It Is Definitley Pee the Estatic Fueled Art of Squirting
Nutrients. 2019 Jul; eleven(7): 1539.
Of Mice and Men—The Physiology, Psychology, and Pathology of Overhydration
Received 2019 May xxx; Accepted 2019 Jul three.
Abstruse
The detrimental effects of dehydration, to both mental and concrete wellness, are well-described. The potential adverse consequences of overhydration, even so, are less understood. The difficulty for most humans to routinely ingest ≥2 liters (Fifty)—or "eight glasses"—of h2o per day highlights the likely presence of an inhibitory neural excursion which limits the deleterious consequences of overdrinking in mammals simply tin be consciously overridden in humans. This review summarizes the existing data obtained from both creature (mostly rodent) and human studies regarding the physiology, psychology, and pathology of overhydration. The physiology section will highlight the molecular force and significance of aquaporin-2 (AQP2) h2o channel downregulation, in response to chronic anti-diuretic hormone suppression. Absence of the anti-diuretic hormone, arginine vasopressin (AVP), facilitates copious gratis water urinary excretion (polyuria) in equal volumes to polydipsia to maintain plasma tonicity within normal physiological limits. The psychology section will highlight reasons why humans and rodents may volitionally overdrink, probable in response to feet or social isolation whereas polydipsia triggers mesolimbic advantage pathways. Lastly, the potential acute (water intoxication) and chronic (urinary bladder amplification, ureter dilation and hydronephrosis) pathologies associated with overhydration will be examined largely from the perspective of human case reports and early on animate being trials.
Keywords: hydration, dehydration, hypohydration, hyponatremia, polydipsia
1. Introduction
Hydration and the evolving search for an adequate universal daily water intake recommendation remains elusive [1] and somewhat contentious [ii,3]. Nearly of the disagreement over an adequate index for fluid intake, however, likely revolves effectually the disparate and non-standardized metrics normally utilized to ascertain both normal and abnormal hydration status (HS) [four]. For case, the clinical definition of dehydration is cellular dehydration from extracellular hypertonicity [v,6] while scientists often use the term dehydration to describe the procedure of losing h2o [4]. Alternatively, the term hypohydration refers to a negative water remainder [vii] or state of water deficit [4]. Regardless of which hydration terminology is utilized to ascertain HS, the vast majority of the scientific and lay literature highlights the well-recognized detrimental furnishings of dehydration and/or hypohydration on a variety of weather such as kidney stones [3], obesity [8], recurrent urinary tract infections [ix], knowledge [10], and athletic performance [xi].
At the opposite end of the hydration spectrum, a paucity of information exists on the topic of overhydration. In 1923, Rowntree published a series of animal and human information exploring the detrimental effects of "water intoxication" [12]. Rowntree successfully induced water intoxication (characterized by restlessness, lethargy, polyuria, diarrhea, salivation, frothing at the mouth, nausea, retching, vomiting, muscle twitching, seizures, coma and decease) in dogs, cats, rabbits and guinea-pigs by speedily administering tap or distilled water (50 mL/kg bodyweight every thirty min) rectally, intravenously, through a stomach tube and/or ureteral catheter to induce water overload [12]. Combined with similar human cases of water intoxication [13,14,15,sixteen,17], it appears clear that extreme fluid administration in excess of excretion rates—or more modest intakes when coupled with pathological anti-diuretic hormone secretion—are indeed detrimental (and sometimes toxic) to health [12].
