One of the things I hope to do in this space is facilitate communication between scientists and science writers about how to best describe complex scientific research to the public. After hearing some concern from University of Iowa neuroscientist and Behavioral Neuroscience Editor-in-Chief Mark Blumberg about Nicholas Wade's recent New York Times story, "Speech gene shows his bossy nature," I invited Blumberg to submit an open letter to Wade. Here it is, along with Wade's response:
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Dear Nicholas Wade,
I'm very sympathetic to the terrific challenges you face in making new scientific research appealing and digestible to the public. But I have some specific concerns about your latest report on the FOXP2 gene, beginning with the headline, "Speech gene shows his bossy nature."
Can we really still call FOXP2 a "speech gene"? As you know, this FOXP2 mutation was originally identified in a London family, many of whose members exhibited profound language impairments. From that single observation, it became known as the "speech gene." But there was always the distinct possibility that the mutation influenced a myriad of other brain and body functions that, in turn, affected speech. Indeed, given all that we know about how genes work - as well as our sad history with grandiose claims about single-gene effects on behavior - wouldn't it be wise for all of us to be more cautious when communicating these findings to the public? As for people with FOXP2 mutations, a well-informed colleague has told me that they do indeed exhibit a variety of problems beyond those related to speech, just as we would expect. I fear that these other problems have not been adequately studied precisely because they detract from the preferred "speech gene" narrative.
As to its "bossy" nature, you write that FOXP2 "does not do a single thing but rather controls the activity of at least 116 other genes." That's true, but let's put it in context. As you know, such distributed effects are nothing new; genes are always part of complex networks and therefore are hardly ever expected to do a single thing. Thus, FOXP2 is part of a large, complex network of genetic and non-genetic factors that, under the right developmental conditions, appear to contribute to the human faculty for language - and a lot of other things as well. In fact, many studies have now shown conclusively that mice with the FOXP2 mutation exhibit changes in a myriad of organ systems, including the lung and brain. And yet FOXP2 is called a "speech gene" rather than a "lung gene" or a "brain gene."
I suggest that the better alternative is to describe FOXP2 in less dramatic terms - which you do very nicely when you write that "the whole network of [language-related] genes has evolved together in making language and speech a human faculty." It's frustrating, then, to read references in the same article to a simplistic and outmoded view of gene action - for instance, when you write of "genes under FOXP2's thumb" and FOXP2 as "a maestro of the genome." The new Nature findings actually portray a more sober view of FOXP2's powers.
This is not the first time that you have written about FOXP2 in the Times. Last May, you wrote an article entitled "A human language gene changes the sound of mouse squeaks." The subject of your piece was another scientific article, this one published in Cell, that reported on changes to brain and behavior in mice engineered to express the human version of the FOXP2 gene. One of the authors of that paper is quoted by you as promising that "We will speak to the mouse." An extraordinary promise coming from a scientist, don't you think?
It was the link to human language that garnered that mouse study so much acclaim. And what did they find: that the "humanized" infant mice emit vocalizations of a slightly lower pitch than typical infant mice. Having researched similar vocalizations in rats for many years, I knew before reading the Cell paper that the findings almost certainly had nothing to do with human language. In fact, any manipulation that alters the body size or respiratory system or larynx or a host of other factors in these animals could account for the small change in pitch of the mouse vocalizations. Given FOXP2's influence on so many organ systems, it would have been astonishing if their vocalizations had not been affected.
Trumping up FOXP2 as yet another star gene in a series of star genes (the "god" gene, the "depression" gene, the "schizophrenia" gene, etc.) not only sets FOXP2 up for a fall; it also misses an opportunity to educate the public about how complex behavior - including the capacity for language - develops and evolves.
Regards,
Mark S. Blumberg, Ph.D.
F. Wendell Miller Professor, Department of Psychology, University of Iowa
Editor-in-Chief, Behavioral Neuroscience
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REPLY FROM NICHOLAS WADE:
Dear Mark,
I'm a little puzzled by your complaint, which seems to me to ignore the special dietary needs of a newspaper's readers and to assume they can be served indigestible fare similar to that in academic journals.
You question whether FOXP2 can be called a speech gene and you suggest it could equally well be called it a lung gene. But language is more interesting to most people, scientists included, than is lung function. It's because of FOXP2's connection with language that so many labs are working on it. So I cannot see any reasonable objection to calling it "a gene that underlies the faculty of human speech."
The role of this article was to update readers on a new finding, not to review the history of ideas about FOXP2. So there's no space to go into the argument about the gene's precise involvement with speech and language, much of which we have covered in earlier articles.
I won't comment on the headline on the article - reporters don't write headlines and are generally not consulted about them.
I don't see what's wrong in calling FOXP2 a "maestro of the genome," a phrase that would apply to many transcription factors. Yes indeed the gene is expressed in several other tissues besides the brain. But I had 550 words in which to set the story up in non-technical language, explain why it was interesting, and give general readers a flavor of what the researchers had found. There was simply no space for the qualifications you mention and they are not essential to the story.
