(ME) outbreaks can be modelled as an infectious disease: a mathematical reconsideration of the Royal Free Epidemic of 1955, 2020, Waters et al

strategist said:
Toxic poisoning can happen much more easily than one would expect. All that needs to happen is a farmer being distracted for a moment or choosing the wrong product. We all have made errors like these.

Another way for it is to grains being affected by fungal toxins while in storage. And probably there are many other ways.

Toxic poisoning cases might be overlooked when they aren't severe enough and don't occur in clusters. In the Aldous paper, the poisoning was discovered because by chance, it happened to affect many people at once and because some effort was put into investigating this possibility.

In countries like Ethiopia and Malaysia they might not have resources to investigate the toxicological angle.
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Modern farming methods in developing countries may be a link. Pesticide and herbicide use is often higher than recommended use ( organophospgates feature heavily) in the belief that more chemicals = more crop when in fact it negatively affects soil fertility over time unless you keep applying .
Perhaps it us no surprise at increasing levels of arsenic in rice.

Link to a study as background which looked at chemical use in rice farming.
https://www.researchgate.net/publication/265404371_Farm_Pesticide_Rice_Production_and_Human_Health

The farmers attitude is interesting, as is the health effects on farmers..

I suspect that the cumulative combination of residual chemicals over the life of a crop has not been studied much and could gave significant impacts.

It's not just a developing country issue , here the average potato crop is sprayed with a combination of herbicide and pesticide 32 times. Though there are targeted delivery methods ( satellite technology looks at leaf cover and senesence to enable dosing to be area specific ie only the plants that require it- this is done automatically via download to the tractor) very few farmers use it and just blanket spray.

There was a paper a few years ago tracking hormonal issues in children in india to agricultural chemical use.

Still looking for the toxic rice article.
 
It is interesting to reread the Moss and McEvedy paper on the Blackburn School alleged hysteria

https://www.bmj.com/content/bmj/2/5525/1295.full.pdf

What became epidemic was a piece of behaviour consequent on an emotional state: excitement or, in the latter stages, frank fear led to overbreathing, with its characteristic sequelae-faintness, dizziness, paraesthesiae, and tetany. Once learned, this selfreinforcing piece of behaviour restarted spontaneously whenever the school was assembled. By day 12, however, the hysterical nature of the epidemic was generally accepted, and a firm line prevented the behaviour propagating as extensively as it had on the previous occasions.

A question arises as to whether it was claimed this explanation was consistent throughout the alleged cases or whether the supposed cause of hysteria varied from case to case., suggesting that "hysteria" is just a word for whatever it is that happens.
 
I am afraid I think this paper tells us nothing useful. Nevertheless, all credit to the authors for getting something published and trying a fresh approach.

The problems I see:

1. The fact that some thought-to-be-hysterical outbreaks do not fit an empirically derived formulator infectious outbreaks does not imply that something that does fit is not hysteria. The argument does not follow. A mathematical formula for wings describes birds pretty well and not mammals. But it describes bats OK. As has already been said we would need evidence that hysterical outbreaks less than one time in a hundred, fit the infection formula. I also doubt that the infection formula is very robust. The complete failure of mathematical modelling of an epidemic to provide useful information in recent months highlights the problem!

2. My memory of the M&B study is that they did not deny that there might have been an infectious outbreak. What they claimed was that the patterns of signs and symptoms that Ramsay had interpreted as evidence of encephalomyelitis in a small number of cases did not fit well with encephalitis. They suggested that instead these might be psychogenic. If psychogenic symptoms occurred as complications of an infection then that presumably would be entirely compatible with there having been an epidemic, for which overall figures would likely be typical.

3. Although Ramsay thought there was evidence of encephalomyelitis the consensus now is that there is no evidence for encephalomyelitis in people with a diagnosis of ME as a whole. From what I can see M&B were very likely right about the signs not being right. Ramsay may have made a big contribution in getting the illness recognised but he was probably wrong about its nature and we should take that on board.

