Polydipsia, chronic or intermittent, with or without hyponatremia, frequently occurs among chronic patients with schizophrenia. The pathogenesis of polydipsia remains poorly understood. The key assumption of our hypothesis is that in some of these patients, polydipsia and hyponatremia are consequences of patients' adjustment to a prolonged intake of an insufficient diet, dominantly poor in potassium. Deficits of potassium, without significant hypokalemia, may cause impairment of the urine-concentrating ability with polyuria-polydipsia. A fall of intracellular tonicity, dominantly due to a decreased amount of K(+) and attendant anions in cells, should be accompanied with a fall of extracellular osmolality. Because of the diminished content of ions that may diffuse out of cells and because osmotic equilibrium between the ECF and ICF compartments cannot be established in a short period of time, these patients have a diminished ability to adapt to an excessive intake of fluids. These mechanisms might be related to the development of polydipsia and water intoxication in patients with different mental and somatic disorders. The experiences with the therapeutic effects of diets containing an sufficient amount of potassium in two patients with schizophrenia are described. Further investigations are needed, and we suggest a possible approach to test our hypotheses.