1.
A Journey through the Early Evidence Linking Hydration to Metabolic Health.
Vanhaecke, T, Perrier, ET, Melander, O
Annals of nutrition & metabolism. 2020;:4-9
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Abstract
The idea that water intake or hydration may play an intrinsic, independent role in modulating metabolic disease risk is relatively recent. Here, we outline the journey from early experimental works to more recent evidence linking water and hydration to metabolic health. It has been known for decades that individuals with existing metabolic dysfunction experience challenges to body water balance and have elevated arginine vasopressin (AVP), a key hormone regulating body fluid homeostasis. Later, intervention studies demonstrated that altering fluid balance in these individuals could worsen their condition, suggesting that hydration played a role in modulating glycemic control. More recently, observational and interventional studies in healthy individuals have implicated the hydration-vasopressin axis in the pathophysiology of metabolic diseases. Individuals with higher AVP (or its surrogate, copeptin) are at higher risk for developing type 2 diabetes and components of the metabolic syndrome, an association that remains even when controlling for known risk factors. Supporting preclinical work also suggests a causal role for AVP in metabolic dysfunction. It is known that individuals who habitually drink less fluids tend to have higher circulating AVP, which may be lowered by increasing water intake. In the short term, water supplementation in habitual low drinkers with high copeptin may reduce fasting glucose or glucagon, generating a proof of concept for the role of water supplementation in reducing incident metabolic disease. A large randomized trial is ongoing to determine whether water supplementation for 1 year in subjects with low water intake can meaningfully reduce fasting glucose, risk of new-onset diabetes, and other cardiometabolic risk factors.
2.
Distinguishing Low and High Water Consumers-A Paradigm of Disease Risk.
Armstrong, LE, Muñoz, CX, Armstrong, EM
Nutrients. 2020;(3)
Abstract
A long-standing body of clinical observations associates low 24-h total water intake (TWI = water + beverages + food moisture) with acute renal disorders such as kidney stones and urinary tract infections. These findings prompted observational studies and experimental interventions comparing habitual low volume (LOW) and high volume (HIGH) drinkers. Investigators have learned that the TWI of LOW and HIGH differ by 1-2 L·d-1, their hematological values (e.g., plasma osmolality, plasma sodium) are similar and lie within the laboratory reference ranges of healthy adults and both groups appear to successfully maintain water-electrolyte homeostasis. However, LOW differs from HIGH in urinary biomarkers (e.g., reduced urine volume and increased osmolality or specific gravity), as well as higher plasma concentrations of arginine vasopressin (AVP) and cortisol. Further, evidence suggests that both a low daily TWI and/or elevated plasma AVP influence the development and progression of metabolic syndrome, diabetes, obesity, chronic kidney disease, hypertension and cardiovascular disease. Based on these studies, we propose a theory of increased disease risk in LOW that involves chronic release of fluid-electrolyte (i.e., AVP) and stress (i.e., cortisol) hormones. This narrative review describes small but important differences between LOW and HIGH, advises future investigations and provides practical dietary recommendations for LOW that are intended to decrease their risk of chronic diseases.
3.
Effect of water drinking on sympathetic nervous activity and blood pressure.
Jordan, J
Current hypertension reports. 2005;(1):17-20
Abstract
Recent studies suggest that water drinking elicits acute changes in human physiology. Water drinking profoundly increases blood pressure in patients with autonomic failure. Water drinking also increases blood pressure in quadriplegic patients, cardiac transplant recipients, and older healthy subjects, but to a lesser extent. Blood pressure does not change in healthy young subjects. More recently, water drinking was shown to increase energy expenditure. The acute changes in cardiovascular regulation and in energy expenditure with water drinking appear to be mediated through activation of the sympathetic nervous system. The sympathetic activation may involve a spinal reflex-like mechanism. The stimulus that causes the sympathetic activation is not known. The acute water pressor response can be exploited in the treatment of patients with impaired orthostatic tolerance caused by autonomic failure, postural tachycardia syndrome, or, perhaps, neurocardiogenic (vasovagal) syncope. The increase in energy expenditure with water drinking should be recognized as an important confounding variable in metabolic studies and may hold some promise as an adjunctive measure in the prevention or treatment of obesity.