The Vertebrate Eye

[bob b]

Someone called the vertebrate eye "bad design" (in favor of an octopus eye). Here is one rebuttal. I have more.

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Someone who does know about eye design is the ophthalmologist Dr George Marshall, who said:

The idea that the eye is wired backward comes from a lack of knowledge of eye function and anatomy.

He explained that the nerves could not go behind the eye, because that space is reserved for the choroid, which provides the rich blood supply needed for the very metabolically active retinal pigment epithelium (RPE). This is necessary to regenerate the photoreceptors, and to absorb excess heat. So it is necessary for the nerves to go in front instead. The claim on the program that they interfere with the image is blatantly false, because the nerves are virtually transparent because of their small size and also having about the same refractive index as the surrounding vitreous humor. In fact, what limits the eye’s resolution is the diffraction of light waves at the pupil (proportional to the wavelength and inversely proportional to the pupil’s size), so alleged improvements of the retina would make no difference.

It’s important to note that the ‘superior’ design of Miller [Ken] with the (virtually transparent) nerves behind the photoreceptors would require either:

The choroid in front of the retina—but the choroid is opaque because of all the red blood cells, so this design would be as useless as an eye with a hemorrhage!

Photoreceptors not in contact with the RPE and choroid at all—but the photoreceptors would be slow to regenerate, so it would probably take months before we could drive after we were photographed with a flashbulb.

Some evolutionists claim that the cephalopod eye is somehow ‘right,’ i.e., with nerves behind the receptor, and the program showed photographs of these creatures (e.g., octopus, squid) during this segment. But no one who has actually bothered to study these eyes could make such claims with integrity. In fact, cephalopods don’t see as well as humans, and the octopus eye structure is totally different and much simpler. It’s more like ‘a compound eye with a single lens.’

Ophthalmologist Peter Gurney gives a detailed response to the question ‘Is the inverted retina really “bad design”?’2 He addresses the claim that the blind spot is bad design, by pointing out that the blind spot occupies only 0.25% of the visual field, and is far (15°) from the visual axis so that the visual acuity of the region is only about 15% of the foveola, the most sensitive area of the retina right on the visual axis. So the alleged defect is only theoretical, not practical. The blind spot is not considered handicap enough to stop a one-eyed person from driving a private motor vehicle. The main problem with only one eye is the lack of stereoscopic vision.

The program also alleges that the retina is badly designed because it can detach and cause blindness. But this doesn’t happen with the vast majority of people, indicating that the design is pretty good. In fact, retinal detachment is more due to the vitreous (‘glassy’) humor liquefying from its normally fairly rigid gel state with advancing age. Then the remaining gel pulls away from the retina, leaving tiny holes, so the other liquefied humor can lift off the retina. So one recently devised treatment is draining the liquid and injecting magnetized silicone gel, which can be moved into place with a magnetic field, to push the retina back and block the holes.3 The occasional failures in the eye with increasing age reflect the fact that we live in a fallen world—so what we observe today may have deteriorated from the original physically perfect state, where, for example, deterioration with age didn’t occur.

To answer other alleged ‘bad design’ arguments, there are two principles to consider:

Do we have all the information/knowledge on the issue?

Could this particular biological system have gone downhill since the Fall?

Related evolutionary arguments are used to attack so-called vestigial organs (see appendix), the panda’s thumb, and so-called ‘junk’ DNA.

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[Jukia]

Do you have a cite for Dr. Marshall's comments? Are they all his or were you editorializing about the fallen nature of man, etc. Thanks so much bob b. We all await your call to Stockholm. Perhaps if you jump on this eye issue it will speed your trip.

 

[eisenreich]

Do you have a cite for Dr. Marshall's comments?

No bias at all here..

" Do you [George Marshall] believe that accepting creation as portrayed in Genesis is essential to your Christian faith?

Yes! On not literally accepting the Genesis account of creation one is left with a major problem—what Scriptures do you accept as true and what Scriptures do you reject as false? Only by accepting the whole of Scripture as the inspired Word of God does one avoid this dilemma."

How useful do you find Creation magazine?

Its principal value is that it challenges what is uncritically accepted. Watch any TV program involving nature and you would think that evolution is an established fact. [No wonder Bob loves this guy, they're both out to take down the pseduoscience that is evolution..]

