I ran across an interesting little article in a trade mag e-newsletter. I tracked down the original research article, which is sadly pay-walled-in. Color vision depends upon having different photoreceptors that maximally respond to different light frequencies. The brain then recombines the the different color inputs into the color imagery that most of us are familiar with. There are many fun vision tests that can diagnose vision deficits, some of which I used to have on my i-Pad (now gone). (I consider them fun because knowing how they work, I can often guess the answer for particular color blind conditions.) They are usually interpreted as to which of the color pigments in the photoreceptor cells are lacking, usually indicative of a particular genetic deficiency. This study I discovered, has found a different way to make distort the usual mix of differeent photorecptors sensitive to different colors. Turns out that during retinal development (in humans), retinal photoreceptors maximally sensitive to different colors develop in a sequence (first blue, then red, then green; sequencing is not too surprising) and that the changes in which cells develop is controlled by Thyroid Hormone (TH). This mechanism was confirmed by treating human retinal organoids in culture with different levels of TH so only particular color sensitive classes of photoreceptors developed. Organoids are one of the few ways to do actively manipulative human biological studies that is considered ethical. In this way, it is proposed that TH could affect color vision without affecting the genetics of the photorecptor pigments. For example derangements of maternal TH production could lead to unusual color vision in infants. In addition, TH is most active when it has 3 iodine atoms (T3) bound to it and less so in the T4 form. T0, T1 and T2 not so active. They bind to the TH receptor in induce actions in different cells that have the TH receptor in their surface. Lacking the TH receptor also affects color photoreceptor development, as I might guess would iodine deficiencies and selenium deficiencies (selenium is part of another enzyme which regulates the iodine levels in TH). Normally TH's signally function is thought of a general regulation of metabolism in a variety of ways, but it is also the trigger for metamorphosis in amphibians (tadpole to frog transition) and (some people claim) humans also. Also, important changes in the fetal blood circulation (such as shifting blood flow away from the placenta to the lungs) occur just prior to/during/after birth.