Abstract
Universal salt iodisation (USI) plays an essential role in the provision of iodine (I) to populations worldwide. Countries adopting USI programmes, adhering to strict criteria laid down by expert organisations such as the Iodine Global Network, are estimated to have reduced the prevalence of I deficiency by 75% (protecting 720 million individuals worldwide). Despite this success, doubts have been raised as to the desirability of continuing such programmes because of (a) the need to reduce salt intake for cardiovascular prevention and (b) the induction of thyroid autoimmunity. We present current evidence from cross-sectional studies in several disparate populations of the possible short-term modulation of thyroid autoimmune markers, thyroid peroxidase (TPOAb) and thyroglobulin antibodies (TgAb), with minimal disruption of biochemical thyroid function. We also present evidence from longer term, mainly cross-sectional studies, that indicate a reduction in the prevalence of TPOAb and TgAb, and the persistence of normal biochemical thyroid function over as long as two decades of USI. We believe these studies indicate that USI is safe, and that long-term salt iodisation does not cause an increase in autoimmune thyroid disease in the populations studied and should not be a safety concern based on current evidence. More long-term and better-designed studies are required.