- answersingenesis.org

 

[bob b]

On the Design of the Vertebrate Retina
George Ayoub, Department of Biology
Westmont College, Santa Barbara, CA 93108-1099

Abstract: It has been commonly claimed that the vertebrate eye is functionally suboptimal, because photoreceptors in the retina are oriented away from incoming light. However, there are excellent functional reasons for vertebrate photoreceptors to be oriented as they are. Photoreceptor structure and function is maintained by a critical tissue, the retinal pigment epithelium (RPE), which recycles photopigments, removes spent outer segments of the photoreceptors, provides an opaque layer to absorb excess light, and performs additional functions. These aspects of the structure and function of the vertebrate eye have been ignored in evolutionary arguments about suboptimality, yet they are essential for understanding how the eye works.
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Editorial Introduction: A Popular Argument
It has been widely argued in both the technical (Thwaites 1984, Williams 1992) and popular evolutionary literature (Diamond 1985, Dawkins 1986, Miller 1994) that the vertebrate eye is poorly designed. "In fact it is stupidly designed," writes the influential neo-Darwinian theorist George Williams, "because it embodies many functionally arbitrary or maladaptive features" (1992:73). Chief among these features, Williams claims (1992:72), is the inversion of the retina.

"The retina is upside down," he writes. "The rods and cones are the bottom layer, and light reaches them only after passing through the nerves and blood vessels." These structures, claims UCLA evolutionary biologist Jared Diamond (1985:91) aren't located behind the photoreceptors, where any sensible engineer would have put them, but out in front of them, where they screen some of the incoming light. A camera designer who committed such a blunder would be fired immediately.

The capstone of this argument is held to be the cephalopod (squid and octopus) retina, which is putatively "wired correctly," with its photoreceptors facing towards the light, and with its nerves "neatly tucked away behind the photoreceptor layer" (Miller 1994:30; see also Diamond 1985:91 and Williams 1992:74). The cephalopods, it is said, got it right.

In considering this argument, we may dispense immediately with optimality comparisons between cephalopod (invertebrate) and vertebrate retina designs. None of the authors cited above provides any evidence that the cephalopod retina is functionally superior to the vertebrate retina: a claim that, in any case, seems unreasonable on its face. Would hundreds of thousands of vertebrate species -- in a great variety of terrestrial, marine, and aerial environments -- really see better with a visual system used by a handful of exclusively marine vertebrates? In the absence of any rigorous comparative evidence, all claims that the cephalopod retina is functionally superior to the vertebrate retina remain entirely conjectural. In short, there is no reason to believe them.

But we should consider a more basic point. Why refer to the cephalopod retina at all? The claim that the cephalapods got it right assumes that the vertebrates did not, and that the latter are making the best of a bad situation -- but, of course, it remains to be demonstrated that, in fact, the vertebrate retina is suboptimal.

And this has not been demonstrated: not by the authors cited above, nor by other evolutionary biologists. "One of the difficulties with the hypothesis of optimality," note Farnsworth and Niklas (1995:355), "is the availability of observations to test it." That goes as well for hypotheses of suboptimality, as exemplified by the evolutionary literature on the vertebrate retina. The biological world is full of puzzling systems. While it is not readily apparent why vertebrate photoreceptors face away from the light, nor why other cell layers intervene, a good many things in science are not apparent at first glance. We need to look more deeply.

In this case, we need not look far. There are excellent functional reasons for vertebrate photoreceptors to be oriented as they are. These aspects of retinal structure and function have been ignored in evolutionary arguments about suboptimality, yet they are essential for understanding how the eye works.

The Structure of the Vertebrate Retina
First, some anatomy. Figure 1 depicts a vertebrate eye in cross section. Light passes first through the cornea, the primary focussing element, then through the iris, which controls how much light will enter the eye, and lastly, through the lens, which provides the adjustable focussing element. The light, now adjusted for intensity, is focused onto the thin tissue lining the back of the eye: the retina.

