Journalist Brandon Keim has a smart post about how he approached last week’s over-hyped schizophrenia genetics story, the latest in a long string of them.
Basically, some high-tech efforts to scan the genome for links to schizophrenia turned up thousands of rare gene variants, each of which might account for some tiny fraction of all schizophrenia cases, and together explained only about 30 percent of all cases. (Papers here, here and here.)
Given that researchers had been looking for meatier schizophrenia genes for years and years without finding anything substantial, this was to be expected, especially if you’re the kind of person who questions whether there are very many genes “for” anything.
Brandon notes that a number of web stories uncritically hyped the journal’s spin, namely, that this was a big, juicy, pharmacologically relevant finding, which it wasn’t. He uses NYTimes reporter Nicholas Wade as his stalking horse, following Wade’s transformation from “gene-whiz” kid to genomics realist.
Here’s Brandon’s point of view:
From a journalistic perspective, there are two possible stories here. First, the straight story: schizophrenia is extraordinarily complicated, and genetics can’t now explain it in any useful way. And two, the contextual angle: for years, the public has expected, and scientists have sometimes promised, that genetics would illuminate this disease — and it failed, just as it has for nearly every disease.
(Useful perspective: search Eurekalert for “schizophrenia” and “gene.”)
When these studies showed up in my pre-embargo pipeline, I made a quick note of them — see above — and moved on. I’m already reporting for a long-form article on the disappointment of genomics, and this didn’t feel like a Wired daily news story. It would require at least a half-dozen interviews, and ultimately produce a narrative preaching caution, tempered expectations and patience. Instead I chose to write about an interesting finding on salamander limb regeneration, and waited for the inevitable onslaught of “Schizophrenia! Unlocked!” stories.
Brandon links to a number of such stories. He wants to portray this as a failure of science journalists — his subject line calls the story a debacle — which I’m inclined to second-guess. As journalists, we tend to critique ourselves from the supply side: we look at the world and see bad things, then look at what our colleagues are doing and see bad things, and then try to link the two, because it reinforces our sense of efficacy. And that’s probably appropriate here.
The other half of the story is the demand side. Can we prevent uncritical science stories from being published? Not by ourselves as journalists. It’s a structural issue that journalists can and should address in the only way they can — by directing skepticism at their own motivations, at least where times allows, and it doesn’t allow much these days for a working journalist. If I was living in a Brooklyn apartment right now instead of my mom’s place in Nashville, you probably wouldn’t be reading these words, although who knows.
I’d argue that Brandon inadvertently makes my point for me.
Knowing that others news outlets would herald the finding uncritically, and assuming that was a bad thing — which calling the coverage a “debacle” implies — what should Brandon have done? By passing on this story in favor of salamander limb regeneration, he passed on an opportunity to confront scientists in real web time about the unmet promise of genomics in understanding complex disease. It could have started something like “Studies appearing in Nature today will be trumpeted as a triumph for the genetics of schizophrenia, and they shouldn’t be,” similar to Nick Wade’s blog post about the coverage, which Brandon says was the only piece to get the story right.
As someone who’s been there, I know what I’m suggesting is easier said than done, although Brandon obviously had the chops to write the tougher story. I’ll forgive him (this time), if for no other reason than because, like he says above, he’s working on a bigger story about the failed promise of genomics, which I can’t wait to read.
So what to make of the schizophrenia coverage? Barring demand-side evidence to the contrary, it was hardly a debacle. The subtext of Brandon’s post is that it’s actually the culmination of a long story arc. It reflects an underlying attitude of scientists and journalists. Attitudes take time to change, and rightly so. I wish I was in a better position to argue about whether the human genome project was oversold, and whether the big daddy gene assumption represents an institutionalized failure of a masculinist theoretical assumption, to paraphrase Evelyn Fox Keller.
We need journalists to step up, in part so other journalists will step up. I am Spartacus, right? With than in mind, I take Brandon’s critique of Wade as a positive.
Not long ago, Wade could be relied upon for reductionist coverage of genetic links to disease. (On the subject of genes and schizophrenia, here’s Wade in July 2002: “Researchers hope they are now starting to close in on some of the genes that go awry in schizophrenia.” In December 2002: “The long search for a gene that helps cause schizophrenia may at last be bearing fruit after many false starts and disappointments, scientists are reporting.” In April 2006: “Researchers have made progress in understanding how a variant gene linked to schizophrenia may exert its influence in the brain.”)
But Wade, who arrived at the Times in 1981, seems to have finally lost patience with the “gene-linked-to-(fill in the blank)” narrative that he and so many others told, and were sold, for so long.
That’s called intellectual honesty! And it’s something all science journalists should aspire to, starting… now.
Question for somebody: To what extent do genetic studies reflect a desire to treat the disease, as opposed to wishing we could find a gene to make it go away?