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How you see colours and your thyroid gland's health


 Thyroid Regulates How We See Colours!

 

Turns out our sensitivity to seeing in colour is not only due to cone cells in the retina, but also through the thyroid gland by controlling which visual pigment is produced in the cones. Research conducted on mice and rats has revealed that the production of visual pigment present in mature cones is regulated by the thyroid hormone. The team of researchers at the Max Planck Institute for Brain Research in Frankfurt/M., along with colleagues at the University of Frankfurt and universities in Vienna, assumed that this process must be present in all mammals, including humans. If this were the case, the adult-onset of thyroid hormone deficiency would affect colour vision. Most mammals have two types of spectral cones, which contain two different visual pigments (opsins). The first opsin is sensitive to shortwave light (UV/blue opsin), and the second is sensitive to middle-to-long wave light (green opsin). These cones are receptive to the thyroid hormone, and when activated by the hormone, the cones will suppress the production of UV/blue opsin, and activate the synthesis of green opsin. It was long believed that the thyroid only controlled opsin production during developmental stages; in mature and established cones, the opsin had reached its plateau, needing no further regulation. However, this theory is now challenged. A study carried out by lead authors Martin Glösmann and Anika Glaschke in Leo Peichl's team at the Max Planck Institute for Brain Research in Frankfurt, along with their colleagues at the universities of Frankfurt and Vienna, conducted a study which proves opsin production in mature cones continually depend on the thyroid at a hormone level past developmental stages. The researchers had started with an analysis of thyroid hormone involvement in the early postnatal development of mouse cones.

"We wanted to know how long the time window for the hormone effect was, at what point the hormone's influence on opsin production stopped," Glaschke was quoted saying. "To our surprise we did not find such an endpoint, even several weeks after birth there was a hormone effect". A treatment was administered to several adult mice and rats that caused an insufficient production from the thyroid hormone. During the treatment, the functions of the opsin switched: the production of UV/blue opsin was activated, and green opsin production was suppressed. When the treatment ended, hormone levels returned to normal and the cones reverted to their regular production of opsin. The results of the study led researchers to conclude that the two types spectral cones, which are defined by the opsin they express, are dynamically and reversibly controlled by thyroid hormone past the developmental stages, and throughout life. "In addition to their importance for basic retinal research, our findings may also have clinical relevance," Martin Glösmann, who currently examines the genetic foundations of the process at the University of Veterinary Medicine, Vienna was quoted as saying. "If this mechanism also acts in human cones, the adult-onset of thyroid hormone deficiency - e.g. as a consequence of dietary iodine deficiency or removal of the thyroid - would also affect the cone opsins and colour vision." SOURCE: Max Planck Institute for Brain Research, March 29, 2011

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