The retina (see Figure 2) comprises cells from the central nervous system (CNS), and converts or transduces light into electrical signals, the "medium" of the CNS. A highly complex tissue, the retina contains cells of several different types:

Photoreceptors (the rods and cones, labelled as "R" and "C" in Fig. 2) which actually convert the light energy into an electrical signal. These are the first cells directly involved in communicating information within the visual system, sending signals via a chemical synapse to:

The Bipolar Cells (B in figure), the second order cells in the retina; the bipolar cells synapse onto:

The Ganglion Cells (G in figure), at the inner surface of the retina; these cells have axons which travel together from the eye, exiting via the optic disk, and forming the optic nerve en route to the brain.

The Amacrine Cells (A in figure) mediate lateral interactions, transmitting information between adjacent bipolar cells and ganglion cells; and the horizontal cells (H in figure) which communicate laterally in the outer retina.

Now observe the path of light in Figure 2. The light must pass first through all the auxiliary cells before arriving at the photoreceptors -- which at first glance hardly seems sensible. If the design problem to be solved by any eye is forming a maximally accurate image of the world, then degrading the light before it reaches the "business end" of the photoreceptors seems self-evidently a poor solution. "This is equivalent to placing a thin diffusing screen directly over the film in your camera; it can only degrade the quality of the image" (Goldsmith 1990: 286).

And that is where evolutionary accounts leave the story.

The Critical Role of the Retinal Pigmented Epithelium (RPE)
But there is much more to be said. Lying directly behind the retina is an epithelial tissue which maintains the photoreceptors (see Fig. 2). This tissue, called the retinal pigmented epithelium (hereafter, RPE), is critical to the development and function of the retina. Indeed, volumes have been dedicated to understanding the role of the RPE (see, for instance, Steinberg 1985, Zinn and Marmor 1979), because when it malfunctions, the eye as a whole malfunctions.

1. Regenerating photoreceptive pigments
When light strikes a photoreceptor, it sets in motion a chain of molecular events which eventually culminate in forming an image in the brain. Here, let's focus on just the first characters in the story.

The first player on stage is the photosensitive molecule rhodopsin. Rhodopsin consists of a protein, opsin, and another molecule, 11-cis-retinal. Found at the distal ends of the photoreceptors -- the portion closest to the RPE, called the outer segment -- rhodopsin is embedded in membranous discs. [An important note about some potentially confusing terminology. The "business end" of the photoreceptor cell, where the membranous discs occur, is called the outer segment. In vertebrates, however, this segment is actually inner, i.e., at the back of the retina, pointing in towards the center of the organism.] When light strikes rhodopsin, the energy changes the shape of its molecular component 11-cis-retinal, into an all-trans conformation, a process called isomerization. This conformational change in retinal starts a complex cascade of reactions in several other molecules, causing the hyperpolarization (or shift in electrical charge) of the outer segment membrane. Molecular transmitters then carry this electrical signal from the synapse at the photoreceptor's base to the next neurons, the horizontal cells and bipolar cells -- thus beginning the process by which we see.

This process depends critically on the isomerization of 11- cis-retinal. Each photon of light striking a photoreceptor can isomerize retinal, and since many billions of photons constantly strike the eye, retinal must be replaced regularly to maintain the cycle, and overall photoreceptor function. That job of replacement falls to the RPE. The RPE cells collect the used retinal from the photoreceptors, and employ vitamin A to make fresh retinal, transporting it back to the photoreceptors (Bridges 1989; Hewitt and Adler 1994).

2. Recycling of photoreceptive material
Next on the list of RPE responsibilities is a related function: recycling the used outer segments. Outer segment membranes are very active, and thus must be continually replaced.

Each day, new outer segment membrane grows at the base of the outer segment (where it intersects with the inner segment, the cell region containing the nucleus), adding to the length of the photoreceptor. As the outer segment lengthens from its base, its distal end -- the oldest membrane -- sheds in segments. These segments are picked up by the RPE, which phagocytizes the material, recycling all of the molecules present (Bok and Young 1979).

Thus, spent photoreceptive membranes are removed from the optical path, to be replaced by new material. This process, which goes on continually, maintains the high sensitivity of the photoreceptors (Bok 1994).

3. Absorption of excess light
In addition to these active functions, the RPE also has an important passive role. Because it is heavily pigmented, it forms an opaque screen behind the optical path of the photoreceptors.

It thus absorbs light which is not collected by the photoreceptors, light which would otherwise decrease the resolution of images. This absorptive property of the RPE is important to maintaining high visual acuity.

