A couple of weeks ago, an interesting article appeared in Scientific American, titled “Evolution Of The Eye.” The subheading of the article makes the bold claim, “Scientists now have a clear vision of how our notoriously complex eye came to be.” When I saw that this article had been published, I was immediately filled with a sense of intrigue. I looked forward to reading a proposed solution to a fiendishly vexing problem. What the article actually provided, however, was largely disappointing. There was nothing particularly new or original, and (though coated with our modern scientific understanding) the argument took, more or less, the same basic form that has been rehashed for the last century and a half since the publication of Darwin’s On the Origin of Species.
The article actually makes explicit mention of intelligent design (ID) and offers the pertinent argument as a rebuttal to the concept of irreducible complexity. The author of the article, Trevor D. Lamb, claims that
… [B]iologists have recently made significant advances in tracing the origin of the eye–by studying how it forms in developing embryos and by comparing eye structure and genes across species to reconstruct when key traits arose. The results indicate that our kind of eye–the type common across vertebrates–took shape in less than 100 million years, evolving from a simple light sensor for circadian (daily) and seasonal rhythms around 600 million years ago to an optically and neurologically sophisticated organ by 500 million years ago. More than 150 years after Darwin published his groundbreaking theory, these findings put the nail in the coffin of irreducible complexity and beautifully support Darwin’s idea. They also explain why the eye, far from being a perfectly engineered piece of machinery, exhibits a number of major flaws–these flaws are the scars of evolution. Natural selection does not, as some might think, result in perfection. It tinkers with the material available to it, sometimes to odd effect.
In a nutshell, the claims made by Lamb are as follows:
1. By comparing eye structures and embryological development of the eye in vertebrate species, one can infer that our camera eye has very ancient evolutionary roots.
2. Prior to acquiring the elements required for its operation as a visual organ, its function was simply the detection of light for modulating the circadian rhythms of our distant ancestors.
3. The eye has various design flaws and this is evidence for its evolutionary / dysteleological origin.
4. There are clues in developing embryos which indicate how the eye formed from a light-sensing but nonvisual organ into an image-forming one by around 500 million years ago.
Lamb’s article is chiefly concerned with rebuffing intelligent design (and not merely demonstrating common ancestry). In this critique of the article, therefore, I want to focus primarily on the fourth of those points (which I deem to be the crux of the matter), and will also weigh in briefly on the apparent suboptimality of the eye’s design.
Folding A Patch Of Photoreceptors
Lamb tells us,
Early in development, the neural structure that gives rise to the eye bulges out on either side to form two sacs, or vesicles. Each of these vesicles then folds in on itself to form a C-shaped retina that lines the interior of the eye. Evolution probably proceeded in much the same way. We postulate that a proto-eye of this kind–with a C-shaped, two-layered retina composed of ciliary photoreceptors on the exterior and output neurons derived from rhabdomeric photoreceptors on the interior–had evolved in an ancestor of vertebrates between 550 million and 500 million years ago, serving to drive its internal clock and perhaps help it to detect shadows and orient its body properly.
This insight is hardly novel. The idea has been espoused by many of the great evolutionary biologists of the 20th century (e.g. Richard Dawkins). Nilsson and Pelger (1994) also articulated a very similar argument (see David Berlinski’s critique here).
In such models, it is thought that visual acuity might be improved first by the initially flat patch of photoreceptors becoming concave, and subsequently by increasing the level of indentation. The argument is, of course, predicated on the critical assumption that the change is both hereditable and able to be continued indefinitely (no matter how much indentation and selection has occurred previously).
Moreover, once the indented patch of photoreceptors is equally as deep as it is wide, visual acuity is most effectively enhanced, not by becoming deeper, but by constricting the orifice of the depression until an optimum is achieved with respect to the trade off between visual acuity (as a result of the narrowing of the angle of incident light to each respective photocell) and the reduction in light admitted to the photocells.
