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The Evolution of the Human Eye
Sean D. Pitman M.D.
© Aug. 2001
No discussion of evolution seems complete without bringing up the topic of the human eye. Despite its deceptively simple anatomical appearance, the human eye is an incredibly complicated structure. Even in this age of great scientific learning and understanding, the full complexity of the human eye has yet to be fully understood. It seems that with increased learning comes increased amazement in that the complexity that once seemed approachable continues to be just as incomprehensible as ever, if not more so. It is well documented that Darwin stood in wonder at the complexity of the eye, even from what little he knew of it in comparison to modern science. And yet, though he could not explain exactly how, he believed that such amazing complexity could be developed through a naturalistic process of evolution. Very small changes, selected as advantageous, could be passed on and multiplied over many generations to produce major miracles of complexity… such as the human eye.
Numerous Gradations
Obviously, Darwin was not crazy. His proposed theory of evolution and his basic explanations concerning the gradual development of complex structures, such as the eye, have convinced the vast majority of modern scientists. So, what exactly did he propose to explain the complexity of such structures as the human eye? Consider the following quote from Darwin.
Reason tells me, that if numerous gradations from a simple and imperfect eye to one complex and perfect can be shown to exist, each grade being useful to its possessor, as is certainly the case; if further, the eye ever varies and the variations be inherited, as is likewise certainly the case and if such variations should be useful to any animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, should not be considered as subversive of the theory.1
Darwin was at a loss to explain exactly what was happening, but he proposed a stepwise evolution of the human eye by showing examples of differences in the eyes of other creatures that seemed to be less complex. These differences were ordered in a stepwise fashion of progression from the most simple of eyes to the most complex. There did in fact appear to be a good number of intermediaries that linked one type of eye to another type in an evolutionary pattern. Some of the “simplest†eyes are nothing more than spots of a small number of light sensitive cells clustered together. This type of eye is only good for sensing light from dark. It cannot detect an image. From this simple eye, Darwin proceeded to demonstrate creatures with successively more and more complex eyes till the level of the complexity of the human eye was achieved.
This scenario certainly seems reasonable. However, many theories that initially seem reasonable on paper are later disproved. Such theories need direct experimental evidence to support them before they are accepted outright as “scientific.†Do complex structures such as eyes actually evolve in real life? As far as I could find, there is no documented evidence of anyone evolving an eye or even an eye spot through any sort of selection mechanism in any creature that did not have an eye before. Also, I have not seen documented evidence for the evolution of one type of eye into a different type of eye in any creature. As far as I can tell, no such evolution has ever been directly observed. Of course the argument is that such evolution takes thousands or even millions of years to occur. Maybe so, but without the ability for direct observation and testing, such assumptions, however reasonable, must maintain a higher degree of faith.
A Closer Look
The necessary faith in such a scenario increases even more when one considers the fact that even a simple light sensitive spot is extremely complicated, involving a huge number of specialized proteins and protein systems. These proteins and systems are integrated in such a way that if one were removed, vision would cease. In other words, for the miracle of vision to occur, even for a light sensitive spot, a great many different proteins and systems would have to evolve simultaneously, because without them all there at once, vision would not occur. For example, the first step in vision is the detection of photons. In order to detect a photon, specialized cells use a molecule called 11-cis-retinal. When a photon of light interacts with this molecule, it changes its shape almost instantly. It is now called trans-retinal. This change in shape causes a change in shape of another molecule called rhodopsin. The new shape of rhodopsin is called metarhodopsin II. Metarhodopsin II now sticks to another protein called transducin forcing it to drop an attached molecule called GDP and pick up another molecule called GTP. The GTP-transducin-metarhodopsin II molecule now attaches to another protein called phosphodiesterase. When this happens, phosphodiesterase cleaves molecules called cGMPs. This cleavage of cGMPs reduces their relative numbers in the cell. This reduction in cGMP is sensed by an ion channel. This ion channel shuts off the ability of the sodium ion to enter the cell. This blockage of sodium entrance into the cell causes an imbalance of charge across the cell’s membrane. This imbalance of charge sends an electrical current to the brain. The brain then interprets this signal and the result is called vision. Many other proteins are now needed to convert the proteins and other molecules just mentioned back to their original forms so that they can detect another photon of light and signal the brain. If any one of these proteins or molecules is missing, even in the simplest eye system, vision will not occur.2
The question now of course is, how could such a system evolve gradually? All the pieces must be in place simultaneously. For example, what good would it be for an earthworm that has no eyes to suddenly evolve the protein 11-cis-retinal in a small group or “spot†of cells on its head? These cells now have the ability to detect photons, but so what? What benefit is that to the earthworm? Now, lets say that somehow these cells develop all the needed proteins to activate an electrical charge across their membranes in response to a photon of light striking them. So what?! What good is it for them to be able to establish an electrical gradient across their membranes if there is no nervous pathway to the worm’s minute brain? Now, what if this pathway did happen to suddenly evolve and such a signal could be sent to the worm’s brain. So what?! How is the worm going to know what to do with this signal? It will have to learn what this signal means. Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems. Now the earthworm, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring. If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them. All of these wonderful processes need regulation. No function is beneficial unless it can be regulated (turned off and on). If the light sensitive cells cannot be turned off once they are turned on, vision does not occur. This regulatory ability is also very complicated involving a great many proteins and other molecules… all of which must be in place initially for vision to be beneficial.
Now, what if we do not have to explain the origin of the first light sensitive “spot.†The evolution of more complex eyes is simple from that point onward… right? Not exactly. Every different component that requires unique proteins doing unique functions requires a unique gene in the DNA of that creature. Neither the genes nor the proteins that they code for function alone. The existence of a unique gene or protein means that a unique system of other genes and proteins are involved with its function. In such a system, the absence of any one of the system genes, proteins, or molecules means that the whole system becomes functionless. Considering the fact that the evolution of a single gene or protein has never been observed or reproduced in the laboratory, such apparently small differences suddenly become quite significant.