This brief summary does not exhaust the functions of the RPE. Note, for instance, that the RPE "is required for the normal development of the eye" (Raymond and Jackson 1995), a function that, while not directly related to vision, certainly undergirds the very possibility of seeing at all. In short:

Considering the diverse functions of the RPE cells...there is no doubt that the integrity of the RPE metabolic machinery is essential for the normal functioning of the outer retina. Because of the nature of these interactions, it is essential that the RPE and photoreceptors be in close proximity for normal retinal function (Hewitt and Adler 1994: 67).

There are excellent reasons for vertebrate photoreceptors to be oriented as they are.

A Thought Experiment
But still: there sits a blind spot in each retina. To be sure, the blind spots are displaced laterally from each other, so that "with both eyes open, we can see everything in the visual field" (Williams 1992: 73), as one eye sees what the other does not. However, we can imagine situations where this wouldn't work:

Our retinal blind spots rarely cause any difficulty, but rarely is not the same as never. As I momentarily cover one eye to ward off an insect, an important event might be focused on the blind spot of the other (Williams 1992: 73).

So, as a thought experiment, let's fix the blind spot. We will start by turning the photoreceptors around, so their wiring isn't in the way.

We have eliminated the blind spot, providing slightly better sight in one portion of the eye. Now, however, the blood vessels and RPE, needed to maintain the photoreceptors, must be located on the inner side of the retina, between it and the lens. This places a large capillary bed (containing many red blood cells) and an epithelial tissue in the path of the light, significantly degrading the visual information passing to the photoreceptors.

Furthermore, since the photoreceptors continually shed material from their outer segments, dumping this opaque waste in the path of the light would greatly diminish the amount of light reaching the photoreceptors. Our proposed change also reduces the quality of the light, by refracting it with the opaque pieces of shed outer segment membrane.

We might imagine simply placing the RPE at the back of the retina, but this raises the problem of how to dispose of spent outer segment membranes, so that the photoreceptors can be quickly regenerated. Or, perhaps, we could surround each photoreceptor cell by RPE cells, but this would need increase the space between the photoreceptors, thus decreasing the resolution of vision.

These design changes may force temporal or spatial decrements in vision.

Are these improvements? Hardly; indeed, our thought experiment has taken the vertebrate eye rapidly downhill. In trying to eliminate the blind spot, we have generated a host of new and more severe functional problems to solve. Our "repair" seems far worse than the apparent flaw we wanted to fix.

Conclusion
The vertebrate retina provides an excellent example of functional -- though non-intuitive -- design. The design of the retina is responsible for its high acuity and sensitivity. It is simply untrue that the retina is demonstrably suboptimal, nor is it easy to conceive how it might be modified without significantly decreasing its function.


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References
Bok, D. 1994. Retinal photoreceptor disc shedding and pigment epithelium phagocytosis. In S.J. Ryan, ed., Retina, 2nd ed., Volume 1: Basic Science & Inherited Retinal Disease (St. Louis: Mosby), pp. 58-71.
Bok, D. and Young, R.W. 1979. Phagocytic Properties of the Retinal Pigment Epithelium. In The Retinal Pigment Epithelium, eds. K.M. Zinn and M.F. Marmor (Cambridge, MA: Harvard University Press), pp. 148-174.
Bridges, C.D.B. 1989. Distribution of retinal isomerase in vertebrate eyes and its emergence during retinal development. Vision Research 12: 1711-1717.
Dawkins, R. 1986. The Blind Watchmaker. New York: W.W. Norton.
Diamond, J. 1985. Voyage of the Overloaded Ark. Discover, June, pp. 82-92.
Farnsworth, K.D. and Niklas, K.J. 1995. Theories of optimization, form and function in branching architecture of plants. Functional Ecology 9:355-363.
Goldsmith, T.H. 1990. Optimization, Constraint, and History in the Evolution of Eyes. Quarterly Review of Biology 65: 281-322.
Hewitt, A.T. and Adler, R. 1994. The retinal pigment epithelium and interphotoreceptor matrix: Structure and specialized functions. In S.J. Ryan, ed., Retina, 2nd ed., Volume 1: Basic Science & Inherited Retinal Disease (St. Louis: Mosby), pp. 58-71.
Miller, R.F. 1994. The physiology and morphology of the vertebrate retina. In S.J. Ryan, ed., Retina, 2nd ed., Volume 1: Basic Science & Inherited Retinal Disease (St. Louis: Mosby), pp. 58-71.
Raymond, S.M. and Jackson, I.J. 1995. The retinal pigment epithelium is required for the maintenance of the mouse neural retina. Current Biology 5: 1286-1295.
Steinberg, R.H. 1985. Interactions between the retinal pigment epithelium and the neural retina. Documenta Opthalmologia 60:327-346.
Thwaites, W. 1992. Design: Can we see the hand of evolution in the things it has wrought? In Evolutionists Confront Creationists, Proceedings of the 63rd Annual Meeting of the Pacific Division, AAAS, Volume 1, part 3 (San Francisco: Pacific Division, AAAS), pp. 206-213.
Williams, G.C. 1992. Natural Selection: Domains, Levels, and Challenges. Oxford: Oxford University Press.
Zinn, K.M., and Marmor, M.F. 1979. The Retinal Pigment Epithelium. Cambridge, MA: Harvard University Press.

