Normal human water intake spans a large range owing to the body’s ability to excrete large volumes of water in times of excess and conserve in times of scarcity. Recently, chronic intakes of either large volumes (HIGH) or small volumes (LOW) of water have been investigated. Adaptations within the renal regulation of water through the secretion and reabsorptive actions of the hormone arginine vasopressin and the thirst mechanism have been observed to differentiate these 2 groups during normal living. Increases or decreases in daily fluid intake in LOW and HIGH resulted in appropriate arginine vasopressin and perception of thirst changes, which enabled fluid balance in both of these populations. However, future research should establish if the chronic adaptive mechanisms, by which fluid is regulated have long-term negative outcomes.
Evan C. Johnson, MA, is a doctoral candidate at the Human Performance Laboratory, University of Connecticut. His research focuses on human fluid balance as well as the prescription and benefits of exercise.
Lawrence E. Armstrong, PhD, is a professor candidate at the Human Performance Laboratory, University of Connecticut, with joint appointments in Nutritional Sciences and in Physiology & Neurobiology. His research interests include human fluid-electrolyte balance and assessment of hydration status.
Dr Johnson has received reimbursement of travel expenses from Danone Research, Palaiseau, France.
Dr Armstrong serves as a member of the Scientific Advisory Board, has received grant funding and serves as a consultant to Danone Research, Palaiseau, France.
Correspondence: Evan C. Johnson, MA, Human Performance Laboratory, Department of Kinesiology, University of Connecticut, 2095 Hillside Rd, Box U-1110, Storrs, CT 06269-1110 ( firstname.lastname@example.org).
Water is an essential dietary nutrient. Although some water is endogenously produced through metabolic utilization of substrates, it must be consumed as part of the human diet to sustain life.1 In the modern world, the importance of water is commonly overlooked as a nutrient requiring recommendations.2 Claude Bernard postulated in the mid-19th century that we, as a species, are at an extreme advantage due to le milieu intérieur (the internal environment), which maintains normalcy around all vital organs despite external fluctuations.3 This attribute allows for the most complex form of life, referred to as la vie constante ou libre (constant life or freedom). It is surely true that this freedom has enabled our species to venture far from water, or to go relatively long periods of time without drinking. However, because of our complex and dynamic body water regulatory capacity it is difficult to identify either the optimal volume of water needed each day, or if beneficial or detrimental adaptations to chronic large or small daily water intake exist.4
Daily water intake varies greatly across and within populations because of physical activity level; environmental, cultural, and social factors; fluid accessibility; and risk of contamination.5 For example, the average intake in Hungary is 720 mL/d, whereas in Denmark, the average is 2621 mL/d,6 more than 3.5 times higher. Despite this range, given free access to fluids, daily total body water is regulated within most individuals.5 This remarkable regulation is explained by Walter Cannon’s expansion of Bernard’s milieu intérieur, with his theory of homeostasis.7 One of the 6 proposals of this theory is that “If the state remains steady there is an automatic arrangement whereby any tendency toward change is effectively met by increased action of the factor or factors which resist the change.”8,9 Therefore, although wide ranges of water intake exist, responses within the organs of the body, specifically the kidney, occur to ensure a constant internal environment. Serum osmolality is 1 such metric that exemplifies this theory, measured as a part of the Third National Health and Nutrition Examination survey.10
In women aged 19 to 50 years, water intake was found to range from 1400 to 5280 mL/d from the 5th to the 95th percentiles. However, within that same range, serum osmolality was constant at 277 mOsm/kg. Referring to Cannon’s theory above, if the state (osmolality) remains steady, a regulating mechanism must change. As fluid intake is altered, small changes in blood concentration are sensed by osmoreceptors in the brain, which in turn modulate the release of the hormone vasopressin.11 Higher plasma concentrations of vasopressin increase the translocation of aquaporin-2 water channels to the surface of cell membranes in the renal tubules, whereas lower concentrations result in the resequestration of these water channels.12 As a result, the “state” is stabilized by either an increase in water reabsorption from filtrate traveling through the kidney in times of low water intake or, conversely, an increase in urine production (ie, less reabsorption) decreases concentration in times of large daily water intake. For this reason, urinary indices such as osmolality, specific gravity, and color successfully predict hydration status4,13–15 in cases where serum osmolality is tightly regulated. Although urinary indices are not direct measures of total body water, they yield valuable information about the strength of the stimulus for water conservation within the body.
Another question important to body water maintenance involves regulation of fluid intake via the sensation of thirst. Sufficient intake for bodily functions and removal of waste is vital to human existence. In that sense, should not the drive to drink be consistent across individuals who exhibit similar fluid loss? However, regulation of body water involves more than just physiological drives for consumption of water.
