Sage Journals: Discover world-class research

Abstract

Few previous review articles have focused on the associations between inadequate daily water intake (LOW) or urinary biomarkers of dehydration (_UD; low urine volume or high urine osmolality) and multiple diseases. Accordingly, we conducted manual online searches (47 key words) of the PubMed, Embase, and Google Scholar databases with these inclusion criteria: English language, full-text, peer reviewed, no restriction on research design, and three publications minimum. Initially, 3,903 articles were identified based on their titles and abstracts. Evaluations of full length .pdf versions identified 96 studies that were acceptable for inclusion. We concluded that the evidence is insufficient or conflicting for seven disorders or diseases (i.e. suggesting the need for additional clarifying research) and it is lacking for all-cause mortality. Differential characterizations among women and men have been reported in the results of nine studies involving five diseases. Finally, the evidence for associations of LOW or _UD is strong for both kidney stones and type 2 diabetes with hyperglycemia. This suggests that great public health value (i.e. reduced disease risk) may result from increased daily water intake—a simple and cost-effective dietary modification.

Keywords

Low water intake disease risk urinary biomarkers kidney stones type 2 diabetes mortality hyperglycemia

Introduction

Water is essential for metabolism, digestion, circulation of essential cellular substrates, movement of substances across cell membranes, regulation of intracellular–extracellular concentration, and it accounts for 55–75% of body weight depending on body composition and age. Although these physiological and biophysical processes rely on the volume of water consumed each day to maintain whole body fluid-electrolyte balance, relatively little is known about the long-term health consequences of chronic mild underhydration (Armstrong, 2012; Armstrong et al., 2020; Kavouras, 2019; Negoianu and Goldfarb, 2008) and few previous review articles have focused on the associations of inadequate daily water intake or urinary biomarkers of dehydration with multiple diseases and disease mortality.

Recognizing the importance of daily water intake to a healthy lifestyle, the United States National Academy of Medicine (NAM) (Institute of Medicine USA, 2004), the European Food Safety Authority (EFSA) (Agostoni et al., 2010), and the Australian National Health and Medical Research Council (ARC) (Australian National Health and Medical Research Council, 2006) published daily water consumption Adequate Intake (AI) values for men (3.7, 2.5, and 3.4 L·d⁻¹, respectively) and women (2.7, 2.0, and 2.8 L·d⁻¹). These AI guidelines were created with the understanding that physiological requirements for water vary widely according to environmental conditions, physical activity, individual differences of metabolism, and sensitivity to the detrimental effects of water intake deficiency (Agostoni et al., 2010; Australian National Health and Medical Research Council, 2006; Institute of Medicine USA, 2004). The respective methods of deriving AI values employed by NAM, EFSA, and ARC are different among these organizations. However, they all sought a daily water intake that was expected to maintain good health for both sexes and representative age groups (i.e. men, women, children, adolescents, and older adults). Two fundamental assumptions supported these AI values: water and adequate hydration are essential for health, and insufficient daily water intake may lead to medical disorders or diseases (Agostoni et al., 2010; Australian National Health and Medical Research Council, 2006; Institute of Medicine USA, 2004). Lending support to these assumptions, Allen et al. (2019) subsequently analyzed data from the Atherosclerosis Risk in Communities study (ARIC investigators, 1989) and determined that human hydration status predicted the development of multiple age-related degenerative diseases and that even subclinical mild hypohydration may affect long-term health outcomes.

No international consensus exists regarding the precise definition of dehydration and no single biomarker allows a convincing clinical diagnosis of dehydration (Armstrong, 2007; Armstrong et al., 2013, 2016; Kavouras, 2019; Lacey et al., 2019; Perrier et al., 2013a, 2013b; Shirreffs, 2000). This is true in part because total body water and extracellular concentration fluctuate continuously throughout life in a circadian pattern (Perrier et al., 2013a) and because water-electrolyte losses vary across individuals, medical conditions, physical activity levels, and environments (Armstrong et al., 2020). In the present review, we represent dehydration in the form of four measured variables, as designated in previously published studies (Armstrong, 2007; Armstrong et al., 1994; Perrier et al., 2013a, 2013b): low daily water intake, low daily fluid intake (i.e. water + beverages + food moisture), plus the human biomarkers low urine volume and high urine osmolality.

Accordingly, the present review evaluates research articles that have reported associations of (or lack thereof) low daily water and fluid intake (LOW) or urinary biomarkers of dehydration (_UD; low urine volume and high urine osmolality) (Johnson et al., 2015, 2016; Kavouras, 2019; Perrier et al., 2013a, 2013b; Stookey et al., 2020) with an increased disease risk, incidence, recurrence, or mortality. This is important because 25–35% of adults in the United States and Europe habitually consume considerably less than the AI for water recommended by EFSA and NAM (Armstrong et al., 2020; Johnson et al., 2015; Perrier et al., 2013b). The present review also identifies relevant gaps in the literature, diseases that warrant future research, and novel research questions. In terms of public health benefits, clarifying the associations (or lack thereof) between LOW, _UD, diseases, and mortality is essential for developing suitable consumer dietary guidelines that effectively reduce the risk and incidence of multiple diseases.

Search methods

Our review began with the discovery and consideration of potential medical disorders or disease types (i.e. that may be influenced by hydration status) and key search terms that involved a preliminary review of government reports (Agostoni et al., 2010; Australian National Health and Medical Research Council, 2006; Institute of Medicine USA, 2004), relevant narrative reviews, systematic reviews, meta analyses, interventional research, and observational studies (Allen et al., 2019; Armstrong, 2012; Dmitrieva et al., 2023; Enhörning et al., 2019a; Kolasa et al., 2009; Lacey et al., 2019; Manz, 2007; Manz and Wentz, 2005; Perrier et al., 2021; Popkin et al., 2010). Manual searches for relevant articles were performed within the PubMed, Embase, and Google Scholar electronic databases using advanced search operators (e.g. and, or, quotation marks, pertinent phrases). Inclusion criteria for searches included English language, full-text, and peer-reviewed articles with no restriction on research design types or year of publication. Combinations of the following keywords during these searches emphasized the associations of medical disorders and diseases (i.e. including risk, incidence, recurrence, and mortality) with LOW (i.e. low daily water intake and low daily fluid intake) and _UD (i.e. low urine volume and high urine osmolality). The following keywords focused on hydration state: “water consumption”, “water intake”, “low water intake”, “total water intake”, “water turnover”, “fluid restriction”, “fluid deprivation”, “urine osmolality”, “urine volume”, “dehydration”, “intracellular dehydration”, “extracellular hypovolemia”, and “osmolality”. The following keywords focused on the type of disease or mortality: “disease”, “chronic disease”, “urinary tract infection”, “uti”, “chronic kidney disease”, “autosomal dominant polycystic kidney disease”, “bladder cancer”, “urinary tract cancer”, “colorectal cancer”, “colon cancer”, “rectal cancer”, “breast cancer”, “diabetes mellitus”, “type 1 diabetes”, “insulin-dependent diabetes”, “type 2 diabetes”, “non-insulin-dependent diabetes”, “hyperglycemia”, “metabolic syndrome”, “calcium oxylate stones”, “renal stones”, “kidney stones”, “urolithiasis”, “chronic lung disease”, “hypertension”, “heart failure”, “cardiovascular disease”, “dementia”, “Alzheimer's Disease”, “depression”, “major depression”, “fatal coronary heart disease”, “stroke mortality”, and “all-cause mortality”. Although polycystic kidney disease is one form of chronic kidney disease, we separated these two diseases because the former arises from a genetic mutation whereas other forms of chronic kidney disease have no widely recognized genetic basis, and the research studies identified in the present manuscript specifically focus on one or the other disease.