 

[bob b]

Where'd Johnny go?

 

[l0progression]

Could this particular biological system have gone downhill since the Fall?

There is a major problem with this. The ID movement claims that certain aspects of biology are too complex or too perfect to be created by accident. When something is found to be less than perfect, and the above question is used, how is that testable? How do you lend evidence towards the above position as opposed to the position that life in general is not too perfect or complex.

In other words, what validates the assumption that a biological system has become less perfect since the fall?

 

[Lord Vader]

A good designer would have given us micro wave vision so we could cook our food by looking at it. Did you think of that!? No? I didn't think so!

 

[bob b]

There is a major problem with this. The ID movement claims that certain aspects of biology are too complex or too perfect to be created by accident. When something is found to be less than perfect, and the above question is used, how is that testable? How do you lend evidence towards the above position as opposed to the position that life in general is not too perfect or complex.

I have never heard or read where anyone in the ID movement said that certain aspects of biology were too complex or too perfect to be created by accident. The argument is more precisely stated than that. The argument is about "specified complexity".

In other words, what validates the assumption that a biological system has become less perfect since the fall?

It is well known that organisms can continue to function even when they experience harmful mutations. This is due to the redundancy and "fail soft " design easily recognized by engineers who try to mimic such natural systems and apply the principles to human-engineered/designed devices.

From the Human Genome Project data is rapidly accumulating which supports the hypothesis that all humans suffer to some degree from "genetic disease", i.e. imperfect genomes caused by harmful mutations. Skeptical? Look it up yourself.

 

[Johnny]

Where'd Johnny go?

I'm here, and I'm rather unimpressed. First, I'm growing weary of your copy and paste style of argumentation. If you can't argue for yourself don't take up the argument. Shall I, as a response, post an argument someone else wrote in response to the aforementioned? Do we make progress this way? Highly unlikely. Any argument that I form is not against your argument, but is instead against the authors of these papers. Even if I effectively dismantle their argument, you escape unshaken because it was not your argument.

Furthermore, I've become convinced that, in the course of these copy and pastes, you don't always understand the arguments presented or the implications. As such, I'm rather disinclined to take the time to understand the author's argument, check his sources, and form a rebuttal where warranted. If you didn't understand the article in the first place what good will my rebuttal be? I can play mouthpiece for articles all day. But I'm of the opinion that forming one's own conclusion based on other's work is more valuable than pasting a conclusion I happen to agree with. Nonetheless, I have read both of the articles you pasted.

Both arguments you pasted seek to argue good design by assuming the static positioning of nearby structures while trying to change the position of the optic nerve. The feat of rearranging the eye so that the optic nerve could originate behind the photoreceptors would undoubtedly require repositioning of other nearby structures. Both authors have effectively argued that this is the best design because of the positioning of other parts. This is as absurd as arguing that a car with its engine in the trunk is the best design because the fuel lines happen to run to the back of the car instead of the front. Of course moving the engine to the front would require repositioning of the fuel lines, but this is in no way an argument that it cannot be done nor that rear-engines are the best design.

