The Eye

Figure 1: Some of the parts of the eye

The eye is an amazing sensory organ that works a lot like a camera. However, given the chronology it’s more proper to say that it’s the camera that works a lot like an eye. The eye lets light pass through the cornea, the opening in the iris called the pupil, the lens and vitreous humor while being focused on the retina. The photoreceptor cells of the retina (rods and cones) when stimulated by light form electrical impulses which produces an “image” of sorts that is processed and then passed on to be interpreted by the visual cortex in the brain (occipital lobes).

When looking at the eye, most people see what Dr. Michael Behe, a Senior Fellow at the Discovery Institute’s Center for Science and Culture, calls a “purposeful arrangement of parts”. This usually leads most of them to conclude that the eye and its ability to provide us with the special sense of vision shows evidence of intelligent design.

However, the presence of conditions like myopia (nearsightedness), presbyopia (old age farsightedness) and cataracts have led some scientists to raise doubts about this conclusion. In particular, to prove their point neo-Darwinian critics often point to the human (vertebrate) retina as being “wired backwards” compared to some invertebrates like the octopus. Please carefully look at the three figures below and read the accompanying explanations to understand their point.

Figure 2: Note the “yellow” layer of photoreceptor cells lining the back of the octopus and human eyes. In the octopus, the “wires” from the photoreceptor cells for each eye move away from the incoming light to make up the optic nerve which then goes back to the optic lobe (not shown) where the visual sensory information is processed and then sent to the brain. In the human, the “wires” from the photoreceptor cells of each eye instead of going backwards like in the octopus move forward toward the incoming light to the inner layer of nerve cells called the bipolar cells. It is here where the visual sensory information begins to be processed and is sent on to the ganglion cells (not shown: see Figure 3). In the human retina, it’s the” wires” from the ganglion cells, not the photoreceptor cells like in the octopus, which make up the optic nerve. So, one can see that the visual sensory information travelling along the optic nerve of the octopus has not yet begun to be processed whereas it has within the optic nerve of the human (keep this in mind!).

Figure 3:The set-up of the vertebrate (human) retina shows that the visual sensory information goes from the photoreceptor cells forward toward to the light to the bipolar cells while it begins to be processed by the horizontal cells and then onto the ganglion cells while being further processed by the amacrine cells. Notice, that it’s the “wires” from the ganglion cells (as opposed to the “wires” coming directly from the photoreceptor cells in the octopus retina) that make up the human optic nerve.

Figure 4: In both graphics the arrow indicates the incoming light. The photochemicals that react to light are located opposite the nuclei (black dots) of the photoreceptor cells. So, you can see that the photochemicals in the cephalopod (octopus) retina come in direct contact with the photons of light whereas the ones in the vertebrate (human) retina are potentially blocked from the light by the contents of photoreceptor cells and the auxiliary nerve cells that begin to process the visual sensory information and their” wires” (in addition to the blood vessels that supply them). Recall that the “wires” coming from the “nucleus end” of the photoreceptor cells that make up the optic nerve in the vertebrate retina come from the ganglion cells after the visual information is processed by the bipolar and other cells (see Figure.2 above) whereas the “wires” in the octopus retina come directly from the photoreceptor cells without having been processed (see below).

As the figures above show, due to our photoreceptor cells having been put in “backwards” (their business end being away from the incoming light), their “wires” leave the retina through the optic nerve through an opening in the retina which also allows blood vessels to bring in nutrients to the auxiliary cells that process the visual information thus creating a “blind spot” which the octopus doesn’t have to contend with. Essentially, in the human retina for the light to reach the photochemicals it has to pass through the auxiliary nerve cells and their “wires”, their blood supply and the contents of the photoreceptor cells as well. It’s set up like a digital camera with a film put in front of its image sensor.

The neo-Darwinian critics claim that no experienced engineer would ever commit such an obvious blunder. And so, despite everything else that needs to be in place and in proper working order for human vision (see below), they conclude that the human eye must have come about solely from the unguided and purposeless forces of natural selection acting on random variation. Here’s how a few of them have put it.

The Critics Speak

"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 backwards with its wire sticking out on the side nearest the light. The wire has to travel over the surface of the retina, to the point where it dives through a hole in the retina (the so-called “blind spot”) to join the optic nerve...(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)." (The Blind Watchmaker: Richard Dawkins: W.W. Norton 1986)

"The human eye for all its effectiveness has a major design flaw. The optic nerve, after accumulating information from our rods and cones, does not travel directly inward from the retina toward the brain, as any minimally competent engineer would demand. Rather, for a variety of reasons related to the accidents of evolutionary history plus the vagaries of embryonic development, optic-nerve fibers first head away from the brain into the eye cavity, before coalescing and finally turning 180 degrees, exiting at last through a hole in the retina and going to the brain’s optic regions." (The Mammal in the Mirror: Understanding Our Place in the Natural World: Barash and Barash: W.H. Freeman, 2000)