Using these search terms within PubMed, Embase, and Google Scholar, 3,903 articles were initially identified based on the title and the abstract (i.e. expressing a focus on associations of LOW or _UD with human medical disorder or disease). After removing duplicate records, the abstracts and titles of the remaining records were evaluated to determine which studies should be assessed further. We subsequently performed manual searches of each relevant article's reference list, as well as the bibliographies found in germane systematic reviews and meta-analyses. Finally, we investigated full text (.pdf) versions of all remaining articles to ascertain if they each fit the purposes of this review. Neither a systematic literature review nor a systematic assessment of study quality or bias was performed for this review. Alternatively, a scoping literature review approach was employed to determine the scope and types of relevant research meeting our water intake, dehydration, and disease association criteria. This method was more suitable, as we did not intend to estimate the unbiased effects of rectifying dehydration or increasing daily water intake in the prevention and therapy of any medical disorder or disease.

Results

The manual screenings of full length .pdf versions identified the articles that were acceptable for inclusion in Table 1. These articles examined associations of LOW or _UD with the risk, incidence, recurrence, or mortality of 10 diseases. The general effects of “dehydration” (i.e. without measurements of LOW or _UD) are not included because no international consensus exists regarding the precise definition of dehydration (Armstrong, 2007; Armstrong et al., 2013, 2016; Kavouras, 2019; Lacey et al., 2019; Perrier et al., 2013a, 2013b; Shirreffs, 2000). Columns 2 and 3 in Table 1 characterize the types of research (i.e. prospective cohort study, retrospective cohort study, cross-sectional study at a single point in time, randomized controlled trial, counterbalanced experimental design with a control trial, systematic review, meta-analysis, narrative review, practice guidelines produced by a panel of experts that outlines current best practices, case–control study, or quasi-experimental study). Column 4 of Table 1 provides the references of nine studies that reported different associations for women and men. Eleven articles in Table 1 described associations of LOW or _UD with multiple diseases and thus are referenced more than once. Similarly, because six of the studies in Table 1 completed a systematic review and a meta-analysis (Cheungpasitporn et al., 2016; Fink et al., 2009; Janbozorgi et al., 2021; Lin et al., 2019; Majdi et al., 2021; Xu et al., 2015), they are cited in both research classifications.

Table 1.

Findings of research studies that evaluated the associations of low water or fluid intake (LOW), urinary biomarkers of dehydration (_UD), and human disorder or disease risk, incidence, recurrence, or mortality.^a,b

Medical condition or disease mortality	Associations were identified	No associations were identified	Studies reporting different associations for men and women	Assessment of the evidence^c (ratio of studies showing an association to those showing no association)
Kidney stones	CoP (Curhan et al., 1993, 1998, 2004; Daudon et al., 2005; Strauss et al., 1982) CoR (Curhan and Taylor, 2008) RCT (Borghi et al., 1996) CS (Wang et al., 2022) SysR (Cheungpasitporn et al., 2016; Fink et al., 2009, 2013; Lin et al., 2019; Prasetyo et al., 2013; Qaseem et al., 2014; Xu et al., 2015) Meta (Cheungpasitporn et al., 2016; Fink et al., 2009; Lin et al., 2019; Xu et al., 2015) NarR (Borghi et al., 1999; Lotan et al., 2013; Manz and Wentz, 2005; Perrier et al., 2021; Siener and Hesse, 2003; Wang et al., 2013a) CC (Embon et al., 1990) Q-E (Frank and De Vries, 1966; Frank et al., 1959; Hosking et al., 1983)	CS (Scales et al., 2012) SysR (Bao et al., 2020)	(Curhan and Taylor, 2008)	Strong evidence for an association (25:2)
Bladder/urinary tract cancer	CoP (Michaud et al., 1999; Zhou et al., 2014) CoR (Ahmad et al., 2012) CS (Braver et al., 1987) CC (Bruemmer et al., 1997; Hemelt et al., 2010; Jensen et al., 1986; Jiang et al., 2008; Radosavljevic et al., 2003; Villanueva et al., 2006; Wilkens et al., 1996) LtrEd (Bar-David et al., 2004)	CoP (Ros et al., 2011; Zeegers et al., 2001; Zhou et al., 2012) SysR (Brinkman and Zeegers, 2008; Zeegers et al., 2004) Meta (Bai et al., 2014) NarR (Altieri et al., 2003; Lotan et al., 2013; Manz and Wentz, 2005) CC (Bianchi et al., 2000; Di Maso et al., 2016; Dunham et al., 1968; Geoffroy-Perez and Cordier, 2001; Slattery et al., 1988; Wang et al., 2013b; Wynder et al., 1963)	(Brinkman and Zeegers, 2008; Hemelt et al., 2010; Jiang et al., 2008; Villanueva et al., 2006; Wilkens et al., 1996)	Conflicting evidence (12:16)
Chronic kidney disease	CoP (Clark et al., 2011; Plischke et al., 2014; Tabibzadeh et al., 2019; Wagner et al., 2022) CoR (Bankir et al., 2015) CS (Sontrop et al., 2013; Strippoli et al., 2011; Wang and Jiang, 2021) NarR (Clark et al., 2016; Wang et al., 2013a) LONG (Wu et al., 2016)	CoP (Lee et al., 2019) CoR (Hebert et al., 2003) RCT (Clark et al., 2018) NarR (Lotan et al., 2013)		Conflicting evidence (11:4)
Autosomal dominant polycystic kidney disease	NarR (Wang et al., 2013a) PG (Torres, 2009)	RCT (Rangan et al., 2022) Q-E (Higashihara et al., 2014)		Insufficient evidence to determine an association (2:2)
Type 2 diabetes, hyperglycemia	CS (Carroll et al., 2015, 2016) CBC (Johnson et al., 2017; Seal et al., 2022) SysR (Janbozorgi et al., 2021; Naumann et al., 2017) Meta (Janbozorgi et al., 2021) LONG (Roussel et al., 2011) RCT (Enhörning et al., 2019b)	CoP (Carroll et al., 2024; Pan et al., 2012) CS (Jang et al., 2016)	(Carroll et al., 2016)	Strong evidence for an association (8:3)
Colorectal cancer	CC (Bitterman et al., 1991; Lubin et al., 1997; Shannon et al., 1996; Slattery et al., 1999; Tang et al., 1999; Wilkens et al., 1996) LtrEd (Bar-David et al., 2004)	NarR (Altieri et al., 2003; Manz and Wentz, 2005) CC (Simons et al., 2010)	(Shannon et al., 1996)	Conflicting evidence (7:3)
Urinary tract Infection	CS (Nygaard and Linder, 1997) RCT (Hooton et al., 2018) NarR (Perrier et al., 2021)	NarR (Beetz, 2003; Lotan et al., 2013; Manz and Wentz, 2005)		Insufficient evidence to determine an association (3:3)
Stroke mortality	CoP (Cui et al., 2018)	CoP (Leurs et al., 2010; Loomba et al., 2016)		Insufficient evidence to determine an association (1:2)
Fatal coronary heart disease	CoP (Chan et al., 2002; Cui et al., 2018) SysR (Majdi et al., 2021) Meta (Majdi et al., 2021)	CoP (Leurs et al., 2010; Lim et al., 2017; Loomba et al., 2016) LONG (Wu et al., 2016)	(Cui et al., 2018)	Insufficient evidence to determine an association (3:4)
All-cause mortality	LONG (Wu et al., 2016)	CoP (Kant and Graubard, 2017; Lim et al., 2017; Loomba et al., 2016) SysR (Majdi et al., 2021) Meta (Majdi et al., 2021)		Evidence suggests lack of an association (1:4)

Eighty-nine percent of these 96 studies evaluated only 1 disease.

LOW was measured in these studies as low plain water intake or low total fluid intake (water + beverages + food moisture).

