Professor Ron Maughan, Emeritus Professor of Sport and Exercise Nutrition, Loughborough University (UK)
Humans can, by conscious effort, over-ride many of the signals that drive the regulatory processes involved in water balance. Thirst tells us that we should drink, but we can choose not to do so. Likewise, we can drink when not at all thirsty, as when offered drinks in a social situation where it might cause offence to refuse. Occasionally, however, the regulatory processes may fail, leading to serious disturbances of water homeostasis. Overhydration may be chronic, in which case it is generally mild, or it may be acute, in which case it may be severe. Chronic mild overhydration is generally considered to be harmless, resulting only in frequent trips to the bathroom. There is emerging evidence, however, that this condition may not be entirely benign. Chronic hyponatraemia appears to increase the risk for both falls and fractures in the elderly. Hyponatraemia may contribute to falls and fractures by two mechanisms: (i) it produces mild cognitive impairment, which can result in unsteady gait and falls and (ii) it contributes directly to increased bone fragility by increasing bone resorption, which may be a way to mobilise sodium (Ayus et al, 2012). Moritz and Ayus (2010) reported that the risk of developing osteoporosis was almost three times higher in those who were mildly hyponatraemic than in those whose plasma sodium levels were within the normal range. This followed an earlier report that elderly patients with long bone fractures were more than twice as likely to be hyponatraemic as patients without fractures (Harminder et al, 2009).
Chronic mild overhydration occurs in some patients with mental illness (most commonly in schizophrenia) but mild forms, commonly referred to as “habit polydipsia” may occur in apparently healthy individuals. Acute severe overhydration results in potentially fatal disturbances of water and electrolyte balance. Osmotic forces balance water and solute concentrations between the intracellular and extracellular spaces. When the extracellular solute concentration falls, water is drawn into the intracellular space, causing the cells to swell. Brain swelling leads to a rise in intra-cranial pressure that can result in symptoms of headache, nausea confusion, drowsiness and also in personality and behavioural effects. Further increases in intracranial pressure can restrict blood flow, leading to central nervous system dysfunction (hyponatraemic encephalopathy) and ultimately to seizures, coma or death (Moritz and Ayus, 2003).
The potential for adverse effects of overhydration has long been recognised in various stressful environments. In a report published in the British Medical Journal in 1923, JS Haldane wrote that “Men working in hot mines . . . suffer greatly from a sensation of thirst. They are therefore induced to take large quantities of water – so large as to be in excess of the real requirements of the body. [This] is a form of water poisoning of the muscles brought about by a combination of great loss of chloride by sweating, excessive drinking of water, and temporary paralysis of renal excretion”. This prescient and perceptive report draws attention to the key factors that are commonly observed in the development of overhydration:
- A large intake of plain water in excess of the body’s actual requirement.
- An electrolyte deficit – in the example above, the loss is caused by high sweat losses.
- An inability of the kidneys to adequately compensate by increasing the rate of urine formation.
These different factors may contribute to varying degrees in different situations, but it is clear that overhydration is unlikely to occur without ingestion of a large volume of water or another beverage in a short period of time. Loss of electrolytes, particularly sodium losses in sweat, may not be a major factor, but will result in a reduction in plasma volume and this may in turn, increase secretion of anti-diuretic hormone (ADH) and thus reduce water excretion by the kidneys. ADH secretion is not normally initiated until the plasma osmolality has been substantially elevated, but in the Syndrome of Inappropriate ADH Secretion (SIADH), high levels of ADH may cause what Haldane referred to as a “temporary paralysis of renal excretion” (Verbalis et al, 2007). The kidneys normally secrete about 1-1.2 ml of urine per minute under basal conditions (to give a total daily output of about 1200-1500 ml), but this can rise to over 20 ml/min when large volumes of fluid are ingested. Some young men routinely ingest 5-10 litres of beer over the course of a few hours without any apparent ill effects (other than temporary intoxication caused by the alcohol).
A small number of cases of fatalities occurring as a result of overhydration are reported each year. Many of these involved assorted competitions or challenges, such as the student fraternity initiation rites (Wikipedia, 2013). In recent years, a few deaths have also been reported in participants in marathon events and other long duration sports events. These appear to be the consequence of an intake of water or other hypotonic drinks far in excess of the sweat losses incurred (Rosner and Kirven, 2007), but these few cases should not divert attention from the fact that the overwhelming majority of participants incur a fluid deficit in the same situation.
*Ayus JC, Negri AL, Kalantar-Zadeh K, Moritz ML (2012) Is chronic hyponatraemia a novel risk factor for hip fracture in the elderly? Nephrology Dialysis Transplantation 27(10), 3725-3731. DOI: 10.1093/ndt/gfs412.
*Boron WF (2005). Medical Physiology: A Cellular and Molecular Approach. Elsevier/Saunders. P 829.
*Cheuvront SN, R Carter, Montain SJ, et al (2004) Daily body mass variability and stability in active men undergoing exercise-heat stress. International Journal of Sport Nutrition and Exercise Metabolism 14(5), 532-540.
*Haldane JS (1923) Water poisoning. BMJ June 9, 986.
*Harminder S, S Sandhu et al (2009) hyponatraemia associated with large-bone fracture in elderly patients. Int Urol Nephrol 41, 733-737.
*Harris JB, RC LaRocque, F Qadri et al (2012) Cholera. Lancet 379(9835), 2466-2476.
*Maughan RJ, SM Shirreffs (2010) Dehydration and rehydration in competitive sport. Scand J Med Sci Sports 20 (Suppl 3), 40-47.
*Moritz ML, JC Ayus (2003) The pathophysiology and treatment of hyponatraemic encephalopathy: An update. Nephrology Dialysis Transplantation 18 (12): 2486-2491. doi:10.1093/ndt/gfg394.
*Moritz ML, JC Ayus (2010) Bone disease as a new complication of hyponatraemia: moving beyond brain injury. Clinical Journal of the American Society of Nephrology 5, 167-168.
*Rosner MH, J Kirven (2007) Exercise-Associated hyponatraemia. Clinical Journal of the American Society of Nephrology 2, 151-161.
*Verbalis JG, SR Goldsmith, A Greenberg, RW Schrier, RH Sterns (2007) hyponatraemia treatment guidelines 2007: expert panel recommendations. American Journal of Medicine 120(11 Suppl 1), S1–21. doi:10.1016/j.amjmed.2007.09.001.
*Wikipedia (2013) Water intoxication. http://en.wikipedia.org/wiki/Water_intoxication. Accessed 17 Sept 2013.