Thanks again to Patrick for letting Health Rising publish his blog. In it Patrick opens up new ground on a topic that hasn’t received the attention it deserves – the unusual thirst that many people with ME/CFS experience. Please note this is a long (but very well-written) blog. You might want to take it in chunks and check out the Gist. 


Water – it’s the stuff of life – but drinking too much can be dangerous.

It’s not in the guidelines. Nor is it in most symptom lists, but it’s hard to ignore the fact that many people with ME/CFS patients suffer from could be termed “excessive thirst”.

The now-retired Dr. David Bell said that his ME/CFS patients could drink up to three gallons (11.5 litres) daily. Meanwhile, Dr. Jacob Teitelbaum more colourfully states that ME/CFS patients can ‘drink like fish and pee like racehorses’.

Searches for terms like ‘thirst’ and ‘dehydration’ on ME/CFS forums such as phoenixrising.me will return hundreds of posts in which patients discuss this symptom. I’ve read through the majority of these. The nature of the thirst is described similarly across the board: it tends to be unquenchable, to involve dilute urine and to get worse during episodes of post-exertional malaise.

While these factors seem to be nearly constant, some patients can also develop hyponatremia (low blood sodium) and some suffer from the symptom more severely than others. Indeed, while some patients might ‘only’ drink four or five litres of water per day, a minority of others are so severely affected that they might drink up to 20. But why is this thirst happening and what can be done about it?

This was a question that, at one time, I had to answer urgently.

Patrick’s Story with Life-Threatening Hyponatremia (Low Blood Sodium Levels)

I have had ME/CFS for five years. For the first half of that time, I certainly experienced increased thirst, typically drinking around four litres of water per day. It was unpleasant at times but it didn’t bother me too much.

In mid-2020 however, that all changed and, for a six-month period, I entered into a personal hell. My ‘good’ days involved drinking around eight litres but when I crashed, the thirst was so extreme and all-encompassing that I could drink 20 litres (over 5 gallons) of water in a 24-hour period.

The symptoms were worse at night. There were around a dozen nights over this period when the thirst prevented any sleep at all. On one occasion, I did not sleep for three nights out of four. But it wasn’t just thirst in isolation. I felt that I was drying up inside and that blood was not reaching my skin and brain in a profound way (although I did not understand the significance of this at the time). I am not at all exaggerating to say that I felt like I was fighting for the morning light at those times and that I feared that my body could not sustain the strain that it was under for much longer.

One of the most difficult things about this nightmare was that I had no idea what to do about it. And so, in January 2021, feeling like I had no other option, I packed a bag and presented myself to my local A&E in Dublin. There, it was found that I had a profound hyponatremia of 116 (normal range: 135-145). Such a severe level of hyponatremia is strongly associated with the development of cerebral edema, something which can induce a coma and lead to death.


At the hospital, Patrick was found to have hyponatremia – dangerously low blood sodium levels.

That week in hospital was very challenging: blood tests were taken morning and night every two hours. Early on in my stay, my blood sodium levels auto-corrected too quickly. This is a known risk factor for serious forms of brain damage and I had to be put on a drip along with desmopressin injections to bring my sodium levels back down again (desmopressin is a medication that has essentially the same effect as vasopressin/antidiuretic hormone, the hormone that conserves water). As I read later in my medical records, I was being treated, for the most part, like an intensive care patient albeit in a standard ward. My case was considered ‘tenuous’ which, in medical terms, means ‘touch and go’.

Throughout that time, I tried to tell the doctors that ME/CFS patients tended to suffer from excessive thirst. I told them about a paper (by Dr. Miwa from 2016) that had found reduced levels of salt and water-retention hormones in the illness. Perhaps that was something to do with what I was experiencing? No one listened though and later my medical records stated simply (and inaccurately on every count): ‘Patient was admitted with self-diagnosed ME due to having non-specific symptoms’.

In the hospital, I was diagnosed as having a mental health condition called ‘psychogenic polydipsia’ (also known as ‘primary polydipsia’). In this condition, it is assumed that people are drinking enormous quantities of water in the absence of any physiological need and only because of mental illness.

I knew that I was being treated like a mental case throughout my stay. At various times, I was told: ‘You’re only in here because of drinking so much water’ and ‘Will we have to go with you to the toilet in case you drink behind our back?’ At one point, standing near to the hallway, I overheard the doctor and nurse talking about my case. ‘So, in this ward, we have Patrick. And he’s been diagnosed with… primary polydipsia’. And then they laughed.