_UD was measured in these studies as low urine volume, high urine osmolality, or both.

Assessment criteria are described in the Results section.

Research designs (columns 2 and 3): CBC, counterbalanced experimental design with a control trial; CC, case–control study; CoP, prospective cohort study; CoR, retrospective cohort study; CS, cross-sectional at a single point in time; LONG, longitudinal study; NarR, narrative review; PG, practice guidelines produced by a panel of experts that outlines current best practices; Q-E, quasi-experimental study; RCT, randomized controlled trial; SysR, systematic review; Meta, meta-analysis of a systematic review.

Column 5 of Table 1 presents the numerical ratio of studies showing an association to those indicating no association. This column also notes our assessments of the evidence for each medical condition, using the following four classifications: strong evidence for an association, conflicting evidence, insufficient evidence to determine an association, and evidence suggests lack of an association. These classifications (column 5) represent the unanimous consensus of all authors and are based on consideration of three criteria: (a) the ratio of studies showing an association (column 2) to those showing no association (column 3); (b) the total number of studies for each medical condition (columns 2 and 3); and (c) the strength of research designs, with randomized clinical trials, systematic reviews, and meta-analyses providing the strongest evidence (Bigby, 2014; Brighton et al., 2003; Cooper, 2016; Hooper et al., 2015; Lichtenstein et al., 2021; Song and Chung, 2010; Spill et al., 2022).

A minimum of three relevant publications were required for inclusion of any disease in Table 1. Our searches in the PubMed, Embase, and Google Scholar databases disclosed that 11 medical disorders and diseases did not reach this minimum inclusion criterion. Shown in parentheses is the number of articles found for each: breast cancer (0), type 1 diabetes (0), metabolic syndrome (0), dementia (1), Alzheimer's disease (0), depression (0), chronic lung disease (0), coronary artery disease (1), heart failure (0), mitral valve prolapse (0), and hypertension (0). In addition, two articles were initially considered for inclusion in Table 1 but were excluded (Palmer et al., 2014; Strippoli et al., 2011) because both employed a 145-item food frequency questionnaire which surveyed beverages (e.g. tea, coffee, milk, juices, sweetened drinks, and alcohol) but did not include a specific question about water consumption.

Discussion

This review highlights research studies in the extant literature that have reported associations of LOW (i.e. low water or fluid intake) or _UD (i.e. urine volume or urine osmolality) with an increased risk, incidence, recurrence, or mortality of multiple diseases. Our scoping search of the literature indicated that 89% of the 96 identified studies examined only one disease. In contrast, Table 1 uniquely describes the strength of evidence for 10 disorders or diseases that were identified during extensive searches in three electronic databases that are highly utilized in medical and health fields. The clarification of the associations (or lack thereof) of LOW or _UD with medical conditions and disease mortality is (a) valuable for the development of practical consumer dietary guidelines (notably including daily water intake) that effectively reduce the risk, incidence, and recurrence of disorders or diseases and (b) provides informed guidance for future research investigations. For example, the Table 1 evidence for kidney stones and for type 2 diabetes/hyperglycemia (T2D/H) is strong (column 5), based on the three criteria described above in the Results section. Using the same assessment criteria, the evidence regarding all-cause mortality suggests a lack of association with LOW or _UD.

We recommend additional future investigations of the three diseases for which the evidence is conflicting (i.e. bladder/urinary tract cancer, chronic kidney disease, and colorectal cancer) and for four medical conditions for which evidence is insufficient to determine an association (i.e. urinary tract infection, autosomal dominant polycystic kidney disease, stroke mortality, and fatal coronary heart disease). All of these limited findings suggest that corresponding research is warranted. Similarly, 11 medical conditions (see Results section above) did not reach the minimum inclusion criterion for Table 1 (i.e. ≥ 3 publications), hence these diseases are worthy of future research.

Kidney stones

Strong evidence of association is presented in Table 1 (column 5) for kidney stones. It is noteworthy that kidney stones deposit at multiple anatomical sites (i.e. renal pelvis, ureters, bladder, and urethra) and have varied mineralogical compositions; calcium oxylate (CaOx) and calcium phosphate (CaP) are the most common. Regardless of composition, kidney stone formation is a complex and multistep phenomenon that includes urinary supersaturation, crystal nucleation, growth, and aggregation (Aggarwal et al., 2013; Hamamoto et al., 2011). Recent theories suggest that the following factors influence kidney stone formation: sex hormones, intestinal and renal microbiomes, and the immune response to urinary crystals (Wang et al., 2021). In addition, laboratory models have demonstrated that artificial stone formation and size are influenced by the supersaturation and pH of a solution as well as energy input which affects seed particle movements (Werner et al., 2021). Because supersaturation and crystal formation are the indispensable first steps in every type of urinary stone disease, enhancing urine dilution is the primary goal of investigators (Borghi et al., 1999; Daudon et al., 2005; Eccles et al., 1998; Finkielstein and Goldfarb, 2006; Pak et al., 1980) who accordingly recommend consuming ≥ 2 L of water per day to prevent kidney stones from recurring. This volume of water increases the minimum supersaturation required to elicit spontaneous crystallization of calcium salts (Pak et al., 1980; Siener and Hesse, 2003). Also, the American Urological Association (Pearle et al., 2014), American College of Physicians (Qaseem et al., 2014), European Association of Urologists (Skolarikos et al., 2023), and a consensus conference sponsored by the National Institute of Diabetes and Digestive & Kidney Diseases (Consensus Conference, 1988) recommend sufficient water intake to achieve a urine volume of 2.0–2.5 L·d⁻¹. Combining this range with the fact that 24h urine volume is 0.8–1.4 L less than 24h total water intake (Cheungpasitporn et al., 2016; Johnson et al., 2015; Xu et al., 2013), the amount of total water/fluid intake needed per day for stone prevention is approximately 2.8–3.9 L·24⁻¹ h, depending on daily activities, fluid losses, environmental heat stress, and body size. Whereas multiple strong recommendations support routine sufficient daily water intake to prevent the formation/reformation of kidney stones (Consensus Conference, 1988; Pak et al., 1980; Pearle et al., 2014; Qaseem et al., 2014; Siener and Hesse, 2003; Skolarikos et al., 2023), the recommended water intake to meet the urine volume threshold appears to be inadequate (Cheungpasitporn et al., 2016; Johnson et al., 2015; Xu et al., 2013).

Type 2 diabetes/hyperglycemia

Regarding the strong evidence for T2D/H, it is important to note that Table 1 does not include studies that assessed the effects of replacing caloric or noncaloric beverages with plain water. This is not surprising, as such effects typically are studied regarding obesity or weight loss during long-term studies (Daniels and Popkin, 2010; Naumann et al., 2017; Tate et al., 2012). Thus, row 5 of Table 1 presents only research that evaluated the associations of LOW or _UD with T2D/H. However, although the process by which LOW or _UD may affect glucose metabolism is not known (Carroll et al., 2015; Jansen et al., 2019), four theoretical mechanisms have been proposed. For example, LOW stimulates the secretion of arginine vasopressin (AVP) (Johnson et al., 2015, 2016; Perrier et al., 2013b) which is a vasoconstrictor and antidiuretic hormone. Because increased circulating AVP results in hyperglycemia, induces gluconeogenesis, and increases plasma glucagon concentration in humans and animals, LOW theoretically in turn increases T2D/H risk (Roussel et al., 2011; Spruce et al., 1985). Supporting this theory, blood AVP concentration is known to be elevated in T2D patients (Roussel et al., 2011; Zerbe et al., 1979). Similarly, the renin-angiotensin-aldosterone system can be activated by LOW or measurable body water loss, resulting in a rise of blood aldosterone concentration (Johnson et al., 2016). Elevated aldosterone has been shown to interrupt normal insulin signaling, consequently slowing the removal of glucose from the bloodstream (Verbalis, 2006). Also, LOW or chronic appreciable loss of body water may disrupt cell metabolism (Haussinger et al., 1994) in a way that leads to insulin resistance (Carroll et al., 2015; Tsai et al., 2005; Uribarri et al., 2007). Further, high glycemic load diets have been associated with an increased risk of T2D (Malik et al., 2010). Because water has no calories, its consumption with meals may reduce the glycemic load of food, dampen the postprandial glycemic response, and lead to reduced risk of T2D (Carroll et al., 2015). Finally, since only 10 research studies in Table 1 associated T2D/H with LOW and or _UD, it is possible that a suitable mechanism has not yet been proposed and that future theories may offer viable explanations (Carroll et al., 2015; Jansen et al., 2019).

