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Did the introduction of the polio vaccine cause the massive rise in ME/CFS incidence in the 1980s?

Hip

Senior Member
Messages
17,824
Nietzsche once wrote: "what does not kill me, makes me stronger". When it comes to natural poliovirus infection, this could indeed be the case.

Before the introduction of the polio vaccine in the late 1950s, most children naturally caught poliovirus. Around 70% of poliovirus infections were completely asymptomatic and resulted in no long-term problems; but around 0.5% of infections caused paralysis, and out of that 0.5%, around 1 in 30 cases were fatal (ref: 1).

Thus the introduction of the poliovirus vaccine undoubtedly saved numerous lives and prevented numerous disabilities. However, in spite of these considerable benefits, it is possible that poliovirus vaccine may also have a dark side, and may have inadvertently created some major health negatives.

It has been suggested that natural infection from wild poliovirus conferred some cross-immunity against the ill effects of other enteroviruses such as coxsackievirus B — a virus linked to ME/CFS and type 1 diabetes (T1D).

But poliovirus vaccine may not confer the same cross-immunity as natural poliovirus infection, and so individuals who were vaccinated and never caught poliovirus as a child may have reduced immunity to coxsackievirus B, and to related enteroviruses such as echovirus.

Decades later in life, when those vaccinated individuals catch coxsackievirus B or echovirus, their immune system may thus have more trouble fending off these infections, and this conceivably could increase the chances of developing ME/CFS or T1D from the infection.

So the introduction of the poliovirus vaccine in the late 1950s might potentially be the cause of the explosive 5- to 8-fold increase in the incidence of ME/CFS that appeared two decades later, in the 1980s. And the introduction of the poliovirus vaccine may have also caused the great increase in type 1 diabetes that appeared in the decades subsequent to introduction of the poliovirus vaccine.



Prior infection with poliovirus most likely does provide immunological cross-protection against coxsackievirus B, as this paper from Estonia talks about the differences between Estonian children immunized with the live attenuated polio vaccine, versus Finnish children immunized with the inactivated polio vaccine.

It was found that the Estonian children given the live vaccine have a stronger T-cell responses against coxsackievirus B4, which the authors suggest may explain why type 1 diabetes (linked to coxsackievirus B4) is 3 times lower in Estonia compared to its neighbor Finland.

So even with the two types of polio vaccine, the live virus vaccine seems to ramp up T-cell immune responses against other enteroviruses like coxsackievirus B more than the inactivated virus vaccine does. Presumably then, natural wild poliovirus infections in childhood will provide even stronger T-cell responses against other enteroviruses later in life.

Thus the loss of natural polio infections in the general population may have resulted in everyone becoming more susceptible to the ill effects of related enteroviruses.



It is a fascinating possibility that the introduction of the polio vaccine could have inadvertently led to a subsequent rise in the incidence of ME/CFS and T1D, because natural poliovirus infections in children were providing cross-immunity to ME/CFS- and T1D-triggering enteroviruses like coxsackievirus B.

To test this theory, it would be interesting to compare the prevalence of ME/CFS and T1D in individuals given the live attenuated polio vaccine (Sabin vaccine) as a child, versus the prevalence in those given the inactivated polio vaccine (Salk vaccine). That paper perhaps suggests that ME/CFS and T1D would be more prevalent among those give the inactivated polio vaccine.

The Sabin live polio vaccine is given orally on a sugar cube; the Salk inactivated vaccine is given by injection.



If it turned out to be true that the introduction of the polio vaccine has weakened our immunity to other enteroviruses, then this would only reinforce the need to develop a coxsackievirus B and echovirus vaccine with urgency, to be added to the vaccine schedule. By preventing natural poliovirus infection via the polio vaccination program, this may have allowed other enteroviruses to move in. So we need to developed vaccines for these other disease-causing enteroviruses too.

More info about the rationale for introducing a coxsackievirus B vaccine here: Coxsackievirus B vaccine appears feasible, and might conceivably abolish ME/CFS in future



Some keywords useful for Google searching on this topic: cross-immunity | cross-protection | cross-reactivity | cross-neutralization
 
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Mary

Moderator Resource
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17,334
Location
Southern California
To test this theory, it would be interesting to compare the prevalence of ME/CFS in individuals given the live attenuated polio vaccine (Sabin vaccine) as a child, versus the ME/CFS prevalence in those given the inactivated polio vaccine (Salk vaccine). That paper perhaps suggests that ME/CFS would be more prevalent among those give the inactivated polio vaccine.

