The Science Stories that Fizzled (and the one that Might Have Been)
There were three kinds of stories that could have developed from the news that Science magazine released a paper by professors at the University of Oregon's Center for Ecology and Evolutionary Biology that supposedly falsifies Michael Behe's theory of irreducible complexity (as an indication of intelligent design). That Science accompanied the paper with an interpretive piece by Christoph Adami of Claremont, underscores the coup Science hoped it had accomplished. What, studying the paper and commentary, should be done with this news?
The first possible story was the one that Science hoped: that finally someone in the science world had done actual research to refute Behe's theory. Hence, intelligent design could be dismissed conclusively as bad science.
Trouble was, in preparing this first story line, the New York Times and the Wall Street Journal science writers contacted us and asked for our scientists' reaction. Mike Behe did answer and conclusively. So did Steve Meyer. There was no way thereafter to say that Thornton et al had made a conclusive case.
Both the Times and the Journal ran stories, all right, and there was a tone in both stories that this was important research, but both papers also downplayed it. After all, if it had been a Darwinist knockout punch, it might have warranted the big story treatment. But the fact that the study was very well refuted by Discovery scientists meant that both the Science article claim and our refutation would have to be covered in some detail in any big story. And that would reveal to any objective observer that Thornton, et al, had failed.
The second option, therefore, was the one chosen: run the story, but downplay it. Story one became story two--the minor leagues account.
However, the third way to cover this story--and the superior way if you think that readers have a right to know what actually is going on in the science world--would have been to tell the truth: the Darwinists, having failed to show (despite Judge John E. Jones' contention, following the ACLU, in the Dover case) that ID is "not science", determined to answer it--as science--after all. This finally concedes that Behe and his colleagues have been doing science all along (see also Behe's essay in Traipsing Into Evolution). So, we now at last see the hope of moving the ID and evolution debate away from Darwinian name calling and motivation mongering and engage it where it deserves to be debated: in science. So, score one for ID.
But, in addition, the fact that the Thornton paper so manifestly fails in its aim to falsify irreducible complexity should alert true science-followers that there not only is a debate going on in science, but that the ID people are winning it. Ten years ago, Behe could not get science journals to let him reply to the captious rebuffs of his critics. Now, days after publication of the tenth anniversary edition of Darwin's Black Box--a tremendously popular book for a science subject, with a quarter million copies in print-- with added material by Dr. Behe, Science magazine has attempted to refute Behe's main scientific contention--and failed.
But does the Oregon Center for Ecology and Evolutionary Biology (with all its public funding) really fail? How would the readers of Science, or the New York Times for that matter, know?
The only way is if the editors of Science invite Behe to reply on their pages. Since they have not been known to be very open to real scientific debate--only ideological assertions--on this topic in the past, we decided to print on our website the replies to the Science article that Dr. Behe and Dr. Meyer gave to the reporters for the New York Times and the Wall Street Journal. Since, reading their resulting articles, you can see for yourself that Behe's and Meyer's points are hardly acknowledged at all, you also can conclude that those publications are as self-referential and fearful of fair debate as is Science itself. Thank goodness for the blogosphere and the 20,000- 25,000 or so of you who follow this site each day!
But, let's hope. Science, the Times and the Journal are edited by human beings and human beings can learn and change their minds. (What human beings do not do, of course, is evolve.)
MEMO from Rob Crowther: Behe and Meyer spent a long time on the phone with the Times and Journal writers providing ten major and relevant criticisms of the Oregon paper. They also sent the reporters some follow-up emails, including the one below from Meyer to Kenneth Chang of the Times. Again: see our lengthy response at ID The Future. Also, follow all the relevant links to responses, as well as some additional reading material from this page on the Discovery website. At some point, if it hasn't happened yet, it will dawn on the reader that the reporters ducked the real story.
-----Original Message----- From: Steve Meyer Sent: Wednesday, April 05, 2006 10:21 AM To: email@example.com Cc: Robert Crowther Subject: Our Conversation/Quotes
I wanted to come back to you the point you raised in the interview. You claimed that because there had been a gene duplication event the loss of binding strength in the cortisol-binding receptor didn¹t matter‹the duplicated gene would maintain that function. But on re-examination of the paper I think this is incorrect. The duplicated gene is being specialized to acquire a different function‹in particular, aldosterone-binding in support of electrolyte homeostasis (cortisol-binding supports other physiological processes such as immunity and inflamation, etc.). Thus, a 100-fold loss of cortisol binding strength in the cortisol-binding receptor is, as I first said, certain to be disruptive of the function of the overall signal transduction circuit in which it operates. In any case, the authors have done no studies on the effect of such a change in an organismal context that would show otherwise.
I include three quotes below which you may use in your story. I also include a longer explanation of the point I make in the second quote.
Doug may contact you by e-mail with a reaction/quote of his own.
The Bridgham et. al. study is trivial. ID theorists have long known that a few mutations can slightly alter an existing protein fold. What we question is whether mutation and selection are sufficient to search the enormous combinatorial space of possibilities necessary to finding fundamentally new protein folds and structures. This study does nothing to allay our skepticism on that score.
Contrary to what the authors assume receptor-hormone pairs do not constitute irreducibly complex systems. The receptor-hormone pair is only a small component of a signal transduction circuit that regulates other complex physiological processes. For such pairs to have any selective or functional advantage many other protein components have to be present, including the other components of a signal transduction circuit and the physiological processes that such circuits regulate. If this is the best that Behe¹s critics can do after ten years of trying to refute him, then neo-Darwinism is deep trouble.
The really interesting thing about this paper is not the science it contains‹its scientific results are trivial--but the sociological dynamics surrounding the publication of these papers. The AAAS has repeatedly insisted that is no scientific controversy about intelligent design. Now Science, the AAAS¹s flagship journal, publishes two scientific articles taking positions on a controversy that the AAAS says doesn¹t exist. Will Science now allow Behe to respond or will it only publish articles examining about the controversy claiming that ID is wrong?‹Stephen C. Meyer, Discovery Institute
Amplification of points in quote #2
First, the receptor-hormone pairs that Bridgham et. al. study are not irreducibly complex systems. According to Behe, a system is irreducibly complex if it contains many well-matched parts that perform a function such that the removal of any one of those parts would cause the system as a whole to lose function. Given that natural selection favors only functionally advantageous variations, Behe has made clear that ³function² in a biological context necessarily means a selectable functional advantage. Unfortunately, these receptor-ligand pairs do not meet Behe¹s definition of irreducible complexity for a simple reason: receptor-ligand pairs do not by themselves confer any selective advantage. Instead, the receptor-ligand pair is only a small component of the genetic regulation of complex physiological processes such as metabolism, inflammation, immunity, and electrolyte homeostasis. For such pairs to have any selective advantage as part of the regulation of larger physiological processes, many other protein components have to be present. In particular, all the other components of a complete signal transduction circuit have to be present as well as the component parts of the physiological process that such circuits regulate. (Even the ligand itself doesn¹t exist apart from a separate enzyme that produces it and the authors¹ gene duplication scenario does not account for the origin of this necessary component either.) In short, ligand and receptor systems do not by themselves perform selectable functions and thus do not qualify as irreducibly complex systems. Thus, in offering their work as an argument against Behe, the authors have fashioned an elaborate straw-man critique.