"The human eye is fraught with functional problems...(many people)have myopia, (others) are farsighted, progressive loss of flexibility of the lens begins around age forty, leading everyone to have difficulty making out close objects, then add cataracts and a pattern begins to emerge. Our species is supposed to be the most highly evolved, but our eyes are rather lacking....One of the all-time most famous examples of quirky designs in nature is the vertebrate retina. The photoreceptor cells of the retina appear to be installed backward, with the wiring facing the light and the photoreceptor facing inward....This is not an optimal design for obvious reasons. The photons of light must travel around the bulk of the photoreceptor cell in order to hit the receiver tucked in the back. Furthermore, light must travel through a thin film of tissue and blood vessels before reaching the photoreceptor, adding another layer of needless complexity to this already needlessly complicated system. To date there are no working hypotheses about why the vertebrate retina is wired in backwards. It seems to have been a random development that then stuck because correcting it would be difficult to pull off with sporadic mutations—the only tool evolution has in its toolkit. During the evolution of the cephalopod eye, the retina took shape in a more logical way, with the photoreceptors facing outward toward the light. Vertebrates were not so lucky." (Human Errors: Nathan Lents: Houghton, Mifflin, Harcourt, 2018)

Filling in the Gaps

Although it’s the retina where incoming light stimulates nerve cells resulting in electrical impulses going to your brain to be interpreted as vision, there are many other parts which play an important role in letting light pass through to the retina and provide the eye with support and protection from injury. If any one of them were not present or working properly your vision would be severely impaired or non-existent. In addition, although it is the retina that provides the sensory information that will be interpreted by the brain as vision, there are many other interconnecting cells needed and the final pattern of neural impulses that the brain “sees” may surprise you. How all of this is interpreted as vision is, as yet, poorly understood. So, let’s take a closer look at how your eyes allow you to see.

The five skull bones that make up the orbital cavity protect about two-thirds of the eyeball and provide the base for the origin tendons of the six different muscles responsible for rapid and precise eye motion in tandem. When you want to look at something you use these muscles to move your eyes in the right direction. But if you keep moving your head and body what you’re focusing on will become blurry. The vestibulo-ocular reflex (doll’s eyes reflex), using data on angular head motion provided by the semicircular canals in your ears, automatically makes your ocular muscles move your eyes to keep things in focus. Look in a mirror and focus on your eyes. Then move your head from side to side and up and down, and you’ll see this reflex in action.

The eyelids and eyelashes protect the eye from exposure to too much light in addition to dust, dirt, bacteria and other foreign objects. We know that a bright light, a threatening motion or something touching the eye will all automatically trigger a protective reflex to close it quickly.

A film of tears, consisting of oil, water and mucus are produced by the oil glands of the eyelids, the lacrimal gland and the conjunctiva that overlies the sclera, the white outer protective coating of the eyeball. The tear film lubricates the eye, protects it from infection and injury, nourishes the surrounding tissue and preserves a smooth surface to aid in light transmission.

The cornea is a convex (curved outward) transparent connective tissue that protects the front of the eye while allowing light to enter. To remain transparent it is absent blood vessels and receives oxygen, water and nutrients from the tears that constantly wash across it by the blinking eyelids and the clear fluid (aqueous humor) within the anterior chamber that sits behind the cornea and in front of the lens. Light rays that reflect from an object more than twenty feet away enter parallel and those closer diverge, so they must be bent (refracted) to focus them on the areas in the retina for sharp and sharpest vision (macula and fovea). The curvature of the cornea provides about two-thirds of this refractive power.

The lens is an elastic biconvex (doubly curved outward) transparent structure made of connective tissue that is kept in place by suspensory ligaments. Like the cornea, it is absent blood vessels. It obtains its oxygen, water and nutrients from the aqueous humor in the anterior chamber which sits in front of it and behind the cornea. To focus the light rays entering the eye on the area for central vision in the retina the curvature of the lens provides about one-third of the needed refractive power. And since what the eye focuses on close-up often changes, the curvature of the lens can be reflexively adjusted by automatic contraction or relaxation of the ciliary muscle. This causes an increase or decrease in the curvature of the lens resulting in more or less refraction as the object moves closer or farther away. This process is called accommodation. By looking at something far away and then suddenly close up, you can literally feel the tugging sensation in your eyes as the ciliary muscles contract to allow you to focus.

As Figure 5 below illustrates, the distance behind a lens where the light comes together in what is called a “focal point” is dependent on the degree of curvature. It’s important to note here that for most people, the combined refractive power of the cornea and lens results in a focal point that exactly matches the distance from the front of the eye to the area for central vision in the macula and fovea. In other words, as light enters the eye it is first bent by the cornea and then by the lens which together focus on the area for central vision in the retina. This is what lets you to have your sharpest vision so you can read and do close-up work.

Figure 5: It is the cornea and lens that together refract the light as it goes through the eye which, for most people, makes it come to a focal point in the area for central vision (macula and fovea).