You cite an earlier article about the mouse which Svante Paabo genetically engineered to carry a human FOXP2 gene. Then you ask if I didn't realize that Paabo was making "an extraordinary promise" in saying "We will speak to the mouse." Well, no, I didn't - I thought it was obvious he was making a joke. He's surely implying the mouse is rather unlikely to speak to him.
Your view is that Paabo's paper on his FOXP2 mouse was of little interest, and it's true that he and Wolfgang Enard only found a large number of rather subtle changes, including slightly different isolation whistles. But I think most people would say the experiment was important and needed to be done, even if we don't really understand yet what all the changes mean. That's why I thought it was worth writing up.
I don't understand your complaint that FOXP2 is being given star treatment. It's in the limelight because it's a really interesting gene that may provide the entryway to a major human faculty. If it fails to do so, we'll write that up too. Are you suggesting we should tell our readers nothing about FOXP2 for the next 10 years until we have a definitive answer? - That's the role for encyclopedias and review articles.
As for missing an opportunity to educate the public, that, with respect, is your job, not mine. Education is the business of schools and universities. The business of newspapers is news.
Nicholas Wade
Reporter, The New York Times
Author, The Faith Instinct
David Shenk
It is indeed quite irritable to read Mr. Wade's response. Especially, his claim that journalists' job is not to educate the public. First of all, there is no such thing like pure news, that is, neutral news that do not carry educational impact. Second of all, news about science ought to be educational. Otherwise, what is the news? That a speech gene has been discovered? Who cares! And lastly, a journalist writing about science has to be less ignorant than Mr. Wade about the complexity of scientific discovery, scientific communication ,and the essence of genetics.
His responses are simplistic and disclose his ignorance, even worse, his superficiality. He did not understand the point Professor Blumberg was making, namely, that genes cannot and should not be assigned names, because the causal relationship between a gene and the phenotype associated with it is never direct and in no case definitively demonstrated. By calling a gene "speech", lung" or 'hair color" one implies the zero hypothesis: gene is there--the feature is there or gene is not there---the feature is not there. Which is never the case in complex biological systems. Had Mr. Wade educated himself about how complex the gene machinery along the chromosome was, he would have had more respect toward what knowledge about it represents news and what not.
Instead, he seems too busy with publishing flashy news reports competing with his colleagues for sensations rather than educating the public. It is sad that all kind of journalistic writing in this country, beyond science journalism, is characterized by the same flaw so well revealed--almost innocently--by Mr. Wade: sucking up to a generally uneducated public.
Zlatko Anguelov, MD
I'm no doctor, but as a fellow journalist, it sounds much like Mr. Wade is justifying his contortion of the spirit of the study by pleading audience ignorance. It is true that most of us laypeople might not understand scientific jargon. But while it is all right for Wade to simplify the language, it is not all right to narrow an article's focus because he feels that readers could not grasp the whole picture. That's called "only telling part of the story," and is a rather egregious breach of journalistic responsibility.
Imagine if we applied similar principles to our coverage of politics, and provided only part of the picture. How many Americans would make political judgments based on incomplete information? How many already do? It's a shame that we cannot trust even an institution as revered as the New York Times not to cut corners in the name of dumbing down to readers.
I think Wade simply had a bad day and didn't want to admit any fault or agree with anything Blumberg had to say. It's too bad, because Wade often explains biochemical concepts deftly. As examples, I can think of stories he's written explaining research on chromatin and the "histone code."
Many of the phrases Wade uses in his reply are rote formulas many journalists could recite in their sleep.
I'm a PhD in biochemistry who later went to work as a reporter at a newspaper, so I've heard many of those formulas before.
They essentially mean: "Go away and leave me alone."
Probably an almost-instinctual thought for someone who works at the New York Times, but not wise to express in this case.
I can't say I'm very impressed by Nicholas Wade's response, and his parting comment in particular. Complaints about journalists misinterpreting and sensationalising scientific results are rife in the scientific community (and other technical communities, too, I should note) and are in many cases quite justified. Journalists labour under their own limitations as well, and many of us more technical folks would do better to try to understand those.
Dr. Blumberg's criticism struck me as not only atypically polite, but a rare attempt to reach out and try to bring scientists and journalists closer together in what I see as a joint responsibility to educate the public about the scientific enterprise and its results. That a reporter, especially one reporting on science, should think that it's not his role to help educate the public about the real import of the news he's reporting I find, frankly, rather shocking. To essentially brush off what appears to be a reasonable criticism from a scientist on the reporting of results in his field can only contribute to increasing, rather than decreasing, the lamentable friction between scientists and reporters, make his own job more difficult, and in the long run, reduce the quality not only of his own reporting, but that of any other journalist who has to deal with scientists watching this exchange.
I enjoyed reading this interesting back and forth between Dr. Blumberg and Mr. Wade, but I was surprised by some of the content in Mr. Wade’s response...