Of course repositioning of the optic nerve would require repositioning of the RPE. I do not deny this. However, you cannot form a convincing argument that there is no other way, especially in a biological system. Why does the RPE even need to exist? You might argue that without it, the availability of retinal would diminish. But this is simply an argument from static design. What if the photoreceptors themselves could store vitamin A? Why restrict that functionality to the pigmented epithelium? I might also argue that direct contact with the pigmented epithelium be eliminated simliar to the way it is eliminated with cone cells. Cone cells do not directly appose the pigmented epithelium, yet they rely on the availability of vitA just as rods do. Here is a simple proposed solution: Have the rods and cones embedded in the RPE so that, while they are sufficiently exposed to photons, the axons can form behind the RPE. Furthermore, they retain their direct apposition to the epithelial layer. Intercellular tight junctions could then drastically reduce the incidence of non-traumatic retinal detachment. As you can see, the possibilities are endless. To suggest that it is impossible to be any other way is quite abusrd, considering the extreme flexibility of living organisms and a Creator in charge of it all.

 

[fool]

What if the photoreceptors themselves could store vitamin A? Why restrict that functionality to the pigmented epithelium? I might also argue that direct contact with the pigmented epithelium be eliminated simliar to the way it is eliminated with cone cells. Cone cells do not directly appose the pigmented epithelium, yet they rely on the availability of vitA just as rods do. Here is a simple proposed solution: Have the rods and cones embedded in the RPE so that, while they are sufficiently exposed to photons, the axons can form behind the RPE. Furthermore, they retain their direct apposition to the epithelial layer. Intercellular tight junctions could then drastically reduce the incidence of non-traumatic retinal detachment.

:squint:
Can we go back to talking about cars?

 

[Lord Vader]

:squint:
Can we go back to talking about cars?

Todays cars are engineered into the next century. My wife has a car that does everything automatically. The headlights turn off automatically and they turn on automatically! It has a chip that reads her mind so that it knows when she is about to go to the store and starts itself automatically to warm itself up. If there is snow on the windows, mechanical arms with three fingered white gloved hands pops out of a little trap door in the hood and wipes the snow away - there is even a vanity feature that causes them to slap their hands together in a gesture of a job well done before they slip back inside their compartment. There is a professional massuese in the back seat on stand by. When the doors open and close a serene voice whispers, "glad to be of service". The rear view mirror digitally alters the images of people behind you so that they are smiling and waving in a friendly manner at you. You can set the radio to "only good news". There are three missile launchers and a torpedo for under water excursions.

 

[bob b]

I'm here, and I'm rather unimpressed. First, I'm growing weary of your copy and paste style of argumentation. If you can't argue for yourself don't take up the argument. Shall I, as a response, post an argument someone else wrote in response to the aforementioned? Do we make progress this way? Highly unlikely. Any argument that I form is not against your argument, but is instead against the authors of these papers. Even if I effectively dismantle their argument, you escape unshaken because it was not your argument.

Furthermore, I've become convinced that, in the course of these copy and pastes, you don't always understand the arguments presented or the implications. As such, I'm rather disinclined to take the time to understand the author's argument, check his sources, and form a rebuttal where warranted. If you didn't understand the article in the first place what good will my rebuttal be? I can play mouthpiece for articles all day. But I'm of the opinion that forming one's own conclusion based on other's work is more valuable than pasting a conclusion I happen to agree with. Nonetheless, I have read both of the articles you pasted.

Both arguments you pasted seek to argue good design by assuming the static positioning of nearby structures while trying to change the position of the optic nerve. The feat of rearranging the eye so that the optic nerve could originate behind the photoreceptors would undoubtedly require repositioning of other nearby structures. Both authors have effectively argued that this is the best design because of the positioning of other parts. This is as absurd as arguing that a car with its engine in the trunk is the best design because the fuel lines happen to run to the back of the car instead of the front. Of course moving the engine to the front would require repositioning of the fuel lines, but this is in no way an argument that it cannot be done nor that rear-engines are the best design.

