Field of Science

Sex, gender, and gender identity

The ongoing discussion about Women Who Write Science has had me thinking a lot lately about sex, gender, and gender identity and the differences among these terms. I've seen a couple of posts that make mention of characteristics that go beyond primary sex, and ever since the "women who write science" topic exploded in the science writer echo chamber, I've had one major point knocking around in the echoes of my mind. Women are not somehow a monolith, one giant representative ovary pumping estrogen all over everything they do and womanifying it. Yes, to be a woman born, we have ovaries. That's what makes our sex female. But that does not mean that we gender identify as Woman.

I've seen the conflation in quite a few posts of the terms sex and gender. I spend my days as an editor correcting the use of "gender" in research papers, often in the context of mice, to "sex." Mice, as far as I know, don't express a gender identity, so all we have to go on is their sex, and that's based on the presence of specific physical and physiological characteristics. If they have ovaries, they're female. If they have testes, they're male. If they have both, they're intersex.

As always, translating anything from rodent to human is an iffy business. I'll keep saying it: Humans are not giant, tailless rodents, and because of social constructs and our ability to articulate what's in our heads, we are not simply the sum of our gonads. Gender is a cultural construct, what is considered in the social context to be masculine or feminine. For example, Google has, in a cultural context, decided I am male because I seem to, based on their cookies record, like things that men like (see image, above). Those things include science, politics, and baseball. But hark, ye may be thinkin' if you're female and you like those things, too: "I am female, and I like those things, too!" Agreed, and I just have to say, Up yours, society. Science is not masculine, dammit. Not any more.

We have gender identities that can be quite clear cut or be hazy and complicated, and we get to self identify as gender, while our sex is something that conception determined for us. Of course, being the able little primates we are, we can go so far as to change our secondary sexual characteristics to match our gender identity if it seems like a fit. Our gender identities encompass various expressions of masculinity or femininity along a spectrum, from the "metrosexual" male who makes up and "manscapes" to the Diane Keatons of the world who really, really like to wear pants and started a fad once upon a time involving women in neckties.

The gender identity variable brings much more depth to any discussion of "women in science" or "men in science" or "GLBTQ in science." Anyone who reads enough Dan Savage will realize that the expression of masculinity and femininity in sexuality is an intricate tapestry of culture, behaviors, and a spectrum of the masculine and feminine. I submit that creating anything--whether it's a great sex act or a great piece of writing--involves this intricate weave of factors, and the presence or absence of ovaries is only one of those factors.

Certainly, people do things that may be in lockstep with the organization and activation hypothesis of sex-based behaviors. But we're not mice, and I'm pretty sure that for humans, lordosis is more likely to be used to describe the spine that to describe a sex posture. Our brains and our gonads may, for many of us, be a reasonably close match, but never try to anticipate the multitude of gender-identity layering that stacks up in our agile, imaginative minds.

As I recently noted somewhere out there on the interWebz, I once participated for a full year in a message board using a gender-neutral name. The other participants, for whatever reason, concluded for themselves that I was male and thought that until I mentioned, after a year, that I am a woman. They went from the initial assumption based on my gender-neutral handle to the default "Male" conclusion, and there was nothing in the way I wrote or what I said that indicated otherwise, evidently.

Curious about my ability to "pass, " sight unseen, as a man, I began examining these notions of masculinity and femininity. Obviously, the other users on this board thought I was male because of some inherently masculine presentation in my writing, my arguments (we argued a lot), and my tone. I began to question the context of their assumptions and the context of these seemingly masculine products of my own brain. And I realized that I've never entered any situation carrying with me the subtext, "I am a woman." Indeed, my subtext is more likely, "I'm bringing this brain with me, and I'm going to use it."

Once upon a time, women who had powerfully analytical minds would be referred to as being "masculine" or having "muscular" brains. The implication was that the male brain, like the male body, had more strength and muscle and less soft, feminine fat (not true, of course), and that any woman co-opting these characteristics was behaving in a masculine, unwomanly way. Today, in the social context of gender, I carry that unwomanly flag, and my experience with this group on that argumentative message board made me aware of what I had in my hands.

I don't come to any table--not a writing table, a dinner table, or a pool table--as a woman. That's not the identity I bring with me. Yes, I show up with ovaries, having still held onto those things even though I don't need them any more. Yes, I show up with a variety of secondary sexual characteristics that announce that indeed, my sex is female. But I bring with me to these tables who I really am, my gender identity, and it's a complex one, hard to define. There's a masculinity there filtered through my experiences in traditional womanly roles like mother and wife, but there's also a total lack of interest in much of what my society defines as feminine (see Google, above). I lived in a men's dorm for awhile in college, all my roommates have been men, and I'm married to a man. It's possible that I could identify as a homosexual male of the non-flamboyant type who spends his time non-flamboyantly in a woman's body. Sure, that's possible. Like I said, it's complicated. What I do know is this: I'm not writing as a Specific Binary Sex Representative in Science, and I bet no other women--or men--who write about science are, either.

The mysterious reproductive life of the aphid

[poplar petiolegall aphid, a gall cut open with aphids of the Pemphigus genus visible. Photo courtesy of and the Texas Forest Service]

I've studied sex determination and development for about 15 years now but for some reason have never stumbled across the mysterious reproductive lives of the Pemphigus aphids. These insects, which preferentially interact with poplars as their host plant, go through one part of their life cycle in bisexual populations, which may not mean what you think: It just means they exhibit two sexes. They are bisexual on their primary host, where they bust out with their bisexuality in the autumn. The resulting eggs spend the winter in diapause (a kind of insect "hanging fire"), and in spring, the foundresses emerge. I love the vocabulary of entomology, and I think "foundresses" is my new favorite word.

These female founders attack their primary host after hatching and snack on various plant soft parts. Their snacking triggers the plant to pump out hormones that cause overgrowth in each tiny area under siege. The result is a gall, those bumps you sometimes find on the underside of leaves.

The snacking foundresses are parthenogens, meaning they don't need no males around to take care of the breeding business. They're certainly not alone in this practice, which occurs among many vertebrates, too (grad advisor alert), including Komodo dragons on occasion. Within the galls that the plant forms, each foundress starts to reproduce, mitotically making more little foundresses. These foundressettes have wings, and they wing their way with them to their secondary host, where they colonize the root systems. There at the roots, they pop out a few more parthenogenetic generations before a final winged form wings back to the primary poplar host and starts that whole sexual thing over again. The official term for spending some of your parthenogenetic species life cycle being sexual is holocyclic.

As if words like "foundress" and "parthenogen" and "holocyclic" weren't sexy (or a-sexy?) enough, in looking around at papers about aphids, I came across this title from Current Biology: "Behavioural ecology: the menopausal aphid glue-bomb." Evidently, the aphids described in this awesomely titled paper have a kind of insectopause in which the adults become "glue-packed warriors" whose job is to defend the aphid colony, giving them something to do in their golden years. I've never seen a glue-packed bundle of aphids, but..."female science writer" alert...I'm pretty sure it probably beats hot flashes.

Mitochondria and autism: the behemoth review

Results of a large analysis of existing studies addressing the interaction of autism spectrum disorder and mitochondrial disorder have drawn together an enormous amount of data and pulled from it a list of take-home results. If you'd like to skip the lesson, kids, leap to the last subsection for the take-home.

[At left: Mitochondria, of course. Courtesy of Wikimedia Commons.]

About those mitochondria
First, a little bit about mitochondria. The review paper, published in Molecular Psychiatry and open access, gives a fine and detailed overview, so my summary here is brief. The mitochondria do the heavy lifting for the cell's energy needs. They take the chemical remains of what we eat and transfers their energy into molecules that the cell can use. This process is complex and involves many steps and dozens of proteins.

Each of those proteins traces its code back to genes in the mitochondria themselves, which have the distinction of being the only mammalian cell organelle with its own DNA. It also makes it own proteins, just like a tiny cell-within-a-cell. And just like any DNA, mutations can happen. These changes in the mitochdondrial DNA can translate into changes in the proteins they encode. Given the mission-critical job that each protein has in building energy-containing molecules, these changes can be bad. Very bad.

The level of bad that results can vary from scarcely noticeable to all-out devastating disease. What complicates things is that the mitochondria in our cells can be genetically different from each other. We inherit our mitochondria from our mothers. In making the egg that will eventually fuse with a sperm and become us, she makes three other unused cells. Her mitochondria are allocated into each of these three unused bits as well as into the egg itself. This allocation can be a bit of a gamble, as not all of the mitochondria are created equal: Some may carry some bad-protein baggage with them, and if the egg gets a walloping dose of these faulty organelles, then the resulting individual may have a walloping dose of mitochondrial disorder.

Mitochondria and autism
Thus, it's entirely possible for a mother to be carrying around a few not-so-great mitochondria in her cells and be relatively unaffected because the healthy mitochondria make up for the gaps, while any offspring who end up with the bulk of the badly functioning organelles will show more signs of disease. Indeed, this scenario seems to have played out in the case of Hannah Poling, whose mother appears to have a low-level mitochondrial disorder while her daughter manifests it much more dramatically.

Poling's family entered the national spotlight when they revealed that her autism-like symptoms may have been linked to a reaction to several childhood vaccines at once and her mitochondrial dysfunction. Her case was not the first revelation of a possible mitochondrial disorder (MD)-autism spectrum disorder (ASD) link, but because of her ultimately successful vaccine injury suit, she became the avatar of the vaccines-cause-harm movement, which almost eclipsed the real scientific and therapeutic feature of her case: the mitochondria.

For that reason, it's a relief to see a review of this subject, especially given recent studies suggesting a link between even subtle, asymptomatic mitochondrial dysfunction and ASD. This resulting review paper is long and covers a lot of ground, so I've broken my discussion of it into bits that I hope the reader--if you're still here--can digest easily.

ASD-MD prevalence
The first issue worth noting--and one that's been noted before--is the much higher prevalence of MD in the ASD population. It's 5% among people with ASD, and only 0.01% in the general population. That's a huge difference and strongly suggests a much closer look at mitochondria in people with ASD and their families. The authors note that even this prevalence may be underestimated given that many studies didn't do what they'd consider to be a thorough enough evaluation for ASD, the exclusion of children with other disorders known to be linked with mitochondria, and the lack of appropriate screening markers in some cases. These markers are usually measures of chemicals that result from mitochondrial activity, and if their levels are higher or lower than normal, that can be a flag, or marker, of a disease state.

They report that almost one third of the children with ASD in these marker studies had such flags, and that for every marker they examined, the ASD population had a significantly higher prevalence of abnormal marker levels. The authors say that these findings are "consistent with the notion that a subgroup of ASD children has abnormal mitochondrial biomarker values or that the range much larger for the ASD population." They go so far as to use the word spectrum, saying that the analysis results suggest "that children with ASD might have a spectrum of mitochondrial dysfunction."

Mutations, mitochondria, and ASD
Most of those markers are proteins, and their code lies locked in the mitochondrial DNA (or in the nuclear DNA for a few). One natural place to look when there's a suspected dysfunction is at the genetic code for those markers. The authors examined papers that analyzed gene sequences and turned up very little in the way of known, disease-linked mutations and ASD. They note that very few ASD individuals have been identified who have specific mitochondrial DNA mutations; for example, in a study of 129 people with Asperger syndrome and 138 mothers looking at one well-established mitochondrial mutation, not one single participant carried it. Another study that grouped individuals based on their mitochondrial DNA sequences--a common way of tracing ancestry--found no link between specific groups and ASD. Examinations of the few nuclear DNA genes for mitochondrial proteins also have found no links.

Thus, tracking down mitochondrial dysfunction in the context of ASD to a specific mutation has remained an elusive goal. Two scenarios are likely for this lack of mutational findings: (1) there are mutations, but we just haven't found them yet; or (2) the environment is largely responsible for any mitochondrial dysfunction that abnormal marker levels might indicate.

Naturally, with genetics studies, family history carries some weight. Eighteen studies have examined a total of112 children with ASD and MD, and of these, only eight studies reviewed the family histories of its cases. Three of these eight identified a family history of MD, but nothing about these findings can be conclusive because of differences in diagnostic criteria or a total lack of information about diagnostic criteria. Sigh. When will we ever learn?

Mitochondria and the brain
The brain is an energy hog, and the mitochondria do all the work required to keep the brain developing and functioning. Some studies have used imaging techniques to visualize the map of marker activity in the brains of people with ASD. They've found that the way the brain produces and uses these markers is distinctive in ASD brains compared to non-ASD brains.

ASD and MD: the overlap
Here's where things really start to get interesting. Yes, I made you wade through all that tough molecular stuff to get to this point. The authors make two relevant comparisons in this paper. The first is between people with both ASD and MD and people diagnosed only with ASD. The second comparison is between the ASD+MD population and people diagnosed only with MD. Classic Design 101, right there. Let's look first at the ASD+MD vs ASD comparison.

The review of published papers showed that children who have ASD+MD also have distinct characteristics compared to children diagnosed with ASD only. Among these are developmental regression (a loss of acquired developmental milestones), seizures, motor delay (such as significantly delayed walking), and, of great interest to many autism parents, gastrointestinal (GI) abnormalities (reflux, diarrhea, inflammation, or constipation). For the ASD+MD population, these features are significantly more prevalent compared to the ASD-only population. Also of interest was the crossover finding: hyptonia, or low muscle tone, had the same prevalence in the two groups.

GI and ASD
GI problems are an oft-reported complaint among autism parents. The authors note that the prevalence of these GI problems was 74% in the ASD+MD population and describe a report linking mitochondrial dysfunction and inflammatory bowel disease (although that work was done in mice, which are not, it bears repeating, tiny humans with tails). They also say that it's possible that products of the digestive tract, including bacterial products, might be toxic to mitochondria and even contribute to seizure activity. Finally, they hypothesize that mitochondrial dysfunction can lead to breaches in the barriers between the GI tract and the rest of the body and between the brain and the blood. In other words, they took the GI results and used them to seed an entire acre of hypotheses to investigate.

The authors also evaluated how markers of MD differ between the two groups and found some evidence of a greater prevalence of marker abnormalities in children with ASD+MD vs those with ASD only.

Males and ASD
Finally, and this one's a big wow: The ASD+MD population had a "significantly more balanced male:female ratio than children from the general ASD population." We've likely all heard about how autism affects boys at far higher rates than girls. Not so in the ASD+MD population, which, if it holds up, implies a completely different or additional way that the ASD develops. The heavily male-biased ratio in the autism population--which probably will drop some as our understanding of autism and girls increases--still strongly implies involvement of "male" hormone pathways. The lack of this imbalance in the ASD+MD population suggests a non-hormone-based path to the disorder.

ASD+MD vs MD only
In this comparison, the male-biased ratio was the same between the groups; in other words, MD also showed a male bias. That doesn't jibe too well with the idea of a non-hormonal cause underlying ASD if the MD-only population also shows that bias. It may be that the MD-only population here also has ASD but that their MD has attracted all of the attention, leaving alone any questions of an ASD diagnosis.

Based on studies done so far, these two groups do not differ in prevalence of developmental regression, seizures, hypotonia, cardiomyopathy (heart disease), or myopathy (muscle disease). They did differ, however, for prevalences of fatigue/lethargy, ataxia, GI abnormalities, and one marker of mitochondrial disease, all of which were more frequent in the ASD+MD population. MD children were more likely to have visible cellular abnormalities compared to ASD+MD children.

No child in any of the reviewed studies who had an ASD+MD diagnosis presented with what the authors refer to as "classic mitochondrial syndrome." They speculate, as I have above, that some children with MD may not ever be evaluated for ASD, as their MD is front and center to family and health professionals. Or, it may be that children who have MD don't have typical ASD symptoms.

An important diagnostic and therapeutic question
The authors ask the important question: Are children with ASD+MD a distinct subgroup of children with ASD, or do they represent a distinct MD syndrome? Their analysis showed an overall prevalence of ASD or ASD features in 4.5% of children with MD, almost the mirror image of the 5% prevalence of MD in the ASD population. They describe two studies that have found a correlation the presence of MD markers and ASD symptom severity, suggesting a continuum for mitochondrial dysfunction that seems to mirror the spectrum, or continuum of ASDs.

Regression, MD, and ASD
Regression is an important part of the autism discussion. Some parents report a noticeable regression in their children, while others report having observed autism symptoms almost from birth. Thus, a look at regression and what might be associated with it can help resolve some of these questions and distinctions.

Regression prevalence was twice as high in children with ASD+MD compared to children with children diagnosed with ASD only, and this finding requires a closer look. Regression also has been identified in people with MD, often in association with stressors like dehydration, fever, or infection. In the case of Hannah Poling, for example, her parents describe her having developed a very high fever following a series of shots in one physician visit, and then exhibiting regression. The review authors here suggest that regression is likely related to MD in at least a subset of people with an ASD diagnosis. They point out that being able to identify the presence of MD could help families avoid exposure to some of the stressors known to have triggered regression in children with established MD.

MD, ASD, and the environment
The authors identify one study that linked exposure to thimerosal with changes in negative mitochondrial outcomes in cells from ASD individuals compared to cells from individuals without ASD. This single in vitro study does not implicate thimerosal in ASD or MD, and childhood exposures to thimerosal have lessened, not increased, over time.

What is of greater interest are the suggestions that exposure to diesel exhaust particles can inhibit mitochondrial function, along with exposure to other environmental toxicants, including heavy metals, polychlorinated biphenyls, and pesticides. Indeed, even as childhood exposure to thimerosal has dropped to zero, exposures to these other factors has likely increased.

Studies on PCB mobilization in breastmilk are one example of how our children may be increasingly exposed to these demonstrably hormonally active contaminants. The review paper authors also mention abnormal calcium signaling and, in an interesting note, report that chelating for high calcium levels led to improvements in levels of one biomarker. Yep. Chelation for high calcium. They also describe animal models in which products of GI bacteria and GI processes are associated with social interaction problems and mention propionic acid and Clostridia overgrowth as potential culprits in GI symptoms.

Limitations and caveats
A meta-analysis (analyzing beyond the original analyses) and a review (meaning a review of the relevant published data on a specific topic) like this obviously is going to have a long list of caveats. The first one that leaps out to me is this: Where is the evaluation of diagnostic criteria for ASD? I can't find that the authors examined papers to see which criteria were reported (if any) or which "kind" of ASD was present in the populations measured. That leaves a lot of question marks in my mind. The leading question mark ends this sentence: "Is MD associated more strongly with 'classic' autism symptoms?"What they describe seems to suggest that the answer is, "Yes," but that analysis is not presented.

The limitations the authors note are many and relevant and include the large variability in how markers were measured and reported and in diagnostic criteria used and reported for MD, and the small populations of the studies, some of which were just cases or small case series. Finally, there is the issue of referral bias, in that there was no prospective, before-the-fact evaluation for either ASD or MD; rather, the children diagnosed with likely were referred because they seemed to have one or the other.

Phew, and a take home
If you skipped straight to here, take heart. There is a take-home. Yes, there seems to be solid information suggestion a link between MD and ASD, especially ASD that manifests with specific symptoms such as seizures, GI abnormalities, regression, and motor delay. Yes, there is likely an environmental involvement in these mitochondrial disruptions, but I could say that about any disorder that shows variability in symptom intensity. Potential triggers that obviously require investigation include PCBs and heavy metals. The ability to identify mitochondrial deficits before a fever or illness strikes might benefit what adds up to a substantial number of children and their families. In sum, let's keep looking at these mitochondria, people.

[Source paper: Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis
D A Rossignol1 and R E Frye2
1International Child Development Resource Center, Melbourne, FL, USA
2Division of Child and Adolescent Neurology and Children's Learning Institute, Department of Pediatrics, University of Texas Health Science Center at Houston, Houston, TX, USA]

Women who write about science

[At left: Anna Brassey, nee Allnut) (1839-1887) was an English traveler and writer. Her bestselling book: A Voyage in the Sunbeam, our Home on the Ocean for Eleven Months was published in 1878. This illustration is from that book, courtesy of Wikimedia Commons.]

What advances have women made in the sciences? Well, we're here, for starters, which you couldn't say about us in general even half a century ago. Strangely enough, women entered the field of writing in substantial numbers well before they had such representation in the sciences. Yet now we're having a (great) conversation about women science writers and how they seem to remain hidden while male science writers allegedly engage in a mutual boys' club of promotion and back slapping and otherwise perpetuating their version of the Athanaeum Club, no women allowed (well, not until 2002, anyway). This reversal of fortune for women in science and writing seems ironic, as though somehow science writing had suddenly joined forces with ESPN and precipitated a discussion about women in the locker room. Cover up, gentlemen, because here we come.

In the many posts I've now read on this topic, I've seen a careful explication with some fabulous comments, a "bring it, I refuse to hide" attitude, and a "Sure this is great for women to discuss, but the men need to get involved, too" call to participate. It's been a great discussion. Kate Clancy has rounded up a variety of posts addressing this topic of women who write science, especially women who blog it.