Thus, while the electric current evidence suggests that pocket-sized hypohydration and extreme overhydration have deleterious health consequences, the question remains whether modest overhydration is benign or detrimental to wellness. This review will explore the physiology, psychology, and pathology of overhydration. Both animal (generally mice) and human studies will be detailed, with an emphasis placed upon the psychogenic polydipsia literature to more conspicuously evaluate: (1) long-term physiological changes associated with concomitant and sustained polyuria and (2) the putative neurogenic pathways which may differentially drive high (anxiolytic) versus low habitual fluid consumption. We will refer to the term polydipsia to represent excessive drinking (beyond regulatory need) without whatsoever known medical crusade [xviii].
ii. Physiology
As comprehensively described elsewhere [i,19,20,21,22], water balance is exquisitely regulated in all mammals (and some non-mammals) [22,23] in physiological defense of both osmotic rest (plasma tonicity) and circulatory book. Plasma tonicity dictates cellular size, and is tightly regulated by a coordinated arrangement of osmosensors, neural networks, endocrine mediators, and physiologically-driven behaviors which cooperatively serve to sustain extracellular fluid osmolality effectually a remarkably abiding set-point of 300 mOsmol/kgHtwoO [20] (or, plasma sodium concentration ~140 mmol/Fifty) [21]. Central to this evolutionarily stable feedback-loop controlling osmotic regulation is the kidney, whose immediate ability to retain or excrete free h2o is vital to the overall maintenance of fluid homeostasis [19,24]. For clinical convenience, we volition refer to a plasma sodium concentration ([Na+]) between 135–145 mmol/Fifty as the "normal" range for extracellular fluid osmolality/plasma tonicity since sodium is the master extracellular cation found within the plasma [21].
When modest amounts of water (or other hypotonic fluids) are ingested in a higher place osmotically-driven thirst stimulation (overhydration), osmoreceptors located inside the highly vascularized circumventricular organs (CVO'southward) within the brain notice a (dilutional) decrease in plasma [Na+] once water is absorbed into the circulation from the gastrointestinal (GI) tract [xx,25]. These CVO'due south, located outside of the blood encephalon barrier, suppress both the release of the body'south main anti-diuretic hormone, arginine vasopressin (AVP), from the posterior pituitary gland and suppress the sensation of osmotically-driven thirst to forestall farther dilution of plasma [Na+]. Oropharyngeal receptors, activated by concrete contact with ingested fluids [26,27,28], likewise as gastrointestinal sensors responding to stretch receptors sensing fullness [29,30,31,32] serve to terminate drinking behavior, perhaps as an anticipatory measure out to prevent the pathophysiological consequences of overdrinking (i.east., cellular swelling). In fact, recent electrophysiological and optogenic studies performed on mice confirm the presence of a distinct neuronal network, mediated past cantankerous-talk between the brain and gastrointestinal tract, through activation of the subfornical organ within the CVO [32]. The subfornical organ appears to coordinate a multifariousness of neuronal inputs that conceptualize the homeostatic consequences of food and fluid intake well earlier changes in plasma tonicity are observed [32,33].
Functional magnetic resonance imaging (fMRI) studies further propose that the brain senses h2o intake in response to thirst equally "pleasant", while overdrinking suppresses this hedonic response [34,35,36]. The alliesthesia associated with drinking while thirsty mainly activates the anterior midcingulate cortex and orbitofrontal cortex, suggesting that drinking to thirst is pleasurable and involuntary [35,36]. In contrast, continued drinking after thirst satiation (+ane L higher up thirst suppression) [34] activates encephalon areas associated with swallowing inhibition too as cortical areas associated with unpleasantness ratings [34,35]. Activation of the motor cortex, striatum and thalamus suggests that voluntary motor activeness is required to keep drinking to a higher place thirst satiation [34]. Every bit such, drinking to a higher place thirst requires a threefold increase in volitional try compared to drinking when thirsty [34]. Independent information nerveless from a clinical trial, where 316 participants with stage iii chronic kidney disease were "coached" to increase daily h2o intake by ane–1.5 50/mean solar day, corroborate these fMRI findings and confirm that drinking above thirst is difficult and unpleasant [37]. The average increase in h2o intake in the participants randomized into the "coached hydration" group, could only increment their daily water intake by ~0.half dozen L relative to the command grouping [37]. Thus, the disability for free-living adults to voluntarily sustain even modest 500 mL (~2 cup) increases in daily water consumption (higher up thirst) underscores the strength of the central inhibitory pathways that serve to forestall the deleterious and life-threatening consequences of fluid overload.
