This reduction, combined with reduced renal water-conservation capacity, may predispose the elderly to dangerous dehydration when illness increases water losses or physical incapacity prevents access to water.
The reasons for the thirst deficit are not clear. The elderly have a reduced capacity to excrete a water load, which means they are predisposed to water overload and hyponatremia.
Scientists have been studying the neurological mechanisms of thirst for decades. The hypothalamus also receives inputs from sensors in the blood vessels that monitor blood volume and pressure. When blood volume or pressure falls too low—from bleeding, for example, or from the excessive loss of fluid in sweat or diarrhea, or when blood sodium concentration rises too high from eating salty snacks, or as the result of certain diseases, the hypothalamus sends out a strong message: Drink something.
In rare cases, when an aneurysm or other brain injury has destroyed the sensors in the hypothalamus that regulate blood sodium concentration, people can lose their sense of thirst completely. They must be prescribed a fixed amount of fluids daily to keep their body safely hydrated. When the body gets low on water, the hypothalamus increases the synthesis of an antidiuretic hormone called vasopressin, which is secreted by the pituitary gland and travels to the kidneys.
There, it causes water to be reabsorbed from the urine, thus reducing urine flow and conserving water in the body until more fluids are consumed. If the pituitary gland becomes damaged, however, or if the kidneys are unable to respond to vasopressin, the body is unable to conserve fluids. The result can be diabetes insipidus, a condition marked by excessive urination and extreme, uncontrollable thirst. Diabetes insipidus should not to be confused with diabetes mellitus, which also causes excessive thirst and urination, but which results from an insulin deficiency or resistance that leads to high blood glucose.
Until scientists understood the structure of vasopressin and its role in diabetes insipidus, people with the condition had to drink up to 20 quarts of water daily to stay healthy.
Today, however, diabetes insipidus can be successfully treated with the synthetic drug demopressin, which mimics the action of vasopressin. Recently, scientists have discovered that vasopressin secretion increases and, thus, less body fluid is lost during periods of physical stress. For that reason, many medical experts are now recommending that healthy runners drink only when thirsty during marathons to avoid retaining excess water with potentially dire consequences.
Although much has been learned about the neural regulation of thirst, research continues. Scientists are exploring, for example, why such factors as swallowing and the emptying of fluids from the stomach appear to inhibit thirst even before the body becomes fully hydrated.
Studies into the thirst mechanism also are helping unravel some of the mechanisms by which the brain motivates sleep, appetite, and other basic human instincts. Clear evidence suggests that the perception of thirst occurs in higher-order centres, such as the anterior cingulate cortex ACC and insular cortex IC , which receive information from midline thalamic relay nuclei.
Thirst has long been thought of as a negative homeostatic feedback response to increases in blood solute concentration or decreases in blood volume.
However, emerging evidence suggests a clear role for thirst as a feedforward adaptive anticipatory response that precedes physiological challenges.
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