I said nothing about this diagnosis at the time. My blood sodium levels eventually normalized and I just wanted to get home.

Two weeks after I had left the hospital, I experienced another episode of post-exertional malaise. At the exact same time, the thirst came raging back. As before, drinking more water only made it worse. I didn’t want the same old vicious cycle to start up again: I had to work out what was really going on. Had I been drinking so much because I was mentally ill? Or was there something about ME/CFS that caused the thirst?

Five gallon bottle of water

At one point, Patrick was drinking over 20 litres (5 gallons) of water a day.

I had been reading a book about hyponatremia by Prof. Tim Noakes. Titled ‘Waterlogged:The Serious Problem of Overhydration in Endurance Sports’, it examines the common problem of overhydration in professional athletes. Early in the book, there was a diagram about thirst physiology. Most of it was dedicated to the ‘osmotic thirst’ centre. This is the most common reason for thirst. It is triggered by classical dehydration and the answer is simply to drink more water.

But something else also caught my eye: the ‘hypovolemic thirst centre’. The brain’s second, and much lesser known, thirst centre is triggered when the plasma blood volume drops by 10% (c. 280 ml). And, in order to quench it, you need to drink something appropriately salty. Blood is salty stuff, after all, and pure water alone can never sustainably boost blood volume. It is, after all, the prerogative of the kidneys to filter water out. (For articles that describe hypovolemic thirst in more detail, see this paper and the relevant sections in this paper).

My mind raced furiously. I knew that ME/CFS patients routinely didn’t have enough blood because of mechanisms within their illness. Was this the reason why I had been so thirsty? And I had just been mistakenly – but understandably – applying the wrong solution to my problem?

I then remembered a study by Prof. Medow in which it was found that drinking Oral Rehydration Solution was as effective as a Saline IV for boosting blood volume. In Ireland, these little packets of salt, glucose, and potassium are sold under the brand name ‘Dioralyte’. I immediately went out to the nearby chemist, bought a box, and drank 600ml of the stuff.

My thirst reduced profoundly. I could feel blood getting back into my skin and brain. I could walk up a staircase without having to stop every step. The lights had switched back on.

At last, I had worked out the main reason for my extreme thirst. I wasn’t a mental case, after all. I had fought through the most horrendous symptoms, symptoms that had been created because my illness had reduced the amount of blood in my body. I had tried to resolve the resulting thirst signal in the wrong way. My thirst had never been looking for more water. Instead, you could say, that I had been thirsty for blood.

I was so glad to have mitigated my thirst that I simply tried to put a lid over my hospital experience and over the severe symptoms that I had suffered in the preceding months. To this day, I am still traumatized by the life-threatening symptoms that I experienced over that time, and for a long period afterwards, I just tried to move on with my life as best as I could. But later, as we shall see, I would come to revisit the whole experience – and my diagnosis as a ‘psychogenic water drinker’ – with a very different purpose in my mind.

So much for my personal story. How can we map out, in more precise and theoretical terms, why extreme thirst might be occurring in ME/CFS? Let’s consider this question now, first reminding ourselves of the findings on low blood volume in the illness and then mapping these findings onto thirst physiology.

Low Blood Volume in ME/CFS: A Summary of the Key Findings To-Date

While this is not a problem that affects all patients, it has been known for a long time that low blood volume is a central characteristic of ME/CFS. For example, back in 2002, a Harvard study found that ME/CFS patients had a 9% reduction in plasma blood volume in comparison to healthy controls.

However, later studies found that, when you categorise ME/CFS patients according to their illness severity, the more seriously ill patients tend to have an even more profound drop in blood volume. A 2018 study by Prof. Visser and Dr. Van Campen found that housebound ME/CFS patients with orthostatic intolerance had 23% less total blood volume than the physiological norm, a finding that echoes a 2010 study by Prof. Hurwitz et al. that had found a similar blood volume reduction among severe ME/CFS patients. Given that a healthy person tends to have around five litres of blood, this means that severe ME/CFS patients can be well over one litre short.

But why is this happening? Research has indicated that it is seemingly primarily because ME/CFS patients suffer from a physiological abnormality which goes against standard medical orthodoxy and teaching.