The "Design Flaw" Argument
Oh, but what about the “design flaws†of the human eye? It is a common argument in favor of evolution that no intelligent designer would design anything with flaws. Evolution on the other hand, being a naturalistic process of trial and error, easily explains the existence of flaws in the natural world. Although many are convinced by this argument, this argument in and of itself assumes the motives and capabilities of the designer. To say that everything designed should match our individual conceptions of perfection before we can detect design, is clearly misguided.
Some might question the design of a Picasso painting, but no one questions the fact that it was designed, even having never met Picasso. A child might build a box car for racing the neighborhood kids in a box car derby. His car might not meet anyone’s idea of perfection, but most would not question the idea that it was designed. Or, someone might deliberately alter the design of a previous designer for personal reasons. This alteration itself is designed by a new designer and can be detected as such. Although not “beneficial†to overall function or the intentions of the original designer, the alteration might still be understood to be designed. For example, if someone slices the tires on a car with a razor blade, would it be accurate for someone walking by afterward to automatically assume that an evolutionary process was at work because of the presence of this current supposed design flaw? While a sliced up tire might not seem logical for a designer of tires to create, the flaw itself does not automatically rule out a designer. A very intelligent designer of flaws might be at work and the calling card might be the abundant evidence of high intelligence and purpose. Or, design flaws might be the result of natural decay and not representative of the original purpose or creation of the designer. A car tire that has 50,000 miles on it might have a few more “flaws†than it had when it was first made. Everything wears out. People grow old, have low back pain, arthritis, senile dementia, and dental decay. Are these design flaws or the wearing out of a great design that just did not last forever? Simply put, just because someone can think of a better design or an improvement upon an old design, does not mean that the old design was not… designed.
Another problem with finding design flaws in nature is that we do not know all the information there is to know. What seems to us to be a design flaw initially, might turn out to be an advantage once we learn more about the needs of a particular system or creature… or designer. In any case, lets take a closer look at the supposed design flaws in the human eye.
In his 1986 book, “The Blind Watchmaker,†the famous evolutionary biologist Richard Dawkins posses this design flaw argument for the human eye:
“Any engineer would naturally assume that the photocells would point towards the light, with their wires leading backwards towards the brain. He would laugh at any suggestion that the photocells might point away, from the light, with their wires departing on the side nearest the light. Yet this is exactly what happens in all vertebrate retinas. Each photocell is, in effect, wired in backwards, with its wire sticking out on the side nearest the light. The wire has to travel over the surface of the retina to a point where it dives through a hole in the retina (the so-called ‘blind spot’
to join the optic nerve. This means that the light, instead of being granted an unrestricted passage to the photocells, has to pass through a forest of connecting wires, presumably suffering at least some attenuation and distortion (actually, probably not much but, still, it is the principle of the thing that would offend any tidy-minded engineer). I don’t know the exact explanation for this strange state of affairs. The relevant period of evolution is so long ago.†3
Dawkins’s argument certainly does seem intuitive. However, the problem with relying strictly on intuition is that intuition alone is not scientific. Many a well thought out hypothesis has seemed flawless on paper, but in when put to the test, it turns out not to work as well as was hoped. Unforeseen problems and difficulties arise. New and innovative solutions, not previously considered, became all important to obtaining the desired function. Dawkins’s problem is not one of reasonable intuition, but one of a lack of testability of his hypothesis. However reasonable it may appear, unless Dawkins is able to test his assumptions to see if in fact “verted†is better than “inverted†retinal construction for the needs of the human, this hypothesis of his remains untested and therefore unsupported by the scientific method. Beyond this problem, even if he were to prove scientifically that a verted retina is in fact more reasonable for human vision, this still would not scientifically disprove design. As previously described, proving flaws in design according to a personal understanding or need does not disprove the hypothesis that this flawed design was none-the-less designed.
Since a designer has not been excluded by this argument of Dawkins, the naturalistic theory of evolution is not an automatic default. However true the theory of evolution might be, it is not supported scientifically without testability. This is what evolutionists need to provide and this is exactly what is lacking. The strength of design theory rests, not in its ability to show perfection in design, but in its ability to point toward the statistical improbability of a naturalistic method to explain the complexity of life that is evident in such structures as the human eye. Supposed flaws do not eliminate this statistical challenge to evolutionary theories. Dawkins’s error is to assume that the thinking, knowledge and motivation of all designers are similar to his thinking, knowledge and motivation.
Dawkins’s problems are further exacerbated by his own admission that the inverted retina works very well. His argument is not primarily one that discusses the technical failures of the inverted retina, but of aesthetics. The inverted retina just does not seem right to him regardless of the fact that the inverted retina is the retina used by the animals with the most acute (image forming) vision systems in the world.