4. Although M&B are charged with shifting opinion to a psychogenic view of ME I am not sure this is realistic. ME had probably previously been classified as psychogenic under neurasthenia or effort syndrome for 100 years. For sporadic ME, which is the majority, the mass hysteria versus epidemic debate does not even arise. What I think M&B did was to quash the idea that there is some specific epidemic encephalomyelitis illness about that can be used to explain ME. I agree with them that there isn't as far as we know.

I think what is unfortunate about M&B's intervention is that they described what happened in psychiatric terminology in such a way that psychiatrists felt they could take ownership. The origin of the signs they described I would prefer to describe in terms of suggestibility. I don't think it makes sense to deny the existence of suggestibility in both patients and health professionals. The belief held by psychologists that CBT works for ME/CFS is ample evidence for suggestibility - the reality is that they cannot possibly know if it does base on their practice (as explained in my evidence to NICE). The belief held by patients that they are miraculously cured of ME by rituximab, the Lightning Process or various other methods that are unlikely to have and real effect on physiology indicates the same. But there is no reason to think suggestibility has anything to do with ME/CFS as we now understand it.
 
The difficulty which this argument faces is that a number of cases were excluded from the paper on the basis that they were thought to be suffering "hysteria". This suggests that those cases and perhaps all the cases were properly assessed by a psychiatrist, better qualified than McEvedy and at least equally qualified to Beard. That non diagnosis was overturned merely on reading the notes and without experience of the patient, Is that any way to diagnose hysteria?
 
If suggestibility was the cause of the Royal Free "epidemic" what is proposed as the cause of the more sporadic outbreak in North West London which started before the Royal Free outbreak and finished after it (Compston 1978). What also was the cause of the Dalston outbreak occurring slightly earlier but unknown to those at the Royal Free.
 
chrisb said:
If suggestibility was the cause of the Royal Free "epidemic" what is proposed as the cause of the more sporadic outbreak in North West London which started before the Royal Free outbreak and finished after it (Compston 1978). What also was the cause of the Dalston outbreak occurring slightly earlier but unknown to those at the Royal Free.
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I suspect that everybody agrees that it is highly likely that all these outbreaks were mini-epidemics of infection. The issue of suggestibility merely relates to certain patterns of symptoms picked out by Ramsay as indicating encephalitis which probably didn't. In an age when unknown infection raised the worry of polio the possibility of the clinical picture being clouded by suggestibility was quite likely to be a general but variable quantity depending on all sorts of more or less random contextual factors.
 
Yes, I agree with some of the difficulties surrounding encephalitis, but I don't understand the need to add the additional layer of suggestibility, for which there is no more evidence than there is for encephalitis, when the infectious epidemic in the neighbourhood is a possible explanation of all the cases.

Myalgic encephalitis was something of a hostage to fortune allowing the likes of Straus and Eisenberg, enthusiastically followed by our BPSers, to call it a spurious disease construct, but that failed to explain away the facts.
 
Jonathan Edwards said:
The issue of suggestibility merely relates to certain patterns of symptoms picked out by Ramsay as indicating encephalitis which probably didn't.
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Do you mean Ramsay was looking for symptoms of encephalitis, so misinterpreted their real symptoms as suggesting that diagnosis? Or do you mean the patients were suggestible and somehow created symptoms that weren't real?
 
Trish said:
Do you mean Ramsay was looking for symptoms of encephalitis, so misinterpreted their real symptoms as suggesting that diagnosis? Or do you mean the patients were suggestible and somehow created symptoms that weren't real?
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I am sure the symptoms were real. But it is easy to misinterpret realities. I suspect the main problem is that Ramsay thought he was looking for signs of encephalitis. On the other hand patients worried that they might have a polio like illness might have misinterpreted sensations.