The Paradox

There is a hormonal system in the body known as the Renin-Angiotensin-Aldosterone System (RAAS). The RAAS is tasked with retaining salt according to the body’s needs. In a healthy person, any excessive loss of salt (e.g. through sweating, vomiting or minor blood loss) will lead to the ramping up of RAAS activity in order to instruct the kidneys to preserve salt.

In ME/CFS, however, this mechanism does not work normally. Termed the RAAS ‘paradox’ by researchers, not only does it lead to excessive salt loss in the urine but even when a state of low blood volume has been established, the RAAS activity remains blunted. Outside of ME/CFS specialists, most doctors are unaware that this irregularity is even physiologically possible. The basic facts of the RAAS paradox in ME/CFS were described in a paper by Dr. Miwa in 2016, building on his earlier 2014 paper.

The Wirth-Scheibenbogen Hypothesis

Why is this downregulation occurring in the first place? Prof. Scheibenbogen and Prof. Wirth, in their 2020 big picture hypothesis for ME/CFS, suggest that the RAAS downregulation is occurring because of an upregulation of a competing system known as the Kallikrein-Kinin-System (KKS).

They propose that ME/CFS patients have blood vessels that, for both autoimmune and autonomic reasons, cannot vasodilate normally. This lack of normal vasodilatory function leads to the creation of an overall state of ‘global hypoperfusion’ within the illness (i.e. the blood just doesn’t perfuse adequately throughout the body, including into the muscles and brain).

The body tries to correct this vasodilation impairment by creating its own endogenous vasodilatory substances. These are manufactured by the KKS and include bradykinin. Unfortunately, this attempt is ultimately unsuccessful and comes with side effects. As the KKS and RAAS act in opposition to each other, the upregulation of one will lead to the downregulation of the other. As a result, the RAAS becomes suppressed, leading to salt loss, lowered plasma volume, and ultimately to a state of low blood volume that the body cannot correct itself. (For a very helpful write-up of this research by Prof. Scheibenbogen and Prof. Wirth, see the article by Cort)

Hypothesis Predicts Major Failure Point in Chronic Fatigue Syndrome (ME/CFS)

I should mention that the RAAS blunting is not the only possible reason for the lowered blood volume in the illness. Prof. Wirth and Prof. Scheibenbogen also propose ‘vascular microleaks’ which might result in the loss of blood from the circulation into the interstitial space.

In addition, it has been noted that, in addition to lowered plasma volume, ME/CFS patients can have less red blood cell (RBC) volume than normal as well. There are two likely reasons for this. One is that the activity of the RAAS also modulates the activity of erythropoietin (EPO), the hormone responsible for creating red blood cells (RBC). If the RAAS activity is lowered, it is possible that EPO activity will also be reduced, thereby lowering RBC volume. Secondly, it is also feasible that the body might ‘sense’ the overall reduction in plasma blood volume and reduce RBC production in order to stay in some kind of physiological balance.

Both of these ideas were suggested by Prof. Satish Raj in his 2005 paper on the renin-angiotensin ‘paradox’ in POTS, a condition in which a similar phenomenon seems to occur. In general, it seems safe to suggest that, one way or another, the RAAS downregulation is the primary driver for the lowered blood volume within ME/CFS.

Thirsty for Blood? An ME/CFS Model of ‘Hypovolemic Dehydration’

Having explored the low blood volume within ME/CFS, how can we map that onto the excessive thirst within the condition?

The small hypothalamus plays an important role in the hypovolemic thirst center.

The small hypothalamus plays an important role in the hypovolemic thirst center.

First, we need to remember that the hypovolemic thirst centre is triggered when the plasma volume drops by 10%. Studies indicate that such a reduction is common in ME/CFS – suggesting that the hypovolemic thirst centre may be being triggered regularly.

Secondly, we also need to remember that the hypovolemic thirst centre is not ‘asking’ for water. Blood is salty stuff, and the ingested fluid needs to be capable of boosting blood volume. This is a crucial point. If someone is experiencing thirst, they will naturally assume that their body is ‘asking’ for them to drink water. Outside of researchers who specialize in thirst physiology, most people have no idea that the brain has two thirst centres and that each has quite different requirements in order to be ‘satisfied’.