The Sabin live polio vaccine is given orally on a sugar cube; the Salk inactivated vaccine is given by injection.

Very interesting @Hip. But, FWIW, I had the sugar cube Sabin live vaccine as a child and still had high Cocksackie B viral titers, as well as a couple of echoviruses.
 

lansbergen

Senior Member
Messages
2,512
Wild poliovirus did not disappear straight away when the vaccination program was started. .Anyway. I was exposed to the wild virus soon after I was vacinated.
 

CCC

Senior Member
Messages
457
It's an interesting thought.

I could be annoying and point out that smallpox vaccinations dropped out at around the same time.

That we had little ME/CFS pre-vaccination might have as much to do with the rise and rise of antibiotics at the same time, which allowed people to survive childhood who otherwise wouldn't have. A few on PR have noted this about themselves.
 

CFS_for_19_years

Hoarder of biscuits
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2,396
Location
USA
There was a discussion here three years ago about the polio vaccine giving rise to the ME/CFS epidemic in the 1980's: http://forums.phoenixrising.me/inde...been-ill-with-cfs-me-for-over-20-years.29818/

More here: http://forums.phoenixrising.me/inde...me-for-over-20-years.29818/page-4#post-458478

There may be a cluster of individuals vaccinated for polio in the late 1950's and early 1960's who later developed ME/CFS.

http://www.wellwithin1.com/polio.htm
The complication researchers had isolated in 1960 was a viral contaminate. It seems that when the live polio virus grown on monkey tissues was extracted for vaccine production another virus was extracted as well, SV-40. When this monkey virus was injected into research animals it produced brain cancer. It appears our government didn't wish to create a public panic or discredit the public health service, because instead of recalling the tainted vaccines, it quietly ordered the manufacturers to find a monkey free of SV-40 and continue production. As of 1963, the rhesus monkey had been replaced with the African green monkey for production of a safer polio vaccine, but between the years of 1955 and 1963 as many as 98 million Americans had received doses of live polio virus vaccines tainted with SV-40.
 

Hip

Senior Member
Messages
17,824
I am wondering whether this possible enterovirus cross-immunity obtained from wild poliovirus infection, and also perhaps to a lesser extent from the Sabin live attenuated polio vaccine, might have any therapeutic benefits in ME/CFS patients.

Is the enterovirus cross-immunity only conferred to infants, or might adults given the live polio vaccine also acquire increased immunity against enteroviruses? If it works for adults too, then I wonder if live polio vaccine might be useful for stimulating the immune response against the chronic coxsackievirus B and echovirus infections often found in ME/CFS patients?

There is some info on enterovirus cross-immunity in this paper:
In this study, the nature of the T-cell response to seven picornaviruses, including polioviruses, coxsackieviruses B3 and B4, human rhinovirus 14, and encephalomyocarditis virus, was determined.
...
The majority of T-cell lines established in response to viruses, other than encephalomyocarditis virus, were cross-reactive to each other.



There was a discussion here three years ago about the polio vaccine giving rise to the ME/CFS epidemic in the 1980's: http://forums.phoenixrising.me/inde...been-ill-with-cfs-me-for-over-20-years.29818/

You are referring to the SV40 virus that contaminated the early batches of polio vaccine. SV40 though has not been linked to ME/CFS; it may have some link to cancer. And SV40 was already present in the human population prior to the introduction of the polio vaccine.
 

lilpink

Senior Member
Messages
988
Location
UK
I had the live 'sugar cube' vaccine also. I was aged 9/10 when I developed ME. I believe coxsackie B virus has played a role in my ME over time (though annoyingly notations of this in my GP records are missing ..I haven't checked my hospital records.). I was also given smallpox vaccine when I was 17 months old. I do ponder the effect of that vaccine at such a young age.
 

Snow Leopard

Hibernating
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South Australia
Anecdotal, but I became very very ill (acute flaccid paralysis) just a few weeks after the Sabin vaccine, though I had a Diptheria/Tetanus vaccine at the same time, so it is hard to know which was the trigger.

These days. the Sabin vaccine is the only source of the Polio virus, (vaccine-derived Polio virus infection) in many countries. hence why there is a worldwide shift towards the Salk vaccine, since we want to cut the number of Polio infections down to zero, the live-attenuated vaccine is still a risk compared to the Salk vaccine that has similar efficacy (for preventing Polio).
 

