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Our inverted retina: Not a bad design

Evolutionists frequently maintain that the vertebrate retina exhibits a feature which indicates that it was not designed because its organisation appears to be less than ideal. They refer to the fact that for light to reach the photoreceptors it has to pass through the bulk of the retina’s neural apparatus, and presume that consequent degradation of the image formed at the level of the photoreceptors occurs. In biological terms this arrangement of the retina is said to be inverted because the visual cells are oriented so that their sensory ends are directed away from incident light. It is typical of vertebrates but rare among invertebrates, being seen in a few molluscs and arachnids.

 

 

 

 

 

 

As usual, evolutionists like to point this out as an evidence of “bad design”, thus, being supposedly more explainable under the light of natural, unguided view. Dawkins, while admitting that light traversing the inverted retina is not disturbed significantly during its passage to the photoreceptors, writes as follows :

‘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.’ 1

First, we must review some things about ocular anatomy:

 

Figure 2Light enters the human eye via the transparent cornea, the eye’s front window, which acts as a powerful convex lens. After passing through the pupil (the aperture in the iris diaphragm) light is further refracted by the crystalline lens. An image of the external environment is thus focused on the retina which transduces light into neural signals and is the innermost (relative to the geometric centre of the eyeball) of the three tunics of the eye’s posterior segment. The other two tunics of the eye’s posterior segment are the white tough fibrous sclera which is outermost and continuous with the cornea anteriorly, and thechoroid, a pigmented and highly vascular layer which lies sandwiched between the retina and sclera.

The retina consists of ten layers, of which the outermost is the dark retinal pigment epithelium (RPE) which because of its melanin pigment is opaque to light. The RPE cells have fine hair-like projections on their inner surface called microvilli which lie between and ensheath the tips of the photoreceptor outer segments. There is thus a potential plane of cleavage between the RPE and the photoreceptors which is manifested when the neurosensory retina becomes separated from the RPE, e.g. as a result of injury, a condition known as retinal detachment.

Each photoreceptor, whether rod or cone, consists of an inner and an outer segment, the former having organelles (intracellular apparatus) for manufacturing the visual pigment present in the latter. The rod and cone layer and all eight layers internal to it constitute (in distinction from the RPE) what is known as the neurosensory retina which is virtually transparent to light. By means of many complex nerve connections within the neurosensory retina, electrical impulses generated by light reaching the photoreceptors are processed and transmitted to the retina’s nerve fibre layer and thence pass up the optic nerve to the brain.

In many species for whom vision in very low levels of illumination is important, a layer of reflective crystalline material, the tapetum (Latin: carpet) is incorporated in the RPE or choroid.1 Acting as a mirror, the tapetum reflects light which has passed between the photoreceptors, so augmenting the light bombarding the photoreceptors. Hence the proverbial ‘cat’s eyes’ when caught by a beam of light in the dark.

The retinal pigment epithelium

Fundamental to understanding the inverted retina is the crucial role played by the RPE. Many of its important functions are now well known. Each RPE cell is in intimate contact with the tips of 20 or more photoreceptor outer segments which number over 130 million. Without the RPE the photoreceptors and the rest of the neurosensory retina cannot function normally and ultimately atrophy.

The outer segment of a photoreceptor consists of a stack of discs containing light-sensitive photopigment. These discs are being continually formed by the inner segment from where they move in succession outwards in the outer segment towards the RPE which phagocytoses (Greek: φάγω (phagō) = eat) them and recycles their chemical components.

The RPE stores vitamin A, a precursor of the photopigments, and thus participates in their regeneration. There are four photopigments which are all bleached on exposure to light: rhodopsin (found in the rods, for night vision) and one for each of the three different types of cones (one for each of the primary colours). It synthesises glycosaminoglycans for the interphotoreceptor matrix, i.e. the material lying between and separating the photoreceptors.