Discussions like these always leave me in reaction limbo. I don't discount that people have blown me off throughout my life because I'm female. In fact, I know they have. They've also blown me off because I'm somewhat short, have a cherubic face, and speak with a long Texas drawl. But I'm always at least briefly confused about how to respond to such brushings away that are based on my sex. If I respond by following my instinct, which is to surge forward, push it, show what I can do and do well, ovaries be damned, then won't I be perceived as a woman not acting quite womanly enough and get the cold shoulder as a result? If I don't do that and instead put my head down and persevere, but quietly, what the hell good is that doing anyone, women, cherubics, short people, or Texans?

Thus, I've often chosen to be who I am, which is a woman with a blunt voice, a sharp mind, an expansive interest in science, and a way with words that I've been cultivating since 1972. If this somehow belies me as a woman, then I can live with that, because it doesn't compromise me as a writer. Being female just is what it is, and it happened to me when I was conceived. I had no control over it. But being a writer and a scientist? That took work. That took ambition. That took years.

Lying in my wake are years of education and experience with both science and words and yes, some of the accouterments that often come with being a woman: a spouse, children, cooking dinner, driving a minivan, derailing from the tenure track. All of these aspects of my life percolate through my writing and my writing choices just as much as my thousands of hours at the books and at the bench. With them comes perspective, sometimes a unique perspective that occasionally transmits to the reader. What defines me--woman, mother, scientist, writer, autism parent, endocrinologist, penile and gonad researcher, herp-o-phile, Texan, brunette--has shaped me and will inevitably shape my words, my viewpoints, and what I write about. Any one of my characteristics might contribute something worthwhile to the scientific conversation.

Yes, my voice is a woman's voice. But it speaks with an accent and years of baggage related to many factors other than my sex. What makes it a voice worth hearing is ultimately that it says something worth saying. For that reason, I'll continue to cast aside any worries that by using that voice or promoting that voice, I'm not being "womanly" enough. And I'll continue to listen to and promote the voices of others whose writing and perspective I admire. Oddly enough, many of them are women. I can't imagine why that is.

Did the Egyptians call oxytocin "Isis"?

[At left, an Isis of the Ptolemies, ca. 332-30 BCE; courtesy of Wikimedia Commons and a little museum called the Louvre]

I'm reading Cleopatra by Stacy Schiff right now, which is proving to be a tight, honest, fascinating and scholarly read. On page 86 of the hardback, I came across this description of the Egyptian goddess Isis, whom Cleopatra appears to have tried to copy:

She was tender and comforting, also the mistress of war, thunderbolts, the sea...She presided over love affairs, invented marriage, regulated pregnancies, inspired the love that binds children to parents, smiled on domestic life. She dispensed mercy, salvation, redemption.

In other words...Isis was the ancient Egyptian's deification of oxytocin.

Communication fails in science and health

A roundup of some of today's worst in science communication fails, from the misleading but clickable headline to the loose reportage. Got more? Send 'em along.

Milk Causes Cancer, from VegNewsDaily. And that seriously reflects the entire "content" of the article, except for a cursory mention of a (completely unsupported) link between casein and autism.

Vaccine-autism link proved false? From the Palm Beach Post. Sorry, Headline, Article doesn't support the query.

Friendships determined by DNA marker. Medical News Today! For antidote, see Daniel MacArthur's insights into this study over at Wired.

Weight loss may send pollutants into bloodstream. MyHealthNews/MSNBC. Take a look at the article. Try to find the "balance."

Weaning before six months 'may help breastfed babies.' BBC News Health. The problem here? These reports are based on a literature review, not new studies or new information, and neither article makes that clear. Indeed, the BBC piece is a muddle that makes it difficult for the reader to determine if any of the studies being described are the study being reported as "news." (They are not). At the BMJ site, the lead-in to the review says that in the piece, the researchers ask, "if the time is right for reappraisal of this advice." That is not the same as the conclusive evidence implied in each of the related news reports.

Finally, I bring you this one, complete with major typo:
Why do women shy from competitive jobs? (subhead): Males, not femals (sic), like to best their co-workers, research shows. Then the click-to, strangely in title case: Men Crave Competition, In (sic) Work and Play.

From the piece:
List and his coauthors, Jeffrey Flory, a graduate student in economics at the University of Maryland, and Andreas Leibbrandt, a postdoctoral fellow at Chicago, were intrigued by a number of recent laboratory studies showing that men are, by nature, more competitive than women. Most of us probably don't need scholarly studies to tell us that, because we see it all around us.

Nice. Furthermore....
Women are raised to be understanding and conciliatory; men are raised to slay wild beasts and triumph over their male friends.

Read the article. Note that the job offered is in office support. Note that the researchers did not actually assess reasons for not applying for a job that was described as more competitive (how could they)? All the study offers is a group of people, divided into male and female based on name alone, who applied for an office job. The ones who were presumed to be female were less likely to apply for the job if it was described as competitive. Does that mean that the women--if they were women, and Hilary, Beverly, and Bobby, I'm talking to you--really shied away from a competitive job? Or does it mean that they were smart and declined to take a crappy office job that would require you to compete in a bruising battle with your co-workers for bad pay?

The tease asks, "Why do women shy from competitive jobs?", but this study does not answer that question or demonstrate fully that women do, indeed, shy from such jobs. Furthermore, I don't see "play" mentioned anywhere in this study. Why is it included in the headline?

As much as these last two pieces muddled and befuddled, I'm giving the win for today to VegNewsDaily. Because...just, wow.


This weekend, I attended ScienceOnline2011 to learn how the Web and social media can be used to promote science. This conference delivered everything it promised, but I'm pretty sure I didn't take up everything it delivered. No normal human could have. Highlights and lowlights:

Highlight: Keynote speaker Robert Krulwich. I luv, I lurve, I luff RadioLab, and it was one of the greatest treats of my life to see him talk about his process, hysterically, personally, and personably.

Lowlight: I ran into Krulwich following a session and promptly dropped an f-bomb in present participle form in my excitement to get across how much I like RadioLab. Oh, and I said I'd much rather hear that show than Terry Gross because, while I like Fresh Air OK, RadioLab's discursive, exploratory, personal style fits my mind better. F-bomb!

Highlight: Nerdy Christie's open mic performance and the arsenic blues song. Hearing "trilobite" and "peer review" in songs is...surreal.

Lowlight: I just can't drink like I used to.

Highlight: The entire panel on blogging as a book-writing tool. Tips abounded, things I hadn't thought about before, even as someone who's been blogging for several years. Thanks to Brian Switek, Sheril Kirshenbaum, Maryn McKenna, and Seth Mnookin for an informative panel. And buy their books!

Lowlight: I needed a lot more coffee for all that standing. That room was crowded.

Highlight: Science journalism online session, every single speaker, although Steve Silberman's personal commentary has really stuck with me.

Lowlight: Sitting on the floor behind someone's butt in the science journalism online session. Awkward, and at my age, I was worried about whether I'd ever get back up again. These knees are at least 20 years older than the rest of me.

Highlight: Matching avatars with the rest of the person. That was sometimes quite easy, sometimes not, occasionally surprising, always fun.

Lowlight: Did anyone else feel that disconcerting personal disconnect between online and reality?

Highlight: Friday night author dinner at Pop's, talking with women at the end of the table who waded deep into science and stayed there. Oh, and a little diversion into breast pumps.