Chrisb

Senior Member
Messages
1,051
I like the sound of the theory, but must add myself to the list of those who took the sugar cube.

I do have a vague memory of having a short illness after one vaccination, but am almost certain that was for smallpox.
 

Chrisb

Senior Member
Messages
1,051
As an afterthought, if there were validity in the theory, might one expect those with a diagnosis of ME who received the Sabin vaccine to have presented with different aetiology and symptoms to those who received the Salk vaccine?

Presumably the numbers starting with, say, EBV or CMV might remain fairly constant, with changes in the incidence due to changes in numbers with an enterovirus origin.
 
Messages
1,478
I also had the sugar cube

I wonder how robust the data is to draw these conclusions in terms of instances of me in the 1980s vs any other time period. This could be a factor of population dynamics, I.e the average age of onset vs changes in size of population. The post war baby boomer effect does have a big effect generally.

The other thing to consider is accurate diagnosis generally. Perhaps the instances were just as high previously but remained undiagnosed. ( e.g smelling salts and the So called "hysterical women" that were ignored before the war) ......this might also be a factor? We do seem to have fairly loose diagnostic criteria even now. A lot has been swept under the carpet due to the suppression of women in the past.
 

Dufresne

almost there...
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Location
Laurentians, Quebec
It has been suggested that natural infection from wild poliovirus conferred some cross-immunity against the ill effects of other enteroviruses such as coxsackievirus B and echovirus — two viruses linked to ME/CFS.

However, polio vaccine may not confer the same cross-immunity as natural poliovirus infection, and so individuals who were vaccinated and never had a natural poliovirus infection as a child may have reduced immunity to coxsackievirus B and echovirus.

Decades later in life, when those vaccinated individuals catch coxsackievirus B or echovirus, their immune system may thus have more trouble fending off this infection, and this conceivably could increase the chances of developing ME/CFS from the infection.

So the introduction of the poliovirus vaccine in the late 1950s might potentially be the cause of the explosive international increase in the incidence of ME/CFS that appeared to occur some two decades later, in the 1980s.

Byron Hyde suggested this hypothesis to me many years ago, more or less.
 

HowToEscape?

Senior Member
Messages
626
It's an interesting thought.

I could be annoying and point out that smallpox vaccinations dropped out at around the same time.

That we had little ME/CFS pre-vaccination might have as much to do with the rise and rise of antibiotics at the same time, which allowed people to survive childhood who otherwise wouldn't have. A few on PR have noted this about themselves.

It could also be that 50 years back there was no name for this disease, and if you were unable to work either your family took care of you or you work yourself to death.

We are vastly wealthier than we were a century ago, we expect medicine to fix things rather than just provide an official diagnostic label and some painkillers, and there are fewer people living with chronic, unfixable diseases, so the majority doesn't expect to join them.

I believe the difference that the change in material wealth has made regarding how sickness is recorded and treated is huge. e.g. In 1917 it wasn't uncommon to be hungry, a 12 hour workday was normal for laborers, and somebody with a bit of brain fog or dizziness was likely to fall off a horse or otherwise expire. Such cases were not recorded as medical events, they were unremarkable, part of the noise of life.

It's also possible that this disease has become more prevalent because of some modern phenomena searches exposure to a natural or artificial agent. But first we should look at the simplest explanation which is that when you don't have a name for something you don't look for it, and when you don't look for something you don't find it.
 
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Hip

Senior Member
Messages
17,824
Byron Hyde suggested this hypothesis to me many years ago, more or less.

Would you have any links to that? I read about the possible beneficial effect of natural polio infection on an archived page of Dr Myhill's website; but presumably this idea has an older history, and someone must have originated it. Perhaps is was Byron Hyde's hypothesis?



I like the sound of the theory, but must add myself to the list of those who took the sugar cube.

In individual cases, this is neither here nor there. You would have conduct a ME/CFS prevalence study on people who had the sugar cube oral live polio vaccine, and compare the ME/CFS prevalence in that group to people who had the inactivated polio vaccine by injection, to see if there might be any protective effect from the live vaccine, compared to the inactivated vaccine.

In any case, any protective effect from the live vaccine might be much weaker than the possible protective effect of catching poliovirus naturally, which most children did catch before the introduction of the polio vaccines in the late 1950s.



The other thing to consider is accurate diagnosis generally. Perhaps the instances were just as high previously but remained undiagnosed.