Of course repositioning of the optic nerve would require repositioning of the RPE. I do not deny this. However, you cannot form a convincing argument that there is no other way, especially in a biological system. Why does the RPE even need to exist? You might argue that without it, the availability of retinal would diminish. But this is simply an argument from static design. What if the photoreceptors themselves could store vitamin A? Why restrict that functionality to the pigmented epithelium? I might also argue that direct contact with the pigmented epithelium be eliminated simliar to the way it is eliminated with cone cells. Cone cells do not directly appose the pigmented epithelium, yet they rely on the availability of vitA just as rods do. Here is a simple proposed solution: Have the rods and cones embedded in the RPE so that, while they are sufficiently exposed to photons, the axons can form behind the RPE. Furthermore, they retain their direct apposition to the epithelial layer. Intercellular tight junctions could then drastically reduce the incidence of non-traumatic retinal detachment. As you can see, the possibilities are endless. To suggest that it is impossible to be any other way is quite abusrd, considering the extreme flexibility of living organisms and a Creator in charge of it all.

LOL. The whole subject got started because some evolutionists thought that they had a good argument that the vertebrate eye was a "poor design". It turns out that they spoke too soon because all of their talking points failed to stand up to closer scrutiny. Now you seem to think that those who demolished the evolutionist argument have an obligation to show that the eye couldn't be designed any better than it is. They have no such obligation.

I would say that the evolutionists should be more cautious in their claims of "poor design" unless they can back it up a lot better than they have in the examples seen to date.

 

[Johnny]

The whole subject got started because some evolutionists thought that they had a good argument that the vertebrate eye was a "poor design". It turns out that they spoke too soon because all of their talking points failed to stand up to closer scrutiny.

As usual, the rest of us are left to wonder (some of us aloud) whether or not you actually read what is posted. Please follow this closely.

First, what we are arguing over is whether their "talking points" happen to be valid. You started this thread as a response to the talking points: namely that the optic nerve is poorly placed. I responded to your defenses arguing why I felt they were poor defenses. However, without even responding to what I said, you repeat the conclusion as if it wasn't addressed.

It turns out that they spoke too soon because all of their talking points failed to stand up to closer scrutiny.

As one member recently complained to me, "I have observed bob b move from trying to refute arguments to simply declaring his side is true with no pretense of refutation." Is this another case? Bob, I clearly explained why their defense is poorly constructed, and without even attempting to refute what I said, you restate the conclusion as if there was no question. If you are here to post statements as fact and run from the ensuing discussion, then I am wasting my time. It is like trying to argue with a child who plugs his ears and states his position over and over, contrary to whatever argument the other side is presenting. If you'd like to continue standing their with your fingers in your ears, then you are certainly entitled to, but I must bow out.

As I stated before, I believe those defenses to be poorly constructed. The goal of your defenses was to show that the eye is not poorly designed. The method by which these authors chose to defend this idea was to argue that the design is the best possible solution given the parameters. The second author concluded, "It is simply untrue that the retina is demonstrably suboptimal, nor is it easy to conceive how it might be modified without significantly decreasing its function." This leads to your second quote:

Now you seem to think that those who demolished the evolutionist argument have an obligation to show that the eye couldn't be designed any better than it is. They have no such obligation.

Once again, you conclude they have demolished the evolutionist argument, without so much as a response to what I posted. You are correct, the authors are not obligated to do anything. However, they chose to argue that the eye is optimal design. I believe they did so poorly. I outlined my reasoning. If you're going to stand their with your fingers in your ears, then you are free to do so.

 

[bob b]

Johnny, your posting does not stand up to close scutiny.

The goal of your defenses was to show that the eye is not poorly designed.

Wrong. The authors merely showed the shallowness of the argument for "poor design" by giving the reasons why the design was the way it was and by implication that the critics had not considered all the functions which need to be performed by a real, not simplified hypothetical visual system.

The method by which these authors chose to defend this idea was to argue that the design is the best possible solution given the parameters.

Not true. They simply presented reasons why the eye was designed in the manner in which it is. In fact they specifically stated in the early parts of their paper why one would have a hard time determining hypothetically what an optimal design would be (obviously because it would only be a hypothetical design and so could not be tested).

You even engaged in a bit of hypothetical argumentation yourself which I ignored because hypothetical designs can not be tested.

So please correct yourself for stating that the authors claimed that the current vertebrate eye is "the best possible design given the parameters". In the case of something as awesomely complex as the vertebrate eye how could anyone short of God possibly know such a thing?

As such, I'm rather disinclined to take the time to understand the author's argument

And so it seems.