The Development And Evolution Of The Lens
In the next stage of embryological development, as the retina is folding inward against itself, the lens forms, originating as a thickening of the embryo’s outer surface, or ectoderm, that bulges into the curved empty space formed by the C-shaped retina. This protrusion eventually separates from the rest of the ectoderm to become a free-floating element. It seems likely that a broadly similar sequence of changes occurred during evolution. We do not know exactly when this modification happened, but in 1994 researchers at Lund University in Sweden showed that the optical components of the eye could have easily evolved within a million years. If so, the image-forming eye may have arisen from the nonvisual proto-eye in a geologic instant.
This is all based upon one big assumption: that biological tissues are innately plastic. Little attention is given to the biochemical and molecular conundrums which confront such scenarios. In other words, all that we have learned in the last 50 years of genetics and biochemistry is totally ignored. One cannot help but wonder whether the details of biochemistry are ignored as a result of oversight or whether it is, rather, because it presents such a formidable challenge to conventional evolutionary explanations that to pay it due attention would radically undermine the Darwinian paradigm.
Lamb’s choice of words in the above seems to imply a spontaneous embryological development of the lens, and he suggests that perhaps evolution happened in much the same manner. The problem is that lens formation does not, in reality, possess such spontaneity — far from it. Rather, it is triggered by the release of several chemicals, called “inducers,” from the optic vesicle. In epithelial cells, release of these chemicals triggers the expression of the genes which are involved in implementing lens development. The inducer triggers the epithelial cells to start producing a transcription factor, which is often called the “master control gene” of eye development (known as Pax6). Pax6 subsequently activates the genes that cause the epithelium to form a lens placode and then a lens vesicle.
Pax6 also plays a role in the initial formation of the optic vesicle, and in differentiation of retinal cells. This gives rise to an interesting question — how does the same transcription factor perform different roles in different cell types? Its action is carefully modulated by an array of other factors which are particular to the respective tissues and cell types. In the case of epithelial cells, Pax6 works in collaboration with another transcription factor called Sox2. When these two proteins bind together on a specific DNA sequence, it literally acts as a genetic switch — triggering lens differentiation.
As Lamb himself explains, lens morphogenesis results from “a thickening of the embryo’s outer surface, or ectoderm, that bulges into the curved empty space formed by the C-shaped retina. This protrusion eventually separates from the rest of the ectoderm to become a free-floating element.”
The lens vesicle subsequently morphs into a lens. The cells of the vesicle’s posterior wall become lens fibers, which grow substantially to a length dozens of times greater than their original size (meaning they completely cover the vesicle cavity). There are several important changes which these cells need to undergo in order to take up their role as lens fibers. For one thing, they have to lose their internal organelles to allow the incoming light to be successfully transmitted through them. The lens fibers are also packed very tightly together — hexagonal in cross-section, and aligned parallel to the axis of the eye.
These lens fibers also produce proteins known as crystallins, and Pax6 (the transcription factor which I mentioned previously) is involved in activating the crystallin genes. The high level of production of these proteins confers an extraordinary high density and hence a high refractive index which is responsible for the lens’ light-bending properties.
Now, at this point we potentially run into a problem.
In the case of most proteins, if they accumulated in such a high concentration as this, they would have a tendency to agglomerate and denature. This would entail that the lens would become cloudy and thus lose its transparency. The proteins which are used — crystallins — however, are exceptionally stable, and the largest class of these proteins actually serves to stabilise the other crystallins. This class is known as α-crystallin, and these molecules interact to form hollow balls which are connected by other proteins called CP49 and filensin. This forms a structure called a “beaded filament”. These structures predominate within the lens fibers. They are absolutely critical for facilitating such a dense concentration of proteins to actually enhance visual capabilities. Even more remarkable is the fact that these proteins are never recycled. Unlike most other proteins, these crystallin molecules do not degrade and thereby result in the lens becoming cloudy. The beaded filament structures actually protect the proteins from such degradation and denaturation. Actually, one of the causes of eye cataracts is a faulty beaded filament structure.
But here’s the bottom line: This is not the type of system which one might intuitively expect to be the product of trial-and-error Darwinian-type tinkering. To simply appeal to the addition of a lens is to fundamentally trivialise the matter at hand.