Lowlight: Possibly for the other diners around us, our imitations of how a breast pump sounds.

Highlight: Getting to meet authors of great books and hear them read.

Lowlight: Is there a lowlight to that? Not really. Oh, maybe that hellaciously long beer line.

Highlight: Leaving with a feeling that there's so much left to do, so many ways to do it, so many great people out there doing it.

Lowlight: Delta cancelling my flight and diverting me through Atlanta to arrive home several hours later than expected.

Wrap-up: I'm no social butterfly, and many others I talked to expressed the same feeling. Are most science/writer/science writer types so introverted? It was hard to make introductions and carry a conversation, especially since I seem to have stopped making alcohol dehydrogenase, so my usual social lubricant was MIA. Even so, I managed to have several good discussions, meet some great people, and pick up some energy and excitement and a great deal of thinking touchstones to take home with me. As for the conference technicals, it couldn't have gone more smoothly or been better arranged. And that's always a highlight of any good conference. Oh, that and the swag. There was some dem fine swag, from books to 8-balls. Or, 8-cubes, actually. Well done all around, with special thanks to Bora Z, Anton Zuiker, and Karyn Traphagen for arranging it all so well.

Hey, Neanderthals: Why were your noses so damned big?

[At left: A blue-eyed Neanderthal, intent on butchery, nose not typical. Photo from the Neanderthal Museum, courtesy of Wikimedia Commons.]

The Neanderthals. Mythical in the stories that surround them, a little discomfiting as our closest (dead) relatives, so much like us that sometimes, we seem to seek ways to draw distinctions. They were bigger. Rougher. Heavier bodied. Bigger brained. If they talked, they didn't do it as well as we did. And damn...have you seen their noses? They were so large that one perfectly serious researcher, Peter Brown of the University of New England, Australia, felt compelled to describe them as "humungous."

The Neanderthal nose has been the subject of much discussion. Some ideas have centered on the diet, which may have required a big mouth and a wide jaw, resulting in embiggening of the nose in the process. A pair of researchers who checked this idea, Nathan Holton and Robert Franciscus of the University of Iowa, found only a slight correlation between the size of the mouth and the size of the nose, probably not enough to drive the two together down the evolutionary path. They also analyzed facial projection as another possibility, the jutting of the lower face, a remnant of earlier ancestors, a feature considered more "simian" than "human." See? See how different they must have been from us?

Cold climate adaptation has often cropped up as an explanation for the Neanderthal's "wide piriform apertures," which in commonspeak are the bony openings of the nose. The problem is, big noses are usually associated with living in hot climates--like equatorial Africa--presumably providing a larger internal area for cooling. This paradox of a wide nasal opening in a cold-adapted organism like the Neanderthal has had researchers casting about for ways to unify the two. Think of it as a Unified Theory of the Humungous (but cold) Nose. One idea was that leading from those wide openings were equally wide sinuses, caverns where the body could warm up the cold air before it flowed into the lungs.

The 2008 study by Holton and Franciscus ended with a bit of an emphasis on the non-adaptation of a big nose. In other words, maybe the Neanderthal nose was big was just big. Humungous. New work seems to bear out that possibility, or at least to box away the idea that the oversized Neanderthal nose had anything to do with cold adaptation. As authors Todd Rae, Thomas Koppe, and Christ Stringer note, many animals that live in cold climes often have smaller sinuses, not bigger ones.

Their work, an analysis of imaging study findings, looked at what might seem to be an obvious question: Are Neanderthal noses big because...well, Neanderthals were big? It makes sense as a question: I wouldn't expect, for example, someone a foot taller than I am to have arms the same length as mine.

The authors correlated imaging measurements of the sinuses and skulls of Neanderthals and Homo sapiens. They found that the sinus sizes simply were associated with cranium size. In other words, big head, big sinuses. Not a cold stress adaptation, an idea that one researcher not associated with the study referred to as a "Just-So Story."

Curious about other animals with big noses, I turned to Google U for some examples. There's the moose, famed among the deer family for its supersized proboscis. While other family members have dainty, Bambi-like sniffers, the moose has a honker unmatched in the antlered world. And as with Neanderthals, efforts to explain this adaptation have yielded controversy, including yet another hypothesis associated with temperature adaptation. But the real reason behind the moose's complex schnoz may be its aquatic feeding tendencies. The nostrils may seal up under differential pressure when immersed in water, making the moose a deer with an aquatic adaptation. Not likely to apply to Neanderthals. And just an all-around odd thing in a deer.

Turning to a horseshoe bat with an unusually long nose, we find that this adaptation is related directly to ultrasonic navigation. Unlikely to translate to Neanderthal, especially given that "big nose" in the case of these bats means "9 mm long."

What about that most famous of the big-nosed mammals, the aptly named proboscis monkey? Based on some commentary, that notable nose provides a resonance chamber for vocalizations. Given the differences between juveniles and adults, there's likely an involvement of hormone influence, just as testosterone acts on male vocal cords in us.

And probably in Neanderthals. Who probably did vocalize, or may you think that their big noses might have had anything to do with that?


Did the sib-spacing autism study leave out an analysis?

Study associates being a closely spaced, second-born sib with increased autism risk

A study coming out in Pediatrics reports that second children born soon after their older siblings are at a higher risk of developing autism, a developmental difference or disorder characterized in general by social and communication deficits. Note that even with the increased risk, the overall risk of autism even for these second siblings is still quite small.

The study is based on a large group derived from data maintained by the California Department of Developmental Services. Findings based on this database must include the caveat that anyone included in the database purposely sought and received services, so there can be a bias against and exclusion of people who sought services elsewhere or are living undiagnosed. It may represent about 75% to 80% of people in California with autism. People who have autism spectrum disorders other than autism--such as Asperger's or PDD-NOS--also do not receive services through CDDS and were not included in this analysis. I'm still mulling over how much of a gap that might represent in the analysis.

The authors assessed the rates of autism in second-born children relative to how long after the birth of their older sibling they arrived. They counted the inter-pregnancy interval (IPI) as time between the births of each sibling minus the gestational age of the second sib. Their analysis indicated that those second-borns who were conceived within a year of the older sibling’s birth were more than three times more likely to have autism (OR 3.39; 3.00-3.82). For IPIs of 12 to 23 months, the OR was 1.86 (1.65-2.10), while OR for those with an IPI of 24 to 25 months was 1.26 (1.10-1.45). Thus, they identified an inverse linear relationship between time and autism—the longer the time between the first birth and the conception of the second born, the lower the autism rate.

Is the sex of the second sibling involved?

When they looked at other factors, such as preterm birth or sex of the second sibling, they didn’t find much. In fact, across all time periods, ORs for girls as second siblings were higher than ORs for boys, although none of the differences were significant.

There was no assessment of what might cause this mathematical relationship, but the authors offered that the first pregnancy and birth might have depleted nutrients in the uterus, depriving the second-born of them. The authors comment that these findings are becoming increasingly relevant as the number of closely spaced births has grown from 11% of all births in 1995 to 18% in 2002.