Verted vs. Inverted
The most advanced verted retinas in the world belong to the octopus and squid (cephalopods). An average retina of an octopus contains 20 million photoreceptor cells. The average human retina contains around 126 million photoreceptor cells. This is nothing compared to birds who have as much as 10 times as many photoreceptors and two to five times as many cones (cones detect color) as humans have. 4,5 Humans have a place on the retina called a “fovea centralis.†The fovea is a central area in the central part of the human retina called the macula. In this area humans have a much higher concentration photoreceptors, especially cones. Also, in this particular area, the blood vessels, nerves and ganglion cells are displaced so that they do not interpose themselves between the light source and the photoreceptor cells, thus eliminating even this minimal interference to the direct path of light. This creates an area of high visual acuity with decreasing visual acuity towards the periphery of the human retina. The cones in the macula (and elsewhere) also have a 1:1 ratio to the ganglion cells. Ganglion cells help to preprocess the information received by the retinal photoreceptors. For the rods of the retina, a single ganglion cell handles information from many, even hundreds of rod cells, but this is not true of cones whose highest concentration is in the macula. The macula provides information needed to maximize image detail, and the information obtained by the peripheral areas of the retina helps to provide both spatial and contextual information. Compared with the periphery, the macula is 100 times more sensitive to small features than in the rest of the retina. This enables the human eye to focus in on a specific area in the field of vision without being distracted by peripheral vision too much.6
Bird retinas, on the other hand, do not have a macula or fovea centralis. Visual acuity is equal in all areas. Octopus retinas also lack a fovea centralis, but do have what is called a linea centralis. The linea centralis forms a band of higher acuity horizontally across the retina of the octopus. A unique feature of octopod eyes is that regardless of the position of their bodies, their eyes always maintain the same relative position to the gravitational field of the earth using an organ called a statocyst. The reason for this appears to be related to the fact that octopods retinas are set up to detect horizontal and vertical projections in their visual fields.7 This necessitates a predictable way to judge horizontal and verticalness. Octopods use this ability, not so much to form images as vertebrates do, but to detect patterns of movement. It is interesting to note that regardless of the shape of an object, octopods will respond to certain movements as they would to prey that make similar movements. However, if their normal prey is not moving, an octopus will not generally respond.8,9 In this respect, the vision of octopods is similar to an insect-type compound eye. The octopod eye has in fact been referred to as a compound eye with a single lens.10 In some other respects, it is also more simple in its information processing than is the vertebrate eye. The photoreceptors consist only of rods, and the information transmitted by these rods does not pass through any sort of peripheral processing ganglion cell(s).11 Octopod eyes are not set up for the perception of small detail, but for the perception of patterns and motion thus eliminating the need for the very high processing power seen in human and other vertebrate eyes.
The high processing power of human and other vertebrate eyes is not cheep. It is very expensive and the body pays a high price for the maintenance of such a high level of detection and processing power. The retina has the highest energy demands/metabolic rate of any tissue in the entire body. The oxygen consumption of the human retina (per gram of tissue) is 50% greater than the kidney, 300% greater than the cerebral cortex (of the brain), and 600% greater than cardiac muscle. These are numbers for the retina as a whole. The photoreceptor cell layer, taken alone, has a significantly higher metabolic demand.12,13 All this energy must be supplied quickly and efficiently. Directly beneath each photoreceptor lies the choroid layer. This layer contains a dense capillary bed called the choriocapillaris. The only thing separating the capillaries from direct contact with the photoreceptors is the very thin (one cell thick) retinal-pigmented epithelial (RPE) layer. These capillaries are much larger than average being 18-50 microns in diameter. They provide a huge relative blood supply per gram of tissue and as much as 80% of the total blood supply for the entire eye. On the other hand, the retinal artery that passes through the “blind spot†and distributes across the anterior retina supplying the needs of the neural layer, contributes only 5% of the total blood supply to the retina.15 The close proximity of the choroidal blood supply to the photoreceptor cells without any extra intervening tissue or space such as nerves and ganglion cells (ie: from a “verted†system) allows the most rapid and efficient delivery of vital nutrients and the removal of the tremendous quantities of waste generated. The cells that remove this waste and re-supply several needed elements to the photoreceptors are the RPE cells.
Everyday rods and cones shed around 10% of their segmented disks. Rods average 700 to 1,000 disks while cones average 1,000 to 1,200 disks.16 This in itself creates a very large metabolic demand on the RPE cells who must recycle this huge number of shed disks. Conveniently, these disks do not have to travel too far to reach the RPE cells since they are sloughed from the end of the photoreceptor that directly contacts the RPE cell layer. If these disks were sloughed off in the opposite direction (toward the lens and cornea), their high level of sloughing would soon create a cloudy haze in front of the photoreceptors, which could not be cleared as rapidly as would be needed to maintain the highest degree of visual clarity. This high rate of recycling maintains the very high sensitivity of the photoreceptors. RPE cells also contain retinol isomerase. Trans-retinal must be converted back to 11-cis-retinal in the visual molecular cascade. With the help of vitamin-A and retinol isomerase, the RPE cells are able to do this and then transfer these rejuvenated molecules back to the photoreceptors.17 The funny thing is, the RPE cells in the retinas of cephalopods do not have retinol isomerase.18 However, the retinas of all sighted vertebrates do have this important enzyme. All of these functions require large amounts of energy and so the RPE cells, like the photoreceptor cells, must be in close proximity to a very good blood supply, which of course they are. Also, as the name implies, RPE cells are pigmented with a very dark/black pigment called melanin. This melanin absorbs scattered light, thus preventing stray reflections of photons and the indirect activation of photoreceptors. This aids significantly in the creation of a clear/sharp image on the retina. There is a different system for some other vertebrates such as the cat who have a reflective layer called the tapetum lucidus, which allows for better night vision (six times better than humans) but poor day vision.19
So we see that inverted retinas seem to have some at least marginal if not significant advantages based on the needs of their owners. We also have the evidence that the best eyes in the world for image detection and interpretation are all inverted as far as their retinal organization. As far as the disadvantages are concerned, they are generally not of practical significance in comparison to overall relative function. Even Dawkins seems to admit that his uneasiness is mostly one of aesthetics. Consider the following admission from Dawkins:
With one exception, all the eyes I have so far illustrated have had their photocells in front of the nerves connecting them to the brain. This is the obvious way to do it, but it is not universal. The flatworm … keeps its photocells apparently on the wrong side of their connecting nerves. So does our own vertebrate eye. The photocells point backwards, away from the light. This is not as silly as it sounds. Since they are very tiny and transparent, it doesn’t much matter which way they point: most photons will go straight through and then run the gauntlet of pigment-laden baffles waiting to catch them.20
The Error of Presumption
To say then that the human eye is definite proof of a lack thoughtful design, is a bit presumptuous I would think. This seems to be especially true when one considers the fact that the best of modern human science and engineering has not produced even a fraction of the computing and imaging capability of the human eye. How can we then, ignorant as we must be concerning such miracles of complex function, hope to accurately judge the relative fitness or logic of something so far beyond our own capabilities? Should someone who cannot even come close to understanding or creating the object that they are observing think to critique not to mention disparage the work that that lies before them? This would be like a six-year-old child trying to tell an engineer how to design a skyscraper or that one of his buildings is “better†than the others. Until Dawkins or someone else can actually make something as good or better than the human eye, I would invite them to consider the silliness of their efforts in trying to make value judgments on such things… such things that are obviously among most beautiful and beyond the most astounding works of human genius and art in existence.