The choroid is the layer of tissue located between the sclera and the retina and provides the circulation of blood and its nutrients to the back of the eye. It also contains the retinal pigmented epithelium (RPE) which sits directly behind and adjacent to the retina. One of the many jobs of the RPE is to absorb any light that travels through the retina (escaping the photoreceptor cells) to stop it from reflecting back on them. This prevents visual blurring just like what can happen with an echo for hearing. We will look at some of the other functions of the RPE below.

The extension of the choroid in the front of the eye is the colored iris which consists of two muscles that together control the amount of light that enters through its opening called the pupil. This is done automatically through the brainstem by the pupillary light reflex to make sure the eye has enough light in dark situations and not too much in very bright situations. Too much light can not only cause visual blurring but also injury to the retina. About 20% of the visual sensory impulses that travel along the optic nerve to the visual cortex veer off to provide sensory data to the brainstem to accomplish this and some of the other reflexes mentioned above. While looking in a mirror shine a light into your eyes to see how it makes your pupils automatically contract. Then turn off the light so you can see how they automatically dilate.

The last tissue to look at that allows light to travel to the retina and provides support and protection for the eye is the vitreous humor. It’s the thick, transparent and gelatinous substance that forms and shapes the eyeball. It’s able to be compressed and return to its natural position allowing the eyeball to withstand most physical stresses without serious injury.

The retina itself is a thin ribbon of tissue that sits at the back and lines about two-thirds of the eyeball. It contains the photoreceptor cells (rods and cones) that react to light to start the process of vision. Each eye has about 120 million rods. They are strewn throughout the entire retina but are completely absent in the fovea (Figure 6). The rods contain a chemical called rhodopsin which is very sensitive to all the wavelengths of the visible light spectrum. They “see” only in black and white and provide us with our peripheral and night vision. In contrast, there are only about six million cones which are mostly in the macula with the highest concentration in the cone-only fovea, the area for our sharpest vision. Each cone contains one of three chemicals called photopsins. They react to either the red, green or blue wavelengths and are less sensitive to light than are the rods. They provide color and central vision but to function properly they require much more light than the rods. Both rhodopsin and the photopsins are dependent on Vitamin A which must first be brought into the body through your diet and requires several chemical reactions to produce these photochemicals.

Figure 6: The fovea contains only cones and is the area for sharpest vision in color. You are using it right now as you read these lines. The macula has a high density of mostly cones but some rods too. The optic disc consists of the optic nerve and the blood vessels that supply the vascular network that feeds some of the tissues of the eye.

When photons of light enter the eye and strike the photoreceptor cells, the rhodopsin in the rods and the photopsins in the cones become chemically changed which results in them sending out electrical signals. These signals DO NOT go straight to the brain. As noted above in Figure 3 and below in Figure 7, they first go to the bipolar cells and then to the ganglion cells while being acted upon by the horizontal and amacrine cells respectively. It’s the “wires” of the 1.2 million ganglion cells which send their messages through the optic nerve to the brain. Once again, it’s important to note here that all of these auxiliary nerve cells that begin to process the visual sensory information provided by the photoreceptor cells are located in front of the retina, not behind it. In other words, they can potentially block the incoming light and distort the image.

Figure 7: In the human (vertebrate) retina the visual impulses from the photoreceptors travel to the bipolar cells and then to the ganglion cells which then send the final message through the optic nerve to the brain to be interpreted as vision. Note that these auxiliary nerve cells sit in front of the photoreceptors potentially in the way of the incoming light.

It’s important to note here that from the 126 million photoreceptors providing visual signals in the retina only 1.2 million messages are sent from the ganglion cells along the optic nerve to the brain. This means that, on average, each ganglion cell sends visual sensory information from about one hundred (126/1.2) different photoreceptors along the optic nerve to the brain. This means that most of the visual sensory information coming from the photoreceptor cells in the retina going to the visual cortex in the brain is mixed-up and jumbled. In general, that’s not a good recipe for sharp vision.

However, your retina is set up so that in the cone-only fovea (sharpest vision) the relationship between the cones, the bipolar cells and the ganglion cells is 1:1:1. This means that each cone has a dedicated bipolar and ganglion cell to which it sends its signals. Due to this set-up the visual sensory information from each cone in the fovea is not mixed up with signals from other retinal cells. This allows the visual cortex of the brain to receive highly specific visual sensory data which allows it to provide the sharpest vision which you’re using right now to read this.

In contrast, the rods strewn throughout the rest of the retina do not have the luxury of their own private bipolar and ganglion cells to receive their visual signals. In the outer regions of the retina, one bipolar cell may service several hundred rods and one ganglion cell may service more than one bipolar cell. This means that the visual cortex in the brain receives only one signal from several hundred different rods from the outer regions. This explains why our peripheral vision is not as refined as our central vision and mostly responds to movement in black and white.

Now, just imagine if things were switched around. If the peripheral rods had a 1:1:1 relationship with their bipolar and ganglion cells and the cones in the fovea were set up 600:3:1. Everything in your periphery would be clear but everything right in front of you would be blurry. Just luck?