The complexity of the womb

The idea of nutrient depletion may be a plausible one, but another one comes to mind that the paper does not appear to address: the relationship between the sex of the previous occupant of the uterus and effects on the next occupant. A well-known hypothesis is that autism develops because of an excess of exposure to androgens in the womb, and research has shown that androgenization can occur in siblings that follow a male older sib in the womb. There’s also the “fraternal birth order effect,” in which the more older brothers a man has, the more likely that man is to be homosexual. This hypothesis, coupled with the idea that homosexual men are hyperandrogenized, has led to some speculation about the influence of an androgenized womb on those who experience that environment.

The DES story

The womb is a changeable place, and the changes that happen there can effect changes in its occupants. This connection may have first come into the spotlight with the studies of DES, or diethylstilbestrol, a powerful synthetic estrogen given to women in the 1940s through the 1960s as a miscarriage preventive. Researchers later discovered that the children of these women—specifically the daughters—were developing rare reproductive tumors. The women who initially received it had an increased risk of breast cancer, not surprising given the 100-fold affinity of this estrogen for one of the estrogen receptors compared to our native prevalent estrogen, estradiol. Sons of DES-treated mothers may also have experienced effects on the reproductive system.

And then there are the grandchildren, the offspring of mothers who themselves were exposed to DES in utero. In an almost biblical expansion of the effects of this synthetic hormone, there is concern based on studies with animal models that grandchildren of the women originally treated with DES during pregnancy may experience higher rates of various reproductive abnormalities, thanks to epigenetic influences of DES their parent experienced in the womb.

A call for another analysis

As the data are presented in the Pediatrics paper, we have no way of knowing if there was a relationship between having a male older sibling and risk of autism in this cohort. Based on my review of the paper, the authors provide autism risk broken down by sex for the second siblings, but do not provide information about the sex of the first sibling or about the rate of autism in second siblings who followed a male older sibling. They likely have these data in hand and may be able to perform this analysis; they may have done so and simply not reported it because there was nothing to report. But in my mind, in the context of the prevailing androgen hypothesis of autism, this analysis would be worth pursuing.

And a call for accurate headlines

I posted an article about this over at BlogHer, and the immediate responses—two of them—were from parents who focused more on feeling blamed and feeling guilt, yet again, over yet another potential factor in a child’s autism. This feeling is essentially battle fatigue, as a headline every other day or so seems to pinpoint something a parent coulda-shoulda-woulda done to head off their child’s autism. The burden remains on the news media who report these stories to make the difference between correlation and causation clear. That clarity must begin with the headlines. A sampling of headlines for this story:

Closely spaced pregnancies might up autism risk (Business Week)
Autism study: Timing is everything (Local television station)
Closely spaced pregnancies increase autism risk (CNN)
Age difference between siblings, not parental age, may indicate higher risk for autism (NY Daily News)
Autism Risk: Is timing everything? (Yahoo News)
Another thing to worry about? Closely spaced second sibs at greater autism risk (My piece at BlogHer)

Of these, the ones that use “might” (get that equivocation across right away) and talk about “risk” come closest to reflecting the paper. But the ones that say “Timing is everything” or assert that parental age is not associated with risk are off base. I’m not thrilled with the headline on the piece I wrote for BlogHer, and I’m afraid that in including it, I unconsciously fell into the “catching clicks and eyeballs” trap, imitating what I’ve seen all over the Web. The answer, of course, to the question the headline poses is, in my opinion, “no,” and I indicate that in the piece. But what I’ve just discovered in this foray into women’s health is that reading to the end doesn’t always happen, and my readers—at least the first two—simply came away feeling like crap about it all. Not the point, not my intention.

The best way to write this headline would be to use words like “associated” or “linked” and “risk” and if you could, work in “correlation, not causation.” I know that latter is unlikely, as it makes eyes roll back and elicits drooling, but could we just develop some quick shorthand so readers can immediately identify a correlation study? I think the subhead I used at the top of this piece sufficiently captures the needed accuracy, clickable is that thing, really?

What’s the take-home?

Back to interpretation: The going wisdom on child bearing is that a mother should wait at least two—if not three—years between conceptions. Of course, some of us are older and don’t have the luxury of spacing our children that way. I, for instance, conceived our second son when his older brother was 8 months old and I was 33. They’re just over 16 months apart in age. Based on the risk categorization in this Pediatrics paper, our second son’s risk of autism from this factor alone would have been 3.3. The thing is, his older brother is the one who’s diagnosed with autism. I’ve spoken with other autism parents whose experience better fits the observations from the Pediatrics paper.

But these are all just anecdotes, not data. The best we can do is—the best we can do. We can follow the going medical wisdom to space our children by two years at least—or, we may be older and not have that luxury. At the very least, it’s not time to add sibling spacing to our list of autism causes. This paper simply showed a mathematical association, which does not mean a confirmed physiological connection, and their findings require considerable further study.

Oxytocin: not the "cuddle hormone" you might think

Many of us first learn about oxytocin as the "positive-feedback" hormone from the posterior pituitary, the one that, during labor, builds and builds and forces contractions of the body's most powerful muscle until, in what in retrospect seems ridiculous, a woman pushes a seven-pound baby, headfirst, through a reluctant orifice. This peptide hormone is, with the exception of C-sections, one of the main reasons we make it here.

It's also implicated in the reason parents usually keep their children after they're born, playing a role in parent-offspring bonding across the vertebrate parenting spectrum and in a mother's ability and willingness to breastfeed. Without oxytocin, we'd all be something like furry sea turtles.

To enhance the reputation of this magical hormone, studies have implicated it as the "trust hormone," leading people, possibly against common sense in some cases, to trust others. Who needs Inception (which was dull anyway) when you've got oxytocin?

According to some studies, some people need oxytocin more than others because of native deficits in the signaling molecule. High on the list are autistic people. Maybe. A study published in PNAS almost a year ago found, in a small group of autistic participants, that oxytocin appeared to promote social behaviors in the group. I've discussed some of the potential caveats about the study previously, but the reports sent parents scrambling for oxytocin treatments for their children and the media busting out headlines about oxytocin, autism, and cure. A tad premature.

Before everyone starts snorting oxytocin, though, let's take a look at some more data on this hormone. First, some hormone background. Hormones can be bi. Truly. Their effects can depend on the tissue where they act, turning things on at one place and shutting them down in another. Slippery little hormones like estrogen are associated with the feminine, but they're also hypothesized to be the masculinizer of the mammalian brain. You can't take one finding about a hormone's behavior and extrapolate it across tissues, developmental periods, and species. Sorry.

Oxytocin is no exception (see uterus vs. brain). Sure, huffing it in an experimental scenario seems to increase the reckless trust response. Yes, it works remarkably well in childbirth and has implications for parenting. But, as a new PNAS study notes, it also is associated with turning inward that love-fest uber-trust it generates. According to this work, oxytocin makes us insular, far more likely to trust our own than to trust not-ours. Or, as the authors put it, it promotes "ethnocentrism."

The authors, in their abstract, go so far as to conclude:
These findings call into question the view of oxytocin as an indiscriminate “love drug” or “cuddle chemical” and suggest that oxytocin has a role in the emergence of intergroup conflict and violence.

