This is a dilutional hyponatremia which your body is already working to resolve. The dilute urine is evidence of its efforts; passing free water is its way of concentrating the extracellular fluid. This urine is absurdly dilute. Less than 100mOsm/L is an osmolality which approaches that of "total" diabetes insipidus, or the maximal diluting capacity of the nephron (which seems to be around 40-50mOsm/Kg).
The college has explored this topic a few times:
Let us consider what will happen if you end up with 5 extra litres of water on board.
The water will distribute evenly among all the compartments, and the compartments will now have an osmolality of about 250mOsm/Kg.
Your kidneys are normal, and they are trying to dump dilute urine, but you just keep on taking on more and more fluid, either because you are insane, or the doctor gave you 10 bags of 5% dextrose.
You cannot pass pure water and call it urine. The minimum urinary osmolality is around 40-60mOsm/Kg; it gets no lower than that. Some solute must be present. This solute is sodium, potassium and urea.
So lets say you are a degenerate beer-fiend, and your total nutritional intake consists of carbohydrate-rich, sodium-poor beer. Vast volumes are happily ingested. The carbohydrate from the beer is metabolised preferentially, leading to a suppression of protein catabolism. Low protein catabolism results in low urea levels, and with the sodium dropping, what solute can you excrete? None. The volume of urine drops. Each day you will excrete as little as 4 litres of maximally dilute urine. Obviously if you drink more than 4 litres of beer a day, hyponatremia will ensue. This phenomenon is not limited to American college students; ovolactovegetarians and people trying to lose weight too fast are also susceptible.
One can imagine a situation in which the osmoreceptors of the hypothalamus are "reset" to accept a lower range of serum osmolality. In these situations, vasopressin secretion occurs during times of inappropriately low serum osmolality. Is this "inappropriate ADH secretion"?
No, but it is not SIADH, either. This condition is known from case reports, and there does not appear to be any review article on it; perhaps because more often than not is is described along SIADH as a disorder of vasopressin release.
The key feature of this syndrome is the ability (absent in SIADH) to concentrate urine appropriately in response to dehydration, and to dilute it in response to a fluid challenge. Proper SIADH does not permit one to excrete 80% of the fluid challenge within 4 hours. Additionally, fluid restriction can improve the hyponatremia of SIADH, but it may not accomplish anything in the setting of a reset osmostat.
An additional (and apparently normal) form of reset osmostat hyponatremia occurs in pregnancy (HCG is apparently responsible for the changes in pituitary vasopressin secretion).
With chronic psychogenic polydipsia, a gradual decrease in water intake is required. If allowed to self-correct, the sodium level (concentrated by massive dilute diuresis) will rise too rapidly, and cause pontine myelinolysis.
But ultimately, fluid intake restriction is the key.
With beer or malnutrition related hyponatremia, one sees rapid results with the restoration of normal nutrition.
A reset osmostat very frequently does not call for any sort of treatment.