Putting all of the above factors together, I suggest that the basic model for excessive thirst in ME/CFS looks something like this:

  • Renin-angiotensin-aldosterone axis suppression >>>>
  • Plasma blood volume drops by at least 10% (and ultimately likely stays at an even lower amount) >>>>
  • Triggering of hypovolemic thirst centre (salt + water appetite) >>>>
  • Patient understandably, but mistakenly, drinks pure water in response to their thirst >>>>
  • water is urinated out shortly afterwards >>>>
  • thirst is still present as low blood volume remains >>>>
  • vicious cycle of unquenchable thirst and excessive urination develops.
Vicious circle

Hypovolemic drinking of water can result in a nasty vicious circle – the thirstier you are – the more you drink – and the thirstier you become.

This model explains the key characteristics of thirst within ME/CFS. It is unquenchable as the wrong remedy is being applied. The urine is dilute because of the amount of water ingested. The thirst can worsen in a crash because, during those times, the RAAS suppression increases, resulting in additional solute loss and therefore in a worsening of hypovolemic thirst. And, finally, hyponatremia can develop for two reasons: the ingestion of a large amount of fluid dilutes the bloodstream and also because the RAAS downregulation is pulling sodium out of the body as a matter of course.

I am not suggesting that this model can explain every aspect of the thirst experienced by ME/CFS patients. Mast cell activation issues, inflammatory responses during post-exertional malaise, or neurological dysregulation (such as increased stress chemicals), among other things, likely all play a role. (There is an excellent paper by long-COVID patient and researcher Dr. Carroll on a wide range of possible general contributing factors to thirst that is well worth reading).

I would propose, though, that the ‘big reason’ why patients can end up drinking so many litres of water every day is likely because of their understandably applying the wrong solution to hypovolemic thirst. Indeed, in researching online forums for how patients have managed to ameliorate this symptom, I have observed consistently that the most profound improvement typically comes from efforts to increase blood volume.

If this model is correct, then what can be done to mitigate this symptom?

Treating Hypovolemic Thirst: Oral Rehydration Solution to the Rescue (or “The Solution That’s the Solution…”)

In speaking of treatment options, I will limit myself to discussing what has worked for me personally. The following is not medical advice and each person should determine their own treatments according to their individual needs and in consultation with their doctor.

The most helpful change I have made is to replace pure water with oral rehydration solution (ORS). Initially, I had drunk a mixture of ORS and of normal water daily. However, this approach is problematic as any normal water will work to pull out the electrolytes within the ORS, thereby somewhat negating its effect. By switching to drinking only ORS, I have made sure that all of the fluids I consume are also boosting plasma blood volume.

Oral Rehydration Solution More Effective than Saline IV at Improving Orthostatic Intolerance

ORS achieves this effect because of something called the ‘sodium-glucose co-transporter’ in the gut. This mechanism allows for the gut to pull essentially all of the sodium neatly into the bloodstream, as long as that sodium is accompanied by a physiologically appropriate amount of glucose (or dextrose). In this way, ORS is akin to having a ‘Saline IV in your pocket’.

I do drink some normal water every day, usually a tiny amount to take some supplements and I might also have the occasional cup of tea or decaf coffee. But by switching to only drinking ORS for the vast majority of my fluids, I now only need to sip on around 2.5 litres of fluid per day. Given the nightmarish crash-days of drinking 15 (or more) litres some years ago, this change still feels miraculous to me.

Aside from ORS, my dietary salt consumption is otherwise moderate, at around 3-5 grams per day. I also find this helpful in quenching my hypovolemic thirst. However, I should note that when I experimented with consuming a lot of dietary salt (i.e. eating salty/salted foods rather than drinking ORS), as many ME patients do, I experienced some negative effects.

Drinking Oral Rehydration Solution vs Adding More Salt

Salt can impair vasodilation and, given that many ME patients appear to have problems with vasodilation (according, at least to the theory by Scheibenbogen and Wirth referred to above), excessive dietary salt could worsen that issue. Excessive salt can also interfere with mitochondrial function, can slow down the activity of the sodium-potassium pump (a key bodily process for energy creation within our cells and for muscle strength), and, at amounts of 12 grams daily at least, can cause muscle wasting. For an excellent overview of the potentially harmful effects of a high-salt diet, see this paper.

