[1][2] It involves an increased osmolality or concentration of solute in the urine, which stimulates secretion of antidiuretic hormone (ADH) from the hypothalamus to the kidneys.

[6] It is possible for hypothalamic dysfunction, which may result in adipsia, to be present without physical lesions in the hypothalamus, although there are only four reported cases of this.

In these rare psychogenic cases, the patients have normal levels of urine osmolality as well as typical ADH activity.

Lesions in that region can also cause adipsia because of the extremely close anatomical proximity of the hypothalamus to ADH-related osmoreceptors.

Changes in the brain that are indicative of adipsia include those of hyperpnea, muscle weakness, insomnia, lethargy, and convulsions (although uncommon except in extreme cases of incredibly rapid rehydration).

[12] Measurements of urine electrolytes and osmolality are critical in determining the central, rather than renal, nature of the defect in water homeostasis.

[4] Type A (essential hypernatremia syndrome) involves an increase of the level in which solvent molecules can pass through cell membranes (osmotic threshold) for vasopressin release and the activation of the feeling of thirst.

[13] Patients with Type A adipsia can be at risk of seizures if they rapidly re-hydrate or quickly add a significant amount of sodium into their bodies.

Although adipsic persons must maintain a strict water intake schedule, their diets and participation in physical activities are not limited.

People affected by diabetes insipidus have the option of using the intranasal or oral hormone desmopressin acetate (DDAVP), which is molecularly similar enough to vasopressin to perform its function.

[8] Additionally, some patients who do not successfully complete behavioral therapy may require a nasogastric tube in order to maintain healthy levels of fluids.