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V*, K. Dipsogenic Diabetes Insipidus. Encyclopedia. Available online: https://encyclopedia.pub/entry/9074 (accessed on 16 November 2024).
V* K. Dipsogenic Diabetes Insipidus. Encyclopedia. Available at: https://encyclopedia.pub/entry/9074. Accessed November 16, 2024.
V*, Krishnaraju. "Dipsogenic Diabetes Insipidus" Encyclopedia, https://encyclopedia.pub/entry/9074 (accessed November 16, 2024).
V*, K. (2021, April 27). Dipsogenic Diabetes Insipidus. In Encyclopedia. https://encyclopedia.pub/entry/9074
V*, Krishnaraju. "Dipsogenic Diabetes Insipidus." Encyclopedia. Web. 27 April, 2021.
Dipsogenic Diabetes Insipidus
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This entry is adapted from the peer-reviewed paper 10.3390/healthcare9040406

Dipsogenic diabetes insipidus (DDI) is a subtype of primary polydipsia (PP), which occurs mostly in healthy people without psychiatric disease. 

dipsogenic diabetes insipidus habitual polydipsia polyuria-polydipsia syndrome dipsogenic polydipsia water intoxication

1. Introduction

With the increasing acceptance of lifestyle programs and the common belief that drinking several liters of fluid per day is healthy, the prevalence of this phenomenon is increasing, particularly outside of the psychiatric setting [1][2]. This phenomenon which occurs in healthy people without psychiatric disease, seems to be closely related with dipsogenic diabetes insipidus (DDI). However, data in the overall population have not been studied and yet to be explored. DDI is defined as a rare non-psychiatric syndrome of disordered thirst, in which the osmotic threshold for thirst is abnormally low, below the threshold for antidiuretic hormone (ADH) release [3]. As DDI is not a well-established disease, there is less information available about DDI, and hence less knowledge about its prevalence in aquaholics.

2. Pathophysiology

DDI is a polyuria polydipsia syndrome (PPS) that mostly occurs in healthy people without psychiatric disease, in contrast to primary polydipsia (PP) that occurs in patients with psychiatric disease. Furthermore, as DDI occurs in healthy people without psychiatric disease, it is often confused with partial central diabetes insipidus (PCDI). Moreover, DDI is not a universally recognized PPS. DDI is caused by a disorder in the patient thirst center, where the osmotic threshold to release antidiuretic hormone is abnormally low [4]. It is a subset of PP, and first described in 1987 by Robertson G in patients without psychiatric illness [5]. This PPS has low urine osmolality, normal plasma osmolality, and normal urinary concentrating capacity. In both PP and DDI, the patient consumes an excessive amount of fluid, most frequently water, which decreases plasma osmolality followed by decreased antidiuretic hormone and less aquaporin-2 (AQP2) expression, resulting in hypotonic polyuria. This is in contrast to central diabetes insipidus (CDI), where excessively dilute urine is followed by ingestion of excess fluid [4]. In DDI, if the lower plasma osmolality is maintained for a continuous period, than the body sets this range as the threshold for ADH release [6]. Though there are discrepancies, many authors have reported that in healthy people the thirst sensation would occur at a higher osmotic threshold, compared to ADH release [7][8][9]. In DDI patients, the thirst threshold will be lower than that of ADH release [3].

The etiology could be idiopathic, or due to a structural lesion similar to CDI [3]. Another hypothesis is that it could be due to behavioral aspects, due to a belief that drinking excess water will protect against the formation of nephrolithiasis or have more pathologic benefits [10][11]. Hence, as DDI patients have no signs of mental illness or increased thirst, the disorder could also be named “habitual polydipsia” [10][12]. DDI could be due to lesions in the hypothalamus and is also possible in lifestyle conscious men and women who consume an excess of water to detox the body. 

3. Differential Diagnosis of DDI and Other PPS

Arginine vasopressin (AVP), a antidiuretic hormone (ADH), and thirst are the two factors that maintain water homeostasis. If these two regulatory mechanisms face any disturbance then it leads to PPS, which includes three different conditions: CDI due to insufficient secretion of AVP, nephrogenic DI caused by renal insensitivity to AVP action, and PP/DDI due to excessive fluid intake and a consequent physiological suppression of AVP [13].