I also learned that hunter-gatherer groups, as a general rule, do not have more than 2.5 grams of salt daily (although some, as the last linked paper shows, like the Inuit, have around four grams and we, of course, cannot forget the pastoralist Maasai tribes of Tanzania who regularly drink the blood of their cattle. Although I haven’t tried it myself, perhaps this is the best natural cure for hypovolemic dehydration. 😉 )

High amounts of dietary salt will also cause classical dehydration, pulling water out of your cells via the process of osmosis. This dehydrates them and causes significant cellular stress. The body then must initiate a substantial repair job to get those cells back up and running normally. To take this phenomenon to its most extreme end, this is why drinking seawater can kill you. The resulting dehydration from such a high salt load is simply too severe for the body to recover from. In this way, a high salt diet, while mitigating hypovolemic thirst, will also increase osmotic thirst.

This difference between drinking ORS and just eating salt normally is very important. While, of course, a considerable amount of that salt will end up boosting blood volume (as was shown by this paper which measured the effect of a daily intake of 12 grams of salt on blood volume), high dietary salt can also have a negative effect on cellular function, as we have just explored.

In contrast, and to the best of my understanding, when you drink ORS, the salty solution will remain in the extracellular space, just like a saline IV. It is this ability of ORS to remain in the extracellular space (i.e. the intravascular plasma and the general extracellular fluid compartment) that makes it such a safe and medically neat option.

Drinking ORS not only helps profoundly with my thirst but has also reduced my heavy legs, improved my exercise tolerance, and helped calm down my nervous system. And the feeling of ‘internal volume expansion’, as the blood more easily reaches your brain and skin, offers significant relief.

On the other hand, I do not know if there are any long-term safety issues with drinking so much ORS. But my current thinking is that, in the grand scheme of things, drinking a solution that essentially just contains salt, glucose, and potassium probably falls into the category of more benign medical interventions.

These days, I drink a product called Normalyte, an ORS that was specifically developed for dysautonomia patients and which does not include unnecessary preservatives.

  • Please note – The link to the Normalyte website is an affiliate link. 100% of the proceeds from sales through that affiliate link for the next month will be donated to Health Rising by Patrick.

However, it is important to mention that, whereas before my thirst level was at 100%, nowadays it hovers somewhere between 5% – 20%, depending on flare-ups in my illness. As mentioned earlier, I think it is likely that other issues also contribute to thirst in ME/CFS, although low blood volume is likely responsible for its most extreme – and dangerous – forms.

Ok, so we have now explored what might be causing excessive thirst in ME/CFS. Let us return to ‘psychogenic polydipsia’ and to the idea that some people are drinking so much water just because they are mentally ill.

Is ‘Psychogenic Polydipsia’ a Terrible Freudian Mistake?

Freudian mistake

Is the diagnosis of psychogenic polydipsia in ME/CFS a Freudian mistake?

After I had managed to resolve my extreme thirst through my own research, I tried to forget about the humiliating diagnosis that had been made in the hospital. Eighteen months later, however, a voice in the back of my mind was still nagging away at me: what is the history of this strange condition that suggests that patients, who are drinking enormous quantities of water and say that they are dying of thirst (and in some cases actually do pass away), are instead just stuck in some sort of strange mental compulsion to down as much fluid as possible? On what is it based and are its premises well-founded?

I spent a whole year researching this condition and, in the end, I concluded the following:

Primary polydipsia is a terrible Freudian mistake and what is termed ‘psychogenic water drinking’ has likely always been, at least in most cases, a misreading of the biomedical thirst that is experienced by ME/CFS and POTS patients.

I draw this conclusion for five key reasons.

(1) Firstly, the condition has received only the tiniest amount of research. A lifetime PubMed search for ‘psychogenic polydipsia’ will return less than 300 results. By way of contrast, a lifetime PubMed search for ‘multiple sclerosis’ will yield over 110,000 results. It has simply received very little interest, despite the fact that it is recognized that so-called primary polydipsia patients can die from severe hyponatremia.

(2) Secondly, the understanding of the condition essentially hasn’t budged since the late 1950s. Writing in 2017, Prof. Daniel Bichet of the University of Montreal noted:

‘Our understanding of the pathophysiology of this disease has made little progress since [a 1959 paper by Barlow and De Wardener]’.

At present, the condition is a kind of medical relic, still operating on assumptions that were developed well over six decades ago. Those assumptions made sense in the context of medical knowledge at the time but, as we shall see with reason no. five below, are totally inadequate in light of current medical understanding.