Future research

From the studies presented in Table 1, eight concepts are revealed that are relevant for the design of future research studies. First, among the 96 unique publications cited in Table 1, randomized controlled trials (n = 5), systematic reviews (n = 13), and meta-analyses (n = 7) are in the minority whereas prospective cohort studies (n = 24) represent the most common research design. Future investigations should critically consider experimental designs. Second, both kidney stones (n = 27) and bladder/urinary tract (n = 28) cancer are represented in Table 1 by nearly twice as many studies as any other medical conditions. This suggests that the remaining eight disorders and diseases in Table 1 are understudied and that water intake may not be widely recognized as a possible etiological factor in these conditions. Third, multiple authors designated their research as “longitudinal” but did not classify their research as prospective or retrospective. We recommend that this distinction be clearly stated in the Methods section of each article. Fourth, the literature regarding chronic kidney disease suggests that daily water intake recommendations may be different with regard to prevention than to the progression of existing disease (Tabibzadeh et al., 2019). For example, studies have reported that the risk of chronic kidney disease and the annual decline of kidney function were positively associated with higher urine osmolality (Plischke et al., 2014) but were inversely correlated with lower urine volume (Clark et al., 2011). This suggested that a higher daily water intake would be kidney protective (Tabibzadeh et al., 2019). However, when chronic kidney disease exists, its progression appears to be faster among individuals who sustain a high urine volume and low urine osmolality (Hebert et al., 2003; Higashihara et al., 2014). Importantly, these observational studies should not be construed as an endorsement of water restriction in patients with chronic renal insufficiency (i.e. where water restriction would result in elevated vasopressin levels), but rather should promote the conduct of randomized, long-term studies to reach more definitive conclusions (Hebert et al., 2003; Higashihara et al., 2014). Fifth, in prospective cohort studies, investigators screen patients and utilize statistics to control risk factors that may have influenced the onset and progression of a medical disorder or disease. However, some relevant factors may go unrecognized and uncontrolled. Bladder cancer is a case in point because the characteristics and incidence of this disease are different among racial/ethnic groups with equivalent healthcare (Porter et al., 2002; Wang et al., 2018). Moreover, bladder cancer susceptibility is greater among individuals who possess certain gene polymorphisms (Fontana et al., 2009; Hung et al., 2004; McGrath et al., 2006). Thus, the uncontrolled influences of racial or genetic factors may partly explain why the bladder cancer evidence in Table 1 is conflicting. Sixth, human exposure to surface water disinfection byproducts (DBP) is another influence on bladder cancer that is worthy of future study. DBP in public water systems are unintended consequences of chlorine disinfectants reacting with organic and inorganic compounds. More than 700 DBP are known (Ashbolt, 2004; Weisman et al., 2022; Zwiener et al., 2007) and DBP in public water supplies have been shown to increase bladder cancer risk (i.e. calculated odds ratio) in the United States (McGeehin et al., 1993; Vena et al., 1993; Weisman et al., 2022), Canada (King and Marrett, 1996), Finland (Koivusalo et al., 1998), and Europe (Nieuwenhuijsen et al., 2009; Vena et al., 1993). Seventh, animal research allows clarification of cellular processes that are challenging or unethical to explore in human subjects. The 2019 controlled laboratory investigation of Allen et al. (2019) is an excellent example. Mice were water restricted (WR) for their entire life starting at the age of 1 month, consumed only gelled food containing 30% water and 70% dry food, and received no additional water. During the first 12–14 months of life, despite an absence of obvious clinical symptoms, WR mice exhibited elevated urine osmolality and were in a state of low-grade inflammation and coagulation. This chronic inflammation (i.e. assessed by serum IL-6 level) was accelerated in the WR mice and their lifespan was shortened by about 6 months (18%), compared with control mice that had free access to water and consumed the same diet. This investigation (Allen et al., 2019) illustrates the value of animal research in identifying chronic disease-related effects of LOW and _UD across the lifespan. Our final recommendation for future research focuses on the important topic of differential characterizations for women and men. The underlying causes for the sex differences in Table 1 (column 4) are not yet fully understood, but the following theoretical factors have been proposed: age-related changes of kidney function, diet, and urine electrolyte levels for kidney stones (Curhan and Taylor, 2008); frequency of urination, hormonal effects on micturition (Jiang et al., 2008; Villanueva et al., 2006), and urine specific gravity (Braver et al., 1987) for bladder cancer; female–male hormonal differences unspecified (Carroll et al., 2016) for T2D/H; as well as the volume of water consumed each day, fruit and vegetable intake, and dairy product consumption for colon cancer (Shannon et al., 1996). Considering the variety of these theoretical explanations and the complex disorder and disease etiologies involved, unraveling the underlying causes of sex differences will require a considerable number of comprehensive and strategic investigations across multiple populations that are specific to each medical condition and related influencing factors.

Summary

In summary, the range of medical conditions incorporated in the present review, as well as the strict criteria utilized for inclusion, represent a robust clarification of the associations between LOW, _UD, disorders and diseases, and related mortality. Our findings regarding kidney stones, T2D/H, and all-cause mortality are unique in the medical and scientific literatures, largely because few previous studies have focused on LOW or _UD. The 11 medical disorders/diseases that did not meet our inclusion criteria and the 10 medical conditions described in Table 1 demonstrate that many medical conditions remain understudied. Accordingly, we have provided seven recommendations for future research. Finally, the experimental designs which are employed to study the associations between LOW, _UD, disorders and diseases, and mortality should prioritize randomized controlled trials, systematic reviews, and meta-analyses.

Footnotes

Authors’ contributions

Conceptualization, LEA; methodology, LEA, MFB; literature search, LEA; data interpretation, LEA, MFB, CXM, SAK; writing – original draft preparation, LEA, MFB, CXM; writing – reviewing and editing, LEA, MFB, CXM, SAK; approval of final manuscript, LEA, MFB, CXM, SAK.

Availability of data and materials

Table 1 provides the outcome (final screen) of the literature search (3 databases) for this review. No supplemental materials have been submitted.

Consent for publication

Not applicable.

Declaration of conflicting interests

The authors declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: LEA is a Board of Trustees member and occasional consultant for the Drinking Water Research Foundation, Alexandria, VA; MFB – no conflicts of interest; CXM – is an occasional consultant for and has an active research grant with Kraft Heinz Co.; SAK has active research grants during the past 36 months from the National Science Foundation, USDA, Kraft Heinz, Unilever, and Standard Process. During this time, he was a lead research aerospace physiologist at Luke Air Force Base, AZ and served as a member of the science advisory board for Hyduro Inc, Zico Rising, and Rockley Photonics. He has also provided scientific consultation to the American Beverage Association, Unilever, Pepsico, and Kraft Heinz Co.

