that all the time). This, my friends, is 1950s interpretation of 21st-century findings, and it irritates the hell out of me.

Let's let the ledes and other content speak for themselves, shall we?

From the Telegraph, which had among the more sensible of writeups:

Researchers said that for every 10 hours a week a mother works, the weight of their children increases by on average one and a half per cent.

From the Daily Mail Online (you should check out the story just for the overwrought and truly awful art they included):

Children whose mothers work are six times more likely to be overweight, research shows.

They believe that a diet of fatty ready meals and snacks eaten unsupervised after school is causing them to pile on the pounds.

They are often left to prepare their own dinners which may consist of a high-calorie ready-meal left out in the fridge, as opposed to a family dinner cooked from scratch.

Note here the introduction of the June Cleaver-evoking "cooked from scratch" phrasing. It was not, for the record, a phrase the authors used in the paper. Ah, for the good old days. What did I do with those pearls?

From HealthDay:
As if working mothers don't have enough to feel guilty about, a new study suggests that the more time they spend working, the heavier their children become.
My favorite over-interpretation from MSNBC:
Children whose mothers work continuously over their lifetime are more likely to have a higher body mass index (BMI) than those whose moms work less, according to a new study, but they're not necessarily worse off in terms of their overall health.
From desperate need of a copy editor:
Childhood obesity has been steadily rising in the U.S. in the past 30 years, and a new study from American University in Washington, D.C. has found that a child’s weight may depend on how much their mothers were away at work growing up.
NPR pours salve into the wound, bless 'em:

So does that mean Mom should stay at home and not work? Not at all, says Taryn Morrissey, a developmental psychologist at American University and lead author of the study appearing in the journal Child Development.

For one thing, the difference was small, Morrissey says. For every five months or so a mother was employed while her child was growing up, a kid of average height would gain about a pound more than otherwise expected.

There you have it, straight from a study author's mouth. It's a good study. It's findings are worth discussing, in context. But that context needs to be the 21st century, not some ideal of a time long since passed.

Headline roundup

All you working mothers can quit feeling guilty about leaving your children as you head to the office.

The kids fat and happy. Well, fat anyway.

Researchers say the more years you work outside the home, the more likely your children will sit in front of the TV and say, "Gosh, I miss Mommy. Pass the Cheetos."

H1N1 vax and narcolepsy? Or not...

[Behold, vials of Pandemrix, possibly, potentially, putatively, conceivably, not confirmedly linked to narcolepsy in children. Courtesy of Wikimedia Commons]

Today's big vaccine news is a study out of Finland with findings of increased rates of narcolepsy among children who had received Pandemrix, Glaxo-Smith-Klein's H1N1 vaccine. Reuters, describing the research as "yet to be confirmed," reported that the study found that children receiving the vaccine were nine times more likely to develop narcolepsy than children who had not. Note that this H1N1 vax was used only when H1N1 was declared pandemic in 2009. It is not the combination flu shot being used this year.

Curious about what other entities had to say, I searched around for more information and found this report from the Press Association. Guess what? There is an unexplained increase in narcolepsy in the pediatric populations in Scandinavia, including Iceland and Sweden, where it is not restricted or correlated with children who have received this vaccine. Furthermore, this association, or "signal," as they call it in epidemiology, has not emerged anywhere else.

According to reports, 31 million doses of this vaccine have been administered in Europe and 90 million worldwide, and 162 cases of narcolepsy reported in Europe, most of them in Finland and Sweden. What remains unknown from these reports is whether or not the narcolepsy is chronic.

I can only infer from what I've found so far, including the fact that this issue has been examined in Sweden with, so far, no findings of a correlation. Thus, I infer from the information that in Finland, they found an increase in narcolepsy in the vaccinated population while in Sweden, they did not. In science, we call these results "mixed." As in, they're all mixed up, and we can't draw any conclusions from them.

That won't stop the headline writers of the world, however. Here is a round-up of incoming headlines to accompany this latest hazy, prematurely Internetulated information (will update as needed).

Today's WINNERS (tie):
ETA: Steven Novella has provided the following analysis of the WHO report here. (2/9)

Tonsillectomies and fat kids? Doubt it

I just stumbled across a news report on a study, published in the February issue of Otolaryngology, Head and Neck Surgery, that identified a correlation between having a tonsillectomy and weight gain in children. The authors performed a review of nine studies spanning the last four decades of tonsillectomies and report, according to MSNBC (the paper is not yet available on the journal Website), a "greater than expected" weight gain in children of normal weight and children who were overweight already following the surgery.