Neurological sensations are particularly easy to mis-witness, if you like. Think of the game where you twine your wrist around each other and someone asks you to move the finger they point to and you find you move the one on the opposite hand. The experimental psychologists have all sort of other tricks that prove the unreliability of our witnessing of nerve signals.

But I really don't think it matters because ME has nothing much to do with these acute symptoms occurring during an episode of infection. It is an illness that comes afterwards and seems to have nothing very specific to do with any infection that might trigger it.
 
Whatever one's interpretation, these outbreaks are given too much importance. While it's useful to know that outbreaks can produce a lot of ME/CFS cases, the number of patients that became ill during outbreaks is insignificantly small compared to the number of patients that did not.

The Tahoe outbreak affected less than 200 people, while current estimates put the number of people in the US that meet diagnostic criteria for ME/CFS around 1-2 million.

The real story is that there is a significant public health problem that is not being adressed.
 
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Jonathan Edwards said:
But I really don't think it matters because ME has nothing much to do with these acute symptoms occurring during an episode of infection. It is an illness that comes afterwards and seems to have nothing very specific to do with any infection that might trigger it.
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Does that really apply if the only reason for the original illness was suggestibility leading to a false belief in illness.? Where does that leave the patient when the illness continues?

We have seen that SW carried forward from mass hysteria into sporadic ME the language of abnormal illness behaviour and maladaptive behaviour. Concede too much and they are left with this.
 
a few more interesting snippets from the little red book;
In 1881, when the first polio epidemic of some 12 patients occurred in a school
straddling the Northern Sweden- Norwegian border, it was called mass hysteria. When
in [1990] [1911-1913], over 10,000 fell ill with polio in Oslo and Southern Sweden, one of France's
leading neurologists called it mass hysteria and physicians around the world had a
laugh at the silly Swedes.
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Although Hoagland described glandular fever among West Point students as an infectious disease
with an incubation period of approximately 40 days in 1964, I was taught in medical
school in 1962 that it was a disease of emotionally distraught lovesick adolescent girls.
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eta: referring to Lake tahoe outbreak
Epstein Barr Virus (EBV)
Now anyone who realizes that infectious mononucleosis is caused by the herpes
family virus, Epstein Barr Virus (EBV), and that the incubation period of this illness
is approximately 40 days, should have realized that you simply cannot have a rapidly
spreading viral epidemic with a virus with a latent period of 40 days.
Neither Dr Strauss nor Dr Holmes, senior government physicians, should have fallen
into such a trap. They only had to go to the excellent CDC library to realize that rather
than spending half a million dollars or so on a publication that they should have
known would not have incriminated EBV.
Yet this epidemic and this Holmes paper somehow spread the myth that this illness
was caused by EBV.
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Can that date of 1990 for the Oslo /Sweden polio outbreak be correct.? Does it mean 1890?
 
The original paper under discussion sent me back to look at McEvedy's papers on the schools outbreaks. It occurred to me that one might learn something not only from the rate of spread, but also from the rate of recovery.

Both the Blackburn and RFH conditions were postulated on the ground that illness in a small number of original cases led to a fear of polio and a hysterical reaction in the remainder. It might be reasonable to suppose that once the fear was shown to be unfounded similar rates of recovery could be expected. There seems to be no report of delayed recovery in the Blackburn cases. According to Ramsey 75%, probably of those responding to his questionnaire, continued to have symptoms, some severe, 30 years later.

His Two Schools Epidemics paper ends with

A diagnostic category that is reached only by exclusion will
collect all the errors made at earlier stages in the diagnostic
process-and fall into disrepute. If diagnoses of epidemic
hysteria are to inspire any confidence they must be made on
positive grounds. Nevertheless, it does seem possible to collect
positive data not only in the specially favourable case of mass
admission to hospital but in the ordinary clinically undocumented
instance.

which rather suggests he wanted hospital data to prove his hypothesis.

Edited-typos
 
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