Recently in the Wall Street Journal, science writer Nicholas Wade contributed a review of Bill Nye’s new book, Undeniable: Evolution and the Science of Creation. Wade misrepresented the status of contemporary evolutionary theory, as does Mr. Nye. Both give the impression that only young-earth fundamentalists entertain serious doubts about modern Darwinism, a misunderstanding reinforced by Mr. Nye’s high-profile debate with Ken Ham.
Ignored in the debate (and in Nye’s book) was any serious discussion of the current dispute in mainstream biology journals about the creative power of the natural selection/random mutation mechanism — the mechanism that allegedly renders a designing intelligence unnecessary to explain the complexity of life. Popularizers like Mr. Nye claim the case for Darwinian evolution is “undeniable.”
Yet many scientists, including leading evolutionary biologists, now question (or deny) the ability of the neo-Darwinian mechanism to generate genuine biological novelty — clearly, a significant lacuna in established theory. Scientific discoveries in molecular biology, genomics, developmental biology, and paleontology are not in fact friendly to Mr. Nye’s dogmatic “undeniability” thesis.
Interestingly, in any case, Nicholas Wade is critical of Nye for failing, in Wade’s view, to make the soundest case for Darwinian evolution. He writes:
[Nye] is good on the geological and fossil evidence for evolution, reflecting his background in the physical sciences, but devotes less attention to changes in DNA, which furnish the most direct evidence of evolution. A recent paper in the journal PLOS Genetics, for instance, describes the seven DNA mutations that occurred over the past 90 million years in the gene that specifies the light-detecting protein of the retina. These mutations shifted the protein’s sensitivity from ultraviolet to blue, the first step in adapting a nocturnal animal to daytime vision and in generating the three-color vision of the human eye. Such insights into nature’s actual programming language are surely the most undeniable part of evolution at work.
Readers may be interested in the scientific story that Wade did not report.
In the experiment that Nicholas Wade cites, researchers compared pigment proteins involved in light-detection in mice eyes with similar proteins involved in light-detection in human eyes. They found that the two proteins exhibit seven important differences in the amino acids that make up the two proteins (think of seven crucial differences in the letters in two sentences giving each sentence a slightly different meaning). As a result of these differences, the two proteins detect light across a modestly different range of light wavelengths.
To simulate how random mutations might have produced a human eye pigment protein from an ancestral protein to the one found in mice, the researchers themselves made a series of changes in the sequence of amino acids in the mouse protein, until they eventually produced a protein with the amino acid sequence found in humans. They then found, not surprisingly, that the protein had the same optical properties — i.e., it could detect the same wave lengths of light — as the protein found naturally in humans.
Though Wade and the experimenters assert otherwise, the researchers did NOT establish that seven mutations had actually occurred to produce the differences in the optical properties of the two proteins — i.e., that one had evolved from a common ancestor of the other by random mutation. Instead, they compared amino acid sequences in human eye proteins and mice eye proteins and simply assumed that the differences between the two proteins must have arisen by random mutation (and natural selection).
Since there are other possible ways that these differences could have arisen (intelligent design, for example), and since there are also independent scientific reasons for doubting that the number of coordinated mutations required to produce this change could have occurred randomly in the time available (see below), this assumption is clearly question begging. (The study also assumed that mice and humans share a common ancestor — another questionable assumption.)
Curiously, as the researchers tried to produce a protein with the properties of human eye proteins from the allegedly ancestral protein, they found that changing any one of the amino acids by itself did not affect the protein’s function. To get anywhere, they discovered that they had to make sure that two or more specific mutations occurred together in concert to make it progressively more like the one found in human eyes.
But this poses two problems. First, such a necessarily choreographed procedure would seem to simulate — if it simulates anything — the need for intelligent foresight and design, not the power of an undirected process involving random mutations.
Second, and in support of this conclusion, the calculated “waiting times” for the occurrence of coordinated mutations (i.e., multiple mutations occurring together) far exceeds the available time for the transition from a mouse-like common ancestor and the emergence of humans.
In my book Darwin’s Doubt, I used the Powerball lottery to illustrate the problem of excessively long evolutionary “waiting times.” On average you have to wait much, much longer to get a big winner (with lots of matching numbers) in the lottery than you do to get a smaller winner (with only a few matching numbers). In the same way, the expected “waiting times” for the occurrence of multiple coordinated mutations is vastly longer (usually requiring many hundreds of millions of years) than the expected waiting time for the occurrence of single mutations. Yet, the experiment that Wade sites actually shows that specific coordinated mutations are necessary to make any progress in altering the ancestral proteins into something similar to human eye proteins.
In other words, calculations made based on standard evolutionary assumptions and mathematical models show that there is likely not enough time for the sequence of mutations necessary to produce the human eye protein to have occurred by random mutations (starting from the ancestral eye protein). Such independent mathematical assessments ought to cast doubt on our confidence that the human eye proteins arose by random mutation and selection. But because the researchers (and Wade) simply assume it must have happened that way — and because they are unwilling to consider the possibility that it arose by design — they conclude that these experiments favor their conclusion, when in fact they don’t.
There is one more problem. Even if we assume that mutation and natural selection could and did transform the ancestral eye protein into the human eye protein in the time available, the change involved is extremely modest. In the experiment, the researchers did not produce a fundamentally new protein structure — called a protein fold. Yet, as I show in Darwin’s Doubt, producing new protein folds is a necessary condition of any significant large-scale macro-evolutionary change. All that the experimenters even purported to simulate was a slight modification in the function of the mouse protein without achieving any fundamental alteration in its structure. Such small scale changes are commonplace and do not help solve the real problem in evolutionary biology today — the one addressed in my book — which is the problem of the origin of structural and morphological innovation (or the origin of novel form).
In the experiment, the allegedly ancestral protein functioned as a light detector with a particular stable structure before the alterations to its amino acid sequence. It functioned as a light detector with a slightly different set of optical properties with the same stable structure (i.e., fold) after the alterations. Same protein structure; same basic function (light detection); with a modestly altered range of frequency detection. Even if this experiment had demonstrated what random mutations can do, it would have shown they can not do much. Indeed, the experiment did nothing to address the key problems discussed in Darwin’s Doubt, including explaining how random mutation and natural selection could generate enough new genetic information to build a new protein fold (or system of proteins, tissues, organs, or body plans).
Wade’s review, of course, doesn’t even hint at these problems, but instead misrepresents the status of evolution theory to the readers of the Journal. As usual there is much more going on than you will find reported in the mainstream media, even — on this issue, alas — in the conservative media.