[IMAGE: Yes, children really do receive this "informative" T&A booklet, complete with suggestive imagery and terms, before having that T&A]

In one analysis of 127 children six months to one year after surgery, the average body mass index of the kids increased by about 7 percent. In another analysis of 249 children, 50 to 75 percent of kids had weight gain after surgery. While most weight gain happened in the first year after surgery, scientists don't know definitively whether it levels off after that.
Oh, dear. Alert the media...oh, never mind.

According to the report, the study authors speculate that the recent increase in childhood obesity might trace in part to the 500,000 children who undergo tonsillectomies every year in the United States. I'll get into the problem with that kind of speculation below. Let's just say that someone got to make a checkmark next to "Current buzzword used?" with that bit of imaginative thinking.

What the news report does not clear up is whether or not this "greater than expected" weight gain adds up to a gain into "overweight" or "obese" territory for children who were within normal weight parameters before the operation. As the piece notes, it's likely that children who have tonsillectomies for the usual indications--repeated strep infections, breathing difficulties--might start eating more or using the energy more efficiently post-op.

Furthermore, the report mentions that there are growth spurts and weight gain after tonsillectomy in the pediatric population. That is, in fact, the case: children who have tonsillectomy for sleep-disordered breathing show gains in height, weight, and growth after the surgery.

The piece closes with the standard de rigeur pap that parents should watch their offspring post-op for weight gain and talk to a pediatrician if they're concerned. The closure-satisfying implication is that the findings of this study are so, um, weighty, that they warrant a specific parental eye to those pediatric pounds after a tonsil surgery. Yes, just one more thing to add to the parental worry list, based on this report. Indeed, I'd be more inclined to caution parents to take their children to the pediatrician if the little wee one does not put on some weight post-op.

Here, I'll drag into this the fact that tonsillectomy rates have likely gone down since the 1950s, before the obesity epidemic struck. Indeed, until the 1960s, it was the most frequently performed surgical procedure in the United States. With the decreasing rates of this surgery over the decades, it's hard to come up with a way that it could be responsible for the increasing obesity rates during my lifetime, which began in the 1960s. (Weird coincidence note: The author of the paper I just linked happens also to have authored the introduction to a re-issue of Rats, Lice, and History, my current reading. These random event pairings are happening to me so much lately that I'm starting to get suspicious).

The head and dek of this MSNBC piece are as follows:

Getting tonsils out tied to kids' weight gain

Researchers wonder if common surgery plays role in child obesity epidemic

Oversimplifying headline aside, the dek in particular makes no sense in the harsh light of common sense and facts. What's to wonder about? A child--like mine--has repeated strep infections, which in children can mean fevers, low dietary intake, and vomiting for days, a cycle that repeats the minute every antibiotic treatment ends. Guess what? Post-surgery, that child's going to put on a few pounds once they can (a) swallow again without pain, (b) do so without vomiting, and (c) live for weeks at a time without contributing valuable energy to a fever rather than to growth.

I'd have been surprised if the researchers had not found weight gain following tonsillectomy. It's the obvious hypothesis, unlike the silly speculation that this operation might be contributing to the "obesity epidemic." That's just dropping in a buzz phrase in a desperate grab for clicks and eyeballs, and nothing more. In this case, it looks like the researcher carries some of the load for overreaching. Anyone want to hypothesize whether or not there are gains involved in that?

ETA: Now there is a growing list of links for this story, so I've annotated below. Many include more commentary on "childhood obesity" in the context of these findings (which don't seem to have much to do with obesity), while others gloss over the findings and launch straight into a lot of statistics about childhood obesity.

Leave it to a blogger to get a good headline out of this story and to make a decent point: Tonsil removal possibly linked to weight gain in children. Blogger notes "scratching her head over this one," as either the child needs a tonsillectomy or the child does not; what does this information do for us?

Study citation
Otolaryngology — Head and Neck Surgery is the official scientific journal of the American Academy of Otolaryngology — Head and Neck Surgery Foundation (AAO-HNSF). The study’s authors are Anita Jeyakumar, MD; Nicholas Fettman, MD; Eric S Armbrecht, PhD; Ron Mitchell, MD.