I have written a book about what I believe causes extreme thirst in ME/CFS. The book is available (and always will be available) as a free download from its website. It can also be found on Amazon.
There is a lot to unpack with this book. I will summarise its main arguments as best as I can. Anyone who wants 'the short version', as it were, is encouraged to go to the book's website and read the blurb there.
Why is Thirst Happening in ME/CFS
- ME/CFS patients are often chronically thirsty. Online forums are full of threads discussing this symptom. The most typical symptom presentation involves unquenchable thirst, dilute urine and a tendency towards (mild or sometimes profound) hyponatraemia. Similarly, a recent Long Covid research survey of almost 10,000 patients (Thaweethai et al., ‘Development of a Definition of Post-acute Sequelae of SARS-CoV-2 Infection’, 2023), found that over a third of LC patients report extreme thirst as one of their main symptoms. The story is similar with POTS patients. Why exactly this thirst might be happening has not yet been mapped out however.
- My hypothesis proposes that this thirst represents a new and previously unappreciated kind of polydipsia: 'hypovolemic thirst'.
- The brain actually has two, separate thirst centres: osmotic (water-based thirst) and hypovolemic (triggered when plasma volume drops by 10%, salt + water appetite). And we know that ME/CFS patients are often hypovolemic, largely due to the suppression of the renin-angiotensin-aldosterone axis (a hormonal axis concerned with maintaining salt levels). This hypovolemia can be mild or profound (in Visser and Van Campen's 2018 study ‘Blood Volume Status in Patients with Chronic Fatigue Syndrome: Relation to Complaints’, it was found that ME/CFS patients with orthostatic intolerance had a mean total blood volume reduction of 23%, or around 1.2 litres less than the physiological norm). As a result, it is theoretically possible that the thirst in ME/CFS stems from the triggering of the hypovolemic thirst centre in response to the endogenous hypovolemia that the illness creates.
- Why does this 'hypovolemic thirst' create the aforementioned typical clinical presentation of dilute urine, hyponatraemia and unquenchable thirst? Essentially because the patient is understandably applying the wrong solution to their problem: they just drink water in response to the thirst they feel. The hypovolemic thirst centre can never be quenched by water alone, however. Blood is salty stuff, after all.
- I believe that the sequence of events is this:
RAA axis suppression >>> increased solute loss >>> state of low blood volume created and maintained >>> triggering of hypovolemic thirst centre once plasma volume drops by 10% >>> this is asking for appropriately concentrated fluids but the patient understandably just drinks pure water in response to their thirst >>> water is just urinated out and blood volume remains low >>> thirst remains and so vicious cycle develops
The thirst remains unquenchable as the wrong solution is being applied to the problem; the urine is dilute due to the amount being ingested and the hyponatraemia develops for two reasons: the amount of water consumed and because of the RAA-axis suppression and associated solute loss
- I believe that a better way of treating this thirst is to stop drinking pure water (for the most part) and switch entirely to drinking Oral Rehydration Solution. These sachets rely on the sodium-glucose co-transporter in the gut and effectively boost blood volume, as was shown in a study by Medow (Medow et al., ‘The Benefits of Oral Rehydration Solution on Children with POTS’, 2019.). I believe that it is best, in the main, only to drink ORS as drinking large amounts of pure water will counteract their effect. It is better if the vast majority of fluid consumed is also boosting plasma volume.
- NB: There may be other reasons for thirst in the illness - there probably are - but I think the major reason, the cause of extreme thirst, is likely to be the hypovolemia.
Challenging Psychogenic Water Drinking, aka 'Primary Polydipsia'
-The primary purpose of the book is actually to challenge a condition called 'Primary Polydipsia' or 'Psychogenic Water Drinking'. This condition is currently believed to involve drinking enormous amounts of fluid in the absence of any physiological need and purely because of mental ill-health.
- Despite the fact that 'Primary Polydipsia' is taught about to all medical students, it has actually received very little research. It is currently regarded as something of a medical mystery: its cause is considered to be unknown but, nevertheless, it is also typically regarded as a psychological problem (sound familiar?).