Detecting Design
Then, if and when humans do achieve and surpass this level of creativity and genius and are able to experimentally prove the existence of actual defects in the function of human eyes and other such things, would this evidence rule out a designer? No. Intuitively, such complexity as we see in living things seems to speak for design in that it has the obvious appearance of design. Richard Dawkins as much as admits this in the title of his book, "The Blind Watchmaker." For those who wish to propose a naturalistic mechanism to explain complexity, the burden of proof cannot be relieved by appealing to supposed design "flaws." The best that evolutionist can do to disprove the theory of design is to demonstrate some real examples of evolution in action where a purely naturalistic mechanism actually works to form a comparably complex function of interacting parts. I have yet to see this done. As it currently stands, the theory of evolution is based only on correlation and inference, but not on actual demonstration. The best examples of evolution in action deal with the evolution of very simple enzymatic functions, such as the evolution of the enzyme galactosidase in E. coli... and even this evolution has its clear limitations. I have yet to see an "irreducibly complex" system of function evolve were the function in question requires more than a few hundred fairly specified amino acid "parts" working together at the same time. For example, the flagellar bacterial motility system requires several thousand fairly specified amino acid "parts" in the form of a couple dozen individual proteins, working together in unified haromony at the same time. Of course, there are many different kinds of bacterial motility systems possible, but all of them require several thousand fairly specified amino acids working together at the same time before the function of motility can be realized. Such a level of functional complexity has never been observed to evolve through any sort of naturalistic process.
Not Much Else to Go On . . .
If one looks carefully at the average time required for the evolution of such a multipart system of function, Dawkins and other evolutionists will most likely be waiting for a very long time for any experimental confirmation. No wonder hypothetical claims of design flaws are so common. There does not seem to be too much else to go on as far as a significant example of real evolution in action. The statistics are against such a process actually working in real life (kind of like a perpetual motion machine). So, evolutionists are left with the design flaw argument - an argument that relies upon the assumed understanding of the identity, motives, and abilities of any possible designer or collection of designers. Such arguments prove nothing except for the arrogance of those who use such arguments - especially when the very ones proposing such arguments cannot make anything even remotely comparable to much less better than that which they are disparaging.
1. Darwin, Charles. Origin of Species (1872), 6th ed., New York University Press, New York, 1988.
2. Behe, Michael J., Darwin’s Black Box, Simon & Schuster Inc., 1996.
3. Dawkins, R., 1986. The Blind Watchmaker: Why the evidence of evolution reveals a universe without design. W.W. Norton and Company, New York, p. 93.
4. J. Z. Young, “The Anatomy of the Nervous System,†Octopus Vulgaris (New York: Oxford University Press, 1971), 441.
5. Frank Gill, Ornithology (New York: W. H. Freeman, 1995), 189.
6. Timothy Goldsmith, “Optimization, Constraint, and History in the Evolution of Eyes,†The Quarterly Review of Biology 65:3 (Sept. 1990): 281–2.
7. Robert D. Barnes, Invertebrate Zoology (Philadelphia, PA: Saunders, 1980), 454.
8. H. S. Hamilton, “Convergent evolution-Do the Octopus and Human eyes qualify?†CRSQ 24 (1987): 82–5.
9. Bernhard Grzimek, Grzimek’s Animal Life Encyclopedia (New York: Van Nostrand Reinhold Co., 1972), 191.
10. B. V. Budelmann, “Cephalopod Sense Organs, Nerves and the Brain: Adaptations for high performance and life style,†in Physiology of Cephalopod Mollusks, ed. Hans Portner, et al. (Australia: Gordon and Breach Pub., 1994), 15.
11. Martin John Wells, Octopus: Physiology and Behavior of an Advanced Invertebrate (London: Chapman and Hall, 1978), 150.
12. Futterman, S. (1975). Metabolism and Photochemistry in the Retina, in Adler’s Physiology of the Eye, 6th edition, ed. R.A. Moses. St. Louis: C.V. Mosby Company, pp. 406-419; p. 406.
13. Whikehart, D.R. (1994). Biochemistry of the Eye. Boston: Butterworth-Heinemann, p. 73.
14. J.M. Risco and W. Noanitaya, Invest. Opthalmol. Vis. Sci. 19 [1980]:5.
15. Henkind, P., Hansen, R.I., Szalay, J. (1979). Ocular Circulation, in Physiology of the Human Eye and the Visual System, ed. R.R. Records. Maryland: Harper & Row Publishers, pp. 98-155; p. 119
16. Dean Bok, “Retinal Photoreceptor disc shedding and pigment epithelium phagocytosis,†in The Retinal Pigment Epithelium, 148.
17. T. Hewitt and Rubin Adler, “The Retinal Pigment Epithelium and Interphotoreceptor Matrix: Structure and Specialized Functions†in The Retina, 58.
18. D. B. Bridges, “Distribution of Retinol Isomerase in Vertebrate Eyes and its Emergence During Retinal Development,†Vision Research 29:12 (1989): 1711–7.
19. M. Ali and A. Klyne, Vision in Vertebrates, New York: Plenum Press, 1985.
20. Richard Dawkins, Climbing Mount Improbable (New York: W. W. Norton, 1996), 170.
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The Evolution of the Human Eye
Sean D. Pitman M.D.