Both thirst stimulation and AVP release are centrally coordinated in real-fourth dimension past input largely from the cranial nerve system. Equally such, central integration of neuronal feedback from osmoreceptors (subfornical organ), baroreceptors (tenth cranial nerve), the oral fissure (fifth cranial nervus), tongue (7th cranial nervus), oropharynx (ninth cranial nerve), and stomach (tenth cranial nerve) ultimately results in either the stimulation or suppression of AVP from the posterior pituitary gland [twenty,21,35]. AVP so regulates plasma [Na+]/tonicity by retaining or excreting h2o inside the kidney collecting duct. The permeability of the kidney collecting duct increases when AVP binds to the vasopressin-ii receptors (V2R), which stimulates the insertion of aquaporin 2 (AQP2) water channels into the lumen of the kidney collecting duct [19,24]. The insertion of these AQP2 h2o channels allows for h2o molecules (otherwise destined for urinary excretion) to be reabsorbed back into the circulation when plasma tonicity is high (or circulating plasma volume depression) to conserve full torso water. Conversely, with overdrinking, there is central inhibition of the AVP release, which withdraws AQP2 channels from the lumen of the kidney collecting duct; thereby promoting urinary free water excretion which matches fluid ingestion beyond physiological need.
It is important to emphasize that the neuroendocrine feedback loop coordinating fluid balance betwixt the brain and kidney is highly conserved within the Deoxyribonucleic acid (dna) of vertebrate and invertebrate species dating back 700 one thousand thousand years [23]. Once released into the circulation, AVP can increment kidney collecting duct permeability inside forty s of activation of the V2R in rodent species [38]. Quantification studies of microdissected renal tubule segments, obtained from the middle role of rodent inner medullary collecting duct, estimate that there are ~12 million individual AQP2 water channels present within each kidney collecting duct cell [24]. Thus, the molecular strength and precision of the diuretic renal response to AVP suppression is powerful and allows for urinary excretion rates approximating 1 L/h, as seen in patients with diabetes insipidus [21] and compulsive water drinkers [39,forty].
Interestingly plenty, chronic overhydration (>3 days), triggers the downregulation of AQP2 water channels within the kidney collecting duct cells [19,24]. This phenomenon has been verified directly in a serial of elegant studies performed on water-loaded rats and mice [19,24] and indirectly confirmed in human studies [41,42,43,44]. The sustained suppression of circulating AVP in response to overdrinking enhances urinary free water excretion and teleologically represents the most advisable renal accommodation to a abiding fluid intake load (polydipsia = polyuria). Yet, when loftier fluid intakes are suddenly curtailed [42,43,44], the downregulation of AQP2 water channels triggers a transient inability to reabsorb h2o molecules dorsum through the kidney collecting duct in response to AVP V2R stimulation [xix,24,45]. This renal insensitivity to AVP secretion augments urinary fluid losses (above intake), which is clinically characterized by an inability to concentrate urinary solutes [43,44,46,47] coupled with enhanced trunk water/weight loss [42]. This phenomenon of "water loading", popularized by gainsay sport athletes and body builders before competition as a method to "counterbalance-in lite" [39,45], highlights the dynamic molecular adaptability within the kidney collecting duct cells in response to chronic (>3 days) changes in h2o intake that have been conspicuously demonstrated in rodent models [19,24,48,49,fifty,51]. A render to regulated drinking (osmotically-driven thirst stimulation) and concomitant AVP exposure will restore AQP2 expression within collecting duct epithelium by three–five days [48] and reverse the physiologic nephrogenic diabetes insipidus induced by chronic h2o loading in both mice and men [24].
3. Psychology
At the most extreme range of overhydration, compulsive water drinking has been recognized in emotionally disturbed individuals without neurogenic (i.east., disability of secrete AVP from the posterior pituitary) or nephrogenic (i.eastward., kidneys resistant to AVP stimulation) diabetes insipidus [47]. Sometimes referred to as "psychogenic polydipsia" [52,53], eighty% of compulsive water drinkers correspond neurotic females with a history of schizophrenia [40,54], depression [xiv,45], and/or anxiety [53,55]. Psychogenic polydipsia in schizophrenic patients was first identified in 1936 through investigation of profuse polyuria, which somewhen ceased when the polydipsia was minimized [56].