Having said all of this, we now need to look at the question of which ganglion “wires” go where in the visual cortex of the brain? It would seem to make sense that all of the visual sensory signals from one eye would end up in one visual cortex in the occipital lobe and all of the ones from the other eye would end up in the other. Otherwise, how could the brain interpret all of these visual messages? In considering the nature of the visual sensory data being presented from the eyes to the visual cortex in the brain several points must be kept in mind.

First, as Figure 8 below shows, when light is refracted through a lens the image on the other side is upside down and reversed. Since light must travel through the one curved surface of the cornea and the two curved surfaces of the lens, it is refracted an odd number of times (three) and so the image on the retina is upside down and reversed. This means that what appears in the upper half of the visual field is detected by the lower half of the retina and what appears in the lower half of the visual field is detected by the upper half of the retina. Also, what appears in the left half of the visual field is detected by the right half of the retina and what appears in the right half of the visual field is detected by the left half of the retina.

Figure 8

Second, by looking through one eye at a time you can see that there is an overlap in the nasal visual fields (the inside halves of both eyes). This overlap provides the visual cortex of the brain with two different perspectives allowing for depth perception. It gives us a sense of our three dimensional world allowing us to sense distances and the ability to do close-up fine skilled handiwork. Incidentally, as Figure 9 below shows, with binocular vision the overlapping fields compensates for the tiny blind spots in each eye rendering the “blind spot” argument of our critics as mildly interesting but more or less irrelevant. More on that later!

Figure 9: The designation “temporal” refers to the outer half visual near the temporal bone and “nasal” refers to the inner half visual field near the nose. Note how small the blind spot defect is with regard to the total visual field and that the opposite field covers the other’s blind spot.

Finally, as Figure 10 below shows, the impulses sent along each optic nerve split-up on their way to the brain. The messages from the nasal half of the retina cross over from left to right and from right to left, through what is called the optic chiasm. However the impulses from the temporal half of the retina stay on the same side. Keep in mind that due to refraction the image on the retina is reversed compared to what is actually being seen so the temporal half of the retina receives the light from the nasal half of the visual field and the nasal half of the retina receives the light from the temporal visual field. So, due to the optic chiasm, everything seen by the right half of each eye (the nasal field of the left eye and the temporal field of the right eye) goes to the left occipital lobe (visual cortex) and everything seen by the left half of each eye (the temporal field of the left eye and the nasal field of the right eye) goes to the right occipital lobe. In other words, the left visual cortex “sees” everything in the right half of the visual fields of both eyes and the right visual cortex “sees” everything in the left half of the visual fields of both eyes. Seeing this I’m sure that our third critic would opine that all of this is just “another layer of needless complexity to this already needlessly complicated system.” But in fact, it is consistent with how the sensory and motor regions of the brain work. The right side of the brain senses what is felt on, and controls the muscles of, the left side of the body, and the left side of the brain senses what is felt on, and controls the muscles of, the right side of the body.

Figure 10: “Temporal half” of the left/right retina refers to the “outside half” near the temporal bone and “nasal halves” of the left/right retina refers to the “inside halves” near the nose.

Our brain then takes this upside down, turned around, split-up, black and white, multi-colored and overlapping collection of photon-generated nerve impulses and provides us with what we experience as vision. How it is able to accomplish this feat is as yet entirely unknown.

So, besides how the photoreceptor cells are set up in the retina there’s a lot more to vision than what’s mentioned above by these three critics. Here are three questions to which they don’t even allude, never mind try to answer, which should give the reader pause.

1. In what order and from where did the new genetic information come that specifies the size, shape and position of all the parts of the eye that allow light to pass through to the retina, physically supports all of the associated structures and automatically serves to protect them from injury and what is the real probability that such a system could have come about by undirected forces while remaining functional in intermediate organisms each step along the way?

2. In what order and from where did the genetic information come to let the body bring in enough Vitamin A and be able to use it to make the four different photochemicals housed within the rods and cones, the interconnecting neurons that begin the processing of the visual information and the ganglion cells that send the visual information on to the brain, and what is the real probability that such a system could have come about by undirected forces while remaining functional in intermediate organisms each step along the way?

3. In what order and from where did the genetic information come to bring about the optic pathways sending an upside down, turned around, split-up, black and white, multi-colored and overlapping collection of photon-generated nerve impulses to the visual cortex of the brain allowing us to instantaneously experience vision and what is the real probability that such a system could have come about by undirected forces while remaining functional in intermediate organisms each step along the way?

So, are you willing to accept the undirected forces of natural selection acting on random variation as the definitive answer to the above questions? The “smoke and mirrors” of neo-Darwinism which doesn’t even try to account for how each of the parts needed for sharp vision came together and happened to have the right size and shape, be in the right position, with the right specifications, doing the right things fast enough and at the right times, for survival?

It’s important to realize that natural selection acting on random variation (genetic mutation) means exactly what it says. Over time, life required a gazillion bits of new genetic information (not natural selection) to bring about new structures with new functions. All natural selection did was preserve the life that was up and running properly and able to survive due to these gazillion undirected genetic mutations. But keep in mind, natural selection cuts both ways.