The Gist

  • Many ME/CFS patients suffer from polydipsia – a condition that involves unquenchable thirst, dilute urine, a worsening of thirst during post-exertional malaise (PEM) and, at least in some patients, the development of hyponatraemia (low blood sodium).
  • Patrick Ussher, an Irish ME/CFS patient, used to suffer from this symptom at its most extreme – to the point that he developed life-threatening hyponatraemia and was hospitalised.
  • In the hospital, he was diagnosed with a mental health condition, ‘psychogenic polydipsia’, in which it is assumed that patients drink enormous quantities of water in the absence of physiological needs and because they are mentally ill.
  • After his hospital stay, Patrick managed to resolve his extreme thirst through his own research and later wrote a (free) book about what might be causing thirst in ME/CFS (details to follow).
  • In Patrick’s hypothesis, excessive thirst in ME/CFS is mainly caused by the low blood volume that is characteristic of the illness. Research has consistently found that ME/CFS patients do not have enough blood, with some patients short by a litre or more. The most significant reason for this reduction in blood volume appears to be the suppression of the renin-angiotensin-aldosterone axis, a hormonal system which controls salt levels in the body.
  • The brain actually has two distinct thirst centres: osmotic (triggered when the body’s water content is too low) and hypovolemic (triggered when the plasma blood volume drops by 10%). It is this little-known second thirst centre that is likely being triggered continuously in ME/CFS patients.
  • Crucially, the hypovolemic thirst centre is not ‘looking’ for water in order to be ‘quenched’. Blood is salty stuff and, in order to boost blood volume, the ingested fluids need to be appropriately salty.
  • Patrick believes that most ME/CFS patients fall into the understandable trap of just drinking pure water in response to their thirst (for who doesn’t drink water when they are thirsty?). When this water is excreted by the kidneys, though, the blood volume will remain low and, as a result, the thirst will continue – and even grow – as sodium levels and blood volume continue to drop.
  • When Patrick switched from drinking pure water to drinking ORS (oral rehydration solutions), he experienced a profound decrease in his thirst along with a significant improvement in his quality of life. In previous research, ORS has been shown to increase blood volume as effectively as a saline IV in POTS patients.
  • Later on, Patrick researched ‘psychogenic polydipsia’ in detail. He found that it is a condition which has received little research and which is generally regarded as a ‘medical mystery’. In fact, several leading academics have suggested that the supposed ‘psychogenic’ basis might be a mistake and that the real mechanisms simply haven’t been identified yet.
  • When Patrick researched the earliest papers into the condition from the 1940s and 50s, he came across several intriguing patient case studies. Those patients had symptoms reminiscent of ME/CFS such as ‘aching everywhere’ and profound ‘weakness of the legs’. Among other reasons, this led Patrick to believe that, at least in many patients, what has always been termed ‘psychogenic polydipsia’ may have been a misreading of the biomedical thirst experienced in ME/CFS patients.
  • Patrick’s book challenges the psychogenic basis of ‘psychogenic polydipsia’ (also known as ‘primary polydipsia’) and instead maps out a model of ‘hypovolemic thirst’ which can explain the symptoms in organic terms. The book is called ‘The Myth of Primary Polydipsia: Why Hypovolemic Dehydration Can Explain the Real Physiological Basis of So-Called Psychogenic Water Drinking’. It is available on Amazon and from themythofprimarypolydipsia.com as a PDF download.
  • At its most extreme, this symptom can lead to hyponatraemia-induced coma and death. Despite this, the current diagnosis of ‘psychogenic water drinking’ offers only stigmatisation and no practical help. If ‘hypovolemic dehydration’ could re-explain these symptoms in organic terms, it would not only lead to much-needed medical help but also to greater awareness about the biomedical nature of ME/CFS among future medical students.
  • Patrick is looking for doctors/medical researchers who may wish to work on a hypothesis paper or other similar collaborations.

(3) Thirdly, in most current research papers, the condition is recognized as a medical mystery. Over and over again, academics state some variation along the lines of: ‘we don’t know what actually causes this’. For example, Sailer, in her 2017 paper, writes:

‘The pathogenesis of insatiable thirst and excessive fluid intake as seen in primary polydipsia remains largely unknown’.

Most notably, Prof. Daniel Bichet says: ‘The diagnosis of compulsive water drinking must be made with care and may represent our ignorance of as yet undiscovered pathophysiological mechanisms’. (‘Compulsive Water Drinking’ is yet another term for ‘primary/psychogenic polydipsia’). As all ME/CFS patients will be aware, just because the cause of a medical issue is unknown does not mean that that medical problem is caused by mental illness.

(4) Fourthly, when you return to the early papers which researched so-called ‘psychogenic water drinking’, it seems clear that many of the patients under examination actually suffered from ME/CFS. For example, in the aforementioned 1959 paper by Barlow and De Wardener, titled ‘Compulsive Water Drinking’, patients reported symptoms such as ‘aching everywhere’ and ‘breathlessness upon exertion’ as well as developing their health problems following previous illnesses and other acute stressors, a pattern which matches the typical development of ME/CFS. One patient was even described as having ‘hysterical weakness of the legs’, which would seem to me to be a rather Freudian characterization of post-exertional malaise.

Indeed, Freudianism abounds in that paper. Patients were assumed to drink so much water simply because of being ‘emotionally disturbed’. Their troubled childhoods, adolescences and unsatisfactory sex lives were also scrutinized. An earlier paper about so-called psychogenic polydipsia even concluded that being homosexual was a likely cause as patients supposedly developed a subconscious obsession with the ‘oral libidinal zones’ as a surrogate activity for heterosexual sex. So much for the scientific method in action.

(5) Fifthly and finally, the discovery of the brain’s second thirst centre, the hypovolemic thirst centre, was not made until the 1960s, long after the idea of ‘psychogenic water drinking’ had taken hold. It is this thirst centre that can, along with the hypovolemia within ME/CFS and POTS, explain the typical symptom presentation that is seen in so-called ‘primary polydipsia’.

Indeed, that typical symptom presentation is hyponatremia and dilute urine, exactly the same features that are observed in thirsty ME/CFS patients. Most notably, I have come across several ME/CFS patients in forums who have suffered the (mis)diagnosis of primary polydipsia (see here and here), including an ME/CFS patient from whom fluids were forcibly restricted (as reported in this thread).

Faulty Test?

At the moment, primary polydipsia is diagnosed by using the ‘water deprivation test’. Patients are forbidden from drinking water for an extended period of time to see whether their bodies can produce concentrated urine. If their bodies can, this is taken as evidence that vasopressin/antidiuretic hormone function is intact. If vasopressin, the principal job of which is to conserve water, can work then, or so the thinking goes, there can be no reason for a patient to drink so much water.

But what if the thirst was never about water at all but instead about blood? What if the issue is nothing to do with vasopressin but originates in the suppression of the renin-angiotensin-aldosterone system? In this case, finding that vasopressin can work is the medical equivalent of examining an elbow, declaring it to be in good condition and that all is well, while that patient is actually suffering from a broken leg and screaming in agony.

In fact, my research has uncovered two papers on so-called Primary Polydipsia that found evidence of RAAS suppression. One paper from Japan found a downregulation of the RAAS in so-called psychogenic water drinkers while a paper from Belgium observed that so-called compulsive water drinkers lost large amounts of solute for some kind of endogenous reason. That paper’s author wondered if it was something to do with a problem in the RAAS.

Were these two papers unknowingly just studying thirsty and undiagnosed ME/CFS patients? The implications of both articles were never pursued however and the status quo remained: such patients are just drinking so much water because they are mentally ill.

To be clear, some people do drink excessive fluid for psychological reasons but such people never cite thirst as a motivator. They may do so for health reasons or because of some kind of misplaced advice. For example, one man developed profound hyponatremia as a result of drinking large volumes of water in order to suppress his chronic hiccups.[1]  There may also exist a distinct pathophysiology within schizophrenia that creates excessive thirst and this phenomenon might represent a specific subset of so-called primary polydipsia patients (for more detail, see the section on severe mental illness in this paper).

“The Myth of Primary Polydipsia”

Patrick Ussher book

Patrick’s book challenges the notion that the thirst or polydipsia in ME/CFS and related diseases is “psychogenic” in nature.

I strongly believe that, in general, what has been termed ‘psychogenic water drinking’ has been a misreading of the thirst experienced by ME/CFS and POTS patients. In order to make my case, I have written a book.