To a more modest degree of drinking, social polydipsia—or overdrinking to achieve wellness benefits—has become popularized within western civilisation. The nigh mutual "one-size-fits-all" guideline suggests that all salubrious humans demand to potable at least eight glasses of water daily beyond fluids obtained through foods or other beverages. This popular recommendation persists despite equivocal prove, which supports the claim that water intake maximizes skin heath, digestion, renal, sexual, or neurological function [iii,57,58]. The connected success of this advice is evidenced by robust water bottle sales, which topped 2.78 billion dollars in 2018 within the United States lonely [59]. At farthermost levels (>5 Fifty daily), social polydipsia may upshot in profound dilation of the bladder, ureters and kidneys [60] and at worst, water intoxication (i.e., overconsumption of fluids beyond excretion rates leading to the signs and symptoms of encephalopathy) [12]. Of note, updated (2017) guidelines put forth past the European Nutrient Prophylactic Authorization (EFSA) now defines total h2o intake to include all beverages consumed plus the moisture contained in foods [61].
Drinking beyond the dictates of thirst has been popularized inside able-bodied circles to prevent the detrimental effects of hypohydration on health and performance [11]. Although guidelines have evolved to drink to minimize torso weight losses (<2%) [62], other drinking guidelines recommend drinking before the onset of thirst stimulation to maintain a dilute urine (urine specific gravity <1.020) [11]. Some athletes, unfortunately, have taken this advice to extreme levels (i.e., drinking fourscore–100 cups of fluid during a marathon footrace [63]) and have developed water intoxication [13,64]. Additionally, h2o loading has become a popular practise for combat sport athletes to enhance water weight losses before weigh-ins [42] while actors participating in pornographic films accept begun water loading to raise their squirting performance abilities [58]. The prevalence of symptomatic water intoxication in prolonged endurance races remains relatively rare (<1%), however [65].
Why otherwise healthy people, exterior of sports or social reasons, habitually drink high volumes of fluid [66] above physiological need remains a curious and unanswered phenomenon. Studies performed in mice exposed to chronic stress [67,68] or raised in isolation [69,70], provide psychological insight into this peculiar finding. Male C57BL/half-dozen mice subjected to chronic social defeat stress (i.e., exposure to bigger, meaner, "bully" mice) demonstrate a singled-out phenotype characterized past enhanced fluid intake [67,70] and water retentiveness [68]. Additionally, two-month one-time Sabra mice [70] and adolescent male Sprague-Dawley rats [69] reared (post-weaning) in isolation developed significant polydipsia compared with control animals. Follow-up molecular and electrophysiological studies implicate the mesolimbic dopamine circuit in the manifestation of polydipsia in response to loneliness and social feet [67].
One explanation equally to why anxious mice develop polydipsia, is that water intake may somehow reduce dopaminergic neuron excitability inside the ventral tegmental area (VTA), or the advantage area, of the encephalon. Of note, schizophrenia has been linked to enhanced dopaminergic receptor excitability [67,71], which likely mediates polydipsia as either a reward-seeking [67] or anxiolytic [67,68,seventy] behavior. Farther investigations on drug-induced polydipsia are required to tease out the potential neurochemical circuits linking dopamine, advantage, and drinking. Drugs that demonstrate the virtually promising results, include: methamphetamines (which inhibit dopamine reuptake in the brain) [72] such as 3,4 methyldioxymethamphetamine (Ecstasy) [73], agonists, which downregulate dopamine receptor 2 (DRD2) [74], showtime and second generation antipsychotics [75], and antidepressant medications [76]. All these drugs have been linked to hyponatremia from not-osmotic AVP secretion, just their relationship to polydipsia is under-appreciated. Of note, a variety of drugs and excipients have been shown to affect hydration condition by augmenting fluid losses, affecting thirst and/or appetite, increasing abdominal permeability and/or renal reabsorption rates [7].
