Iodine in Disruption of Thyroid and Thyroid Hormone Receptive Systems

Iodine is an integral component of thyroid hormones. Relationship between the level of iodine intake and the risk of occurrence of thyroid diseases is ‘U’ shaped, that indicates there is an increasing risk with both low and high iodine intake. There are studies to evaluate thyroid functions in iodine deficient regions on humans and animals. To prevent iodine deficiency iodized salt has been introduced through universal salt iodization programme and enormous benefits have been achieved. However, improper monitoring of iodine content in edible salt at consumer level have increased the risk of excessive iodine intake leading serious health consequences to thyroid as iodine induced hypothyroidism, hyperthyroidism, goitre, thyroid gland disruption, thyrocyte apoptosis, thyroiditis, etc. Further, excess iodine induces marked alteration in the morphology and histology of testis along with male accessory sex organs including functional characteristics of sperm which are associated with the antifertility potential; in female cyclic ovarian function changes leading to decreased fertility potential that prevents pregnancy. Hypothyroidism caused by excess iodine impairs glial cell structure causing functional as well as morphological impairment of the major areas of brain developing neurological disorders interrupting connectivity of neural networks that signals early cognitive impairments triggering cognitive weakening, memory impairment and depression. Iodine in excess has the immunomodulatory effect in thyroid developing autoimmunity. Prolonged exposure of excess iodine impairs carbohydrate and lipid metabolic pattern and the histoarchitecture of the pancreas, liver, kidney, as well as skeletal and cardiac muscles. All these show the emergence of several health consequences in post-salt iodization.