Chicken And Egg
I have really only scratched the surface here. Molecular morphogenesis of the eye extends far deeper than this. Once the optic vesicle has contacted the epithelium, it spreads outwards and folds in on itself. This forms the hollow eyeball. The inner layer of this will develop into the retina. What is particularly remarkable is that, while the optic vesicle is absolutely fundamental for the induction of lens development, subsequent development of the eye depends, in large measure, on factors which are secreted by the developing lens! This casts even further doubt on the sorts of scenarios commonly offered to us by Darwinians such as Lamb, wherein the lens is viewed as a relatively late addition to the eye structure.
In his review of Richard Dawkins’ Climbing Mount Improbable, David Berlinski makes the following additional observations:
Light strikes the eye in the form of photons, but the optic nerve conveys electrical impulses to the brain. Acting as a sophisticated transducer, the eye must mediate between two different physical signals. The retinal cells that figure in Dawkins’ account are connected to horizontal cells; these shuttle information laterally between photoreceptors in order to smooth the visual signal. Amacrine cells act to filter the signal. Bipolar cells convey visual information further to ganglion cells, which in turn conduct information to the optic nerve. The system gives every indication of being tightly integrated, its parts mutually dependent.
The very problem that Darwin’s theory was designed to evade now reappears. Like vibrations passing through a spider’s web, changes to any part of the eye, if they are to improve vision, must bring about changes throughout the optical system. Without a correlative increase in the size and complexity of the optic nerve, an increase in the number of photoreceptive membranes can have no effect. A change in the optic nerve must in turn induce corresponding neurological changes in the brain. If these changes come about simultaneously, it makes no sense to talk of a gradual ascent of Mount Improbable. If they do not come about simultaneously, it is not clear why they should come about at all.
The same problem reappears at the level of biochemistry. Dawkins has framed his discussion in terms of gross anatomy. Each anatomical change that he describes requires a number of coordinate biochemical steps. “[T]he anatomical steps and structures that Darwin thought were so simple,” the biochemist Mike Behe remarks in a provocative new book (Darwin’s Black Box), “actually involve staggeringly complicated biochemical processes.” A number of separate biochemical events are required simply to begin the process of curving a layer of proteins to form a lens. What initiates the sequence? How is it coordinated? And how controlled? On these absolutely fundamental matters, Dawkins has nothing whatsoever to say.
Is The Vertebrate Eye Bad Design?
Lamb tells us that,
The vertebrate eye, far from being intelligently designed, contains numerous defects that attest to its evolutionary origin. Some of these flaws degrade image quality, including an inside-out retina that focus light to pass through cell bodies and nerve bodies before hitting the photoreceptors; blood vessels that sprawl across the retina’s inner surface, casting undesirable shadows onto the retina; nerve fibers that gather together to push through a single opening in the retina to become the optic nerve, creating a blind spot.
This argument has been addressed many a time. The bottom line is this: Retinal cells require a very large oxygen supply, and hence a very large blood supply. Blood cells absorb light. If blood cells invade retinal cells, the consequence can be blindness. This entails that the retinal cells need to receive a blood supply from vessels which do not block the light. Since red blood cells readily absorb light, this demand requires that the retina be wired in the manner in which it is. As is often pointed out, squids and octopuses have ‘correctly’ wired retinas that face outward. But these organisms are exothermic — they do not require the same blood supply to the retina.
For a slightly different perspective on this topic, I refer readers to Richard Sternberg’s essay here.
Summary and Conclusions
I have only provided a sketchy overview of a few of the key processes which undergird eye development. I have not even discussed the biochemical and molecular details of vision (for that, I refer readers to Michael Behe’s book, Darwin’s Black Box, or this article). In addition, Casey Luskin has an excellent critique of the Darwinian account of the eye’s origin here. Nonetheless, I hope that this article has given readers a sense for why Darwinists are going to have to do a lot better than they are currently doing if they are to convince us of the plausibility of their model.