© Aug. 2001
No discussion of evolution seems complete without bringing up the topic of the human eye. Despite its deceptively simple anatomical appearance, the human eye is an incredibly complicated structure. Even in this age of great scientific learning and understanding, the full complexity of the human eye has yet to be fully understood. It seems that with increased learning comes increased amazement in that the complexity that once seemed approachable continues to be just as incomprehensible as ever, if not more so. It is well documented that Darwin stood in wonder at the complexity of the eye, even from what little he knew of it in comparison to modern science. And yet, though he could not explain exactly how, he believed that such amazing complexity could be developed through a naturalistic process of evolution. Very small changes, selected as advantageous, could be passed on and multiplied over many generations to produce major miracles of complexity… such as the human eye.
Numerous Gradations
Obviously, Darwin was not crazy. His proposed theory of evolution and his basic explanations concerning the gradual development of complex structures, such as the eye, have convinced the vast majority of modern scientists. So, what exactly did he propose to explain the complexity of such structures as the human eye? Consider the following quote from Darwin.
Reason tells me, that if numerous gradations from a simple and imperfect eye to one complex and perfect can be shown to exist, each grade being useful to its possessor, as is certainly the case; if further, the eye ever varies and the variations be inherited, as is likewise certainly the case and if such variations should be useful to any animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, should not be considered as subversive of the theory.1
Darwin was at a loss to explain exactly what was happening, but he proposed a stepwise evolution of the human eye by showing examples of differences in the eyes of other creatures that seemed to be less complex. These differences were ordered in a stepwise fashion of progression from the most simple of eyes to the most complex. There did in fact appear to be a good number of intermediaries that linked one type of eye to another type in an evolutionary pattern. Some of the “simplest†eyes are nothing more than spots of a small number of light sensitive cells clustered together. This type of eye is only good for sensing light from dark. It cannot detect an image. From this simple eye, Darwin proceeded to demonstrate creatures with successively more and more complex eyes till the level of the complexity of the human eye was achieved.
This scenario certainly seems reasonable. However, many theories that initially seem reasonable on paper are later disproved. Such theories need direct experimental evidence to support them before they are accepted outright as “scientific.†Do complex structures such as eyes actually evolve in real life? As far as I could find, there is no documented evidence of anyone evolving an eye or even an eye spot through any sort of selection mechanism in any creature that did not have an eye before. Also, I have not seen documented evidence for the evolution of one type of eye into a different type of eye in any creature. As far as I can tell, no such evolution has ever been directly observed. Of course the argument is that such evolution takes thousands or even millions of years to occur. Maybe so, but without the ability for direct observation and testing, such assumptions, however reasonable, must maintain a higher degree of faith.
A Closer Look
The necessary faith in such a scenario increases even more when one considers the fact that even a simple light sensitive spot is extremely complicated, involving a huge number of specialized proteins and protein systems. These proteins and systems are integrated in such a way that if one were removed, vision would cease. In other words, for the miracle of vision to occur, even for a light sensitive spot, a great many different proteins and systems would have to evolve simultaneously, because without them all there at once, vision would not occur. For example, the first step in vision is the detection of photons. In order to detect a photon, specialized cells use a molecule called 11-cis-retinal. When a photon of light interacts with this molecule, it changes its shape almost instantly. It is now called trans-retinal. This change in shape causes a change in shape of another molecule called rhodopsin. The new shape of rhodopsin is called metarhodopsin II. Metarhodopsin II now sticks to another protein called transducin forcing it to drop an attached molecule called GDP and pick up another molecule called GTP. The GTP-transducin-metarhodopsin II molecule now attaches to another protein called phosphodiesterase. When this happens, phosphodiesterase cleaves molecules called cGMPs. This cleavage of cGMPs reduces their relative numbers in the cell. This reduction in cGMP is sensed by an ion channel. This ion channel shuts off the ability of the sodium ion to enter the cell. This blockage of sodium entrance into the cell causes an imbalance of charge across the cell’s membrane. This imbalance of charge sends an electrical current to the brain. The brain then interprets this signal and the result is called vision. Many other proteins are now needed to convert the proteins and other molecules just mentioned back to their original forms so that they can detect another photon of light and signal the brain. If any one of these proteins or molecules is missing, even in the simplest eye system, vision will not occur.2
The question now of course is, how could such a system evolve gradually? All the pieces must be in place simultaneously. For example, what good would it be for an earthworm that has no eyes to suddenly evolve the protein 11-cis-retinal in a small group or “spot†of cells on its head? These cells now have the ability to detect photons, but so what? What benefit is that to the earthworm? Now, lets say that somehow these cells develop all the needed proteins to activate an electrical charge across their membranes in response to a photon of light striking them. So what?! What good is it for them to be able to establish an electrical gradient across their membranes if there is no nervous pathway to the worm’s minute brain? Now, what if this pathway did happen to suddenly evolve and such a signal could be sent to the worm’s brain. So what?! How is the worm going to know what to do with this signal? It will have to learn what this signal means. Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems. Now the earthworm, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring. If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them. All of these wonderful processes need regulation. No function is beneficial unless it can be regulated (turned off and on). If the light sensitive cells cannot be turned off once they are turned on, vision does not occur. This regulatory ability is also very complicated involving a great many proteins and other molecules… all of which must be in place initially for vision to be beneficial.
Now, what if we do not have to explain the origin of the first light sensitive “spot.†The evolution of more complex eyes is simple from that point onward… right? Not exactly. Every different component that requires unique proteins doing unique functions requires a unique gene in the DNA of that creature. Neither the genes nor the proteins that they code for function alone. The existence of a unique gene or protein means that a unique system of other genes and proteins are involved with its function. In such a system, the absence of any one of the system genes, proteins, or molecules means that the whole system becomes functionless. Considering the fact that the evolution of a single gene or protein has never been observed or reproduced in the laboratory, such apparently small differences suddenly become quite significant.