Based on what we know about how life actually works neo-Darwinism may explain the survival of the fittest but not the arrival of the fittest. That’s because, when it comes to survival, logic tells us that the same power that natural selection had to preserve human life when its vision worked properly would have also prevented it from surviving if any one of above-mentioned parts of the eye were either missing, defective, misplaced or not working well or fast enough.

The known engineering principles needed to bring about peripheral and sharp enough vision in the dark or in the light of day, that resulted in human survival means that, in principle, not only does Darwin’s theory of gradualism fail, but so do all the other neo-Darwinian attempts to replace it. What do you think?

Comments

The first critic begins by telling us what an engineer would “naturally assume” regarding the positioning of the “photocells” and their “wires”. When it comes to passing judgment on the optimality of a given structure or device an engineer never assumes anything. Unlike evolutionary biologists, who often make conclusions without discussing the physicochemical factors, packaging or functional capacity involved, engineers must always take these and many others into account. So, it is doubtful that a “tidy-minded” engineer would “laugh at” or be “offended” by “any suggestion that the photocells might point away from the light” until (as opposed to this critic) having first considered the location and specifications of each structure, how their function relates to the whole and the physiological ramifications of any suggested changes (none of which were given by the critic).

The critic also mistakenly claims that it is the photocell wire “that dives through (the blind spot) to join the optic nerve” when as noted above, it is the wire from the ganglion cell (not the photocell) that enters the optic nerve after the visual sensory information has begun to be processed by the nearby auxiliary neurons. As we’ll see below, this is a very important distinction when it comes to comparing human and octopus retinal function. Finally, although the light having to “pass through a forest of connecting wires” could potentially suffer distortion, when it comes to attenuation (reduction), the effect of the pupillary reflex on how much light enters through the iris is several orders of magnitude greater, an indication that for visual acuity, being able to see details and retinal protection, since many vertebrates, as opposed to cephalopods, live in very bright environs, maybe a little attenuation of light is a good thing.

The second critic(s), like the first, parroting the standard neo-Darwinian talking point, opine that “The human eye for all its effectiveness has a major design flaw” because the “information from our rods and cones (do) not travel directly inward from the retina toward the brain as a minimally competent engineer would demand”. Here in a nut-shell is the difference between evolutionary biology, a discipline in decline because it just talks about how life looks, and systems biology, a discipline on the rise, because it talks about how life actually works. In contrast to the two evolutionary biologists, a minimally competent systems biologist, rather than dismissing the set-up of the vertebrate retina based on a simplistic view of optimal functionality would ask “Why is this structure in this organism set up the way it is compared to similar ones in others and does it afford it a functional advantage for survival that may not be readily apparent?” In other words, since the structure in question is present in an organism that is surviving, the systems biologist assumes that it has been working well enough whereas evolutionary biologists seem to think that their credentials alone justify their conclusions without any legitimate scientific explanation. It is this attitude that then leads to their answer to the three questions above with respect to origin. Namely that the various structures within the vertebrate retina came about “for a variety of reasons related to the accidents of evolutionary history plus the vagaries of embryonic development”; a neo-Darwinian tale of the highest order; long on rhetoric and short on details.

The third critic rightly points out all of the problems that can arise with human eyesight but fails to explain how, despite them, humanity has somehow been able to survive. From these and other known defects he concludes that “Our species is supposed to be the most highly evolved, but our eyes are rather lacking”. It doesn’t take a PhD in Biology to realize that within the animal kingdom, humans are not the strongest nor the weakest, the fastest nor the slowest, the most nor the least agile. So, one has to look askance at someone who would apply the term “highly evolved” to mere physical abilities (like vision) alone. The author’s ability to investigate, reflect on, and analyze the details of what is required for human vision and then communicate his opinion of its fitness compared to other organisms by using his manual dexterity to write is just one example of how the human ability to reason and communicate through language is actually some of what “highly evolved” is intended to mean.

The critic then moves on to the standard neo-Darwinian talking point that “The photoreceptor cells of the (human) retina appear to be installed backward, with the wiring facing the light and the photoreceptor facing inward...adding another layer of needless complexity to this already needlessly complicated system.” Here, in black and white (not color) is the fatal error of neo-Darwinism; all of the mechanisms that allow for life are assumed by them to be very simple!!

He then states that “To date there are no working hypotheses about why the vertebrate (human) retina is wired in backwards”. Here he ignores all of the scientific research on this topic which, as will be seen below, does provide a reasonable explanation.

He then gives us the usual neo-Darwinian view that the vertebrate retina “seems to have been a random development that then stuck because correcting it would be difficult to pull off with sporadic mutations” without explaining how “sporadic mutations” allowed it to come into being in the first place.