The first step in evaluating patients with PPS is to verify that there is polyuria and that it is hypotonic in nature. For polyuria, the urine output should be in excess of 40 mL/kg/24 h, and to confirm PPS, the urine osmolality should be <300 mOsm/kg. If the urine osmolality is above this value, then other etiologies that are not primarily caused by impaired AVP secretion or action have to be ruled out, such as hyperglycaemia or hypercalcaemia. [14][15][16] Once hypotonic polyuria is confirmed, history has to be taken into account to characterize PPS. This includes onset of polyuria, whether it is gradual or abrupt, craving for ice water, and family history to rule out hereditary DI (diabetes insipidus) [17].

In order to diagnose DDI, the patient should exhibit excessive thirst as the main symptom intact and urine concentrating ability. Moreover, as DDI could be possible due to the similar hypothalamic lesions of CDI, c-MRI scans could be done to diagnose PP as an idiopathic or psychiatric based illness [18]. Currently, in many endocrine centers the water deprivation test is used for diagnosis of PPS. However, this test has some lacuna, as the prolonged water deprivation not only creates discomfort to patients, leading to discontinuation [13], it also creates resistance to desmopressin [19]. In addition to the above mentioned routine analysis, Fenske et al. suggested determination of copeptin, a precursor peptide of AVP and mirrors circulating AVP concentration [20][21]. Hence based on the above data, for the differential diagnosis of PPS, the water deprivation test in combination with copeptin measurement may become a standard test in the future.

4. Treatment

Antidiuretic therapy was the early treatment for DDI. Due to the risk of water intoxication, its usage has not been in practice. In 2011, an animal study showed that GLP-1R (Glucagon-like peptide-1 receptor) agonists have a hypodipsic effect through central activation of GLP-1R [22]. Hence, the potential of GLP-1R agonists like liraglutide and dulaglutide in the treatment of DDI has to be explored. In 2012, Shapiro M et al. suggested that sour candies, ice chips, or gum might be useful, if used as alternatives to fluid intake [17]. A DDI case study reported that in 2018 a 19-year-old male was successfully treated with low dose desmopressin in addition to fluid restrictions [23].

5. Could Excessive Drinking Habits Lead to DDI Associated with Water Intoxication?

There is a strong belief in society that drinking excessive water will purify and cleanse the body by removing harmful waste products. In addition, even scientific studies done on different disease conditions tend to support high fluid intake. A 10-year cohort study (n = 48000 men) done in health professionals reported that fluid consumption is inversely proportional to the risk of bladder cancer [24]. Similar results have been reported for colon cancer, chronic kidney disease, urolithiasis, urinary tract infection, fatal coronary heart disease, venous thromboembolism, and exercise-induced bronchospasm [25][26][27][28][29][30][31][32][33][34]. However, experts believe that we do not require fluid in excess of the amount our body actually signals for. Adding to it, if thirst is an imperfect signal of fluid deficit, than how come everything else in the body could be perfect? Actually, the thirst sensation is triggered when the body loses water by 1–2%, and during which physical and cognitive performance might also decline [35][36][37][38][39][40].

6. Summary

DDI is a little studied and reported disease. As DDI cases have been reported in health-conscious people consuming excess fluid, it could be hypothesized that habitual polydipsia might be a cause of DDI. To substantiate this claim, more detailed studies in habitual over drinkers needs to be done. Moreover, specific research investigating novel treatment strategies is desirable. Most importantly, enhancing the awareness in the general public to rationalize the common belief that drinking excessive water will purify and cleanse the body is the need of the hour.

