Bro myopia is the least stupid part of our eye design problems. Our retinas are built entirely backwards for no other reason besides evolution making a mistake and then duct taping over it too much to fix it later.
If your retina was the right way around (like cephalopod eyes) you would have:
- No blind spots
- Higher fidelity vision even with the same number of receptors since the nerves and blood vessels wouldn’t interfere like they do now
- much lower likelihood of retinal detachment since you could attach it for real in the first place
- possibility for better brightness/darkness resolution since blood supply could be greater without affecting light passage
- possibility for better resolution because ganglion nerves can be packed more densely without affecting light passage
- The ability to regenerate cones and rods because you could, again, ACTUALLY HAVE SUPPORT CELLS WITHOUT BLOCKING LIGHT TO THE RETINA
Our eyes are built in the stupidest way possible.
Another fun fact: retinol is regenerated by your liver. Not your eyes, not some part of your brain, not some organ near your head like your thalamus which could probably get the job done if it tried, your fucking liver. Your eyes taking a while to adjust to the dark has basically nothing to do with your eyes; it’s because of the delay in adjustment by your fucking liver to produce more retinal, dump it into your vascular system and wait for it to hopefully reach your eyes. Why are we built like this?!
Edit: A few comments asked for sources on the relation between dark adaptation and liver vitamin A. So I went looking for sources. It was honestly somewhat difficult to find information, but I was able to find two different case studies showing that night blindness in patients with damaged livers. Specifically these individuals had liver damage that affected their serum Vitamin A levels. And after raising their vitamin A levels, their symptoms improved.
This study details a patient with normal day vision and no other ocular problems besides being unable to see at night.
The patient had a medical history of stage 4 non-alcoholic liver cirrhosis, which led to a malabsorption of vitamin A, as confirmed by the very low vitamin A level in the serum analysis… …Subjective improvement in symptoms, along with better performance on visual field, were noted after initiating oral vitamin A supplementation for 6 months.
This study details a patient with night blindness caused by low levels of vitamin A presumably due to Hepatitis C.
Case description: This case describes a 64-year-old female patient with symptomatic VAD, likely secondary to liver cirrhosis in the setting of Hepatitis C. The patient presented with night blindness and blurry vision. She was successfully managed with direct replacement of Vita-min A.
These studies do show that dark adaptation is dependent on vitamin A produced by the liver, but I’ll be the first to admit it’s not exactly conclusive evidence of my initial claim that the liver must respond to dark conditions increasing retinol concentration in the blood in order for rod cells to function properly in low light conditions. That is a possible explanation for these case studies but not necessarily the only one, so take my last fun fact with a grain of salt.
