Better than any camera—the eye’s response to light
When you emerge from a darkened room out into bright sunlight, your eye mechanically shrinks the pupil, cutting down the amount of light entering the eye. In fact, the eye works marvellously in a wide variety of light intensities, i.e. from hardly any light to very bright light.
The eye can detect a single photon of light, the faintest light possible. Despite some evolutionists claiming that the eye is badly designed, it is impossible to improve on this sensitivity! But the eye can also work with 10 billion photons; that is, its dynamic range is 10 billion to one.
Modern photographic film has a dynamic range of only about 1,000 to one. Also, one of us (JS) performed doctoral research using state-of-the-art light detectors. However, they were so delicate that they needed protection from more normal light intensities using filters that let in only a millionth of the light; otherwise, the detector would have been destroyed. Newer models have an automatic shut-off. Yet the eye easily adjusts to a far wider range without needing such a shut-off.1
The best known way the eye copes with varying light intensity is the iris. This is the coloured ring of the eye. In bright light, muscles contract and narrow the pupil, letting less light in. In dim light, other muscles widen the pupil.
But the biochemists Craig Montell and Seung-Jae Lee have discovered that microscopic machinery is involved, not just the large-scale motion of the iris. They examined fruit fly eyes, which have similar proteins and light detector cells to ours.
These cells have the light-detecting proteins in one end of the cell. But another protein, called arrestin, is moved around in the cell in response to light.
In dim light, arrestin is in a ‘holding area’. But in bright light, it is shuttled so that it can bind and ‘calm’ the light-detecting protein, thus protecting it.
The arrestin doesn’t just drift into place. Rather, it is moved quickly by a motor protein, myosin, along the ‘train tracks’ of the cell’s internal skeleton. The myosin and arrestin are ‘glued’ together with special sticky fats.2
Dr Montell explains, ‘For the cell to properly adapt to bright light, arrestin needs to move. If it doesn’t, the cell remains as sensitive to light as it was when it was dark.’3
Chance or design?
Far from being a poor design, the eye’s dynamic range exceeds that of the best man-made photodetectors. And this latest research shows the intricate microscopic machinery behind it—a motor, glue, ‘calmer’ and internal ‘train tracks’.
All these features would need to be present and coordinated; otherwise, the eye would be blinded by bright light.4 Thus natural selection could not build this system up step-by-step, since each step by itself has no advantage over the previous step, until all steps are complete.
The Bible has a far more cogent explanation: ‘I am fearfully and wonderfully made’ (Psalm 139:14)—an explanation so obvious ‘that men are without excuse’ (Romans 1:20).
- The well-known blink reflex, where our eyelids involuntarily close in the presence of a sudden increase of light intensity, is not strictly analogous, as it is a very temporary protective mechanism. But see also reference 4 below. Return to text.
- Lee, S.-J. and Montell, C., Light-dependent translocation of visual arrestin regulated by the NINAC Myosin III, Neuron 43:95–103, 8 July 2004. Return to text.
- Johns Hopkins Medicine, <www.hopkinsmedicine.org/Press_releases/2004/07_16_04.html>, 2 September 2004. Return to text.
- This includes the aforementioned blink reflex, which may serve to buy sufficient time for these molecular protections described here to ‘kick in’. Return to text.