Besides oxygen, the RPE selectively transports nutrients from the choroid to supply the outer third of the retina and removes the waste products of photoreceptor metabolism to be cleared by the choroidal circulation. By selective pumping of metabolites and the presence of its tight intercellular junctions, the RPE acts as a barrier, called the blood-retinal barrier, preventing access of larger or harmful chemicals to retinal tissue, thereby contributing to the maintenance of a stable and optimal retinal environment.

The RPE has complex mechanisms for dealing with toxic molecules and free radicals produced by the action of light. Specific enzymes such as the superoxide dismutases, catalases, and peroxidases are present to catalyse the breakdown of potentially harmful molecules such as superoxide and hydrogen peroxide. Antioxidants such as a-tocopherol (vitamin E) and ascorbic acid (vitamin C) are available to reduce oxidative damage.

Our photoreceptors thus continually synthesise new outer segment discs with their specific photopigments, recycling materials from used discs digested by the RPE. This prompts the question, ‘Why have such a complicated process?’ The answer must be that it is an example of biological renewal, by means of which tissues exposed to damaging chemicals, radiation, mechanical trauma, etc., are able to survive. Without self renewal, tissues such as the skin, the lining of the gut, blood cells etc would quickly accumulate fatal defects. In the same way, by the continual replacing of their discs the photoreceptors counter the relentless process of disintegration accelerated by toxic agents, particularly short wavelength light.

 

The choroidal heat sink

 

It has been observed that the damage to photoreceptors in an experimental model is strongly related to temperature, and other studies have confirmed that heat exacerbates photochemical injury. Any system designed to protect against the latter should also protect against the former. In 1980, a paper was published which explained for the first time something already known about the choroid.2 That is, its very high rate of blood flow which far exceeds the nutritional needs of the retina, despite the latter being highly active metabolically, as indicated.

The choroidal capillaries (the choriocapillaris) form a rich plexus lying immediately external to the RPE, predominantly its central area, and separated from it by only a very thin membrane (Bruch’s). The absorption of excess light by the RPE produces heat in the outer retina which has to be dissipated if thermal damage to the delicate and complex biological machinery, its own and that of its neighbourhood, is to be avoided.

The authors of this study cogently argue that an important function of the choroid with its torrential blood flow (in local terms) and its close proximity to the RPE, is to act as a heat sink and cooling device. Still more fascinating are the results of further studies by the same workers indicating that there are central (via the brain), light-mediated nervous reflexes regulating choroidal blood flow, increasing the blood flow with increased illumination. Both RPE and choroid are essential for vision, but they are opaque, so it follows that for light to reach the photoreceptors, both RPE and choroid have to be located external to the neurosensory retina; hence we can conclude that there are sound reasons for the inverted configuration of the human and vertebrate retina.

 

The foveola

Although the neurosensory retina is virtually transparent apart from the blood in its very slender blood vessels, there is an additional refinement of its structure in its central region called the macula. The retina and the occipital cerebral cortex (called the visual cortex) of the brain, to which the former transmits visual information, are so organised that the VA is maximal in the visual axis. The visual axis passes through the foveola which forms the floor of a circular pit with a sloping wall, the fovea (Latin: pit) at the centre of the macula. Away from the fovea the VA diminishes progressively towards the periphery of the retina. Thus the colour photoreceptors—the cones for red, green and possibly also blue—have their greatest density of 150,000 per square mm at the foveola, which measures only 300–330 µm across.

 

Xanthophyll pigment

The optical system of the human eye is such that ambient light tends to fall with peak intensity on the macular area of the retina with much less on the retinal periphery. It must be significant therefore that not only is melanin more abundant in the macular region because its RPE cells are taller and more numerous per unit area than elsewhere30 but there is also in the retina’s central area the yellow pigment xanthophyll (Greek: ξάνθος xanthos, yellow). In this region of the retina, xanthophyll permeates all layers of the neurosensory retina between its two limiting membranes and is concentrated in the retinal cells, both the neurons and the supporting tissue cells. Recently attention has been drawn to the presence of a collection of retinal supporting tissue cells (called Müller cells after the person who first described them) over the internal surface of the fovea and forming a cone whose apex plugs the foveolar depression.