Finally, we are told that “During the evolution of the cephalopod (octopus) eye, the retina took shape in a more logical way, with the photoreceptors facing outward toward the light, vertebrates were not so lucky.” Are we to believe that an octopus has better vision than an eagle? When someone is able to see something faraway should we now call him “octopus eye”? After all, the eagle is only one of the tens of thousands of vertebrates living within many different environs with “backward wired” retinas compared to the few marine cephalopods with “logically wired” retinas. Based on the incredible number of organisms with “backward wired” retinas, it would appear that it seems to function pretty well despite our critics’ concerns. Let’s take a closer look.

Laufmann’s Triple Filter

Not understanding the objectives of the designer

Let’s be honest. The main objective for vision, whether in an invertebrate (like the octopus) or a vertebrate (like a human), is to aid in survival. Other organisms may have poorer vision or even none at all, but have other sensory devices that allow them to be aware of and interact with their environment for survival too. So keying on just one aspect of a given organism’s visual sensory device and comparing it with another’s without considering or even understanding how each organism processes and interprets the visual sensory data nor how that set-up fits into what the organism must do to survive, is a bit myopic (pun intended).

Even to the casual observer it is evident that the life of an octopus and a human are quite different. The cold-blooded octopus lives in a darker watery environment and must feed on what keeps it alive and evade and protect itself from predators to survive. To accomplish this, its eyes, which it can move independently, are set further apart and more laterally positioned resulting in a larger field of vision than humans’ with limited (if any) overlap and therefore much less (if any) depth perception. This is very important for animals that are tracking prey and predators. The only octopus that used close-up 3D vision was a fantasy character called Ursula, the sea witch from Walt Disney’s The Little Mermaid.

The diameter of the octopus eye is about the same as a human’s (20 mm). Its retina has about 20 million identical photoreceptor cells which generally provide vision in black and white and is mostly geared to detect vertical and horizontal motion rather than fine detail. Contrast this to the densely packed human retina that has 120 million rods which allow for peripheral and night vision in black and white, and 6 million cones which allow for very detailed sharp central vision in color. Moreover, the human retina has a macula and fovea, for sharp and sharpest vision, the latter containing 200,000 cones/mm², whereas the octopus has only 55,000/mm² in its central horizontal stripe. In his book “Children of Light” Michael Denton, a Senior Fellow with the Discovery Institute’s Center for Science and Culture, tells us that both these pale in comparison to the eagle’s fovea which has 1,000,000/mm².

It’s important to remember that although the eye is absolutely needed to experience vision, the sensory information obtained by the photoreceptors in the retina must be processed with respect to, among other things, light variability, image sharpness and distortion, and then be sent on to the brain for interpretation. And for it to be useful for survival all of this must take place almost instantaneously! The octopus retina contains one layer of identical photoreceptor cells that sends the visual sensory information to the optic lobe behind it to be processed on the way to the brain. In contrast (as noted above) the visual sensory information in the human retina comes from two different types of photoreceptors containing four different types of photochemicals and is pre-processed in the auxiliary cells that sit in front of the photoreceptor cells before being sent on to the brain. How this is actually accomplished in both the octopus and the human is at yet poorly understood.

Needless to say, whatever the differences between the octopus and human retina and their respective visual abilities, they have been sufficient for both of them to survive. The eyes of octopi along with their eight arms and other body features, has afforded them the ability to be powerful predators allowing them to move quickly and grab onto prey as well as evade danger and defend themselves. In contrast, the black and white peripheral and night vision along with the daytime acuity and close-up three-dimensional detailed color vision of humans along with their manual dexterity driven by their intellect affords them not only mere existence but also the ability to create and produce millions of useful objects, read and write, calculate and solve problems and even write and play music on instruments (just to name a few).

Another thing to consider in how vision aids in survival is its importance for balance and motion along with hand-eye (tentacle-eye, wing/talon-eye) coordination and its effect on hunting prey or defending against predators. The octopus buoyed up by its watery environment is at minimal risk of gravity making it fall to cause serious injury and possible death. The same cannot be said for terrestrial and aerial organisms. Human balance and rapid coordinated movements are dependent on not only the pressure sensors in the feet, the vestibular organs in the ears and the proprioceptors in the muscles and joints, but also on visual cues.

Don’t believe me? Start walking toward an object, accelerating as fast as you can, until you are running. Now, try it with your eyes closed and see how more difficult it can be. Consider the eagle, that “unlucky” vertebrate (according to the third critic) that can see its prey from over two miles away as it swoops down at speeds of over 100 m.p.h. to grab it in its talons and fly away again. Without its extraordinary vision and the cues it provides do you think it could accomplish such a precisely coordinated action? Do you think it could even survive at all without its vision?

The suggestion, that an octopus has better vision than a human whether due to the set-up of its retina or other features is pure conjecture. That an invertebrate like an octopus has better vision than a vertebrate like an eagle is laughable. Given the functional objectives that distinguish octopus from human life it is likely that this set-up for the human retina required different specifications as opposed to the set-up for the octopus. Let’s take a closer look.

