Last Monday, Dr.Hasse Walum gave a talk titled "Genetic and Hormonal Influences on Pair Bonding Related Behavior in Humans" at the Center for Translational Social Neuroscience at Emory. I hadn't heard of Walum's work before I saw the e-mail announcement for his talk, but a little googling got me interested. Here's the most titillating version of his findings: Walum found the gene that makes men cheat.
Okay, that is most definitely not what he found, and I got the sense from talking with him briefly that he would be the first one to tell you that. So why am I misrepresenting his results?
|Dr. Hasse Walum: hard-hitting Wired reporter David Ewing Duncan compares him to Kurt Cobain, but my science and rock star senses detect a David Bowie influence|
I want to make some points about how science interacts with the media. Like I said, it was reading news reports that made me want to go hear Walum talk. As a graduate student, in his first published study, Walum reported that different forms of a certain gene are associated with the strength of relationships that men form. As he told me after his talk, he spent the week after the study was published just answering phone calls from the press. On Wired’s site I found an article about the paper that struck me as fairly cautious, even if the author did point out that "Walum did not report if he carries the tell-tale gene". Then again, on the BBC website I found a piece that opened up with a pic of actor George Clooney, pointing confidently at someone off camera, along with a caption that asks if he's "afraid of commitment?" Clearly, the press sensationalized this story. In a recent post on this blog, Emory neuroscience grad student Jordan Kohn put a lot of blame on journalists for the sensationalizing of research results. Unfortunately, there's plenty of blame to go around for the way that science gets represented in the media, and I think some of it should fall squarely on the shoulders of the science establishment.
Let's face it; Dr. Walum's study wouldn't have been published if the title was: "We can't find any evidence that this gene has anything to do with dudes that suck at monogamy". He told me as much after his talk. I don't mean to use Walum's words against him--in fact, I think anyone who's studying anything remotely interesting about the brain faces the same ethical dilemma. I'll say more about that after I sum up the seminar.
|Ratty (actually a water vole)|
What I didn't realize when I got the e-mail announcement was that Dr. Walum was here giving a job talk. The reason for Dr.Walum's visit became obvious when he got to the slide in his Powerpoint presentation featuring a picture of Ratty from Wind in the Willows. Ratty, for the uninformed, is a water vole, and Dr.Walum's childhood love of Ratty establishes that he's wanted to work with voles ever since he was a kid. If that didn't convince us, he also informed us that he wrote a literature review of filial mate bonding for his degree project as an undergrad, and that the inspiration for his work was Larry Young's studies of the vasopressin receptor gene in voles.
As you are no doubt aware if you have spent more than five minutes on Emory's campus doing something besides playing beer pong, a significant component of Emory's neuroscience research revolves around voles. Voles provide a convenient model for understanding how monogamy works in the brain. Species like montane and meadow voles are promiscuous, but the prairie vole is monogamous. Young's group has shown that this difference is due in large part to a 482 base-pair long snippet of DNA which the prairie voles carry. This length of DNA lies in the regulatory region of the vasopressin receptor gene—that is, the DNA near the gene itself that affects how the cell’s machinery churns out vasopressin receptors. As the name implies, these receptors bind vasopressin, a hormone known to play a role in bonding (and in other more mundane physiological tasks, like water retention). By inserting the same length of DNA in the regulatory region of the vasopressin receptor gene in mice, which are easier to manipulate genetically, you can increase affiliative behaviors in males. Male mice carrying the insert show increased levels of olfactory exploration and grooming of females. Now all we have to do is figure out how that change in regulatory regions translates into a change in behavior, and...viola! We've figured out monogamy. And cured autism. Maybe.
Not everyone feels the love for the Young lab's research agenda. Last week this blog also featured an interview with feminist science studies scholar Angela Willey. While at Emory, Dr. Willey problematized the heck out of the Young lab's research on monogamy. I'm still processing that post. The neuroscientist in me wants to defend the Young group's work with adjectives like "elegant". On the other hand, I'm sympathetic to feminist and queer critiques of neuroscience research, and I think it's important for neuroscientists to engage with those critiques. To their credit, the Young lab did just that. I could echo Willey's points about how their definition of monogamy seems to reduce a very complex human behavior to a single number which they assign to vole behavior--a simplification I'm sure the lab is aware of--but let me stay focused on the seminar.