Dr John Richardson, a GP in the UK who had a very longstanding interest in enterovirus infection and ME/CFS, kept meticulous records of his patients that date back to 1954, and these records span 4 decades. With Richardson's keen eye and interest in these matters, he was certainly in a good position to observe any surge in the number of ME/CFS patients thoughout the period of 1950 to 2000.

If you look at the graph in this post, taken from Dr Richardson book, you see that in the 1980s, the number of patients in his GPs surgery experiencing chronic ongoing organ pathology arising after viral infection shot up. So this might be viewed as further corroborating evidence of an explosion of ME/CFS cases in the 1980s.

This increase in chronic organ pathology from viral infection may be a reflection of a weakened immune response — an immune system which is no longer able to keep regular viral infections fully in check.

Perhaps once children were no longer being exposed to natural poliovirus infection and the immune boost it may provide, this resulted in the population as a whole becoming weaker in their immune response to viruses, leading to these cases of ongoing viral organ pathology.

Dr John Richardson's figures for viral organ pathology in his patients are here:
Number of patients with chronic organ pathology following viral infection in each decade:

Decade 1954 to 1963: 22 patients
Decade 1964 to 1973: 56 patients
Decade 1974 to 1983: 245 patients
Decade 1984 to 1992: 571 patients

Source: this post.
You can see that from the late 1970s onwards, there was a huge explosion in the number of patients with ongoing viral organ pathology .

This data from Dr John Richardson's surgery is in addition to the several other sources that found an explosion of the number of new ME/CFS cases in the 1980s — sources detailed in the first post of the thread: Fivefold to eightfold increase in the incidence of ME from 1980 to 1989
 
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Dufresne

almost there...
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1,039
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Laurentians, Quebec
Would you have any links to that? I read about the possible beneficial effect of natural polio infection on an archived page of Dr Myhill's website; but presumably this idea has an older history, and someone must have originated it. Perhaps is was Byron Hyde's hypothesis?

It was quickly mentioned in conversation in his office, and it was somewhat vague. The gist of it was the vaccine had spared us polio, but maybe left us with a greater incidence of ME. I have his old text at my parents' place and I'll try to remember to look up vaccinations in the index the next time I'm there.
 
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1,478
Just thought I would post this to illustrate my earlier point. It would be interesting if there was a control against population for this study so you could see the results per capita. It would also be interesting to see this mapped against average age of ME onset if that exists
image.png
 

Hip

Senior Member
Messages
17,824
It would be interesting if there was a control against population for this study so you could see the results per capita.

The post-war baby boomers will have increased the percentage of younger people in the populace in the 1980s, which conceivably might have an effect on ME/CFS incidence. However, if it were having an effect, the effect would be relatively small, because the birth rate graph shows around a 25% to 30% rise in birth rate in the baby boomer era (1946 to 1964), compared to the pre-war era in the 1930s.

Whereas the apparent increase in incidence of ME/CFS in the 1980s is 5 to 8-fold, that is to say, a 500% to 800% increase in incidence. So the baby boomers could not really explain such a large increase in incidence.

Also, I understand that this huge increase in ME/CFS incidence that began in the 1980s has been maintained in the subsequent decades. Whereas if this increased ME/CFS incidence were due to baby boomers (a two decade phenomenon from 1946 to 1964), you'd expect that increased incidence to drop off after a decade or two, which it didn't.

So it does not look like the baby boomers could explain this increased ME/CFS incidence in the 1980s, although certainly it is the sort of thing that needs to be taken into account when looking at this data.
 
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halcyon

Senior Member
Messages
2,482
@Hip you might find this paper interesting, I found it yesterday while musing about the subject of the thread. Not really sure how it might fit into the hypothesis here, but it was interesting regardless, particularly this part:
The emergence of enteroviruses other than the poliovirus in our group of families accords with the results of most epidemiological studies in that members of the Coxsackie and Echo groups show a degree of communicability which can be as high as that of the polioviruses. They are well able to succeed poliovirus in the individual host, and there is some evidence that subsequent infection with other enteroviruses may actually terminate a poliovirus infection (Hale et al. 1961). Though previous immunisation perhaps complicates the picture, members of families C and D (and others we have recently studied) may have been protected from poliovirus infection by " interference " from Coxsackie B viruses. This has been shown in human and animal studies (Dalldorf 1960, Stern 1961). The high prevalence of such enteroviruses during a large-scale oral poliomyelitis immunisation campaign might prevent satisfactory levels of immunity being achieved in the population (Sabin et al. 1960).