Ethical approval

Not applicable.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

ORCID iDs

Lawrence E Armstrong

Michael F Bergeron

References

Aggarwal

Narula

Kakkar

, et al. (2013) Nephrolithiasis: molecular mechanism of renal stone formation and the critical role played by modulators. Biomed Research International 2013: 292953.

Agostoni

Bresson

Fairweather-Tait

, et al. (2010) Scientific opinion on dietary reference values for water. EFSA Journal 8(3): 42.

Ahmad

Pervaiz

(2012) Non-occupational risk factors of urinary bladder cancer in Faisalabad and Lahore, Pakistan. The Journal of the Pakistan Medical Association 62(3): 236–239.

Allen

Springer

Burg

, et al. (2019) Suboptimal hydration remodels metabolism, promotes degenerative diseases, and shortens life. JCI Insight 4(17): 1–17.

Altieri

La Vecchia

Negri

(2003) Fluid intake and risk of bladder and other cancers. European Journal of Clinical Nutrition 57: S59–68.

ARIC investigators (1989) The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. American Journal of Epidemiology 129(4): 687–702.

Armstrong

(2007) Assessing hydration status: the elusive gold standard. Joural of the American College of Nutrition 26(Suppl 5): 575S–584S.

Armstrong

(2012) Challenges of linking chronic dehydration and fluid consumption to health outcomes. Nutrition Reviews 70: S121–S127.

Armstrong

Kavouras

Walsh

, et al. (2016) Diagnosing dehydration? Blend evidence with clinical observations. Current Opinion in Clinical Nutrition and Metabolic Care 19(6): 434–438.

10.

Armstrong

Maresh

Castellani

, et al. (1994) Urinary indices of hydration status. International Journal of Sport Nutrition and Exercise Metabolism 4(3): 265–279.

11.

Armstrong

Maughan

Senay

, et al. (2013) Limitations to the use of plasma osmolality as a hydration biomarker. American Journal of Clinical Nutrition 98(2): 502–512.

12.

Armstrong

Munoz

Armstrong

(2020) Distinguishing low and high water consumers—a paradigm of disease risk. Nutrients 12(3): 858.

13.

Ashbolt

(2004) Risk analysis of drinking water microbial contamination versus disinfection by-products (DBPs). Toxicology 198(1–3): 255–262.

14.

Australian National Health and Medical Research Council (2006) Nutrient Reference Values for Australia and New Zealand: Including Recommended Dietary Intakes. Canberra, Australia: National Health and Medical Research Council.

15.

Bai

Yuan

, et al. (2014) Relationship between bladder cancer and total fluid intake: a meta-analysis of epidemiological evidence. World Journal of Surgical Oncology 12: 223.

16.

Bankir

Plischke

Bouby

, et al. (2015) Urine osmolarity and risk of dialysis initiation in a CKD cohort. Annals of Nutrition and Metabolism 66: 14–17.

17.

Bao

Wei

(2020) Water for preventing urinary stones. Cochrane Database of Systematic Reviews 2020(2): 1–26.

18.

Bar-David

Gesundheit

Urkin

, et al. (2004) Water intake and cancer prevention. Journal of Clinical Oncology 22(2): 383–385.

19.

Beetz

(2003) Mild dehydration: a risk factor of urinary tract infection? European Journal of Clinical Nutrition 57(Suppl 2): S52–S58.

20.

Bianchi

Cerhan

Parker

, et al. (2000) Tea consumption and risk of bladder and kidney cancers in a population-based case-control study. American Journal of Epidemiology 151(4): 377–383.

21.

Bigby

(2014) The hierarchy of evidence. In: Williams

Bigby

Herxheimer

, et al. (eds) Evidence-Based Dermatology. London: BMJ Publishing Group, pp.30–32.

22.

Bitterman

Farhadian

Abu Samra

, et al. (1991) Environmental and nutritional factors significantly associated with cancer of the urinary tract among different ethnic groups. Urology Clinics of North America 18(3): 501–508.

23.

Borghi

Meschi

Amato

, et al. (1996) Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study. Journal of Urology 155(3): 839–843.

24.

Borghi

Meschi

Schianchi

, et al. (1999) Urine volume: stone risk factor and preventive measure. Nephron 81(Suppl 1): 31–37.

25.

Braver

Modan

Chetrit

, et al. (1987) Drinking, micturition habits, and urine concentration as potential risk factors in urinary bladder cancer. Journal of the National Cancer Institute 78(3): 437–440.

26.

Brighton

Bhandari

Tornetta

, et al. (2003) Hierarchy of evidence: from case reports to randomized controlled trials. Clinical Orthopaedics and Related Research 413: 19–24.

27.

Brinkman

Zeegers

(2008) Nutrition, total fluid and bladder cancer. Scandinavian Journal of Urology and Nephrology 42(218): 25–36. DOI: https://doi.org/10.1080/03008880802285073.

28.

Bruemmer

White

Vaughan

, et al. (1997) Fluid intake and the incidence of bladder cancer among middle-aged men and women in a three-county area of western Washington. Nutrition and Cancer 29(2): 163–168.

29.

Carroll

Betts

Johnson

(2016) An investigation into the relationship between plain water intake and glycated Hb (HbA1c): a sex-stratified, cross-sectional analysis of the UK National Diet and Nutrition Survey (2008–2012). British Journal of Nutrition 116(10): 1770–1780.

30.

Carroll

Davis

Papadaki

(2015) Higher plain water intake is associated with lower type 2 diabetes risk: a cross-sectional study in humans. Nutrition Research 35(10): 865–872.

31.

Carroll

Ericson

Ottosson

, et al. (2024) The association between water intake and future cardiometabolic disease outcomes in the Malmo Diet and Cancer cardiovascular cohort. PLoS ONE 19(1): e0296778.

32.

Chan

Knutsen

Blix

, et al. (2002) Water, other fluids, and fatal coronary heart disease: the Adventist Health Study. American Journal of Epidemiology 155(9): 827–833.

33.

Cheungpasitporn

Rossetti

Friend

, et al. (2016) Treatment effect, adherence, and safety of high fluid intake for the prevention of incident and recurrent kidney stones: a systematic review and meta-analysis. Journal of Nephrology 29: 211–219.

34.

Clark

Sontrop

Huang

, et al. (2016) Hydration and chronic kidney disease progression: a critical review of the evidence. American Journal of Nephrology 43(4): 281–292.

35.

Clark

Sontrop

Huang

, et al. (2018) Effect of coaching to increase water intake on kidney function decline in adults with chronic kidney disease: the CKD WIT randomized clinical trial. JAMA 319(18): 1870–1879.

36.

Clark

Sontrop

Macnab

, et al. (2011) Urine volume and change in estimated GFR in a community-based cohort study. Clinical Journal of the American Society of Nephrology 6(11): 2634–2641.

37.

Consensus Conference (1988) Prevention and treatment of kidney stones. JAMA: The Journal of the American Medical Association 260(7): 977–981.

38.

Cooper

(2016) Evidence ladder and the Journal of the Medical Library Association. Journal of the Medical Library Association 104(4): 262.

39.

Cui

Iso

Eshak

, et al. (2018) Water intake from foods and beverages and risk of mortality from CVD: the Japan Collaborative Cohort (JACC) Study. Public Health Nutrition 21(16): 3011–3017.

40.

Curhan

Taylor

(2008) 24-h uric acid excretion and the risk of kidney stones. Kidney International 73(4): 489–496.

41.

Curhan

Willett

Knight

, et al. (2004) Dietary factors and the risk of incident kidney stones in younger women: Nurses’ Health Study II. Archives of Internal Medicine 164(8): 885–891.

42.

Curhan

Willett

Rimm

, et al. (1993) A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. New England Journal of Medicine 328(12): 833–838.

43.

Curhan

Willett

Speizer

, et al. (1998) Beverage use and risk for kidney stones in women. Annals of Internal Medicine 128(7): 534–540.