The "Design Flaw" Argument
Oh, but what about the “design flaws†of the human eye? It is a common argument in favor of evolution that no intelligent designer would design anything with flaws. Evolution on the other hand, being a naturalistic process of trial and error, easily explains the existence of flaws in the natural world. Although many are convinced by this argument, this argument in and of itself assumes the motives and capabilities of the designer. To say that everything designed should match our individual conceptions of perfection before we can detect design, is clearly misguided.
Some might question the design of a Picasso painting, but no one questions the fact that it was designed, even having never met Picasso. A child might build a box car for racing the neighborhood kids in a box car derby. His car might not meet anyone’s idea of perfection, but most would not question the idea that it was designed. Or, someone might deliberately alter the design of a previous designer for personal reasons. This alteration itself is designed by a new designer and can be detected as such. Although not “beneficial†to overall function or the intentions of the original designer, the alteration might still be understood to be designed. For example, if someone slices the tires on a car with a razor blade, would it be accurate for someone walking by afterward to automatically assume that an evolutionary process was at work because of the presence of this current supposed design flaw? While a sliced up tire might not seem logical for a designer of tires to create, the flaw itself does not automatically rule out a designer. A very intelligent designer of flaws might be at work and the calling card might be the abundant evidence of high intelligence and purpose. Or, design flaws might be the result of natural decay and not representative of the original purpose or creation of the designer. A car tire that has 50,000 miles on it might have a few more “flaws†than it had when it was first made. Everything wears out. People grow old, have low back pain, arthritis, senile dementia, and dental decay. Are these design flaws or the wearing out of a great design that just did not last forever? Simply put, just because someone can think of a better design or an improvement upon an old design, does not mean that the old design was not… designed.
Another problem with finding design flaws in nature is that we do not know all the information there is to know. What seems to us to be a design flaw initially, might turn out to be an advantage once we learn more about the needs of a particular system or creature… or designer. In any case, lets take a closer look at the supposed design flaws in the human eye.
In his 1986 book, “The Blind Watchmaker,†the famous evolutionary biologist Richard Dawkins posses this design flaw argument for the human eye:
“Any engineer would naturally assume that the photocells would point towards the light, with their wires leading backwards towards the brain. He would laugh at any suggestion that the photocells might point away, from the light, with their wires departing on the side nearest the light. Yet this is exactly what happens in all vertebrate retinas. Each photocell is, in effect, wired in backwards, with its wire sticking out on the side nearest the light. The wire has to travel over the surface of the retina to a point where it dives through a hole in the retina (the so-called ‘blind spot’
to join the optic nerve. This means that the light, instead of being granted an unrestricted passage to the photocells, has to pass through a forest of connecting wires, presumably suffering at least some attenuation and distortion (actually, probably not much but, still, it is the principle of the thing that would offend any tidy-minded engineer). I don’t know the exact explanation for this strange state of affairs. The relevant period of evolution is so long ago.†3 Dawkins’s argument certainly does seem intuitive. However, the problem with relying strictly on intuition is that intuition alone is not scientific. Many a well thought out hypothesis has seemed flawless on paper, but in when put to the test, it turns out not to work as well as was hoped. Unforeseen problems and difficulties arise. New and innovative solutions, not previously considered, became all important to obtaining the desired function. Dawkins’s problem is not one of reasonable intuition, but one of a lack of testability of his hypothesis. However reasonable it may appear, unless Dawkins is able to test his assumptions to see if in fact “verted†is better than “inverted†retinal construction for the needs of the human, this hypothesis of his remains untested and therefore unsupported by the scientific method. Beyond this problem, even if he were to prove scientifically that a verted retina is in fact more reasonable for human vision, this still would not scientifically disprove design. As previously described, proving flaws in design according to a personal understanding or need does not disprove the hypothesis that this flawed design was none-the-less designed.
Since a designer has not been excluded by this argument of Dawkins, the naturalistic theory of evolution is not an automatic default. However true the theory of evolution might be, it is not supported scientifically without testability. This is what evolutionists need to provide and this is exactly what is lacking. The strength of design theory rests, not in its ability to show perfection in design, but in its ability to point toward the statistical improbability of a naturalistic method to explain the complexity of life that is evident in such structures as the human eye. Supposed flaws do not eliminate this statistical challenge to evolutionary theories. Dawkins’s error is to assume that the thinking, knowledge and motivation of all designers are similar to his thinking, knowledge and motivation.
Dawkins’s problems are further exacerbated by his own admission that the inverted retina works very well. His argument is not primarily one that discusses the technical failures of the inverted retina, but of aesthetics. The inverted retina just does not seem right to him regardless of the fact that the inverted retina is the retina used by the animals with the most acute (image forming) vision systems in the world.