- Primary Polydipsia was first conceptualised back in the 1930s, 40s and 50s. The papers from those times are happy to attribute the disorder to such Freudian staples as: troubled childhoods, not having enough sex, female hysteria, homosexuality, conversion disorders and delusional hypochondriasis and just, in general, to being emotionally disturbed. All of the central diagnostic tests and physiological assumptions about the condition stemmed from that time: they have never been challenged since. In fact, with some minor changes around the edges, the physiological teaching about Primary Polydipsia is the same now as it was 60 years ago.
- While some people do drink excessive water for psychological reasons, those patients don't tend to experience thirst as a motivator. However, the vast majority of so-called psychogenic water drinkers do say that their primary motivator is extreme thirst.
-It is my belief that what has always been termed 'psychogenic water drinking' has, in the main, been 'hypovolemic dehydration' by another name
- I say this for several reasons.
First, because the typical clinical presentation in so-called Primary Polydipsia is the exact same as what one would expect to see in hypovolemic thirst: dilute urine and hyponatraemia, only that in teaching about Primary Polydipsia it is assumed that these clinical features develop purely because of drinking too much water in the absence of any physiological need. In contrast, the theory I am putting forward can explain these symptoms as stemming from the patient understandably applying the wrong solution to their hypovolemic thirst as well as from the RAA-axis induced solute loss.
Secondly, when you strip the early papers of their Freudian jargon, it is clear that the patients in question were actually suffering from ME/CFS. They 'experienced breathlessness on exertion', 'ached everywhere' and (as the authors put it at the time) had 'hysterical weakness of the legs'. And they developed their health complaints after physiological, medical or psychological traumas.
Thirdly, the hypovolemic thirst centre was not discovered until the 1960s, long after the idea of psychogenic water drinking had taken hold. It could have explained the symptoms from the beginning but early attempts to understand these symptoms were hampered by not having enough information. As a result, a psychogenic cause was assumed: the same old, hubristic error we have seen in so many other cases.
- Prof. Daniel Bichet, a professor of medicine at the University of Montreal, is one of the few medical researchers to have expressed a note of caution about the supposedly psychogenic nature of Primary Polydipsia. Writing in 2017, he said: 'The diagnosis of compulsive water drinking must be made with care and may represent our ignorance of yet undescribed pathophysiological mechanisms'. Primary Polydipsia was always likely to be 'solved' by a blindspot in modern medicine. Has that blindspot been ME/CFS?
My Personal Story
- While for some ME/CFS patients, thirst is an unpleasant, daily nuisance, I once suffered from this symptom at the more extreme end. From August 2020 until January 2021, my life descended into a nightmare of extreme thirst which often felt, and in fact was, life threatening. On 'good' days, my water intake was around 8 litres but if I crashed, that could jump up to 20 litres over a 24 hour period. At those times, I often thought that I was dying and I fought for the morning light (as sleep was not possible at such times). I had no idea why this nightmare was happening to me. I am still traumatised by that time and the severe symptoms I experienced.
- In January 2021, I was hospitalised with profound hyponatraemia of 116. This was enough to be in a hyponatraemia-induced coma or even dead but, although severely ill, I was still conscious. That week in hospital I was often treated as if I were an ICU patient (as my medical records later revealed) although in a standard ward (as ICU space was limited).
- I knew that I was being treated like a mental case throughout my stay. 'Don't drink water behind our back when you go to the toilet' and 'You are only in here because you were drinking so much water' were the kinds of things I was told. I even overheard a doctor and nurse laughing about my supposed diagnosis in the hallway. And yes, I was diagnosed with psychogenic polydipsia. Had I died, I would have had mental illness listed as the cause of death. I tried to tell the hospital team that ME/CFS patients were often thirsty, even if no one had mapped out exactly why. Everything I said about ME was ignored and my medical records later stated 'Patient admitted with self-diagnosed ME due to having non-specific symptoms'. (although I had been diagnosed a few years previously actually and had tried to explain post-exertional malaise).
- My blood sodium was normalised thanks to the hospital stay but as soon as I experienced my next crash, two weeks after leaving hospital, the extreme thirst returned. At that point, I learnt about the existence of the hypovolemic thirst centre and wondered if hypovolemia had been the cause of my thirst. I immediately went to the local pharmacy to buy some Oral Rehydration Solution and drank 600 ml of it. My thirst diminished hugely, the lights switched back on and I felt much better.
-Since that time, two and a half years ago, I have never needed to drink more than 3L per day. For someone who once suffered through 20 litres of fluid in a day, this still seems like a miracle to me.
My Hopes for the Book
- That it might lead to research by ME/CFS researchers into the nature of thirst that occurs in ME/CFS patients, the validation of a new kind of polydipsia (hypovolemic dehydration) along with treatment guidelines so that patients can manage this symptom effectively (and without entering into the kind of, potentially fatal, nightmare that is possible at the more extreme end of the spectrum)
- That it will one day lead to the validation of 'hypovolemic dehydration' as a new kind of polydipsia and one that solves the mystery of so-called 'Primary Polydipsia' (at least in many cases), leading to the mitigation of suffering of those affected with this problem and the ending of current stigmatisation
- That, since Primary Polydipsia is currently taught routinely in medical school, it will have to be replaced / supplemented with teaching on hypovolemic thirst instead. This will necessarily also involve teaching about the core pathophysiological mechanisms in ME/CFS that create such a thirst. This will mean that no future medical student can be under any illusion as to just how serious ME/CFS actually is. In this way, medical minds of the future will be more open to the illness and more may turn their minds to researching it. Put simply: if Primary Polydipsia can be replaced by Hypovolemic Dehydration, then this represents a 'way in' for knowledge about ME/CFS to become more widespread in the medical profession.
I did come across a forum posting (unfortunately I can't find it now) where a carer wrote movingly about the death of a severe ME/CFS patient who had been in her care. The cause of death given was 'psychogenic polydipsia'. The carer however wrote that she knew this was not the case. At the moment, people with the problem of 'hypovolemic thirst' are being held responsible even for their own deaths. This is a medical travesty and it needs to change. I hope that my book can achieve that.
Please forward details of my book to anyone you think might like to read it. As I mentioned, it will always be available for free download on its website.
There is a lot to unpack with this book. I will summarise its main arguments as best as I can. Anyone who wants 'the short version', as it were, is encouraged to go to the book's website and read the blurb there.
Why is Thirst Happening in ME/CFS
- ME/CFS patients are often chronically thirsty. Online forums are full of threads discussing this symptom. The most typical symptom presentation involves unquenchable thirst, dilute urine and a tendency towards (mild or sometimes profound) hyponatraemia. Similarly, a recent Long Covid research survey of almost 10,000 patients (Thaweethai et al., ‘Development of a Definition of Post-acute Sequelae of SARS-CoV-2 Infection’, 2023), found that over a third of LC patients report extreme thirst as one of their main symptoms. The story is similar with POTS patients. Why exactly this thirst might be happening has not yet been mapped out however.
- My hypothesis proposes that this thirst represents a new and previously unappreciated kind of polydipsia: 'hypovolemic thirst'.
- The brain actually has two, separate thirst centres: osmotic (water-based thirst) and hypovolemic (triggered when plasma volume drops by 10%, salt + water appetite). And we know that ME/CFS patients are often hypovolemic, largely due to the suppression of the renin-angiotensin-aldosterone axis (a hormonal axis concerned with maintaining salt levels). This hypovolemia can be mild or profound (in Visser and Van Campen's 2018 study ‘Blood Volume Status in Patients with Chronic Fatigue Syndrome: Relation to Complaints’, it was found that ME/CFS patients with orthostatic intolerance had a mean total blood volume reduction of 23%, or around 1.2 litres less than the physiological norm). As a result, it is theoretically possible that the thirst in ME/CFS stems from the triggering of the hypovolemic thirst centre in response to the endogenous hypovolemia that the illness creates.
- Why does this 'hypovolemic thirst' create the aforementioned typical clinical presentation of dilute urine, hyponatraemia and unquenchable thirst? Essentially because the patient is understandably applying the wrong solution to their problem: they just drink water in response to the thirst they feel. The hypovolemic thirst centre can never be quenched by water alone, however. Blood is salty stuff, after all.