44.

Daniels

Popkin

(2010) Impact of water intake on energy intake and weight status: a systematic review. Nutrition Reviews 68(9): 505–521.

45.

Daudon

Hennequin

Boujelben

, et al. (2005) Serial crystalluria determination and the risk of recurrence in calcium stone formers. Kidney International 67(5): 1934–1943.

46.

Di Maso

Bosetti

Taborelli

, et al. (2016) Dietary water intake and bladder cancer risk: an Italian case–control study. Cancer Epidemiology 45: 151–156.

47.

Dmitrieva

Gagarin

Liu

, et al. (2023) Middle-age high normal serum sodium as a risk factor for accelerated biological aging, chronic diseases, and premature mortality. eBioMedicine 87: 104404.

48.

Dunham

Rabson

Stewart

, et al. (1968) Rates, interview, and pathology study of cancer of the urinary bladder in New Orleans, Louisiana. Journal of the National Cancer Institute 41(3): 683–709.

49.

Eccles

Freemantle

Mason

(1998) North of England evidence based guidelines development project: methods of developing guidelines for efficient drug use in primary care. British Medical Journal 316(7139): 1232–1235.

50.

Embon

Rose

Rosenbaum

(1990) Chronic dehydration stone disease. British Journal of Urology 66(4): 357–362.

51.

Enhörning

Christensson

Melander

(2019a) Plasma copeptin as a predictor of kidney disease. Nephrology Dialysis Transplantation 34(1): 74–82.

52.

Enhörning

Tasevska

Roussel

, et al. (2019b) Effects of hydration on plasma copeptin, glycemia and gluco-regulatory hormones: a water intervention in humans. European Journal of Nutrition 58(1): 315–324.

53.

Fink

Akornor

Garimella

, et al. (2009) Diet, fluid, or supplements for secondary prevention of nephrolithiasis: a systematic review and meta-analysis of randomized trials. European Urology 56(1): 72–80.

54.

Fink

Wilt

Eidman

, et al. (2013) Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Annals of Internal Medicine 158(7): 535–543.

55.

Finkielstein

Goldfarb

(2006) Strategies for preventing calcium oxalate stones. Canadian Medical Association Journal 174(10): 1407–1409.

56.

Fontana

Delort

Joumard

, et al. (2009) Genetic polymorphisms in CYP1A1, CYP1B1, COMT, GSTP1 and NAT2 genes and association with bladder cancer risk in a French cohort. Anticancer Research 29(5): 1631–1635.

57.

Frank

De Vries

(1966) Prevention of urolithiasis. Education to adequate fluid intake in a new town situated in the Judean Desert Mountains. Archives of Environmental Health 13(5): 625–630.

58.

Frank

De Vries

Atsmon

, et al. (1959) Epidemiological investigation of urolithiasis in Israel. The Journal of Urology 81(4): 497–505.

59.

Geoffroy-Perez

Cordier

(2001) Fluid consumption and the risk of bladder cancer: results of a multicenter case-control study. International Journal of Cancer 93(6): 880–887.

60.

Hamamoto

Taguchi

Fujii

(2011) [Molecular mechanism of renal stone formation] in Japanese. Clinical Calcium 21(10): 1481–1487.

61.

Haussinger

Lang

Gerok

(1994) Regulation of cell function by the cellular hydration state. American Journal of Physiology-Endocrinology and Metabolism 267(3): E343–E355.

62.

Hebert

Greene

Levey

, et al. (2003) High urine volume and low urine osmolality are risk factors for faster progression of renal disease. American Journal of Kidney Diseases 41(5): 962–971.

63.

Hemelt

Zhong

, et al. (2010) Fluid intake and the risk of bladder cancer: results from the South and East China case-control study on bladder cancer. International Journal of Cancer 127(3): 638–645.

64.

Higashihara

Nutahara

Tanbo

, et al. (2014) Does increased water intake prevent disease progression in autosomal dominant polycystic kidney disease? Nephrology Dialysis Transplantation 29(9): 1710–1719.

65.

Hooper

Abdelhamid

Attreed

, et al. (2015) Clinical symptoms, signs and tests for identification of impending and current water-loss dehydration in older people. Cochrane Database of Systematic Reviews 4: CD009647.

66.

Hooton

Vecchio

Iroz

, et al. (2018) Effect of increased daily water intake in premenopausal women with recurrent urinary tract infections: a randomized clinical trial. JAMA Internal Medicine 178(11): 1509–1515.

67.

Hosking

Erickson

Van Den Berg

, et al. (1983) The stone clinic effect in patients with idiopathic calcium urolithiasis. The Journal of Urology 130(6): 1115–1118.

68.

Hung

Boffetta

Brennan

, et al. (2004) GST, NAT, SULT1A1, CYP1B1 genetic polymorphisms, interactions with environmental exposures and bladder cancer risk in a high-risk population. International Journal of Cancer 110(4): 598–604.

69.

Institute of Medicine USA (2004) Panel on Dietary Reference Intakes for Electrolytes and Water. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, D.C.: National Academy Press, 1–640.

70.

Janbozorgi

Allipour

Djafarian

, et al. (2021) Water intake and risk of type 2 diabetes: a systematic review and meta-analysis of observational studies. Diabetes & Metabolic Syndrome: Clinical Research & Reviews 15(4): 102156.

71.

Jang

Cheon

Jang

B-H

, et al. (2016) Relationship between water intake and metabolic/heart diseases: based on Korean National Health and Nutrition Examination Survey. Osong Public Health and Research Perspectives 7(5): 289–295.

72.

Jansen

Suh

Adams

, et al. (2019) Osmotic stimulation of vasopressin acutely impairs glucose regulation: a counterbalanced, crossover trial. American Journal of Clinical Nutrition 110(6): 1344–1352.

73.

Jensen

Wahrendorf

Knudsen

, et al. (1986) The Copenhagen case-control study of bladder cancer. II. Effect of coffee and other beverages. International Journal of Cancer 37(5): 651–657.

74.

Jiang

Castelao

Groshen

, et al. (2008) Water intake and bladder cancer risk in Los Angeles County. International Journal of Cancer 123(7): 1649–1656.

75.

Johnson

Bardis

Jansen

, et al. (2017) Reduced water intake deteriorates glucose regulation in patients with type 2 diabetes. Nutrition Research 43: 25–32.

76.

Johnson

Munoz

Jimenez

, et al. (2016) Hormonal and thirst modulated maintenance of fluid balance in young women with different levels of habitual fluid consumption. Nutrients 8(5): 302.

77.

Johnson

Munoz

Le Bellego

, et al. (2015) Markers of the hydration process during fluid volume modification in women with habitual high or low daily fluid intakes. European Journal of Applied Physiology 115(5): 1067–1074.

78.

Kant

Graubard

(2017) A prospective study of water intake and subsequent risk of all-cause mortality in a national cohort. American Journal of Clinical Nutrition 105(1): 212–220.

79.

Kavouras

(2019) Hydration, dehydration, underhydration, optimal hydration: are we barking up the wrong tree? European Journal of Nutrition 58(2): 471–473.

80.

King

Marrett

(1996) Case-control study of bladder cancer and chlorination by-products in treated water (Ontario, Canada). Cancer Causes & Control 7(6): 596–604.

81.

Koivusalo

Hakulinen

Vartiainen

, et al. (1998) Drinking water mutagenicity and urinary tract cancers: a population-based case-control study in Finland. American Journal of Epidemiology 148(7): 704–712.

82.

Kolasa

Lackey

Grandjean

(2009) Hydration and health promotion. Nutrition Today 44(5): 190–201.

83.

Lacey

Corbett

Forni

, et al. (2019) A multidisciplinary consensus on dehydration: definitions, diagnostic methods and clinical implications. Annals of Medicine 51(3–4): 232–251.