But that's not all. High levels of oxytocin have been associated with greater "relational distress and interpersonal difficulties," which might militate against its use as a therapy in autism. In a just-published study of women who'd recently experienced interpersonal harm, researchers found that high oxytocin levels were associated with reduced forgiveness and increased anxiety. Indeed, the oxytocin effect was present regardless of levels of cortisol, the so-called "stress hormone."

This hormone isn't only bi. It's multi, and that's why anyone contemplating it as a therapy should exercise extreme caution.

If God has a plan for you, why do you pray?

photo © Adrian van Leen
for CC:PublicDomain

In the wake of the shootings in Tucson, I've seen countless appeals on Twitter and in the news media--including from our president--for prayer. I understand the motivation to pray, to drop to one's knees in a crisis, either figuratively or in truth, and beg for a certain outcome. How many of us, in suddenly becoming an unwilling participant in something near-fatal have muttered, "Please, God, please, God" (when we're not yelling, "Shiiiiiiiiiiiiit!")? That proximity to approaching death seems to make involuntary believers of us all.

But prayer for the sake of intercession, say to heal a friend's heart trouble or urge a child's recovery from ill health--prayer with the intention of asking for a favor on someone's behalf--that's a more complex animal. One thing that's always beflustered me about intercessory prayer is that most of the people I know who practice it also believe in an omniscient, omnipotent Christian God who "has a plan" for them. I've never been quite able to grasp how exactly a being with that kind of all-knowingness and a plan would just drop the whole thing because someone asks and go, "Oh, OK. Since you asked nicely, I will go ahead and have them accept that offer on the house, even though I'd intended to make you rent for at least another year."

The perils of parsing prayer
The world is full of people who attest emphatically to the power of prayer. And a few scientific types have tried to quantify and test that power, failing miserably overall. As noted over at The Skeptic's Dictionary, trying to link outcome to causality with something as uncontrollable and evanescent as prayer is sheer folly. Plus, as the SkepDic article notes, if one believes in a deity of some sort that would interfere beneficially on one's behalf, then one must accept the possibility of a malevolent deity that might be interfering simultaneously. How in Thor's name could science control for that? According to some researchers, those studies say more about the scientists--and their focus of belief--than they do about prayer.

I'm not here to mock prayer. As someone who grew up in the Big Silver Buckle on the Baptist Bible Belt (a.k.a., Waco, Tex.), I've pondered these issues long, and people I respect enormously practice prayer. Yet in spite of the fact that there are undoubtedly things in heaven and earth that aren't yet dreamt of in my philosophy, I can't reconcile the overall lack of outcome with prayer and that nagging conflict between asking for a change of plans from a deity that already "has a plan" for you anyway.

And the perils of prayer itself
And from a possibly scientific standpoint, intercessory prayer does not appear to be demonstrably useful for the intercessee and was even disadvantageous in one study (although strangely enough, one group has reported that it helped out wound healing in bush babies, no less). In spite of the limited effects on the intercessee, however, prayer has been correlated in many studies with benefits to the intercessor.

Evolution has done a number of funny things to our minds, possibly leading us into magical thinking traps, leading us to forever seek the patterns and make the connections where often there are none. It has been argued that religion is intertwined with our evolution and that we, in turn, drive the evolution of religion. Prayer--that appeal to something beyond our control that helps us feel more in control through articulation and expression alone--likely serves a very material purpose. We're more likely to forgive and feel "selfless concern," for example, when we pray, and at least one researcher argues that prayer is an "imaginary social support interaction" that helps us manage our emotions.

Praying: A people thing
Indeed, prayer appears to be such a common human condition that an alleged 9 out of 10 Americans report doing it. While I'm not a believer in prayer-as-intervention, I am a believer in the benefits of adaptation and resilience, and prayer--as in this time of a national paroxysm of tragedy, vitriol, and loss--may be just one of many ways we've been shaped for self healing. Obviously, this idea is not new and is one even articulated by religion scholars, such as Karen Armstrong, author of The Case for God.
Religion is about helping us to deal with the sorrow that we see in life, helping us to find meaning in life, and helping us to live in relation to that transcendence that I was speaking about earlier. Religious people are ambitious. They want to feel enhanced. They want to feel at peace within themselves.
Many scientists who've analyzed the prayer literature have concluded that efforts at double-blind studies of intercessory prayer are efforts wasted. But identifying the underpinnings of this seemingly near-universal human impulse is a pursuit worth continuing, I'd argue, given its possible adaptive role. I'd like to see what happens with neurotransmitter and hormone levels during prayer (in the intercessor, maybe in a non-blinded intercessee), a causation/mechanistic study I could get behind.

The physiology of prayer: worth a closer look
Some functional/MRI imaging studies of Carmelite nuns and other groups show nonspecific activation in various areas of the brain during prayer or meditation, but (1) meditation and prayer, I'd argue, are not necessarily the same thing, and (2) that doesn't address the physiology--neuro or organismal--of prayer. Correlative studies with stress hormones suggest a link between self-reported "religiosity" and cortisol levels, but that doesn't evaluate direct physiological mediation through the act of prayer. I wonder what researchers would find, for example, about oxytocin levels in prayerful people who are praying versus prayerful folk reading an amusing story.

This post has been submitted to NESCent for their "Best Evolution-Themed Blog Post" contest. The winner receives a travel award to attend Science Online 2012. I think there would be a delicious irony if the winning post for a evolution-themed contest were about prayer.

What motivates individual political violence?

The saying goes that sticks and stones can break your bones but that words cannot hurt you. That saying is, of course, nonsense. Words are powerful. They bring nations to their knees, they've motivated the unmotivated from Agincourt to today. War rhetoric obviously has its place. But hate rhetoric? It's done immeasurable harm in the past--and it's back in full force, inflaming minds and driving what can become a real "lock-and-load", target-minded groupthink.

Today, January 8, 2011, an Arizona U.S. congresswoman was shot in the head, injured along with several other people, some of whom have died. She was one of the "20" placed in the crosshairs on Sarah Palin's Website and had been the target of gun-related rhetoric from her tea-party opponent. As of this writing, no one knows exactly what motivated the reportedly 22-year-old male shooter responsible for this horrific Saturday morning massacre--and it is horrific, certainly for the families of those who have died or lie critically injured, and also for the United States--and as I monitored the flood of tweets updating the situation and linking it (prematurely) to the tone of today's political rhetoric, I had a question: What motivates individual political violence?

Whether specific political rhetoric motivated this act of mass murder, the question is a relevant one for our country today when celebrities like Palin literally place gunsights to represent political targets and when gun-associated campaign rhetoric do-si-dos down the aisle right alongside the hate language spewed across the heartland. This toxic linguistic brew has had many observers on edge, concerned that it would penetrate the wrong mind, trigger a deadly impulse, lead to a horrific outcome.

But what makes that mind more susceptible to acting violently while the other interlocutors merely wave signs and rant in their kitchens over coffee...or tea? According to this article at the UK Register of Trauma Specialists, the answer to that question is extraordinarily complex:
Thinking about political violence, it is important to acknowledge that the issues motivating individual and collective acts of political violence are complex and multi-factorial. Such issues include social injustice, coercion, consensual validation, radicalisation, dehumanisation of the other, abdication of individual responsibility, becoming the voluntary agent of others within a malign authority system, and fear of retribution. Socio-cultural, economic and historical contexts also need to be taken into consideration in understanding political violence.
Words that leap out in today's political context are, of course, "radicalisation" and "dehumanisation of the other," possibly along with "becoming the voluntary agent of others within a malign authority system." All of these burn through our political fabric and leave our national functionality in tatters.

