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The symptom of thirst is familiar to everyone. Thirst is thought to be part of a corrective mechanism which acts as a support to the physiological control of fluid balance in the body. Thirst can also be a prominent symptom in diseases which disrupt fluid balance in the body. It is worth considering the physiology of thirst to understand how different diseases may produce thirst as a symptom and disrupt fluid balance.

  • An important factor in the maintenance of fluid balance is the secretion of antidiuretic hormone (ADH). ADH, also known as vasopressin:
    • Is secreted by the hypothalamus when plasma osmolality increases.
    • Acts mainly on the distal renal tubule, where ADH binds to receptor sites and stimulates the reabsorption of water.[1]
  • The physiological driving force behind the desire to drink liquid is thus the maintenance of blood osmolality.
  • In Western societies this primary mechanism is supplemented by secondary factors such as social convention and the habit of drinking with meals (secondary drinking), which in fact results in most people being in a state of mild water excess.[2]This is compensated for, under normal circumstances, by renal excretion.
  • Sensory osmoreceptors in the lamina terminalis and other areas of the brain stimulate cortical effector regions, principally in the anterior cingulate cortex and insula, to trigger the sensation of thirst in response to a rise in blood osmolality.[3] This sensation usually starts at 280 mOsmol/kg. The intensity of thirst and the amount of water required to quench it are directly proportional to blood osmolality. Other areas of the brain integrate these signals and provide inhibitory responses when thirst is quenched, to prevent fluid overload.[4]
  • Circulating angiotensin II is known to play a role. It is known that the area of the hypothalamus which releases angiotensin II is anatomically close to, and linked neuronally with, the area that releases ADH, so there is clearly a close connection between the two systems.[5]Animal experiments suggest that angiotensin II binds to the angiotensin type 1 receptor, stimulating thirst, sodium appetite and both arginine vasopressin (AVP) and oxytocin (OT) secretion.[6]
  • The gastric hormone ghrelin is thought to play an inhibitory role, helping to prevent the over-consumption of fluid.[7]
  • The mode of consumption appears relevant. One study found that drinking water quenched thirst more rapidly than when the same amount of water was mixed with food (eg, in soup).[8]
  • Acute falls in blood pressure and/or blood volume will also stimulate thirst. 15% or more reduction in circulating blood volume is required for this effect. However, the effects are short-lived and the effect of osmolality changes on thirst is more significant.[9]
  • With increasing age the thirst stimulus becomes blunted (hypodipsia) with a reduction in primary drinking. This is usually compensated for by secondary drinking.[10]However, it may be a contributory factor in causing not just dehydration but also stroke.[11] One study found that elderly patients with heart failure experienced an increase in thirst with such frequency that it could be considered a presenting feature of the condition.[12]
  • In pregnancy, the thirst stimulus is thought to be set at a lower osmolality, which leads to increased intake of water and an increase in circulating blood volume. Vasopressin and human chorionic gonadotrophin are both thought to play a role in these processes.[13]
  • Research has been done in relation to exercise and sport. For example, fluid loading in cyclists can have beneficial effects, whereas one study observed no effect on the running time of athletes completing an 80- to 90-minute run.[14]
  • Excessive thirst, also known as polydipsia, has a number of causes (see Differential diagnosis, below).

Note that within the categories above there are some specific conditions - for example, the nephrogenic syndrome of inappropriate antidiuresis (NSIAD).[15]

Renal function tests and glucose levels should be assessed to rule out chronic kidney disease and diabetes mellitus.

Investigations to exclude diabetes insipidus should be carried out. See separate article Diabetes Insipidus for further details.

Interpretation of results

  • In normal individuals, the urine osmolality is 2-4 times greater than the plasma osmolality. Administration of vasopressin results only in a small increase in urine osmolality (less than 9%). It takes between 4-18 hours to achieve maximal concentration of urine.
  • In central diabetes insipidus (due to decreased production of ADH), there is an excessive increase in plasma osmolality but not in urine osmolality. Administration of vasopressin results in an increase in urine osmolality of 50% or more. ADH levels are minimal.
  • In nephrogenic diabetes insipidus (due to resistance of renal tissue to the action of ADH), ADH levels are normal to elevated and the kidney fails to respond to exogenous ADH during the water deprivation test.
  • In psychogenic polydipsia, water deprivation will show the same changes as normal individuals, although occasionally urine osmolality will increase moderately. There is no response to exogenous ADH. Such patients may have considerable mental health problems and may not be prepared to tolerate prolonged periods of water restriction.

The management of polydipsia depends on the underlying cause. Psychogenic polydipsia is often a difficult condition to treat. In severe cases the phenomenon is often part of a wider psychotic illness. Treatment options include behavioural therapy, beta-blockers, antipsychotics such as risperidone and angiotensin-II receptor antagonists, such as irbesartan.[16]

A distinction has to be drawn between organic and psychogenic polydipsia. In the former, once the underlying condition is treated, complications from the polydipsia per se are few. This is because homeostasis tends to be preserved. In psychogenic polydipsia, however, water continues to be drunk in excess irrespective of the osmotic status of plasma and urine. This can result in water intoxication with subsequent cardiac failure, pathological fractures and urinary tract abnormalities.[17]

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Original Author:
Dr Laurence Knott
Current Version:
Dr Laurence Knott
Peer Reviewer:
Dr Helen Huins
Document ID:
1598 (v25)
Last Checked:
10 June 2016
Next Review:
09 June 2021

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. Patient Platform Limited has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.