Don't try to get me to explain this! Just reporting the direct impact of thyroid hormone on colour vision is an important step.
There have been some posts here which mentioned shifts in colour perception. What has, perhaps, not been clear is where the shift happens. This paper appears to indicate it occurs in the cones of the retina - though additional effects might occur in the parts of the brain that process vision.
(The actual experimentation was done on zebrafish, not humans.)
Endocrine regulation of multichromatic color vision
Robert D. Mackin, Ruth A. Frey, Carmina Gutierrez, Ashley A. Farre, Shoji Kawamura, Diana M. Mitchell, and Deborah L. Stenkamp
PNAS first published August 5, 2019 doi.org/10.1073/pnas.190478...
1. Edited by Robert Johnston, The Johns Hopkins University, Baltimore, MD, and accepted by Editorial Board Member Jeremy Nathans July 8, 2019 (received for review March 25, 2019)
Significance
Primate and fish genomes contain tandemly replicated cone opsin genes. The human long wavelength-sensitive/medium wavelength-sensitive (LWS/MWS) tandem array underlies trichromatic color vision; mutations in this array cause altered color vision and retinal degenerations. Differential expression of human LWS vs. MWS is considered a stochastic event, whereby upstream enhancers associate with the promoter of the proximal or distal gene. We demonstrate that the endocrine signal thyroid hormone (TH) is a potent endogenous regulator of the orthologous zebrafish lws1/lws2 array, and of the tandemly quadruplicated rh2-1/rh2-2/rh2-3/rh2-4 array. TH promotes shifts in spectral sensitivity to longer wavelengths by changing expression of opsins in each array, indicating TH-coordinated control of visual function during organismal growth.
Abstract
Vertebrate color vision requires spectrally selective opsin-based pigments, expressed in distinct cone photoreceptor populations. In primates and in fish, spectrally divergent opsin genes may reside in head-to-tail tandem arrays. Mechanisms underlying differential expression from such arrays have not been fully elucidated. Regulation of human red (LWS) vs. green (MWS) opsins is considered a stochastic event, whereby upstream enhancers associate randomly with promoters of the proximal or distal gene, and one of these associations becomes permanent. We demonstrate that, distinct from this stochastic model, the endocrine signal thyroid hormone (TH) regulates differential expression of the orthologous zebrafish lws1/lws2 array, and of the tandemly quadruplicated rh2-1/rh2-2/rh2-3/rh2-4 array. TH treatment caused dramatic, dose-dependent increases in abundance of lws1, the proximal member of the lws array, and reduced lws2. Fluorescent lws reporters permitted direct visualization of individual cones switching expression from lws2 to lws1. Athyroidism increased lws2 and reduced lws1, except within a small ventral domain of lws1 that was likely sustained by retinoic acid signaling. Changes in lws abundance and distribution in athyroid zebrafish were rescued by TH, demonstrating plasticity of cone phenotype in response to this signal. TH manipulations also regulated the rh2 array, with athyroidism reducing abundance of distal members. Interestingly, the opsins encoded by the proximal lws gene and distal rh2 genes are sensitive to longer wavelengths than other members of their respective arrays; therefore, endogenous TH acts upon each opsin array to shift overall spectral sensitivity toward longer wavelengths, underlying coordinated changes in visual system function during development and growth.
Rest of full paper, including PDF option, available here: