Clinical Science (2015) 128, 225 (Printed in Great Britain) doi: 10.1042/CS20140496
Chronic dehydration is associated with obstructive sleep apnoea syndrome Simon N. Thornton∗ and Marie Trabalon† ∗
Clinical Science
www.clinsci.org
INSERM, U1116, Universit´e de Lorraine, Nancy, France †CNRS-UMR 6552, Universit´e de Rennes 1, Rennes, France
We were interested to read the recent review article in Clinical Science concerning OSA (obstructive sleep apnoea) and its connections to obesity, diabetes and hypertension [1]. That article looked into the evidence supporting the association of OSA with hypertension, and described the different associated health problems of obesity, hypoxia and cardiovascular disease and the difficulty in finding successful treatments, even using animal models. Similar points have been laid out recently in an editorial published in the New England Journal of Medicine [2]. However, one important aspect that appears to have been overlooked in the review [1] and in the editorial [2], is, with sleep apnoea, the mouth is open sometimes for considerable periods of time. With chronic open mouth breathing there is considerable loss of water leading to chronic dehydration. Appropriate physiological responses to intracellular dehydration (increased osmolality) are thirst (drinking) and vasopressin release, and, in response to extracellular dehydration (hypovolaemia) thirst, vasopressin release and activation of the renin–angiotensin–aldosterone system [3]. In cardiovascular disease, antagonists of the renin–angiotensin– aldosterone system make up the majority of treatments [4,5]. As mentioned in many reviews, these same medications are used in patients with apnoea. This would suggest that hypovolaemia, or extracellular dehydration, is a prominent part of OSA. Another problem associated with dehydration, and especially hypovolaemia, is anaemia leading to hypoxia and thus to an increase in viscosity [6]. This is an adaptive mechanism to low blood volume or hypovolaemia. The correct physiological response would be to reduce red blood cell number, which is also observed in obesity and diabetes [7,8] and, of course, to increase arterial stiffness, leading to cardiovascular disease [9]. It would not be surprising then to understand that all of these effects also lead to resistant hypertension. Recommendations to increase water drinking to reduce dehydration would be necessary, and perhaps especially at night,
in order to help reduce any increase in viscosity [9]. An increase in fluid, especially water, intake would over time restore blood volume, which would reduce blood levels of angiotensin, vasopressin and aldosterone, the three major hormones involved in hypertension. Furthermore, increased fluid intake would help improve blood volume and thus red blood cell number, thus assisting in decreasing hypoxia and leading to a possible reduction in obesity and diabetes associated with OSA.
REFERENCES 1
2 3
4
5
6
7 8
9
Ayas, N. T., Hirsch, A. A., Laher, I., Bradley, T. D., Malhotra, A., Polotsky, V. Y. and Tasali, E. (2014) New frontiers in obstructive sleep apnoea. Clin. Sci. 127, 209–216 CrossRef PubMed Basner, R. C. (2014) Cardiovascular morbidity and obstructive sleep apnea. N. Engl. J. Med. 370, 2339–2341 CrossRef PubMed Thornton, S. N. (2010) Thirst and hydration: physiology and consequences of dysfunction. Physiol. Behav. 100, 15–21 CrossRef PubMed Chobanian, A. V. (2009) The hypertension paradox–more uncontrolled disease despite improved therapy. N. Engl. J. Med. 361, 878–887 CrossRef PubMed Zannad, F., McMurray, J. J., Krum, H., van Veldhuisen, D. J., Swedberg, K., Shi, H., Vincent, J., Pocock, S. J. and Pitt, B. (2011) Eplerenone in patients with systolic heart failure and mild symptoms. N. Engl. J. Med. 364, 11–21 CrossRef PubMed Okamura, K., Washimi, Y., Endo, H., Tokuda, H., Shiga, Y., Miura, H. and Nojiri, Y. (2005) Can high fluid intake prevent cerebral and myocardial infarction? Nihon Ronen Igakkai Zasshi 42, 557–563 CrossRef PubMed Fetissov, S. O. and Thornton, S. N. (2009) Hypovolemia-induced obesity and diabetes. Metabolism 58, 1678 CrossRef PubMed Thornton, S. N. (2009) Hypovolaemia-induced mild hypoxia produces subchronic metabolic dysfunction. Int. J. Obes. 33, 605 CrossRef Alberto, E. C., Tanigawa, T., Maruyama, K., Kawasaki, Y., Eguchi, E., Mori, H., Yoshimura, K., Tanno, S., Sakurai, S., Hitsumoto, S. and Saito, I. (2014) Relationships between nocturnal intermittent hypoxia, arterial stiffness and cardiovascular risk factors in a community-based population: The Toon Health Study. J. Atheroscler. Thromb., doi: 10.5551/jat.24505
Received 18 August 2014; accepted 9 September 2014 Published as Immediate Publication 9 September 2014, doi: 10.1042/CS20140496
Abbreviation: OSA, obstructive sleep apnoea. Correspondence: Professor Simon N. Thornton (email [email protected]).
C The Authors Journal compilation C 2015 Biochemical Society
225
Copyright of Clinical Science is the property of Portland Press Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Chronic dehydration is associated with obstructive sleep apnoea syndrome Simon N. Thornton∗ and Marie Trabalon† ∗
Clinical Science
www.clinsci.org
INSERM, U1116, Universit´e de Lorraine, Nancy, France †CNRS-UMR 6552, Universit´e de Rennes 1, Rennes, France
We were interested to read the recent review article in Clinical Science concerning OSA (obstructive sleep apnoea) and its connections to obesity, diabetes and hypertension [1]. That article looked into the evidence supporting the association of OSA with hypertension, and described the different associated health problems of obesity, hypoxia and cardiovascular disease and the difficulty in finding successful treatments, even using animal models. Similar points have been laid out recently in an editorial published in the New England Journal of Medicine [2]. However, one important aspect that appears to have been overlooked in the review [1] and in the editorial [2], is, with sleep apnoea, the mouth is open sometimes for considerable periods of time. With chronic open mouth breathing there is considerable loss of water leading to chronic dehydration. Appropriate physiological responses to intracellular dehydration (increased osmolality) are thirst (drinking) and vasopressin release, and, in response to extracellular dehydration (hypovolaemia) thirst, vasopressin release and activation of the renin–angiotensin–aldosterone system [3]. In cardiovascular disease, antagonists of the renin–angiotensin– aldosterone system make up the majority of treatments [4,5]. As mentioned in many reviews, these same medications are used in patients with apnoea. This would suggest that hypovolaemia, or extracellular dehydration, is a prominent part of OSA. Another problem associated with dehydration, and especially hypovolaemia, is anaemia leading to hypoxia and thus to an increase in viscosity [6]. This is an adaptive mechanism to low blood volume or hypovolaemia. The correct physiological response would be to reduce red blood cell number, which is also observed in obesity and diabetes [7,8] and, of course, to increase arterial stiffness, leading to cardiovascular disease [9]. It would not be surprising then to understand that all of these effects also lead to resistant hypertension. Recommendations to increase water drinking to reduce dehydration would be necessary, and perhaps especially at night,
in order to help reduce any increase in viscosity [9]. An increase in fluid, especially water, intake would over time restore blood volume, which would reduce blood levels of angiotensin, vasopressin and aldosterone, the three major hormones involved in hypertension. Furthermore, increased fluid intake would help improve blood volume and thus red blood cell number, thus assisting in decreasing hypoxia and leading to a possible reduction in obesity and diabetes associated with OSA.
REFERENCES 1
2 3
4
5
6
7 8
9
Ayas, N. T., Hirsch, A. A., Laher, I., Bradley, T. D., Malhotra, A., Polotsky, V. Y. and Tasali, E. (2014) New frontiers in obstructive sleep apnoea. Clin. Sci. 127, 209–216 CrossRef PubMed Basner, R. C. (2014) Cardiovascular morbidity and obstructive sleep apnea. N. Engl. J. Med. 370, 2339–2341 CrossRef PubMed Thornton, S. N. (2010) Thirst and hydration: physiology and consequences of dysfunction. Physiol. Behav. 100, 15–21 CrossRef PubMed Chobanian, A. V. (2009) The hypertension paradox–more uncontrolled disease despite improved therapy. N. Engl. J. Med. 361, 878–887 CrossRef PubMed Zannad, F., McMurray, J. J., Krum, H., van Veldhuisen, D. J., Swedberg, K., Shi, H., Vincent, J., Pocock, S. J. and Pitt, B. (2011) Eplerenone in patients with systolic heart failure and mild symptoms. N. Engl. J. Med. 364, 11–21 CrossRef PubMed Okamura, K., Washimi, Y., Endo, H., Tokuda, H., Shiga, Y., Miura, H. and Nojiri, Y. (2005) Can high fluid intake prevent cerebral and myocardial infarction? Nihon Ronen Igakkai Zasshi 42, 557–563 CrossRef PubMed Fetissov, S. O. and Thornton, S. N. (2009) Hypovolemia-induced obesity and diabetes. Metabolism 58, 1678 CrossRef PubMed Thornton, S. N. (2009) Hypovolaemia-induced mild hypoxia produces subchronic metabolic dysfunction. Int. J. Obes. 33, 605 CrossRef Alberto, E. C., Tanigawa, T., Maruyama, K., Kawasaki, Y., Eguchi, E., Mori, H., Yoshimura, K., Tanno, S., Sakurai, S., Hitsumoto, S. and Saito, I. (2014) Relationships between nocturnal intermittent hypoxia, arterial stiffness and cardiovascular risk factors in a community-based population: The Toon Health Study. J. Atheroscler. Thromb., doi: 10.5551/jat.24505
Received 18 August 2014; accepted 9 September 2014 Published as Immediate Publication 9 September 2014, doi: 10.1042/CS20140496
Abbreviation: OSA, obstructive sleep apnoea. Correspondence: Professor Simon N. Thornton (email [email protected]).
C The Authors Journal compilation C 2015 Biochemical Society
225
Copyright of Clinical Science is the property of Portland Press Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