One thing that may exacerbate the ability of this murderous rhetoric to lead, in fact, to murder, is the idea of sacred values. It is possible for people to transform the issues of dispute into these "sacred values," giving them an almost divine imprimatur. Certainly, with the talk of God and "our founding fathers" and "real America," there is without doubt the attachment of a kind of divinity to much of the language used in rousing up the faithful. Indeed, Glenn Beck proved himself a sort of avatar of this movement of a sacred America when he held his "Take Back America" rally, exhorting his followers to return the United States to its allegedly Christian roots.

In their paper, "What Motivates Participation in Violent Political Action," Jeremy Ginges and Scott Atran discuss collective violent action, but a question is how much of what they discuss could also be attributed to individual motivation. They write about the "cognitive transformation of issues under dispute into sacred values" and describe the actors as declaring a "moral commitment" that can lead to resistance to attempts at compromise of those values, especially for material incentives. They note that the dominant explanatory model for violent collective action is the idea of an individual incentive following the presumed victory, but that with this moral imperative, another possibility is "parochial altruism," in which the actors collectively commit to the violence because of their moral commitment to sacred values.

In other words, things can get pretty damned dangerous--and intractable--when we drag the sacred into it. How much the above might apply to an individual act of political violence, I can't say. Most of the literature I found addressed terrorist recruitment and acts in the Middle East, not the acts of an individual politicized by hate rhetoric into deadly violence. And regardless, as noted in the above quote, the ultimate profile of such a person will be based on a diverse set of potential characteristics.

But what do their brains and their genes look like? A look at the violence literature reveals two rough categories of violent brain and genetics: the brain of the impulsively or hostilely violent and the brain of the proactive, or instrumentally violent--the one who carefully plans the violent act, rather than committing it in the heat of the moment. Impulsive violence, thanks to its unpredictability and relative ubiquity, seems to get the bulk of the attention. Proactive violence, which encompasses the planned violence of war, is a different animal altogether. And psychopathic instrumental violence may well be the most terrifying of them all. The two appear to have very different underlying mechanisms and origins, as well:
Biological models of violence have identified distinct neural patterns that characterize each type of violence. For example, the "low-arousal" aggressor more likely to commit instrumental violence is underreactive and responds sluggishly to stressors. In contrast, the "high-arousal" aggressor who is more prone to hostile violence tends to be hypervigiliant and easily frustrated

In humans, instrumental aggression is roughly analogous to predatory aggression although it is limited to intraspecies behavior....Similarly, emotional or hostile aggression in humans could be considered the analogue of defensive aggression in response to a threat or perceived threat.
Instrumental violence has previously been thought to lie in the domain of planned violence for the sake of individual gain, the kind of violence a predator uses. But based on the observations of Ginges and Atran, it could also be performed because of a dedication to defending that which is perceived as moral and sacred. Indeed, an individual committing an act of political violence on behalf of the sacred is doing so in the instrumental, planned sense, but are they not also reacting in the hostile, impulsive sense? This latter is usually considered reactive, sometimes a defensive or fear response. When your leaders wrap their rhetoric in the sacred while also embedding fear and a sense of threat, can the outcome be violence that is both instrumental and hostile?

There is no way of knowing right now if the allegedly 22-year-old shooter in the Arizona violence is a psychopath. Right now, we don't even know what his motivations were (added: and he may be "mentally ill"). What we do know is that there has been an ocean of free-floating hate rhetoric seeping into the cortices of the susceptible in this country for a very long time, and that if this man is not the embodiment of it, if this atmosphere of making the political into the sacred persists, some susceptible individual may some day soon genuinely become its hostile instrument.

There were two other non-retracting authors on the Wakefield MMR paper. Where are they now?

A question that keeps rising to the surface as I read Andrew Wakefield's name over and over again since yesterday's revelation of a scathing indictment of him in BMJ is, "What happened to those other two authors who DID NOT join in the retraction of the original Lancet paper linking MMR and autism?" Peter Harvey and John Linnell were the other two authors, one actively declining to retract, the other simply gone AWOL.

Of course, we have initially their own words, joined with Wakefield's now apparent lies, published in the Lancet as a response to the retraction. There also is Peter Harvey's 2004 letter to the Lancet just preceding the retraction, in which he wrote (ironically, in retrospect):
"Much is made of the epidemiological studies that have failed to show an association between MMR and autism. However, these studies are open to serious criticism."

Harvey then writes:
I examined the original cohort of children, and they had no physical neurological abnormalities. I have recently seen one of them again. His behaviour is much worse, at times being uncontrollable. He has developed epilepsy and bilateral extensor plantar responses. [From EW: I do not have any idea what a bilateral Babinksi's--an upper motor neuron sign--would have to do with autism]
From investigative journalist Brian Deer's Website, we find this about Harvey, a tidbit published in The Sunday Times:
Another author, Dr Peter Harvey, a board member of Visceral, a registered charity set up to support Wakefield, spoke out in his defence. Harvey said he did not think the funding was relevant and he would have still have put his name to the study if he had known. "I don't think there was any conflict of interest," he said.
Who is Peter Harvey? Why do we not see his name coupled more with Wakefield's in this debacle, as he asserts above that he was involved in examining the children and states here, in this letter, for the record, that they "had no physical neurological abnormalities"? Why is this self-decribed "adult neurologist" examining children for a study in the first place? His moral compass for conflicts of interest, as described in the Times, appears to be on par with Wakefield's.

I've done a Google search on a variety of terms, including Peter Harvey with and without autism, MMR, Brian Deer, General Medical Council, neurologist...and all I find is that Peter Harvey's put his name to a retracted paper and to two letters defending the retracted paper. Yet...his culpability in this "deliberate fraud" must at least be given serious consideration.

That leaves us with John Linnell, the last of the three authors on that debacle of a paper who didn't participate in its retraction. It appears that the reason he didn't participate is that the other 10 authors involved could not find him. I wonder if they looked at the Chelsea & Westminster Hospital in London for him. And unless he's taken to studying carnivores in Norway, his only publications are the MMR-autism-related ones, although his name turns up consistently on biomed-autism/ADHD sites in this form:
Elevated urinary methylmalonic acid and early reports of response to oral B12 from John Linnell, research director at The Children's Medical Charity, U.K. Some reports of response to B12 shots.
This report or whatever it is appears to be quite popular among the DAN! sorts, although it does not appear on PubMed.

Wakefield didn't commit this fraud alone. Ten of his co-authors acknowledged the faults of the original paper and withdrew their names from it. One of his co-authors appears to have vanished, while the other has steadfastly refused to retract and has solidly associated himself with some of the misrepresentations involved in the paper's case histories. Harvey, it seems, has ended up as Wallace to Wakefield's Darwin, except, you know, for the lying and cheating and all that.

Peter Harvey and John Linnell...where are you now?