Titled ‘The Myth of Primary Polydipsia: Why Hypovolemic Dehydration Can Explain the Real Physiological Basis of So-Called Psychogenic Water Drinking’, it traces the early Freudian research into primary polydipsia, explores the findings into low blood volume in ME/CFS and POTS, contains many ME/CFS patient testimonies regarding this symptom and describes possible treatment options. In my view, the ‘medical mystery’ of so-called primary polydipsia was always likely to be explained by a blind spot in medical thinking and that blind spot may well be ME/CFS.

The book is available as a free download here or as a paperback from Amazon.  The book also includes research into long COVID, in which two large survey-based research papers have found that around 35-40% of patients report intense thirst as a symptom (see here and here). It seems highly likely that hypovolemia is a key factor in the thirst experienced by long-COVID patients as well.

Primary polydipsia currently amounts to unintentional medical negligence. Patients who say they are dying of thirst, and in some cases do pass away, are stigmatized by this diagnosis and receive no practical help regarding how to mitigate their symptoms. This is an appalling situation and it must change both so as to save lives and to mitigate intense suffering.

A Boon to ME/CFS?

But if ME/CFS actually holds the clue to demystifying so-called ‘psychogenic water drinking’ then could the current debacle of primary polydipsia contribute to changing the perception towards ME/CFS in the wider medical community?

This is because all current doctors are taught about primary polydipsia while in medical school. If this could one day be replaced with teachings on ‘hypovolemic thirst’, then the mechanisms that create that thirst within ME/CFS would have to be taught instead, alongside other typical causes of thirst, such as Type II diabetes, diabetes insipidus, kidney issues and so on.

Who then would leave medical school, having learned that ME patients are often over a litre short of blood due to their illness, without recognizing the seriousness of ME/CFS? Would such a change not lead to increased interest in the condition and to a much greater likelihood that future ME/CFS patients would be listened to rather than gaslighted, dismissed, and left to suffer on their own?

Such future medical students might well ask why their profession had not been taught, in the first place, about the research into such a debilitating condition. And they would be right to wonder.

Watch a talk that Patrick gave to The Irish ME Trust about thirst in ME/CFS


And a summary video about why Primary Polydipsia might be a terrible, Freudian mistake.


About The Author

Patrick Ussher

Besides having and writing about ME/CFS, Patrick Ussher is a classical composer, a founder of the Modern Stoicism Project, and the author of a book on stoicism and Buddhism.

Patrick Ussher runs a YouTube channel, Understanding Myalgic Encephalomyelitis, aimed at simplifying ME/CFS and Long Covid research as well as sharing treatment strategies he has tried.

He is also a composer of music in a contemporary classical style. His music is part of the Artlist catalogue and can also be listened to on Spotify.

He is the author of Stoicism & Western Buddhism: A Reflection on Two Philosophical Ways of Life He has also recently written a pseudonymous political satire.

While a Classics PhD student, he was a founding member of the Modern Stoicism project, an interdisciplinary collaboration between academics and psychotherapists working to create modern applications of the ancient Greco-Roman philosophy of Stoicism. As part of that project, he started and ran the project’s blog from 2012 to 2016 and he also edited two books: Stoicism Today: Selected Writings, Volumes 1 & 2.

In 2018, he worked with Columba Press on a new edition of a book by his late mother, Mary Redmond-Ussher, on coping with breast cancer under the title Following the Pink Ribbon Path. Patrick has a BA and MA in Classics (Ancient Greek & Latin) from the University of Exeter, UK. His website is: www.patrickussher.com

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Health Rising provides access to a wide range of viewpoints from the ME/CFS/FM/long-COVID communities. If that supports you, please support us.

Thanks to the approximately 200 people who have supported Health Rising thus far. Patrick’s blog demonstrates another feature of Health Rising – the access it provides to the creativity found in our communities. People with ME/CFS, FM, long COVID, etc., are constantly breaking new ground in how we understand and treat these diseases.

During 2023, Health Rising has featured blogs by Patrick (polydipsia, apheresis), Bronc (Armin Alaedini), Efthymios (artificial intelligence), Patrick Allard (recovery), Melissa Wright (cerebral spinal fluid leaks, recovery), Brian Vastag (Intramural research study), Alice Kennedy (languaging long COVID), Adam (BCG vaccination story) and others that are casting new light on ME/CFS and related diseases. If you find this access to the community helpful, please support Health Rising in a way that works for you.






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