Not accounting for the functional requirements, constraints and trade-offs

As noted above, within about the same space, the human retina has 6x the photoreceptors than the octopus, consisting of four different types to the octopus’ one. Also, when it comes to sharp detailed vision, their concentration in the fovea of the human retina is 4x more than anything the octopus has (in the eagle it’s 20x more!). Given the three critics’ comments and what’s actually needed for human vision let’s see how the differences between the set-up for the human and octopus retinas can be reconciled with their functional capacity.

First, when it comes to cell survival and function, the most important thing needed is enough oxygen and nutrients. Besides the cold-blooded octopus having a much lower metabolic rate than the warm-blooded human, because its blood uses hemocyanin, rather than hemoglobin, it has only about one-tenth of the oxygen-carrying capacity. Maybe this physiological truth has something to do with why, compared to the octopus, the human retina can have so many more photoreceptor cells, consisting of more types of photochemicals. in much higher concentrations.

In his book “Zombie Science: More Icons of Evolution”, Jonathan Wells, a Senior Fellow with the Discovery Institute’s Center for Science and Culture astutely noted that “In mammals, they (the rods and cones) have the highest metabolic rate of any tissue in the body. Oxygen and nutrients—including modified Vitamin A—are transported from the blood in the choriocapillaris (choroid blood supply) to the rods and cones by an intermediate layer of specialized cells called the “retinal pigment epithelium (RPE)” (see Figure 11 below).

Figure 11: Note how the rods and cones, which are reported to have the highest metabolic rate of any other tissue in the human body, are literally enmeshed within the finger-like projections of the RPE from whence comes their oxygen and nutrients from the nearby choroid blood supply (choriocapillaris). Also, as noted in the text above, human blood, using hemoglobin can carry 10x the amount of oxygen than octopus blood which uses hemocyanin. In other words, the limited oxygen-carrying capacity of the octopus blood limits its ability to service its retinal cells and precludes it from being able to service a much more complicated retina like the vertebrate’s.

In addition to providing an excellent supply of oxygen and nutrients to the photoreceptors the RPE has many other important functions. After the photons of light cause the rhodopsin and photopsins to chemically change and make the photoreceptor cells send out electrical signals, these molecules must then be chemically put back the way they were to be ready to work again. If this doesn’t happen fast enough you could lose your vision—think of how a flash of light can momentarily blind you. That’s why!! It’s the RPE, using its vast stores of vitamin A and several different enzymes, supported by its lush blood supply that carries out this task.

Also, the rods and cones daily breakdown about 10% of their photoreceptor discs where the rhodopsin and photopsins are made. This causes the release of toxins. The RPE mops up these discarded discs and recycles everything to prevent a toxic build-up of chemicals. And, as noted above, the RPE contains a dark pigment called melanin which absorbs any light that may have escaped through the photoreceptor cells and stops it from reflecting back to blur the image.

If the photoreceptor cells of the human retina were turned around so that their business end was facing the incoming light instead of the RPE, this would impair their ability to receive enough oxygen and nutrients in a timely manner, quickly regenerate the spent photochemicals to allow for continued vision and efficiently breakdown the degenerated discs with their toxins. Since the RPE with its associated blood supply from the choroid capillaries is absolutely necessary for human vision, the only other engineering options would be to place the RPE either at the sides of the photoreceptor cells which would make it less effective and limit their concentration (like in the octopus) or in front of them, which, due to its lush blood supply, would significantly block the entry of light (orders of magnitude more than the present set-up of the auxiliary nerve cells).

Second, given that the human retina has many more photoreceptor cells in a much higher concentration and with more types of photochemicals than the octopus retina, another thing to consider is what it takes to process the human retina’s exponentially more visual sensory information. Think of it like what it would take to process the digital information in a camera with a very low versus a very high pixel density to obtain a sharp image. Which do you think will need more complex and highly sophisticated components requiring more energy (and be more expensive)?

As noted above, the octopus retina is simpler in that it has just one layer of photoreceptor cells consisting of one type of photochemical that send their visual sensory information directly to the optic lobe and from there to the brain. In contrast, the human retina with its many more photoreceptors, in higher concentration and with more photochemicals, begins processing its exponentially more visual sensory information by sending it first to the bipolar cells and then the ganglion cells while being also worked on by the horizontal and amacrine cells respectively. The pre-processed visual sensory data is then sent from the ganglion cells to the brain where it is further processed and interpreted as vision.

Without mentioning the more complex nature of the human compared to the octopus retina and therefore the need for pre-processing, ergo the extra neural layer in the human retina, the critics claim that, by being positioned between the incoming light and the photoreceptor cells the above set-up causes reduced and distorted vision. The nerve cells and the small central retinal vessels are so tiny and thin, and being mostly made of water, barely block any light and even if they do, the pattern in each eye being different would be rendered inconsequential with binocular vision. In particular, all of the auxilary nerves and associated blood vessels skirt around the macula and fovea so that central detailed vision is not impaired. And of course, having too much light entering the eye is a common problem that the iris largely deals with through the automatic pupillary light reflex so a slight blockage by these tissues may actually be a good thing. Of course, the octopus lives in a much darker environment and so may need to get as much light to its photoreceptors as possible. Additionally, when it comes to the definite potential issue of distortion, the human (vertebrate) retina has specialized cells, called Müller cells, which sit between its inner surface and the rods and cones which act like optical fibers to prevent this happenstance.