Walum’s began his with that first paper on the human vasopressin receptor gene that got him all the press. I'll state what he and his colleagues reported in scientific terms. Then I'll explain those terms, just in case anyone finds them as opaque as I once did, before undergoing years of training that allow me to speak complete gibberish to strangers. Their results show a correlation in humans between scores on a Partner Bonding Scale and variations in a microsatellite upstream of the human gene for the vasopressin receptor. Dr. Walum created the Partner Bonding Scale, as he proudly told us, basing it on the behaviors that are measured to put a number to the strength of pair bonds between great apes and other nonhuman primates. By sequencing microsatellites in roughly two thousand Swedes, Walum et al. were able to show an association between scores on his scale and the version of the microsatellite that men carried. Microsatellites are short regions of repeats in DNA. When they occur in the regulatory regions outside of a gene, these microsatellites can affect gene transcription, and by extension the protein that the gene encodes. Case in point: the vasopressin receptor has a different distribution in the brains of the monogamous prairie voles and the promiscuous montane voles. As outlined above, the Young lab has shown that a 428 base pair insert in the genome of the prairie vole, right next to one of the vasopressin receptor genes, causes this change in receptor distribution. Similarly, Walum et al found that men who carried the so-called "334 allele" were significantly more likely to receive lower scores on the Partner Bonding Scale. You might know that alleles are different versions of a gene, or in this case microsatellite. There’s not 334 versions—the number refers to the length of the repeat. The effect they found was “dose-dependent”: men that carried one or two copies of the 334 allele were much more likely to have lower Partner Bonding Scale scores. It’s worth emphasizing, though, that the 334 allele does not show any sequence similarity to the 428 base pairs of prairie vole DNA that supposedly make that species more monogamous, and neither does any other part of the regulatory region flanking any of our vasopressin receptor genes. Different microsatellites, related effects. At least that’s what Walum et al. argue.
|Cyberball: image taken from a study|
of "social exclusion" (Bolling et al. 2010)
Dr.Walum went on to talk about the other studies he carried out as a grad student. One set of experiments looked at the effects of oxytocin, another hormone that some argue increases trust. To try and measure the bond that female subjects formed with males they were partnered with during the experiments, Walum and company used a videogame of sorts they called “cyberball”. In cyberball, the female subjects could choose to “throw” a ball to either an icon of their partner’s face or to an icon of an unfamiliar male. If female subjects that recevied intranasal oxytocin more readily trusted the male partners, it should show up in the cyberball score. After the talk was over, I went up talk with Dr. Walum. I had to know, did the data from cyberball tell them anything? At first he said he couldn’t remember. Then he said something about “trending in the same direction”, only to interrupt himself and say that the scores had only been significant when lumped together with other metrics they’d used. I replied sympathetically. “It’s hard to find a way to measure human behavior.” Then I told him that the Cyberball game reminded me of the Partner Preference Test, a behavioral assay designed by the Young lab to measure monogamy. In the test, voles are put in a three-part cage, with their partner on one side and a stranger on the other. Prairie voles tend to spend more time with their partner. I asked Dr. Walum if he was trying to find a way to do the Partner Preference Test with humans. “Yes, exactly,” he said, “but you can't do that with humans. You can't do the experiments you would like to do." I agreed. "I don't think that an experiment proposing that you put humans in a large plastic tank would make it past the Institutional Review Board." He went on: “With human subjects, it's all about variation. You can do some pharmacological manipulations, like with the intranasal oxytocin, but with our first study [on the vasopressin receptor allele] we had to think more about our story than about our results”, he said. “In a way we published the story that everybody wanted to hear.”
Again, I’m not trying to use Dr. Walum’s words against him. While I might not have the expertise to critique his study’s use of Generalized Linear Mixed Effect Models, I also don’t have any reason to doubt his results. As Dr.Walum made perfectly clear in the Karolinksa Institute press release that the Wired and BBC alike were so quick to quote, “There are, of course, many reasons why a person might have relationship problems.” What am I trying to say is that we should keep the economic realities of science in mind when we talk about how research filters through to the media. Every neuroscientist who complains about how the only things the press can do is cut and paste pretty pictures from fMRI studies should remember that, right now, those are the studies that get published, and by extension, the studies that get media attention. Like it or not, the axiom of “publish or perish” still applies. All these papers that only trot out sexy results “provide strong evidence”, as us science types like to say, that studies should be registered and accepted by journals before the experiments are carried out. Scientists already write their grants this way—they sell the research they’re going to do—so why shouldn’t that be what journals are buying? This is the system that Neuroskeptic has advocated on his blog (here’s a hyperlink by way of citation). If the experiments don’t provide any evidence, then publish that lack of evidence, and save everyone else the effort of pointlessly repeating the same study.
Under this system, if neuroscientists find themselves angry about how the media represents their results, at least they can tell themselves it’s not because they're only publishing what gets them funding. I don't think that system would put an end to press releases that tout tantalizing findings, though. After all, someone has to sell the science so more science can get done. I'm guessing that's the explanation I'd get if I talked with the Man who Voled the World.
Want to cite this post?
Nicholson, D. (2012). The Man Who Voled the World. The Neuroethics Blog. Retrieved on , from http://www.theneuroethicsblog.com/2012/07/man-who-voled-world.html