84.

Lee

Chang

Lee

, et al. (2019) Urine osmolality and renal outcome in patients with chronic kidney disease: results from the KNOW-CKD. Kidney and Blood Pressure Research 44(5): 1089–1100.

85.

Leurs

Schouten

Goldbohm

, et al. (2010) Total fluid and specific beverage intake and mortality due to IHD and stroke in the Netherlands Cohort Study. British Journal of Nutrition 104(8): 1212–1221.

86.

Lichtenstein

Petersen

Barger

, et al. (2021) Perspective: design and conduct of human nutrition randomized controlled trials. Advances in Nutrition 12(1): 4–20.

87.

Lim

Wong

Lewis

, et al. (2017) Total volume and composition of fluid intake and mortality in older women: a cohort study. BMJ Open 7(3): e011720.

88.

Lin

Lieske

, et al. (2019) High water intake in preventing the risk of uric acid nephrolithiasis: a systematic review and meta-analysis. Journal of Clinical Nephrology 3: 126–142.

89.

Loomba

Aggarwal

Arora

(2016) Raw water consumption does not affect all-cause or cardiovascular mortality: a secondary analysis. American Journal of Therapeutics 23(6): e1287–e1292.

90.

Lotan

Daudon

Bruyere

, et al. (2013) Impact of fluid intake in the prevention of urinary system diseases: a brief review. Current Opinion in Nephrology and Hypertension 22: S1–S10.

91.

Lubin

Rozen

Arieli

, et al. (1997) Nutritional and lifestyle habits and water-fiber interaction in colorectal adenoma etiology. Cancer Epidemiology, Biomarkers & Prevention 6(2): 79–85.

92.

Majdi

Hosseini

Naghshi

, et al. (2021) Total and drinking water intake and risk of all-cause and cardiovascular mortality: a systematic review and dose-response meta-analysis of prospective cohort studies. The International Journal of Clinical Practice 75(12): e14878.

93.

Malik

Popkin

Bray

, et al. (2010) Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care 33(11): 2477–2483.

94.

Manz

(2007) Hydration and disease. Journal of the American College of Nutrition 26: S535–S541.

95.

Manz

Wentz

(2005) The importance of good hydration for the prevention of chronic diseases. Nutrition Reviews 63(6): S2–S5.

96.

McGeehin

Reif

Becher

, et al. (1993) Case-control study of bladder cancer and water disinfection methods in Colorado. American Journal of Epidemiology 138(7): 492–501.

97.

McGrath

Michaud

De Vivo

(2006) Polymorphisms in GSTT1, GSTM1, NAT1 and NAT2 genes and bladder cancer risk in men and women. BMC Cancer 6: 239.

98.

Michaud

Spiegelman

Clinton

, et al. (1999) Fluid intake and the risk of bladder cancer in men. New England Journal of Medicine 340(18): 1390–1397.

99.

Naumann

Biehler

Lüty

, et al. (2017) Prevention and therapy of type 2 diabetes—what is the potential of daily water intake and its mineral nutrients? Nutrients 9(8): 914.

100.

Negoianu

Goldfarb

(2008) Just add water. Journal of the American Society of Nephrology 19(6): 1041–1043.

101.

Nieuwenhuijsen

Smith

Golfinopoulos

, et al. (2009) Health impacts of long-term exposure to disinfection by-products in drinking water in Europe: HIWATE. Journal of Water and Health 7(2): 185–207.

102.

Nygaard

Linder

(1997) Thirst at work—an occupational hazard? International Urogynecology Journal 8(6): 340–343.

103.

Pak

Sakhaee

Crowther

, et al. (1980) Evidence justifying a high fluid intake in treatment of nephrolithiasis. Annals of Internal Medicine 93(1): 36–39.

104.

Palmer

Wong

Iff

, et al. (2014) Fluid intake and all-cause mortality, cardiovascular mortality and kidney function: a population-based longitudinal cohort study. Nephrology Dialysis Transplantation 29(7): 1377–1384.

105.

Pan

Malik

Schulze

, et al. (2012) Plain-water intake and risk of type 2 diabetes in young and middle-aged women. American Journal of Clinical Nutrition 95(6): 1454–1460.

106.

Pearle

Goldfarb

Assimos

, et al. (2014) Medical management of kidney stones: AUA guideline. Journal of Urology 192(2): 316–324.

107.

Perrier

Demazieres

Girard

, et al. (2013a) Circadian variation and responsiveness of hydration biomarkers to changes in daily water intake. European Journal of Applied Physiology 113(8): 2143–2151.

108.

Perrier

Vergne

Klein

, et al. (2013b) Hydration biomarkers in free-living adults with different levels of habitual fluid consumption. British Journal of Nutrition 109(9): 1678–1687.

109.

Perrier

Armstrong

Bottin

, et al. (2021) Hydration for health hypothesis: a narrative review of supporting evidence. European Journal of Nutrition 60(3): 1167–1180.

110.

Plischke

Kohl

Bankir

, et al. (2014) Urine osmolarity and risk of dialysis initiation in a chronic kidney disease cohort—a possible titration target? PLoS ONE 9(3): e93226.

111.

Popkin

D'Anci

Rosenberg

(2010) Water, hydration, and health. Nutrition Reviews 68(8): 439–458.

112.

Porter

Voigt

Penson

, et al. (2002) Racial variation in the incidence of squamous cell carcinoma of the bladder in the United States. Journal of Urology 168(5): 1960–1963.

113.

Prasetyo

Birowo

Rasyid

(2013) The influence of increased fluid intake in the prevention of urinary stone formation: a systematic review. Acta Medica Indonesiana 45(4): 253–258.

114.

Qaseem

Dallas

Forciea

, et al. (2014) Dietary and pharmacologic management to prevent recurrent nephrolithiasis in adults: a clinical practice guideline from the American College of Physicians. Annals of Internal Medicine 161(9): 659–667.

115.

Radosavljevic

Jankovic

Marinkovic

, et al. (2003) Fluid intake and bladder cancer. A case control study. Neoplasma 50(3): 234–238.

116.

Rangan

Wong

Munt

, et al. (2022) Prescribed water intake in autosomal dominant polycystic kidney disease. NEJM Evidence 1(1): 1–13.

117.

Ros

Bas Bueno-de-Mesquita

Buchner

, et al. (2011) Fluid intake and the risk of urothelial cell carcinomas in the European Prospective Investigation into Cancer and Nutrition (EPIC). International Journal of Cancer 128(11): 2695–2708.

118.

Roussel

Fezeu

Bouby

, et al. (2011) Low water intake and risk for new-onset hyperglycemia. Diabetes Care 34(12): 2551–2554.

119.

Scales

Jr Smith

Hanley

, et al. (2012) Prevalence of kidney stones in the United States. European Urology 62(1): 160–165.

120.

Seal

Colburn

Suh

, et al. (2022) The acute effect of adequate water intake on glucose regulation in low drinkers. Annals of Nutrition and Metabolism 77: 33–36.

121.

Shannon

White

Shattuck

, et al. (1996) Relationship of food groups and water intake to colon cancer risk. Cancer Epidemiology, Biomarkers & Prevention 5(7): 495–502.

122.

Shirreffs

(2000) Markers of hydration status. Journal of Sports Medicine and Physical Fitness 40(1): 80–84.

123.

Siener

Hesse

(2003) Fluid intake and epidemiology of urolithiasis. European Journal of Clinical Nutrition 57(Suppl 2): S47–51.

124.

Simons

Leurs

Weijenberg

, et al. (2010) Fluid intake and colorectal cancer risk in the Netherlands Cohort Study. Nutrition and Cancer 62(3): 307–321.

125.