- I believe that the sequence of events is this:
RAA axis suppression >>> increased solute loss >>> state of low blood volume created and maintained >>> triggering of hypovolemic thirst centre once plasma volume drops by 10% >>> this is asking for appropriately concentrated fluids but the patient understandably just drinks pure water in response to their thirst >>> water is just urinated out and blood volume remains low >>> thirst remains and so vicious cycle develops
The thirst remains unquenchable as the wrong solution is being applied to the problem; the urine is dilute due to the amount being ingested and the hyponatraemia develops for two reasons: the amount of water consumed and because of the RAA-axis suppression and associated solute loss
- I believe that a better way of treating this thirst is to stop drinking pure water (for the most part) and switch entirely to drinking Oral Rehydration Solution. These sachets rely on the sodium-glucose co-transporter in the gut and effectively boost blood volume, as was shown in a study by Medow (Medow et al., ‘The Benefits of Oral Rehydration Solution on Children with POTS’, 2019.). I believe that it is best, in the main, only to drink ORS as drinking large amounts of pure water will counteract their effect. It is better if the vast majority of fluid consumed is also boosting plasma volume.
- NB: There may be other reasons for thirst in the illness - there probably are - but I think the major reason, the cause of extreme thirst, is likely to be the hypovolemia.
Challenging Psychogenic Water Drinking, aka 'Primary Polydipsia'
-The primary purpose of the book is actually to challenge a condition called 'Primary Polydipsia' or 'Psychogenic Water Drinking'. This condition is currently believed to involve drinking enormous amounts of fluid in the absence of any physiological need and purely because of mental ill-health.
- Despite the fact that 'Primary Polydipsia' is taught about to all medical students, it has actually received very little research. It is currently regarded as something of a medical mystery: its cause is considered to be unknown but, nevertheless, it is also typically regarded as a psychological problem (sound familiar?).
- Primary Polydipsia was first conceptualised back in the 1930s, 40s and 50s. The papers from those times are happy to attribute the disorder to such Freudian staples as: troubled childhoods, not having enough sex, female hysteria, homosexuality, conversion disorders and delusional hypochondriasis and just, in general, to being emotionally disturbed. All of the central diagnostic tests and physiological assumptions about the condition stemmed from that time: they have never been challenged since. In fact, with some minor changes around the edges, the physiological teaching about Primary Polydipsia is the same now as it was 60 years ago.
- While some people do drink excessive water for psychological reasons, those patients don't tend to experience thirst as a motivator. However, the vast majority of so-called psychogenic water drinkers do say that their primary motivator is extreme thirst.
-It is my belief that what has always been termed 'psychogenic water drinking' has, in the main, been 'hypovolemic dehydration' by another name
- I say this for several reasons.
First, because the typical clinical presentation in so-called Primary Polydipsia is the exact same as what one would expect to see in hypovolemic thirst: dilute urine and hyponatraemia, only that in teaching about Primary Polydipsia it is assumed that these clinical features develop purely because of drinking too much water in the absence of any physiological need. In contrast, the theory I am putting forward can explain these symptoms as stemming from the patient understandably applying the wrong solution to their hypovolemic thirst as well as from the RAA-axis induced solute loss.
Secondly, when you strip the early papers of their Freudian jargon, it is clear that the patients in question were actually suffering from ME/CFS. They 'experienced breathlessness on exertion', 'ached everywhere' and (as the authors put it at the time) had 'hysterical weakness of the legs'. And they developed their health complaints after physiological, medical or psychological traumas.
Thirdly, the hypovolemic thirst centre was not discovered until the 1960s, long after the idea of psychogenic water drinking had taken hold. It could have explained the symptoms from the beginning but early attempts to understand these symptoms were hampered by not having enough information. As a result, a psychogenic cause was assumed: the same old, hubristic error we have seen in so many other cases.
- Prof. Daniel Bichet, a professor of medicine at the University of Montreal, is one of the few medical researchers to have expressed a note of caution about the supposedly psychogenic nature of Primary Polydipsia. Writing in 2017, he said: 'The diagnosis of compulsive water drinking must be made with care and may represent our ignorance of yet undescribed pathophysiological mechanisms'. Primary Polydipsia was always likely to be 'solved' by a blindspot in modern medicine. Has that blindspot been ME/CFS?