If the photoreceptors cells were turned toward the light so their “wires” pointed backwards, away from the light, like in the octopus, the neural auxiliary cells that do the needed pre-processing of the visual sensory information would have to be located either behind the retina, but still inside the eye or behind the eyeball itself. Either way, the size of the eye and nearby structures, like the brain, the sinuses the facial muscles and skull, would have to be altered to accommodate this change. After all, there’s not a lot of space there (see Figure 12 below).

Figure 12: Note the eyes above wth the “yellow” optic nerves in addition to the tight placement of all the surrounding tissues: placing the pre-processing neural tissue behind the retina within the eyeball or behind the eyeball in front of the brain (like in the octopus) would necessarily change the anatomy of the head including the skull, the brain, the sinuses and the facial muscles.

Third, the critics rightly note that since the ganglion cell wires and blood vessels that feed the auxiliary nerve cell layer of the retina must pass through a hole in the retina (called the optic disc) this leaves a “blind spot” in each eye. However, what they don’t mention is that this defect doesn’t involve central vision and is a very small area located in the peripheral field. Of course, the blind spot in each eye is in a different location so good binocular vision makes the critics’ claim “much ado about nothing”.

In summary, when it comes to the functional requirements to survive and be able to do what humans can do they must have not only excellent peripheral night and day vision but also three dimensional central vision, in living color, for close-up detail. Compared to the octopus, this required that their retinas have many more photoreceptor cells, in much higher concentration, with more types of photochemicals. But the constraints to service this higher number and concentration of photoreceptors with their ability to detect a much wider visual spectrum required much more highly organized and effective vascular and processing systems. These metabolic and functional requirements made it necessary for the photoreceptor cells to be placed facing away from the incoming light so they could receive enough oxygen and the nutrients they need and do what they need to do in a timely manner through the RPE which was put in the only place where it could accommodate a higher amount and concentration of photoreceptor cells and facilitate these functions without critically blocking light entry. Furthermore, as compared to the octopus, because of this set-up, the auxiliary neural tissue needed to begin pre-processing the exponentially higher amount of visual sensory information needed to be placed somewhere; either in front of or behind the retina within the eyeball or behind the eyeball and in front of the brain, as it is in the octopus. This functional need was constrained by the anatomical limits of the bony skull along with the nearby tissues. The end result being that the neural tissue was placed within the potential space in front of the retina but still within the eyeball. Both of these innovations meant that there would be the trade-offs of a small “blind spot” in each retina which was off center so as not to impact central vision and the light entering the eye could be partially blocked and/or distorted. The inconsequential practical concern of the “blind spot” as it is compensated for by binocular vision, the limited attenuation of light by the cellular and vascular structures in front of the retina being orders of magnitude less than how much light the pupil prevents from entering the eye to preserve visual acuity and protect the retina, and the presence of the Müller cells to prevent visual image distortion seem to be the reasons why we can see a lot better than the critics think we should be able to given such “bad design”.

Failure to acknowledge user abuse and degradation over time

In the last several decades it’s been noted that there is an increasing incidence of myopia (short-sightedness) throughout the world, especially in the young. This happens when the eye focuses the incoming light in front of the retina either (more commonly) because the eye has elongated or (less commonly), the refractive power of the cornea and lens is too strong. Myopia has been around for centuries but its increased incidence particularly in the last several decades may be due to increased screen time. The increase of myopia over the centuries may be due to an increase in the literacy rate which caused people to start reading earlier and earlier in life. Whether our ancient ancestors had this problem is unknown although if it did exist it was likely much less prevalent and therefore would have had little effect on humanity’s survival. After all, with the human ability to reason and create along with family life, a person with myopia would have been cared for and would have been particularly good at close up handiwork. As for presbyopia which is due to stiffening of the lens in mid-life which makes it harder to see things up close up and cataracts that come about usually after the sixth decade of life and blur vision, particularly at night, neither of these would have affected the person’s ability to reproduce.

Conclusion

By their very existence it is evident that the set-up of the retinas in the eye of the octopus and of the human is sufficient for their ongoing survival. When considering the functional requirements of the human eye and in particular its retina, to allow us to be able to do what we need to do to survive within the physical and chemical constraints of nature, the idea that the “backward wiring” of its photoreceptor cells is evidence of “bad design” is not only misguided but, based on engineering principles, totally absurd. What do you think?

Also see Dr. Glicksman's Series on

"Beyond Irreducible Complexity"

"Exercise Your Wonder"

"On Being Alive"

Howard Glicksman M. D. graduated from the University of Toronto in 1978. He practiced primary care medicine for almost 25 yrs in Oakville, Ontario and Spring Hill, Florida. He now practices palliative medicine for a Hospice organization in his community. He has a special interest in how the ethos of our culture has been influenced by modern science’s understanding and promotion of what it means to be a human being.