To prevent iodine deficiency disorders, the universal salt iodization programme has been introduced all over the globe, including environmentally iodine sufficient regions irrespective of their iodine status. As a result, iodine-induced thyroid dysfunctions namely hyperthyroidism, hypothyroidism, autoimmune thyroid diseases, endemic goiter and even thyroid cancer including infertility, still births, abortions and embryo toxicity have emerged as a major public health problem. In other words, the consequence of iodine deficiency and excess is almost 'U'-shaped. Hypothyroidism caused by iodine deficiency affects reproductive functions of organisms; however, such undesirable effects of iodine overload on male gonadal physiology together with hormonal profiles are yet to be adequately explored. The discovery of iodide transporter in the testis justifies an independent role of iodine in male reproductive function, which is not entirely known. Recent studies on human subjects and animal models are now revealing further perceptions into the effect of excess iodine on male infertility with euthyroid status. Excess iodine exposure has been linked with deterioration of structural and functional changes of testis leading to compromised spermatogenesis by affecting various cellular and molecular signaling pathways culminating into disrupted the blood-testis barrier and cytoskeleton. This review provides an update and summarizes various novel insights of excess iodine exposure on reproduction by establishing the independent role of iodine on male reproductive endocrinology, which might help in formulating future strategies to prevent iodine-induced male infertility, an emerging global concern, especially in the post-salt iodization era.