Missed opportunity – not debacle – in bogus schizophrenia genes coverage

July 6, 2009

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.

Related: NYTimes | 1) A Dissenting Voice as the Genome Is Sifted to Fight Disease, 2) Gene-Hunters Find Hope and Hurdles in Schizophrenia Studies

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?

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5 Responses to “Missed opportunity – not debacle – in bogus schizophrenia genes coverage”

  1. John Timmer Says:

    I’d say that, to a certain extent, the hope behind genetic studies is to understand the basic biology. So, prior to these studies, there might be the hope that all the mutations that came out of this screen would affect genes involved in signaling through a specific neurotransmitter, or something involved in synapses. All of that would be likely to assist in therapies and such, but it’s really essential to establish any sort of organized research program.

    In this case, the genetics appear to be suggesting that what we call schizophrenia is probably multiple disorders that we just lump together.

  2. JR Minkel Says:

    John, I was meaning to blog your recent story about rare gene variants combining to cause autism, which was nice because it put the genetic complexity in proper perspective. I think schizophrenia and autism are so multi-factorial because they represent limit-faults in highly optimized cognitive functions that are basic to H. sapiens.

    That said, there’s the separate question of why scientists frame their results the way they do, why the public wants to believe them, and what role journalists should be playing.

    Two points:

    a) Many of us have invested in the idea of science as efficacious, whether or not we understand how science achieves efficacy.

    b) Schizophrenia and autism are burdensome on society. It would be nice if publicly funded science could help us alleviate those burdens. When science doesn’t “cooperate,” parents say things that can be interpreted as wishing autism would go away. Scientists are then perceived as agents of that wishing away.

    I’m positive something like this accounts for some of the shrill discourse around autism — “damn scientists! parents need help!,” and, “damn scientists! auties are people too!” — and I suspect something similar is at work with schizophrenia, where we also have to make hard decisions about how to treat people suffering from the disease.

    Journalists are in a position to negate that discourse in incremental ways.


  3. [...] Missed opportunity – not debacle – in bogus schizophrenia genes coverage [...]


  4. [...] risk factors for disease. See my story on risk factors for schizophrenia, inspired by this exchange with Brandon Keim of Wired [...]


  5. [...] risk factors for disease. See my story on risk factors for schizophrenia, inspired by this exchange with Brandon Keim of Wired [...]


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