Nonhomeostatic,16 discretionary water consumption can be attributed to factors other than regulation of fluid compartments. Therefore, all fluid intake is not regulated, rather fluid intake as a whole aids in the regulation of body water volume and composition.17 Consequently, it is fitting that our current water recommendations outlined by the Institute of Medicine are described as “adequate intakes”18 because, given the vast flexibility of renal water reabsorptive capabilities, 3700 mL/d for men and 2700 mL/d for women are enough to enable all cellular processes that require water and eliminate urinary wastes safely.15 It is important to state that these recommendations have been based upon “median intakes,” which enable the maintenance of serum osmolality. Although serum osmolality is sensitive to exercise-induced dehydration, these guidelines fail to take into account the potential negative consequences of long-term low or high fluid intake compensation.
Nevertheless, ranges of fluid intake still exist. Individuals have been identified as either chronic small volume or chronic large volume water consumers.4 It has been shown that the vasopressin-mediated changes in urinary excretion compensate acutely for increased or decreased fluid intake.11 However, when either high or low fluid consumption is chronic, little research suggests a consequence of, or rationale for, this behavior. New research from our laboratory sheds light on the interesting paradigm that describes the physiology of body water regulation and the wide variations of fluid intake within a population.
DIFFERENCE BETWEEN LARGE AND SMALL VOLUME DRINKERS
A human research study sought to outline the conundrum between different habitual water intake volumes and potential differences in the regulation body water. From a population of 120 women, with an average water intake of 2300 ± 760 mL/d (Johnson and Armstrong), 14 habitual low volume drinkers (LOW; total water intake, 1620 ± 480 mL/d) and 14 habitual high volume drinkers (HIGH; total water intake, 3340 ± 560 mL/d) were chosen to participate in 4 days of modified water intake. During the experiment, participants consumed their usual volume of water during 2 baseline days followed by 4 days where daily water intake was switched between groups by either additional (LOW) or reduced (HIGH) daily bottled water administration (Volvic; Danone, Paris, France). Over the 4 treatment days, LOW averaged 3500 ± 130 mL/d, while HIGH averaged 2000 ± 210 mL/d. Urinary markers of hydration status, plasma vasopressin, and perception of thirst19 were measured each morning and compared with those of the 2 baseline days.
Between baseline and modified water intake, urine volume changed by 1440 and −660 mL/d in LOW and HIGH, respectively. Although both groups showed reduced urine volume when consuming less water, the magnitude of the response by LOW was more than 2 times greater than that of HIGH, for a similar change in total daily water intake. In addition, LOW sharply decreased urine osmolality by 492 mOsm/kg, whereas HIGH increased by only 201 mOsm/kg. When consuming a small volume of water daily, both groups had more concentrated urine but there was no difference between HIGH and LOW with regard to serum osmolalities. Plasma vasopressin was similar between groups when a smaller volume (LOW, 4.78 ± 1.05 pg/mL; HIGH, 3.91 ± 1.28 pg/mL) and larger volume (9.03 ± 2.58 and 8.47 ±3.19 pg/mL) of water was consumed.
Although vasopressin influences urine concentration,11 a significant relationship existed between vasopressin and urine osmolality only in LOW (manuscript currently under review). Therefore, in HIGH, the change from a large volume to a small volume of daily water intake resulted in an increased vasopressin concentration without the corresponding water reabsorption in the kidney. This may have occurred because chronic small or large volumes of daily water intake modulated the expression of the water channels responsible for water reabsorption. Vasopressin acutely stimulates translocation of water channels to the surface of renal nephron epithelial cells20 and chronically stimulates additional expression through the cyclic adenosine monophosphate signaling pathway.21
Hence, those who chronically consume small volumes of water on a daily basis (LOW) may have a greater capacity to concentrate urine than do those who chronically consume large volumes (HIGH) owing to the number of water channels available for translocation. Although neither aquaporin-2 translocation nor expression was directly measured as a part of this study, research supports this theoretical concept.
Finally, the perception of thirst was analyzed. Despite a difference in habitual fluid intake of 1580 mL/d, the mean rating of thirst was identical for LOW and HIGH. However, when the groups were compared at similar volumes of daily water intake, perception of thirst was blunted in LOW. Across days, it was apparent that regardless of water intake, HIGH experienced an elevated thirst when compared with LOW. Returning to Cooper’s statement that fluid intake is regulatory, it is logical that an increased need for fluid consumption in HIGH drives increased thirst.
WATER INTAKE SCHEMATIC
The Figure describes a paradigm that encompasses the findings from our comparison of large and small volume water consumers. For example, when discretionary water intake remains consistently low with no progressive dehydration, LOW displayed an increased ability to reabsorb water. We interpret this to be caused by adaptation in the renal nephron, evidenced by the small amount of concentrated urine that LOW produced while habitually consuming a small volume of water. As a consequence of increased reabsorption, a greater percentage of water was retained on a daily basis and a lower volume was required each day to maintain homeostasis. Thus, the reduced perception of thirst shown in LOW is compensation for the effects of a chronic small daily water volume and a potential cause for future behavioral fluid intake. Conversely, if an individual chronically increases discretionary fluid intake because of cultural influences or a perceived health benefit, the opposite cascade could take place.
