I'd theoretically ascribe it to a dietary poison that effectively shuts down or blocks expression of the NaI symporter, the most likely candidates seemingly being fluoride and bromide, as the symporters are set up to receive and deal with singly-charged anions, and it'd make sense that those isoelectonic with Iodide would fit right in. The stomach is the place that encounters these first, so the symporters there should be expected to be of reduced number or viability than symporters elsewhere, upon their encountering such dietary poison.