Human being observations corroborate these animal findings, as virtually psychogenic polydipsic patients report that drinking makes them experience amend [77]. Patients with hallucinations also written report that drinking fluids suppress the "voices" [78], further suggesting that the act of drinking activates neural circuits associated with primitive coping mechanisms [77]. Other investigators suggest that the inductive hippocampus and nucleus accumbens are involved in polydipsia equally a reward-seeking behavior in psychiatric patients [77]. Alternatively, compulsive water drinking has been documented in non-neurotic individuals seeking to reach a drunken-like state [14,55]. For example, a xvi-year-old female drank copious amounts of water because it fabricated her experience "funny and high, like afterwards a beer" [55] while a 46-year-old homo with a history of depression ran out of money to purchase beer, so drank large amounts of water because it made him feel "slightly boozer" [14]. Therefore, coupled with testify suggesting that drinking fluids improves noesis [10], information technology is possible that polydipsia activates a dopaminergic reward excursion that attenuates feet in susceptible individuals exposed to chronic stress and/or social isolation. A summary of this proposed relationship is detailed in Figure 1. Further investigation on the potential anxiolytic effects of polydipsia, specially in females, warrants further investigation with detail regards to whether this practice is adaptive or maladaptive over the long term.
Summary of information obtained from mice and humans linking polydipsia to mesolimbic reward centers, which serve to reduce anxiety and/or signs and symptoms of psychiatric illness.
four. Pathology
Equally previously summarized, total body fluid regulation is exquisitely regulated in defense of plasma [Na+]/tonicity and circulating volume. Accordingly, complications from overdrinking are rare. The virtually common (and dire) clinical outcome from overdrinking is water intoxication, which is biochemically divers as a plasma [Na+] below the normal range set by the lab performing the test (unremarkably a plasma [Na+] < 135 mmol/L, which is called "hyponatremia", because hypo = depression and natremia = blood sodium) [21]. Equally starting time described by Rowntree in 1923, the fatal consequences of water intoxication occur when fluid administration exceeds the capacity to excrete whatsoever fluid excess and exacerbated by AVP stimulation (water retentiveness) [12]. Hyponatremia causes water to flow down an osmotic gradient from outside of cells to inside of cells and causes all cells inside the body to cracking. Hyponatremia is fatal when cerebral swelling in excess of 5–eight% exceeds the rigid confines of the skull, resulting in brainstem herniation, cognitive hypoxia, and loss of vegetative functions [thirteen,64].
Gross estimations suggest that an acute (<1 h) fluid intake effectually 3–4 L (~i gallon) is enough to induce symptomatic hyponatremia in otherwise healthy individuals at rest [12,52]. Although maximal urine excretion rates allow humans to tolerate water intakes approximating 20 50 per day without ill-effects [79], the actual fluid intake tolerance limit appears to be closer to 10 Fifty per mean solar day in normal individuals [43,79]. De Wardener and Herxheimer each drank 10 L of water per day (250–500 mL every 30–60 min during waking hours) for xi days and reported physical signs of headache, scotoma, skin coldness with pallor, and puffiness of the face [43]. These two subjects also reported that their lips felt dry (without the sensation of thirst), food was tasteless, emotional liability was high, and unproblematic intellectual tasks became increasingly difficult during this period of enhanced water intake [43]. Of note, the pathogenic effects of overhydration are not isolated to oral intake. The starting time water intoxication fatality was reported in 1935, in a fifty-year-former female who received 9 L of fluid over 24-h through the rectum (proctoclysis) following an otherwise uncomplicated gallbladder surgery [17]. Thus, it is hard to commit to recommending a threshold volume of h2o that can be safely consumed (or administered) over time, since both the ~iii L per 60 minutes and ~10 L per twenty-four hour period can be tolerated by some (especially athletes with high sweat rates [fourscore]) only fatal to others. Of note, when not-osmotic AVP secretion is present, or when sodium losses are astringent, modest water ingestion at rates of i–2 L/h can induce symptomatic hyponatremia [13,21]. Non-osmotic stimuli to AVP secretion, sodium losses, a multifariousness of drugs and excipients influencing hydration condition, and type of fluids consumed are beyond the scope of this review and detailed elsewhere [7,81,82].
