Episode Transcript
Welcome to faith and science. I'm Doctor John Ashton. Just a few days ago, I was chatting with a friend and she mentioned that she just had her second cataract operation done.
And when she was talking to the doctor, she said, well, after this first one, I still see this sort of corner thing in this eye. There's something there that I notice in the corner of my eye. And his comment actually really surprised her.
He said, well, we can't actually make lenses as good as the creator can. And she was really pleased and she thought, wow, this person believes in God. My doctor believes in a creator God.
And she felt really good about that. And of course, the origin of the human eye was one of the things that fascinated Darwin as well. And he saw it as a potential major problem for his theory of evolution.
How could an eye evolve? And of course, many, many animals have eyes. And of course, the human eye is quite complex. We can see a lot with our eye.
But we also know quite early in the so called evolutionary model, if we look at things like trilobites, they had extremely complex eyes and they're right down at the bottom of the fossil record and hence believed to be the oldest forms of life. And yet how could these extremely complex eyes have evolved? Major challenge for evolution to explain. And really, when we look at it from the biochemistry and the physiology point of view, from what we know now, it would be absolutely impossible for the eye to have formed, by random chance, blind mutations to some sort of DNA code.
And I'd like to have a look at this now. I'm going to read some things from a summary of the physics, physiology of the eye and the amazing biochemistry of the eye. And as I discuss and talk about and read this information, one of the things we need to bear in mind is that when we look at all these complex structures that make up our visual system, they all work together, they all play a role that sort of harmonises and enables each to function properly and together.
And these components in themselves are extremely complicated. They're controlled by a whole lot of biochemistry that involves a whole lot of particular specific chemical compounds. And we have to remember that all these compounds are formed by complex chemical reactions.
And all these systems, the compounds that are required to make the reactions go and to form the other compounds, all have to be encoded for in the DNA. And what the evolutionary theory is saying is that the codes to set up the biochemistry and the enzymes to make all these reactions occur to assemble these structures to form the eye, because, remember, the components of the eye have to be assembled. And all these instructions have arisen by random, blind chemical changes to a DNA code.
And when we look at that, we can see that's absolutely impossible. Absolutely, and I use that term, it cannot possibly happen. And so what we have is when we look at the eye and the structure of the eye, we have powerful evidence, right, that we can observe today that the theory of evolution must be false.
There must have been a creator, a highly intelligent creator, that was able to put these systems together, make them work. So let's now just review some of the things that are involved in the eye. So the proper function of the eye depends on its ability to receive and process energy from light in the environment, to produce action potentials in specialised nerve cells and relay those potentials through the optic nerve to the brain.
Now, the eye is made of, if you've got the cornea, the iris, the cilia body, then the lenses, and these all play a role in transmitting and focusing light onto the sensory components of the eye, the retina. Now, the structures such as the toroid, the aqueous and vitreous humours, and the lacrimal system, or LT system, are also important pay an important physiological balance. They appropriate pressure maintenance in our eye, maintain the pressure and so forth, and the nourishment of the tissue of the eye.
And so these are a complete system that works together. Now, our ability to see or visual acuity relies on the proper refraction or bending of light passing through structures of various densities as the light is transmitted through the cornea, the aqueous humour, the lens, the vitreous humour, before striking the retina. Now, the lens is adjustable.
It's an adjustable component of this refractive system. And its shape is altered by the contraction or relaxation of the cilia muscle to focus on objects that are near or fast. So again, we've got these muscle structures that are involved that control this.
The retina is composed of two types of photoreceptor cells, rods and cones. The rods are the cells primarily responsible for what is called scotopic vision or low light vision. And the rods are the more abundant cell types of the retina.
They reach their maximum density, approximately 15 to 20 degrees in angle from the favia. And this is a small depression in the retina of the eye, where visual acuity is higher. So again, all these amazing structures make up the eye.
There are approximately 90 million rod cells. So when we think about this, all these cells and 90 million cells, and all these cells have to be made up and assembled in position in the human retina the cones, on the other hand, confer colour vision and high spatial acuity, and are the cell type most activated at higher light levels, where phototopic vision predominates. And the favia has the highest density of cones and is free of rods.
And the human retina contains approximately 6 million cone cells, so 90 million rod cells, 6 million cone cells. And it should be noted that there is a visual field or blind spot at the site where the optic nerve, where the photoreceptor cells are absent in that part. Now, if we compare the photoreceptor cell types, the rods have more photopigment and exhibit high amplification.