Verted vs. Inverted
The most advanced verted retinas in the world belong to the octopus and squid (cephalopods). An average retina of an octopus contains 20 million photoreceptor cells. The average human retina contains around 126 million photoreceptor cells. This is nothing compared to birds who have as much as 10 times as many photoreceptors and two to five times as many cones (cones detect color) as humans have. 4,5 Humans have a place on the retina called a “fovea centralis.†The fovea is a central area in the central part of the human retina called the macula. In this area humans have a much higher concentration photoreceptors, especially cones. Also, in this particular area, the blood vessels, nerves and ganglion cells are displaced so that they do not interpose themselves between the light source and the photoreceptor cells, thus eliminating even this minimal interference to the direct path of light. This creates an area of high visual acuity with decreasing visual acuity towards the periphery of the human retina. The cones in the macula (and elsewhere) also have a 1:1 ratio to the ganglion cells. Ganglion cells help to preprocess the information received by the retinal photoreceptors. For the rods of the retina, a single ganglion cell handles information from many, even hundreds of rod cells, but this is not true of cones whose highest concentration is in the macula. The macula provides information needed to maximize image detail, and the information obtained by the peripheral areas of the retina helps to provide both spatial and contextual information. Compared with the periphery, the macula is 100 times more sensitive to small features than in the rest of the retina. This enables the human eye to focus in on a specific area in the field of vision without being distracted by peripheral vision too much.6
Bird retinas, on the other hand, do not have a macula or fovea centralis. Visual acuity is equal in all areas. Octopus retinas also lack a fovea centralis, but do have what is called a linea centralis. The linea centralis forms a band of higher acuity horizontally across the retina of the octopus. A unique feature of octopod eyes is that regardless of the position of their bodies, their eyes always maintain the same relative position to the gravitational field of the earth using an organ called a statocyst. The reason for this appears to be related to the fact that octopods retinas are set up to detect horizontal and vertical projections in their visual fields.7 This necessitates a predictable way to judge horizontal and verticalness. Octopods use this ability, not so much to form images as vertebrates do, but to detect patterns of movement. It is interesting to note that regardless of the shape of an object, octopods will respond to certain movements as they would to prey that make similar movements. However, if their normal prey is not moving, an octopus will not generally respond.8,9 In this respect, the vision of octopods is similar to an insect-type compound eye. The octopod eye has in fact been referred to as a compound eye with a single lens.10 In some other respects, it is also more simple in its information processing than is the vertebrate eye. The photoreceptors consist only of rods, and the information transmitted by these rods does not pass through any sort of peripheral processing ganglion cell(s).11 Octopod eyes are not set up for the perception of small detail, but for the perception of patterns and motion thus eliminating the need for the very high processing power seen in human and other vertebrate eyes.
The high processing power of human and other vertebrate eyes is not cheep. It is very expensive and the body pays a high price for the maintenance of such a high level of detection and processing power. The retina has the highest energy demands/metabolic rate of any tissue in the entire body. The oxygen consumption of the human retina (per gram of tissue) is 50% greater than the kidney, 300% greater than the cerebral cortex (of the brain), and 600% greater than cardiac muscle. These are numbers for the retina as a whole. The photoreceptor cell layer, taken alone, has a significantly higher metabolic demand.12,13 All this energy must be supplied quickly and efficiently. Directly beneath each photoreceptor lies the choroid layer. This layer contains a dense capillary bed called the choriocapillaris. The only thing separating the capillaries from direct contact with the photoreceptors is the very thin (one cell thick) retinal-pigmented epithelial (RPE) layer. These capillaries are much larger than average being 18-50 microns in diameter. They provide a huge relative blood supply per gram of tissue and as much as 80% of the total blood supply for the entire eye. On the other hand, the retinal artery that passes through the “blind spot†and distributes across the anterior retina supplying the needs of the neural layer, contributes only 5% of the total blood supply to the retina.15 The close proximity of the choroidal blood supply to the photoreceptor cells without any extra intervening tissue or space such as nerves and ganglion cells (ie: from a “verted†system) allows the most rapid and efficient delivery of vital nutrients and the removal of the tremendous quantities of waste generated. The cells that remove this waste and re-supply several needed elements to the photoreceptors are the RPE cells.
Everyday rods and cones shed around 10% of their segmented disks. Rods average 700 to 1,000 disks while cones average 1,000 to 1,200 disks.16 This in itself creates a very large metabolic demand on the RPE cells who must recycle this huge number of shed disks. Conveniently, these disks do not have to travel too far to reach the RPE cells since they are sloughed from the end of the photoreceptor that directly contacts the RPE cell layer. If these disks were sloughed off in the opposite direction (toward the lens and cornea), their high level of sloughing would soon create a cloudy haze in front of the photoreceptors, which could not be cleared as rapidly as would be needed to maintain the highest degree of visual clarity. This high rate of recycling maintains the very high sensitivity of the photoreceptors. RPE cells also contain retinol isomerase. Trans-retinal must be converted back to 11-cis-retinal in the visual molecular cascade. With the help of vitamin-A and retinol isomerase, the RPE cells are able to do this and then transfer these rejuvenated molecules back to the photoreceptors.17 The funny thing is, the RPE cells in the retinas of cephalopods do not have retinol isomerase.18 However, the retinas of all sighted vertebrates do have this important enzyme. All of these functions require large amounts of energy and so the RPE cells, like the photoreceptor cells, must be in close proximity to a very good blood supply, which of course they are. Also, as the name implies, RPE cells are pigmented with a very dark/black pigment called melanin. This melanin absorbs scattered light, thus preventing stray reflections of photons and the indirect activation of photoreceptors. This aids significantly in the creation of a clear/sharp image on the retina. There is a different system for some other vertebrates such as the cat who have a reflective layer called the tapetum lucidus, which allows for better night vision (six times better than humans) but poor day vision.19
So we see that inverted retinas seem to have some at least marginal if not significant advantages based on the needs of their owners. We also have the evidence that the best eyes in the world for image detection and interpretation are all inverted as far as their retinal organization. As far as the disadvantages are concerned, they are generally not of practical significance in comparison to overall relative function. Even Dawkins seems to admit that his uneasiness is mostly one of aesthetics. Consider the following admission from Dawkins:
With one exception, all the eyes I have so far illustrated have had their photocells in front of the nerves connecting them to the brain. This is the obvious way to do it, but it is not universal. The flatworm … keeps its photocells apparently on the wrong side of their connecting nerves. So does our own vertebrate eye. The photocells point backwards, away from the light. This is not as silly as it sounds. Since they are very tiny and transparent, it doesn’t much matter which way they point: most photons will go straight through and then run the gauntlet of pigment-laden baffles waiting to catch them.20
The Error of Presumption
To say then that the human eye is definite proof of a lack thoughtful design, is a bit presumptuous I would think. This seems to be especially true when one considers the fact that the best of modern human science and engineering has not produced even a fraction of the computing and imaging capability of the human eye. How can we then, ignorant as we must be concerning such miracles of complex function, hope to accurately judge the relative fitness or logic of something so far beyond our own capabilities? Should someone who cannot even come close to understanding or creating the object that they are observing think to critique not to mention disparage the work that that lies before them? This would be like a six-year-old child trying to tell an engineer how to design a skyscraper or that one of his buildings is “better†than the others. Until Dawkins or someone else can actually make something as good or better than the human eye, I would invite them to consider the silliness of their efforts in trying to make value judgments on such things… such things that are obviously among most beautiful and beyond the most astounding works of human genius and art in existence.
