The Evolution of the

Human Eye
Sean D. Pitman M.D.
© May. 2007
 Table of Contents
• Introduction
• Numerous Gradations
• A Closer Look
• The Design Flaw Argument
• Verted vs. Inverted
• Living Optical Fibers
• The Error of Presumption
• Detecting Design
• Not Much Else to Go On

Home

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 with 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

Living Optical Fibers

 As it turns out, the supposed problems Dawkins finds with the inverted retina

become actual advantages in light of recent research published by Kristian Franze et.
al., in the May 2007 issue of PNAS (see illustration above; Link). As it turns out, "Müller

cells are living optical fibers in the vertebrate retina." 21 Consider the observations and

conclusions of the authors in the following abstract of their paper:

Although biological cells are mostly transparent, they are phase objects that differ in

shape and refractive index. Any image that is projected through layers of randomly

oriented cells will normally be distorted by refraction, reflection, and scattering.

Counterintuitively, the retina of the vertebrate eye is inverted with respect to its optical

function and light must pass through several tissue layers before reaching the light-

detecting photoreceptor cells. Here we report on the specific optical properties of glial

cells present in the retina, which might contribute to optimize this apparently

unfavorable situation. We investigated intact retinal tissue and individual Müller cells,

which are radial glial cells spanning the entire retinal thickness. Müller cells have an

extended funnel shape, a higher refractive index than their surrounding tissue, and are

oriented along the direction of light propagation. Transmission and reflection confocal

microscopy of retinal tissue in vitro and in vivo showed that these cells provide a low-

scattering passage for light from the retinal surface to the photoreceptor cells. Using a

modified dual-beam laser trap we could also demonstrate that individual Müller cells act

as optical fibers. Furthermore, their parallel array in the retina is reminiscent of fiberoptic

plates used for low-distortion image transfer. Thus, Müller cells seem to mediate the

image transfer through the vertebrate retina with minimal distortion and low loss. This

finding elucidates a fundamental feature of the inverted retina as an optical system and

ascribes a new function to glial cells.21

 And Dawkins would have us believe that no "intelligent" designer would have

done it that way? Really?

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

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 marvels, 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.
21. Kristian Franze, Jens Grosche, Serguei N. Skatchkov, Stefan Schinkinger,
Christian Foja, Detlev Schild||, Ortrud Uckermann, Kort Travis, Andreas
Reichenbach, and Jochen Guck, Müller cells are living optical fibers in the
vertebrate retina, PNAS | May 15, 2007 | vol. 104 | no. 20 | 8287-8292
(Link)
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