They have high convergent retinal pathways, high sensitivity, while the cones have a faster response with shorter integration times, and are all directionally sensitive and exhibit high acuity. And the rods are what we call achromatic, meaning they contain one type of pigment, while the cones are arranged in a chromatic organisation of three different pigments. And so in the favia, this arrangement takes the form of what is referred to as the cone, mosaic and photopigment molecules.
So again, these are special molecules that the body has to make, are embedded in the membranes of the photoreceptors. Now, the photopigment in the rods, and this is where it gets really complicated and really deep. The photopigment in the rods is called rhododopsin and human rhododopsin is a g protein coupled receptor made up of 348 amino acids that have been assembled in particular way.
And when you look at the probability of just that forming by itself, it's astronomical. And they are arranged in seven transmembrane domains and its gene is located on chromosome three. Now raise this, because it's very interesting that some of these parts are quite different parts of our DNA and yet they are all responsible for producing structures of the eye, even though they're widely apart in terms of the DNA.
Rhododopsin consists of a protein called scototopsin and it's covantly bound cofactor retinal. The chromophore retinol lies in a pocket formed in the transmembrane domains of scototopsin. Retinol is a vitamin a derivative from dietary beta carotene, of course, and inactive retinol exists as an isomer, so it's there as well.
But upon exposure to light, retinol is isomerised to all trans retinol, leading to a series of changes in conformation to form meta rhodopsin or meta two. And meta two activates the g protein transducin. So you're noting this.
All this complex biochemistry that follows one after the other, is part of the biochemistry that enables us to see, and these are all specific molecules that have to be made and encoded for in the DNA after transducin, after which its alpha subunit is released, the transducin alpha subunit, bound to guanosine triphosphate, or gtp, then activates the cyclic guanosyanine monophosphate gmp phosphoridase diesterase, and this is hydrolysed by the monophosphate is hydrolysed by the phosphodiesterase, which inhibits its active conservation of the gmp dependent cation channels and causes hyperpolarisation of the rod cells, and consequently the release of glutamate, which depolarises some neutrons and hyperpolarizes others. And so this is all part of really complex chemistry that's occurring in our eyes, that enables us to see. And I could go on talking about the other different compounds and the roles that they play in signalling different proteins and the channels that they travel down and so forth.
But one of the things that's quite fascinating, in contrast to rods and the extreme complex biochemistry in rods, we've also got the chemistry in cones. And so in contrast to rods, there are three different types of cones. You've got the s cones, short wavelength sensitive, the m cones medium wavelength sensitive, the l cones long wavelength sensitive.
So these are all different structures. And it's interesting, the S cone photopigment genes encoded on chromosome seven. Now, remember, we talked about in the rods, its protein gene was okay on chromosome three, so they're quite different, and yet they all work together in quite a different part of the DNA structure, but they work together.
Now, it's interesting that those of the M cones and the L cone cones are on a different chromosome. Again, they're actually on the X chromosome, which is one of the sex chromosomes. Of course, now, all cone receptors contain the protein photosipsin in modified conformations to enable the activation by different wavelengths of light.
And of course, there are different types of photophotopsin as well. We can go through a whole lot of looking at the different types of photopsins. There's phototopsin one, photosopsin two, phototopsin three, which are for the different types of light there.
And then there's another one, melanopsin, which is located on some of the ganglion cells of the retina. And is responsible for non visual responses to light, such as the regulation of circanium, of our circadian rhythms and the pupillary reflex. And so when we look at these amazing structures, the amazing biochemistry that is producing all these different compounds that enable the different signalling, that enable these different photoreceptors work, the information and so forth, to be carried to the optic nerve, we can see that it all functions together.
It's not just a random higgledy piggledy. And we know that there are a lot of eye diseases as well, that once this biochemistry and physiology is altered in some way, that we begin to lose our sight. The structure of the eye is really powerful evidence that we were created by a creator God.
And that's the God that the Bible talks about. And we know. And the Bible said, God said, how you can know that I am God is that I have revealed to you the future, what will happen.
And that's why the Bible contains these prophecies. God revealed what would happen and those prophecies have come true. That gives us faith to believe that the Bible count is the true account of our creator.
You've been listening to faith and science, and if you want to enjoy these programmes and share them, remember to Google Three abnaustralia.org and click on the radio button. I'm doctor John Ashton.
Have a great day.
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