Detecting Design
Then, if and when humans do achieve and surpass this level of creativity and genius and are able to experimentally prove the existence of actual defects in the function of human eyes and other such things, would this evidence rule out a designer? No. Intuitively, such complexity as we see in living things seems to speak for design in that it has the obvious appearance of design. Richard Dawkins as much as admits this in the title of his book, "The Blind Watchmaker." For those who wish to propose a naturalistic mechanism to explain complexity, the burden of proof cannot be relieved by appealing to supposed design "flaws." The best that evolutionist can do to disprove the theory of design is to demonstrate some real examples of evolution in action where a purely naturalistic mechanism actually works to form a comparably complex function of interacting parts. I have yet to see this done. As it currently stands, the theory of evolution is based only on correlation and inference, but not on actual demonstration. The best examples of evolution in action deal with the evolution of very simple enzymatic functions, such as the evolution of the enzyme galactosidase in E. coli... and even this evolution has its clear limitations. I have yet to see an "irreducibly complex" system of function evolve were the function in question requires more than a few hundred fairly specified amino acid "parts" working together at the same time. For example, the flagellar bacterial motility system requires several thousand fairly specified amino acid "parts" in the form of a couple dozen individual proteins, working together in unified haromony at the same time. Of course, there are many different kinds of bacterial motility systems possible, but all of them require several thousand fairly specified amino acids working together at the same time before the function of motility can be realized. Such a level of functional complexity has never been observed to evolve through any sort of naturalistic process.
Not Much Else to Go On . . .
If one looks carefully at the average time required for the evolution of such a multipart system of function, Dawkins and other evolutionists will most likely be waiting for a very long time for any experimental confirmation. No wonder hypothetical claims of design flaws are so common. There does not seem to be too much else to go on as far as a significant example of real evolution in action. The statistics are against such a process actually working in real life (kind of like a perpetual motion machine). So, evolutionists are left with the design flaw argument - an argument that relies upon the assumed understanding of the identity, motives, and abilities of any possible designer or collection of designers. Such arguments prove nothing except for the arrogance of those who use such arguments - especially when the very ones proposing such arguments cannot make anything even remotely comparable to much less better than that which they are disparaging.
1. Darwin, Charles. Origin of Species (1872), 6th ed., New York University Press, New York, 1988.
2. Behe, Michael J., Darwin’s Black Box, Simon & Schuster Inc., 1996.
3. Dawkins, R., 1986. The Blind Watchmaker: Why the evidence of evolution reveals a universe without design. W.W. Norton and Company, New York, p. 93.
4. J. Z. Young, “The Anatomy of the Nervous System,†Octopus Vulgaris (New York: Oxford University Press, 1971), 441.
5. Frank Gill, Ornithology (New York: W. H. Freeman, 1995), 189.
6. Timothy Goldsmith, “Optimization, Constraint, and History in the Evolution of Eyes,†The Quarterly Review of Biology 65:3 (Sept. 1990): 281–2.
7. Robert D. Barnes, Invertebrate Zoology (Philadelphia, PA: Saunders, 1980), 454.
8. H. S. Hamilton, “Convergent evolution-Do the Octopus and Human eyes qualify?†CRSQ 24 (1987): 82–5.
9. Bernhard Grzimek, Grzimek’s Animal Life Encyclopedia (New York: Van Nostrand Reinhold Co., 1972), 191.
10. B. V. Budelmann, “Cephalopod Sense Organs, Nerves and the Brain: Adaptations for high performance and life style,†in Physiology of Cephalopod Mollusks, ed. Hans Portner, et al. (Australia: Gordon and Breach Pub., 1994), 15.
11. Martin John Wells, Octopus: Physiology and Behavior of an Advanced Invertebrate (London: Chapman and Hall, 1978), 150.
12. Futterman, S. (1975). Metabolism and Photochemistry in the Retina, in Adler’s Physiology of the Eye, 6th edition, ed. R.A. Moses. St. Louis: C.V. Mosby Company, pp. 406-419; p. 406.
13. Whikehart, D.R. (1994). Biochemistry of the Eye. Boston: Butterworth-Heinemann, p. 73.
14. J.M. Risco and W. Noanitaya, Invest. Opthalmol. Vis. Sci. 19 [1980]:5.
15. Henkind, P., Hansen, R.I., Szalay, J. (1979). Ocular Circulation, in Physiology of the Human Eye and the Visual System, ed. R.R. Records. Maryland: Harper & Row Publishers, pp. 98-155; p. 119
16. Dean Bok, “Retinal Photoreceptor disc shedding and pigment epithelium phagocytosis,†in The Retinal Pigment Epithelium, 148.
17. T. Hewitt and Rubin Adler, “The Retinal Pigment Epithelium and Interphotoreceptor Matrix: Structure and Specialized Functions†in The Retina, 58.
18. D. B. Bridges, “Distribution of Retinol Isomerase in Vertebrate Eyes and its Emergence During Retinal Development,†Vision Research 29:12 (1989): 1711–7.
19. M. Ali and A. Klyne, Vision in Vertebrates, New York: Plenum Press, 1985.
20. Richard Dawkins, Climbing Mount Improbable (New York: W. W. Norton, 1996), 170.
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The Evolution of the Human Eye