Retinal xanthophyll is a carotenoid, chemically related to vitamin A, whose absorption spectrum peaks at about 460 nm and ranges from 480 nm down to 390 nm It helps to protect the neurosensory retina by absorbing much of the potentially damaging shorter wavelength visible light, i.e. blue and violet, which is more scattered by small molecules and structures.

 

The blind spot

Because of the retina’s inverted arrangement, the axons (nerve fibres) transmitting data to the brain pass under cover of the retina’s inner surface to converge to a small area which is the optic nerve head, where they all exit the eye together as the optic nerve. The optic nerve head has no photoreceptors and so is blind, thereby producing a small blind spot in the visual field. No surprise, evolutionists criticized that. As Williams puts it:

‘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.’ 3
Notwithstanding, this issue has to be viewed in perspective: the blind spot is centred at 15° away from the visual axis (3.7 mm from the foveola) and is very small in relation the visual field of an eye, occupying less than 0.25%. As mentioned above, the further away a point in the retina is from the foveola, the less will be its VA and its sensitivity. The retina surrounding the optic nerve head, in the light-adapted state, has a VA of only about 15% of that at the foveola. We can safely infer that the theoretical risk referred to by Williams arising from the blind spot in a one-eyed person, is negligible; and, in keeping with this, it is considered safe for a one-eyed person to drive a private motor car, i.e. for non-vocational purposes.’ 

Because the two visual fields overlap to a large degree, the blind spot of one eye is covered by the other eye’s visual field. It is true that occlusion or loss of one eye is a handicap, but this is not because of the blind spot of the seeing eye for the reasons given above.

 

Invertebrated eyes

Some claims that the verted retinae of cephalopods, such as squids and octopuses, are more efficient than the inverted retinae found in vertebrates. But this presupposes that the inverted retina is inefficient in the first place, and we’ve seen that isn’t the case. Also, they have never shown that cephalopods actually see better. On the contrary, their eyes merely ‘approach some of the lower vertebrate eyes in efficiency’ and they are probably colour blind. Further, the cephalopod retina, besides being ‘verted’, is actually much simpler than the ‘inverted’ retina of vertebrates; as Budelmann states, ‘The structure of the [cephalopod] retina is much simpler than in the vertebrate eye, with only two neural components, the receptor cells and efferent fibres’.5 It is an undulating structure with ‘long cylindrical photoreceptor cells with rhabdomeres consisting of microvilli’, so that the cephalopod eye has been described as a ‘compound eye with a single lens’. Finally, they live in regions with much lower light intensity than most vertebrates, which contributes to show that cephalopods eyes don’t need to be so complex as it’s usually claimed.

Despite the efforts of evolution promoters, the inverted retina isn’t an evidence of bad design; all the way around, even its “backwards wired” design poses a clear sign of planned origin, as to suit the demands of each living being, in accordance to its environment.

(From the article:  Is our ‘inverted’ retina really ‘bad design’?-Creation Ministries)

 

God bless you!

 

References

 

1 Dawkins, R., The Blind Watchmaker: Why the evidence of evolution reveals a universe without design. W.W. Norton and Company, New York, p. 93, 1986

2 Duke-Elder, S., System of Ophthalmology, Henry Kimpton, London, vol. 1, p. 147, 1958.

3 Parver, L.M., Auker, C., Carpenter, D.O., Choroidal blood flow as a heat dissipating mechanism in the macula, Am. J. Ophthalmol. 89:641–646, 1980.

4 Williams, G.C., Natural Selection: Domains, Levels and Challenges, Oxford University Press, Oxford, pp. 72–73, 1992.

5 Budelmann, B.U., Cephalopod sense organs, nerves and brain, 1994. In Pörtner, H.O., O’Dor, R.J. and Macmillan, D.L., ed., Physiology of cephalopod molluscs: lifestyle and performance adaptations, Gordon and Breach, Basel, Switzerland, p. 15, 1994.

4 responses to “Our inverted retina: Not a bad design

  1. เสริมจมูก April 25, 2014 at 23:45

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  2. rozy sacardo July 15, 2013 at 20:59

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