My Personal Story
- While for some ME/CFS patients, thirst is an unpleasant, daily nuisance, I once suffered from this symptom at the more extreme end. From August 2020 until January 2021, my life descended into a nightmare of extreme thirst which often felt, and in fact was, life threatening. On 'good' days, my water intake was around 8 litres but if I crashed, that could jump up to 20 litres over a 24 hour period. At those times, I often thought that I was dying and I fought for the morning light (as sleep was not possible at such times). I had no idea why this nightmare was happening to me. I am still traumatised by that time and the severe symptoms I experienced.
- In January 2021, I was hospitalised with profound hyponatraemia of 116. This was enough to be in a hyponatraemia-induced coma or even dead but, although severely ill, I was still conscious. That week in hospital I was often treated as if I were an ICU patient (as my medical records later revealed) although in a standard ward (as ICU space was limited).
- I knew that I was being treated like a mental case throughout my stay. 'Don't drink water behind our back when you go to the toilet' and 'You are only in here because you were drinking so much water' were the kinds of things I was told. I even overheard a doctor and nurse laughing about my supposed diagnosis in the hallway. And yes, I was diagnosed with psychogenic polydipsia. Had I died, I would have had mental illness listed as the cause of death. I tried to tell the hospital team that ME/CFS patients were often thirsty, even if no one had mapped out exactly why. Everything I said about ME was ignored and my medical records later stated 'Patient admitted with self-diagnosed ME due to having non-specific symptoms'. (although I had been diagnosed a few years previously actually and had tried to explain post-exertional malaise).
- My blood sodium was normalised thanks to the hospital stay but as soon as I experienced my next crash, two weeks after leaving hospital, the extreme thirst returned. At that point, I learnt about the existence of the hypovolemic thirst centre and wondered if hypovolemia had been the cause of my thirst. I immediately went to the local pharmacy to buy some Oral Rehydration Solution and drank 600 ml of it. My thirst diminished hugely, the lights switched back on and I felt much better.
-Since that time, two and a half years ago, I have never needed to drink more than 3L per day. For someone who once suffered through 20 litres of fluid in a day, this still seems like a miracle to me.
My Hopes for the Book
- That it might lead to research by ME/CFS researchers into the nature of thirst that occurs in ME/CFS patients, the validation of a new kind of polydipsia (hypovolemic dehydration) along with treatment guidelines so that patients can manage this symptom effectively (and without entering into the kind of, potentially fatal, nightmare that is possible at the more extreme end of the spectrum)
- That it will one day lead to the validation of 'hypovolemic dehydration' as a new kind of polydipsia and one that solves the mystery of so-called 'Primary Polydipsia' (at least in many cases), leading to the mitigation of suffering of those affected with this problem and the ending of current stigmatisation
- That, since Primary Polydipsia is currently taught routinely in medical school, it will have to be replaced / supplemented with teaching on hypovolemic thirst instead. This will necessarily also involve teaching about the core pathophysiological mechanisms in ME/CFS that create such a thirst. This will mean that no future medical student can be under any illusion as to just how serious ME/CFS actually is. In this way, medical minds of the future will be more open to the illness and more may turn their minds to researching it. Put simply: if Primary Polydipsia can be replaced by Hypovolemic Dehydration, then this represents a 'way in' for knowledge about ME/CFS to become more widespread in the medical profession.
I did come across a forum posting (unfortunately I can't find it now) where a carer wrote movingly about the death of a severe ME/CFS patient who had been in her care. The cause of death given was 'psychogenic polydipsia'. The carer however wrote that she knew this was not the case. At the moment, people with the problem of 'hypovolemic thirst' are being held responsible even for their own deaths. This is a medical travesty and it needs to change. I hope that my book can achieve that.
Please forward details of my book to anyone you think might like to read it. As I mentioned, it will always be available for free download on its website.
The Maasai tribe in Tanzania though are regular blood drinkers - maybe they are onto something!
