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Adipsia is a condition that can affect both humans and other animals and involves an absence of thirst. Its underlying causes vary but have included anomalies involving the hypothalamus, pituitary and corpus collosum. These abnormalities can occur due to trauma, genetics, or tumors. Although diabetes insipidus usually involves polydipsia, it can also rarely occur not just in the absence of polydipsia but in the presence of such diminished thirst as to fit hypodipsia or adipsia. Adipsia is difficult to study because it is rare; there are only about one hundred researched cases. While adipsia is rare, and may occur in the absence of any structural lesions to the hypothalamus, it may also be seen medically in association with hypothalamus/pituitary involvement in Diabetes Insipidus (adipsic diabetes insipidus) and/or hypernatremia or following pituitary/hypothalamus surgery. Adipsia has been found to increase the risk of infection and death when present in people who are diagnosed with central diabetes insipidus. Although most cases are a result of physical anomalies, there are some cases of psychogenic adipsia. Unlike non-psychogenic adipsic patients, these patients have normal urine osmolarity levels and antidiuretic hormone (ADH) activity.

Characteristics

Type A

Type A (essential hypernatraemia 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. There is no known cause for Type A adipsia. There is debate over whether osmoreceptor resetting could lead to the increase in threshold. Other studies have shown that it is the loss of osmoreceptors, not resetting, that cause the change in threshold.

Type B

Type B adipsia occurs when vasopressin responses are at decreased levels in the presence of osmotic stimuli. Although minimal, there is still some secretion of AVP. This type may be due to some elimination of osmoreceptors.

Type C

Type C adipsia (type C osmoreceptor dysfunction) involves complete elimination of osmoreceptors, and as a result have no vasopressin release when there normally would be. Type C is generally the adipsia type found in patients with adipsic diabetes insipidus.

Type D

Type D is the least commonly diagnosed and researched type of adipsia. The AVP release in this subtype occurs with normally functioning levels of osmoregulation.

Relationship with dopamine

Dopamine, a neurotransmitter, has been linked with feeding behaviors. In an experiment, scientists measured how much food and water mice consumed when they did not have dopamine in their systems. They found that without dopamine, the mice would starve and be dehydrated to the point of death. The scientists then injected the mice without dopamine with its precursor, L-DOPA, and the mice started eating again.

Relationship with hypothalamus

The area of the brain that regulates thirst is located in the anterior part of the hypothalamus. The anterior hypothalamus is in close proximity to osmoreceptors which regulate the secretion of antidiuretic hormone (ADH). ADH secretion is one of the primary mechanisms by which sodium and osmolar homeostasis are regulated, ADH is also secreted when there are small increases in serum osmolality. Thirst is triggered by increases in serum osmolality and along with increases ADH secretion. Both serum osmolality and ADH maintain normal ranges of serum osmolality.

Adipsia tends to result from lesions to hypothalamic regions involved in thirst regulation. These lesions can be congenital, acquired, trauma, or even surgery. Lesions or injuries to those hypothalamic regions cause adipsia because the lesions cause defects in the thirst regulating center which can lead to adipsia. Lesions in that region can also cause adipsia because of the extremely close anatomical proximity of the hypothalamus to ADH-related osmoreceptors.

Testing

Initial testing for adipsia involves electrolyte, blood urea nitrogen and creatinine levels, serum and urine osmolality, blood hormone levels, like vasopressin. In patients who have defects in thirst regulation and vasopresin secretion, serum vassopresin levels are low or absent. Measurements of urine electrolytes and osmolality are critical in determining the central, rather than renal, nature of the defect in water homeostasis. In adipsia, the fractional excretion of sodium is less than 1%, unless a coexisting defect in AVP secretion is present. In salt intoxication, the urine sodium concentrations are very high and fractional excretion of sodium is greater than 1%. Initial test results may be suggestive of diabetes insipidus. The circulating AVP levels tend to be high, which indicate an appropriate response of the pituitary to hyperosmolality. Patients may have mild stable elevations of serum sodium concentrations, along with elevations in both BUN and creatinine levels and in the BUN/creatinine ratio.

Management

People affected by adipsia lack the ability to feel thirst, thus they often must be directed to drink. Adipsic persons may undergo training to learn when it is necessary that they drink water. Currently, there is no medicine available to treat adipsia. For people with adipsia because of hypothalamic damage, there is no surgical or medicinal option to fix the damage. In some cases where adipsia was caused by growths on thirst centers in the brain, surgical removal of the growths was successful in treating adipsia. 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. In this case, desmopressin helps the kidneys to promote reabsorption of water. Some doctors have reported success in treating psychogenic adipsic patients with electroconvulsive therapy.