Regarding the “indigestible fare” in Dr. Blumberg’s essay, I found it all quite tasty--his argument was cogent and easy to understand. What’s so “indigestible” about the idea that genes interact in complex ways? And why would we expect that something complex like speech would have a simple underlying genetic cause? That strikes me as rather simple-minded--has Mr. Wade ever watched a child learn language?
Regarding the "special dietary needs" of the New York Times readers, I have to say (as a New York Times reader) that this is one of the most condescending things I’ve read in a while. So as a reader of the Times, it's not possible for me to understand that genes do complex things?
Next, I agree with Mr. Wade that language is more interesting to people than lungs, but isn’t that why special care is needed when describing phenomena claimed to be uniquely human? If journalists are always feeding our expectations about the specialness of human abilities and the specialness of genes, doesn't that create a barrier to understanding the reality of genetic and non-genetic systems? Might journalists be creating a blind spot by feeding our biases? Is that objective reporting?
Finally, Mr. Wade’s purported lack of understanding about the "star treatment" of FOXP2 strikes me as disingenuous, as is the claim that he'll write about research that fails to find evidence of a link between FOXP2 and language per se. For instance, Scharff, Jarvis, Wada et al. (2004) reported that FOXP2 is linked to the learning of rapid vocal movement sequences and their timing rather than being linked to the production of bird song or a “song module”. It would be interesting to apply the FOXP2 star treatment to evidence like this.
But then Mr. Wade might run the risk of educating his readers. Wouldn’t want that to happen...
And by the way, I made all my comments in 333 words ;)
There is no doubt that Mr. Wade’s job is a difficult one. How does one explain a complex phenomenon in a brief article and at the same time give it sufficient pizzazz to garner it’s audience’s attention? What could be better but talk about genes and their direct link to language and then, for good effect, start off with an attention-grabbing headline? In point of fact, what would be better is either not write the article that Mr. Wade wrote at all or write an article that captures the complexity of the issue.
I agree with Dr. Blumberg that Mr. Wade and his editors have committed a great injustice to a public that they purport to educate: they have badly misinformed the intelligent and curious readers of the New York Times and have lent their considerable respectability to the discredited and outmoded nature vs. nurture framework. I’m afraid that I don’t buy Mr. Wade’s protestations that it is difficult to explain complex concepts to a lay public that is not conversant with the intricate details of a particular discipline. It is actually not very difficult to do it at all.
When I try to get across the key idea that is part-and-parcel of developmental systems thinking, namely that everything matters in development and that developmental outcomes are the result of exceedingly complex interactions among many factors at different levels of organization (i.e., genetic, neural, behavioral, environmental), I resort to some commonly used metaphors that the lay public can readily grasp. Take, for example, the “science” of bread-making. To bake a good and tasty bread one must first use the proper mix of all the required ingredients (flower, water, oil, yeast, and salt). The ingredients must be combined in the correct order, the dough must be properly worked to develop the gluten, the dough must rise at the correct temperature (if the water is too cold the yeast won’t grow but if too hot it will kill the yeast), and the bread must be baked at the proper temperature for a specific amount of time. Encapsulated in this example are the important principles of development. No single factor is determinative in a developing system. For example, simply placing the 46 chromosomes of a newly fertilized human egg in a petri dish will not produce a human infant; they need to be inside a cell and that cell needs to be inside a uterus.
The interactions among all the factors in a complex biological system are at the heart of the developmental process, the quantity and quality of each of those factors is crucial, the conditions under which the interactions occur are key, and the proper timing of those interactions is essential. Voluminous empirical evidence from developmental biology and psychology is consistent with these general principles. Unfortunately, much of this evidence lacks the cachet that evidence purportedly linking a single gene mutation with something as important to the human species as language possesses.
I doubt that Mr. Wade and his editors would be willing to point out that language acquisition is an enormously complex process that involves, at a minimum, exposure to the maternal voice prior to birth, the countless utterances that infants are exposed to in their daily lives, the babbling that infants produce, the feedback that their babbling elicits in adults, the social interactions that not only encourage infants to communicate but also serve to correct their incipient speech productions, and the years of subsequent schooling during which children learn to read and write and the syntactic structure that governs the way they can use their language. If we are to take Mr. Wade’s article at its face value then none of these factors and their interactions really matter because for him the master is a single gene that, like a conductor of an orchestra, drives the whole process. This is simply wrong! Genes code for proteins and nothing else. If that is the case then how does one get from a protein all the way to one of the most complex of all human cognitive skills: language? Obviously, the path is extremely complex and the principles of development listed earlier are one way to begin to conceptualize the process. Single-factor explanations such as those suggested in Mr. Wade’s article are simply wrong-headed.
David J. Lewkowicz, Ph.D.
To suggest that changes in a couple of amino acids could be responsible for the stunning phenomenon of speech is unspeakable and a sad comment on modern science.
D J Wray
http://www.atotalawareness.com/documents/atotalawareness.pps
“Darwinian evolution creates primitive creatures with an ability to host visitors with language skills.”