Skolarikos

Jung

Neisius

, et al. (2023) EAU guidelines on urolithiasis. Available at: http://uroweb.org/guidelines/compilations-of-all-guidelines/ (accessed 1 August).

126.

Slattery

Caan

Anderson

, et al. (1999) Intake of fluids and methylxanthine-containing beverages: association with colon cancer. International Journal of Cancer 81(2): 199–204.

127.

Slattery

West

Robison

(1988) Fluid intake and bladder cancer in Utah. International Journal of Cancer 42(1): 17–22.

128.

Song

Chung

(2010) Observational studies: cohort and case-control studies. Plastic and Reconstructive Surgery 126(6): 2234–2242.

129.

Sontrop

Dixon

Garg

, et al. (2013) Association between water intake, chronic kidney disease, and cardiovascular disease: a cross-sectional analysis of NHANES data. American Journal of Nephrology 37(5): 434–442.

130.

Spill

English

Raghavan

, et al. (2022) Perspective: USDA nutrition evidence systematic review methodology: grading the strength of evidence in nutrition-and public health-related systematic reviews. Advances in Nutrition 13(4): 982–991.

131.

Spruce

McCulloch

Burd

, et al. (1985) The effect of vasopressin infusion on glucose metabolism in man. Clinical Endocrinology 22(4): 463–468.

132.

Stookey

Kavouras

Suh

, et al. (2020) Underhydration is associated with obesity, chronic diseases, and death within 3 to 6 years in the U.S. population aged 51–70 years. Nutrients 12(4): 905.

133.

Strauss

Coe

Deutsch

, et al. (1982) Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study. The American Journal of Medicine 72(1): 17–24.

134.

Strippoli

Craig

Rochtchina

, et al. (2011) Fluid and nutrient intake and risk of chronic kidney disease. Nephrology 16(3): 326–334.

135.

Tabibzadeh

Wagner

Metzger

, et al. (2019) Fasting urinary osmolality, CKD progression, and mortality: a prospective observational study. American Journal of Kidney Diseases 73(5): 596–604.

136.

Tang

Wang

, et al. (1999) Physical activity, water intake and risk of colorectal cancer in Taiwan: a hospital-based case-control study. International Journal of Cancer 82(4): 484–489.

137.

Tate

Turner-McGrievy

Lyons

, et al. (2012) Replacing caloric beverages with water or diet beverages for weight loss in adults: main results of the Choose Healthy Options Consciously Everyday (CHOICE) randomized clinical trial. American Journal of Clinical Nutrition 95(3): 555–563.

138.

Torres

(2009) Vasopressin in chronic kidney disease: an elephant in the room? Kidney International 76(9): 925–928.

139.

Tsai

Leitzmann

Willett

, et al. (2005) Glycemic load, glycemic index, and carbohydrate intake in relation to risk of cholecystectomy in women. Gastroenterology 129(1): 105–112.

140.

Uribarri

Stirban

Sander

, et al. (2007) Single oral challenge by advanced glycation end products acutely impairs endothelial function in diabetic and nondiabetic subjects. Diabetes Care 30(10): 2579–2582.

141.

Vena

Graham

Freudenheim

, et al. (1993) Drinking water, fluid intake, and bladder cancer in western New York. Archives of Environmental Health 48(3): 191–198.

142.

Verbalis

(2006) Whole-body volume regulation and escape from antidiuresis. American Journal of Medicine 119(7): S21–S29.

143.

Villanueva

Cantor

King

, et al. (2006) Total and specific fluid consumption as determinants of bladder cancer risk. International Journal of Cancer 118(8): 2040–2047.

144.

Wagner

Merkling

Metzger

, et al. (2022) Water intake and progression of chronic kidney disease: the CKD-REIN cohort study. Nephrology Dialysis Transplantation 37(4): 730–739.

145.

Wang

Grantham

Wetmore

(2013a) The medicinal use of water in renal disease. Kidney International 84(1): 45–53.

146.

Wang

Jiang

(2021) Higher volume of water intake is associated with lower risk of albuminuria and chronic kidney disease. Medicine (Baltimore) 100(20): e26009.

147.

Wang

Kamat

, et al. (2013b) Fluid intake, genetic variants of UDP-glucuronosyltransferases, and bladder cancer risk. British Journal of Cancer 108(11): 2372–2380.

148.

Wang

Chiang

Chen

, et al. (2022) Association of water intake and hydration status with risk of kidney stone formation based on NHANES 2009–2012 cycles. Public Health Nutrition 25(9): 2403–2414.

149.

Wang

Chang

(2018) Racial differences in urinary bladder cancer in the United States. Scientific Reports 8(1): 12521.

150.

Wang

Zhang

, et al. (2021) Recent advances on the mechanisms of kidney stone formation (review). International Journal of Molecular Medicine 48(2): 1–10.

151.

Weisman

Heinrich

Letkiewicz

, et al. (2022) Estimating National Exposures and Potential Bladder Cancer Cases Associated with chlorination DBPs in U.S. Drinking Water. Environmental Health Perspectives 130(8): 1–10.

152.

Werner

Bapat

Schobesberger

, et al. (2021) Calcium oxalate crystallization: influence of pH, energy input, and supersaturation ratio on the synthesis of artificial kidney stones. ACS Omega 6(40): 26566–26574.

153.

Wilkens

Kadir

Kolonel

, et al. (1996) Risk factors for lower urinary tract cancer: the role of total fluid consumption, nitrites and nitrosamines, and selected foods. Cancer Epidemiology, Biomarkers & Prevention 5(3): 161–166.

154.

Chen

Liaw

, et al. (2016) Association between fluid intake and kidney function, and survival outcomes analysis: a nationwide population-based study. BMJ Open 6(5): e010708.

155.

Wynder

Onderdonk

Mantel

(1963) An epidemiological investigation of cancer of the bladder. Cancer 16: 1388–1407.

156.

Zhang

Wang

X-L

, et al. (2015) Self-fluid management in prevention of kidney stones: a PRISMA-compliant systematic review and dose-response meta-analysis of observational studies. Medicine 94(27): e1042.

157.

Zisman

Coe

, et al. (2013) Kidney stones: an update on current pharmacological management and future directions. Expert Opinion on Pharmacotherapy 14(4): 435–447.

158.

Zeegers

Dorant

Goldbohm

, et al. (2001) Are coffee, tea, and total fluid consumption associated with bladder cancer risk? Results from the Netherlands Cohort Study. Cancer Causes and Control 12(3): 231–238.

159.

Zeegers

Kellen

Buntinx

, et al. (2004) The association between smoking, beverage consumption, diet and bladder cancer: a systematic literature review. World Journal of Urology 21(6): 392–401.

160.

Zerbe

Vinicor

Robertson

(1979) Plasma vasopressin in uncontrolled diabetes mellitus. Diabetes 28(5): 503–508.

161.

Zhou

Kelsey

Giovannucci

, et al. (2014) Fluid intake and risk of bladder cancer in the Nurses’ Health Studies. International Journal of Cancer 135(5): 1229–1237.

162.

Zhou

Smith

Giovannucci

, et al. (2012) Reexamination of total fluid intake and bladder cancer in the Health Professionals Follow-up Study Cohort. American Journal of Epidemiology 175(7): 696–705.

163.

Zwiener

Richardson

De Marini

, et al. (2007) Drowning in disinfection byproducts? Assessing swimming pool water. Environmental Science & Technology 41(2): 363–372.

Low daily water intake profile—is it a contributor to disease?

Abstract

Keywords

Introduction

Search methods

Results

Discussion

Kidney stones

Type 2 diabetes/hyperglycemia

Future research

Summary

Footnotes

Authors’ contributions

Availability of data and materials

Consent for publication

Declaration of conflicting interests

Ethical approval

Funding

ORCID iDs

References