The body'due south appropriate fluid homeostatic response to polydipsia is polyuria (i.east., excessive urine production). For individuals with normal kidney function, any excess fluid that is ingested (across osmoregulatory need) is promptly excreted by the body. For example, the ten L of water ingested by De Wardener and Herxheimer resulted in a daily urine output of 10 L [43]. Polyuria is as well the characteristic characteristic of diabetes insipidus (both neurologic and nephrogenic), whereas chronic urinary gratis water excretion (from AVP suppression or renal insensitivity) is counterbalanced by osmotic thirst stimulation and concomitant water intake, which matches urinary fluid losses (to maintain plasma [Na+] within the normal physiological range) [21,47,83]. As such, sustained polyuria has been shown to cause profound urinary tract changes such equally float distension, dilation of the ureters, renal dorsum force per unit area atrophy, hydronephrosis, traumatic rupture of the urinary tract, and renal failure [threescore,84,85,86,87,88]. One such case of (reversible) hydronephrosis occurred in an otherwise healthy 53-year-old female who drank 4.5–five.5 L of fluid daily over the subsequent three years to "stay salubrious" and because "all her friends practise then" [60]. Another possible mechanical consequence of polydipsia is gastric amplification [89], which may exist advantageous in those trying to lose weight (producing the sensation of tum fullness ahead of meals) [8]. Figure 2 summarizes the astute and chronic physiological effects of overhydration while Effigy three summarizes the astute and chronic physiological effects of water intake when hypohydrated.
Summary diagram of acute (A) and chronic (C) physiological responses integrating potential pathologies and benefits associated with overdrinking in the satiated condition (above thirst stimulation).
Summary diagram of astute (A) and chronic (C) physiological responses and potential pathologies associated with drinking to thirst when hypohydrated.
With specific regards to kidney role, individuals with a history of kidney stones (nephrolithiasis) have a reduced take chances of recurrent rock formation if they consume more than than 2 Fifty of h2o per day [iii,57]. Ane hypothesis is that increased water intake (>2 L/day for 12-months) reduces renal papillary density, which may precipitate calcium oxalate stone formation [90]. Conversely, excessive fluid intake may exacerbate proteinuria [91], take no consequence [37] or accelerate [92] the progression of chronic renal illness.
It has been demonstrated in a randomized-control trial that premenopausal women with a history of recurrent urinary tract infections (UTI), who potable less than one.5 L of h2o daily (low volume drinkers), can reduce the recurrence rate of UTI's from three to two episodes/yr past increasing water consumption past +1.iii L/mean solar day [9]. However, increased fluid intake has not been equivocally shown to raise peel complexion or kidney function [3,57], while data are unclear regarding constipation [57,93]. Information regarding the event of water intake on weight loss are mixed. Some studies demonstrate positive associations between h2o intake, weight management and body composition [94,95,96], while others demonstrate an increment in energy intake when pre-meal water ingestion was removed [97,98]. Alternatively, a randomized command trial performed on obese and overweight adolescents did not demonstrate enhanced weight loss with increased water consumption [8].
Information technology is important to note that water intake is not completely benign. Otherwise healthy individuals take died or developed significant encephalon swelling (hyponatremic encephalopathy) from drinking too much fluid to foreclose kidney stones [99], sooth a toothache [100], dilute ingested poison [16], counter a UTI [101], treat gastroenteritis [fifteen], and alleviate constipation [46,102], as shown in Table 1. These cases highlight the demand to dampen overzealous (just well-intended) advice to "stay hydrated".