References

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  3. Perkins, R.M.; Yuan, C.M.; Welch, P.G. Dipsogenic diabetes insipidus: Report of a novel treatment strategy and literature review. Clin. Exp. Nephrol. 2006, 10, 63–67.
  4. Robertson, G.L. Differential diagnosis of polyuria. Annu. Rev. Med. 1998, 39, 425–442.
  5. Robertson, G.L. Dipsogenic diabetes insipidus: A newly recognized syndrome caused by a selective defect in the osmoregulation of thirst. Trans. Assoc. Am. Phys. 1987, 100, 241–249.
  6. Goldman, M.B.; Robertson, G.L.; Luchins, D.J.; Hedeker, D. The influence of polydipsia on water excretion in hyponatremic, polydipsic, schizophrenic patients. J. Clin. Endocrinol. Metab. 1996, 81, 1465–1470.
  7. Wolf, A.V. Osmometric analysis of thirst in man and dog. Am. J. Physiol. 1950, 161, 75–86.
  8. Baylis, P.; Robertson, G. Plasma vasopressin response to hypertonic saline infusion to assess posterior pituitary function. J. R. Soc. Med. 1980, 73, 255–260.
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  10. Valtin, H. “Drink at least eight glasses of water a day.” Really? Is there scientific evidence for “8 × 8”. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2002, 283, R993–R1004.
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  13. Rogers, P.W.; Kurtzman, N.A. Renal failure, uncontrollable thirst, and hyperreninemia. Cessation of thirst with bilateral nephrectomy. JAMA 1973, 225, 1236–1238.
  14. Baylis, P.H.; Thompson, C.J. Osmoregulation of vasopressin secretion and thirst in health and disease. Clin. Endocrinol. 1988, 29, 549–576.
  15. Weiss, J.P.; Blaivas, J.G. Nocturia. J. Urol. 2000, 163, 5–12.
  16. van Kerrebroeck, P.; Abrams, P.; Chaikin, D.; Donovan, J.; Fonda, D.; Jackson, S.; Jennum, P.; Johnson, T.; Lose, G.; Mattiasson, A.; et al. The standardisation of terminology in nocturia: Report from the Standardisation Subcommittee of the International Continence Society. Neurourol. Urodyn. 2002, 21, 179–183.
  17. Robertson, G.L. Diabetes Insipidus. Endocrinol. Metab. Clin. N. Am. 1995, 24, 549–572.
  18. Shapiro, M.; Weiss, J.P. Diabetes Insipidus: A review. J. Diabetes Metab. 2012, S6, 2–11.
  19. Cadnapaphornchai, M.A.; Summer, S.N.; Falk, S.; Thurman, J.M.; Knepper, M.A.; Schrier, R.W. Effect of primary polydipsia on aqua-porin and sodium transporter abundance. Am. J. Physiol. Renal Physiol. 2003, 285, F965–F971.
  20. Fenske, W.; Quinkler, M.; Lorenz, D.; Zopf, K.; Haagen, U.; Papassotiriou, J.; Pfeiffer, A.F.; Fassnacht, M.; Störk, S.; Allolio, B. Copeptin in the differential diagnosis of the poly-dipsia-polyuria syndrome—Revisiting the direct and indirect water deprivation tests. J. Clin. Endocrinol. Metab. 2011, 96, 1506–1515.
  21. Szinnai, G.; Morgenthaler, N.G.; Berneis, K.; Struck, J.; Müller, B.; Keller, U.; Christ-Crain, M. Changes in plasma copeptin, the c-terminal portion of arginine vasopressin during water deprivation and excess in healthy subjects. J. Clin. Endocrinol. Metab. 2007, 92, 3973–3978.
  22. McKay, N.J.; Kanoski, S.E.; Hayes, M.R.; Daniels, D. Glucagon-like peptide-1 receptor agonists suppress water intake independent of effects on food intake. Am. J. Physiol. Integr. Comp. Physiol. 2011, 301, R1755–R1764.
  23. Idowu, A.O.; Ajiro, T.O.; Odusan, O.O. Dipsogenic form of primary polydipsia in a young man and an emerging treatment modality. Int. J. Med Pharm. Case Rep. 2018, 11, 1–6.
  24. Michaud, D.; Spiegelman, D.; Clinton, S.K.; Rimm, E.B.; Curhan, G.C.; Willett, W.C.; Giovannucci, E.L. Fluid intake and risk of bladder cancer in men. N. Engl. J. Med. 1999, 340, 1390–1397.
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