Two mirror image cycles are shown in the Figure, which displays the differences between 2 separate groups that were studied. However, in a randomly sampled population, this figure can be interpreted as a continuum of adaptation. The midpoint (not shown) theoretically represents the volume of daily water consumption that neither stimulates nor suppresses renal water reabsorption. However, this point has yet to be defined because of the complexity of the known and unknown inputs to and effects of body water regulation.
Our research does not address the long-term health outcomes of consuming a low or high volume of water each day. However, the findings suggest that physiological adaptations occur that enable body water balance across a range of fluid intakes. In addition, these adaptations may include perceptual differences between large and small volume water consumers. We propose that persons previously assumed to have a lower “set-point” for thirst may in fact maintain total body water similar to individuals who chronically consume a larger volume. For both HIGH and LOW, the volume of water habitually consumed was appropriate to maintain a euhydrated state (ie, normal and similar serum osmolality) because each employed unique thirst perception and renal responsiveness to arginine vasopressin (AVP). However, given some of the known ill-effects related to the actions of AVP,22 the chronic high levels of AVP present in HIGH necessitate further research. Although fluid balance is maintained, the overall health cost has yet to be determined.
1. Jequier E, Constant F. Water as an essential nutrient: the physiological basis of hydration. Eur J Clin Nutr. 2010; 64: 115–123.
2. EFSA Panel on Dietetic Products, Nutrition, and Allergies. Scientific opinion on dietary reference values for water. EFSA J. 2010; 8: 1459.
3. Bernard C, ed. Leçons Sur Les Phénomènes De La Vie Communs Aux Animaux Et Auxvégétaux. Paris, France: Bailliere; 1878.
4. Perrier E, Vergne S, Klein A, et al. Hydration biomarkers in free-living adults with different levels of habitual fluid consumption. Br J Nutr. 2013: 109: (9) 1678–1687.
5. Sawka MN, Cheuvront SN, Carter R 3rd. Human water needs. Nutr Rev. 2005; 63: S30–39.
6. Vergne S. Methodological aspects of fluid intake records and surveys. Nutr Today. 2012; 47: S7.
7. Cannon WB. Organization for physiological homeostasis. Physiol Rev. 1929; 9: 399.
8. 8. Wolfe EL, Barger AC, Benison B. Walter B. Cannon. Science and Society.
Vol 2. Cambridge, MA: Boston Medical Library in the Francis A Countway Library of Medicine; 2000.
9. Cooper SJ. From Claude Bernard to Walter Cannon. Emergence of the concept of homeostasis. Appetite. 2008; 51: 419–427.
10. US Department of Health and Human Services, National Center for Health Statistics. Third National Health and Nutrition Examination Survey (NHANES III). 1988–1994
. Washington, DC: The National Academies Press; 2005.
11. Robertson GL, Athar S. The interaction of blood osmolality and blood volume in regulating plasma vasopressin in man. J Clin Endocrinol Metab. 1976; 42: 613–620.
12. Fenton RA, Moeller HB. Recent discoveries in vasopressin-regulated aquaporin-2 trafficking. Prog Brain Res. 2008; 170: 571–579.
13. Armstrong LE, Maresh CM, Castellani JW, et al. Urinary indices of hydration status. Int J Sport Nutr. 1994; 4: 265–279.
14. Armstrong LE. Assessing hydration status: the elusive gold standard. J Am Coll Nutr. 2007; 26: 575S–584S.
15. Tack I. Effects of water consumption on kidney function and excretion. Nutr Today. 2010; 45: S1.
16. Rolls BJ, Rolls ET. Thirst. New York, NY: Cambridge University Press; 1982.
17. Booth DA. Physiological regulation through learnt control of appetites by contingencies among signals from external and internal environments. Appetite. 2008; 51: 433–441.
18. Panel on Dietary Reference Intakes for Electrolytes and Water, Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate
. Washington, DC: The National Academies Press; 2005.
19. Engell DB, Maller O, Sawka MN, Francesconi RN, Drolet L, Young AJ. Thirst and fluid intake following graded hypohydration levels in humans. Physiol Behav. 1987; 40: 229–236.
20. Nielsen S, Chou CL, Marples D, Christensen EI, Kishore BK, Knepper MA. Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane. Proc Natl Acad Sci U S A. 1995; 92: 1013–1017.
21. Hozawa S, Holtzman EJ, Ausiello DA. cAMP motifs regulating transcription in the aquaporin 2 gene. Am J Physiol. 1996; 270: C1695–C1702.
22. Bankir L, Bouby N, Ritz E. Vasopressin: a novel target for the prevention and retardation of kidney disease? Nat Rev Nephrol. 2013; 9 (4): 223–239.