Tabular array one
Cases of hyponatremic encephalopathy (and expiry) in otherwise good for you people who overdrank to treat another medical status (L = liters).
| Field of study | Corporeality of Fluid Consumed | Reason for Polydipsia | Report |
|---|---|---|---|
| Not described | 3 L/xx min | Examination pare elasticity | Rowntree 1923 [12] |
| 16 yo female | 20 L/day | Facial acne | Lee 1989 [55] |
| 44 yo male person | 12 50/twenty-four hour period | Kidney stones | Berry 1977 [99] |
| 9.5 yo male person | 10–15 L/24 h | Soothe toothache | Pickering 1971 [100] |
| * 40 yo female | "plenty of h2o" | Dilute toxicant (ingested) | Sarvesvaran 1984 [xvi] |
| 59 yo female | "plenty of water" | Urinary tract infection | Lee 2016 [101] |
| * 27 yo female | "lots of h2o" | Gastroenteritis | Sjoblom 1997 [fifteen] |
| 52 yo male | 6 50/2 h + 1 L enema | Constipation | Swanson 1958 [102] |
| 74 yo female | 10–14 glasses water/day | Soften stool | Walls 1977 [46] |
The potential for abnormal thirst regulation to contribute to pathological water consumption has been documented in a few select scenarios (one in humans and another in cattle). Compulsive water drinkers demonstrate abnormal thirst regulation, whereas the osmotic threshold for thirst stimulation is paradoxically lower than the osmotic threshold for AVP release [83]. Whether or not this reverse in osmotic thresholds for thirst and AVP stimulation is a cause or upshot of psychogenic polydipsia remains unclear. Additionally, the animal studies suggest that most mammals will not voluntarily develop h2o intoxication, unless artificially induced in the laboratory to investigate hyponatremia [12,103]. The just confirmed exception are calves (and in rare instances, adult cattle) who develop fatal h2o intoxication only after given access to water following a period of water deprivation for reasons which remain unclear [104].
Finally, in contrast to the potential beneficial effects of polydipsia in healthy humans detailed elsewhere [one,iv,57], fluid overload is conversely associated with an increase in mortality in unhealthy animals and humans. More specifically, hyponatremia is associated with an increased mortality rate in hospitalized dogs and cats [105]. Schizophrenic patients with polydipsia demonstrate a higher mortality rate [18] while fluid retentiveness/overload predicts thirty-solar day mortality rate in geriatric patients [106] while increasing morbidity and mortality in critically ill children [107]. One proposed mechanism to explain the increased mortality in compromised patients is a plausible human relationship between fluid overload and inflammation, which has been observed in patients with chronic kidney disease [108,109]. Whether or not fluid overload or hyponatremia is a cause or outcome of disease progression remains unclear [110].
5. Conclusions
Studies performed in mice and men collectively suggest that modest overhydration results in modest urine production (which matches fluid intake volumes) in homeostatic defense of plasma tonicity and intracellular size. In the chronic condition (>3 days) sustained AVP suppression results in the downregulation of AQP2 water channels within the kidney collecting duct, which results in a transient (3–5 days) disability to concentrate urine or reabsorb kidney water back into the circulation in response to AVP stimulation. Complications from astute (>3 L/h) or chronic (5–10+ 50/day) water intakes at rest are uncommon but may issue in acute h2o intoxication or chronic urinary tract abnormalities such as urinary bladder distention, ureter dilation, and hydronephrosis. Modest overhydration (>2 Fifty/day in sedentary individuals of average size in temperate environments) may prevent kidney stones in individuals with recurrent nephrolithiasis or reduce the number of urinary tract infections in susceptible premenopausal females. The anxiolytic effects of copious water intake on a subset of vulnerable individuals, with or without mental illness, has been demonstrated along with data suggesting that overhydration enhances cognitive function. Further studies assessing the benefits and detriments of water intake higher up thirst are required, as long every bit h2o intakes are not extreme and warnings of the potentially fatal consequences of water intoxication are duly noted.
Author Contributions
T.H.-B. contributed to the conceptualization, data curation, and writing–original draft preparation; T.H.-B., V.S.-H., A.P.-Yard. and M.V. contributed to the resource and writing–reviewing and editing of this manuscript.
Funding
This enquiry received no external funding.
Conflicts of Interest
The authors declare no conflicts of involvement.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682940/
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