Postulated human sperm count decline may involve historic elimination of juvenile iodine deficiency: A new hypothesis with experimental evidence in the rat

Human sperm count studies, historic dietary iodination, and an animal model where neonatal goitrogen administration causes unprecedented testis enlarg ement, together suggest an hypothesis relevant to the postulated fall in hu man sperm counts. We present the hypothesis with a supporting study extendi ng the model to include iodine deficiency. In a one-generation rat reproduc tion study, dams were fed an iodine sufficient (control, 200 ppb I) or defi cient (low iodine diet [LID], <20 ppb I) diet from prebreeding through wean ing, when male offspring were divided into three groups: 1) controls from i odine sufficient darns, 2) neonatal LID (NLID) from the LID dams, fed contr ol diet postweaning, and 3) chronic LID (CLID) from LID dams, fed a moderat e LID (40 ppb I) postweaning. F1 males were euthanized on postnatal day (PN D) 133 +/- 1. Each of the three diet groups comprised two subgroups in whic h testicular parameters were evaluated: 1) daily sperm production (DSP), sp erm motility, morphology, and histopathology, and 2) Sertoli cell and round spermatid morphometry. In the first subgroup, NLID and CLID testes weights were 8.5% and 14.0% heavier than their unusually heavy controls (3.921 g; historical control mean congruent to 3.5 g), with proportional DSP increase s. Sperm motility, morphology, and testis histopathology were unaffected. I n the morphometry subgroup, respective increases in NLID and CLID rats incl uded testes weights (+28.6% and +20.3%), Sertoli cells (+24.8% and +23.9%), and round spermatids (+20.4% and +15.8%). The results indicate that neonat al iodine deficiency can significantly increase spermatogenic function in r ats, and support our hypothesis concerning human sperm counts.