Is there any research into vaccinations being a trigger for ME/CFS?

I have heard of several people being assessed or diagnosed with ME/CFS and they and their GP believe that vaccination may have been the cause. In this instance, the Pfzier covid-19 vaccination.

Are there any studies that confirm a link between vaccination and ME/CFS, or is it still or anecdotal stories?

I note that:

• This 2020 paper from Amerian Autonomic Society suggests perhaps not...
  https://www.s4me.info/threads/human...an-autonomic-society-2020-barboi-et-al.13259/
  
  
• The International Consensus Primer states vaccination may be a trigger and refers to a survey "Onset Survey 1,000+ patients 75.6%: infection alone or infection + 1 or more factors: environmental exposure, physical trauma, vaccinations, other stressors"
  Vernon SD. CFIDS of America, which I haven't found yet.
  http://www.investinme.org/Documents/Guidelines/Myalgic Encephalomyelitis International Consensus Primer -2012-11-26.pdf
  
  
• ME/CFS/PVFS: An Exploration of the Key Clinical Issues: The ME Association's clinical and research guide also mentions that vaccination is reported as a trigger, but no refs.

 

There was this study last year: Infections in temporal proximity to HPV vaccination and adverse effects following vaccination in Denmark..., 2021, Krogsgaard et al.

It is not simply about vaccination though but it examined vaccination and infection happening relatively close to each other in time and the CFS-like symptoms this combo might have triggered.

 

Interesting question.

When I was diagnosed in 2020, the proximity of my first becoming ill to the flu vaccine received (it was 24 hours almost to the minute that I noted initially feeling unwell), was cited as the trigger for my ME. The doctor said that 10%-15% of the patients he diagnosed with ME were triggered by vaccines. No idea how representative that % is more widely, especially given many patients will go many years before diagnosis.

Whilst a vaccine is not typically a live virus (as I understood it), the body must still react to an outside agent being introduced and trigger some kind of response to fight it - presumably, why many will have felt ill after one or more of their Covid vaccinations.

I guess now, with the number of vaccinations happening with Covid, the likelihood of an increase in vaccine triggered illnesses such as ME is going to increase - though, has likely not been acknowledged amid the overall focus on core Covid stats.

 

Charles Shepherd was interested into a link between hep B vaccination and ME at one point but I don't know if anything was published.

 

Thought it might be useful to post this related article here https://www.science.org/content/art...avirus-vaccines-may-cause-long-covid-symptoms

Extracts:

Personal accounts:

• Brianne Dressen's personal story of feeling like she had Long Covid symptoms after getting the AstraZeneca vaccine.
• Jana Ruhrländer, personal experience with symptoms after single dose of the Moderna vaccine... She played detective, realizing her symptoms overlapped with a hormonal system called the renin-angiotensin-aldosterone system that regulates blood pressure and fluid balance—and in which ACE2 plays a key role.

Research at NIH
"researchers at the National Institutes of Health (NIH) began to hear about such reports and sought to learn more, bringing Brianne Dressen and other affected people to the agency’s headquarters for testing and sometimes treatment"
"The research was small in scale and drew no conclusions about whether or how vaccines may have caused rare, lasting health problems. The patients had “temporal associations” between vaccination and their faltering health, says Avindra Nath, clinical director at the National Institute of Neurological Disorders and Stroke (NINDS), who has been leading the NIH efforts. But “an etiological association? I don’t know.” In other words, he does not know whether vaccination directly caused the subsequent health problems."
...
"The NIH data, which documented the patient cases, haven’t been reported yet. Two top medical journals declined to publish a case series of about 30 people, which Nath first submitted in March 2021. Nath says he understands the rejection. The data weren’t “cut and dried; it was observational studies.” This month, the scientists submitted a case series of 23 people to a third publication, and Nath says his group has submitted an amendment to a Long Covid protocol to include patients with postvaccine side effects."

The dilemma for Researchers:
"Probing possible side effects presents a dilemma to researchers: They risk fomenting rejection of vaccines that are generally safe, effective, and crucial to saving lives. “You have to be very careful” before tying COVID-19 vaccines to complications, Nath cautions. “You can make the wrong conclusion. … The implications are huge.” And complex and lingering symptoms like Dressen’s are even more difficult to study because patients can lack a clear diagnosis."

"At the same time, understanding these problems could help those currently suffering and, if a link is nailed down, help guide the design of the next generation of vaccines and perhaps identify those at high risk for serious side effects. “We shouldn’t be averse to adverse events,” says William Murphy, an immunologist at the University of California, Davis."

Autoimmune mechanism triggered?
"In November 2021 in The New England Journal of Medicine, he (William Murphy) proposed that an autoimmune mechanism triggered by the SARS-CoV-2 spike protein might explain both Long Covid symptoms and some rare vaccine side effects, and he called for more basic research to probe possible connections. “Reassuring the public that everything is being done, researchwise, to understand the vaccines is more important than just saying everything is safe,” Murphy says. Like others, he continues to urge vaccination."

Physiologist observe chronic problems following vaccination
"Pretorius says she and her colleagues have also seen patients—fewer than 20, she estimates—with chronic problems following vaccination. She says these include Long Covid–like symptoms such as brain fog as well as other clotting concerns such as deep vein thrombosis. The cause of the very rare but severe clotting after the AstraZeneca and Johnson & Johnson vaccines remains unknown, but Pretorius suspects all COVID-19 vaccines might also sometimes trigger subtler clotting issues. She says she has preliminary evidence that vaccination can lead to microclots, although in most cases they go unnoticed and quickly disappear—an effect she and a colleague saw in their own blood and that of eight other healthy volunteers, which they sampled after their vaccinations."

Pfizer monitoring:
"Science contacted regulators and vaccinemakers about any information they’d gleaned on these side effects. A Pfizer spokesperson wrote, “We can confirm it’s something we’re monitoring.”

Current research projects:
"... Prüss has detected autoantibodies in some patients with postvaccine symptoms, although not in others. Several groups are studying whether a patient’s post vaccination symptoms are due to autoantibodies to the angiotensin-converting enzyme 2 (ACE2) receptor, which the spike protein targets. Cheng and her colleagues are planning a case series that includes sophisticated imaging and diagnostic tests from a mix of Long Covid patients and those with postvaccine side effects. And Pretorius and her colleague Chantelle Venter are hoping to recruit at least 50 people to study clotting patterns before and after vaccination."

Patients in the middle:
"People with lasting health problems after vaccination welcome any attention to their plight. “You have this ugly stain on you, and you’re marginalized and abandoned,” Brianne Dressen says. At first, “I was really afraid of causing vaccine hesitancy,” she adds."

Vaccine still considered less risk than covid infection:
"Researchers exploring postvaccine side effects all emphasize that the risk of complications from SARS-CoV-2 infection far outweighs that of any vaccine side effect. “You see 10, 100, 1000 times less risk from the vaccine,” Prüss says. But understanding the cause of postvaccine symptoms—and whether early treatment can help prevent long-term problems—could be crucial for designing even safer and more effective vaccines, Murphy says, as well as potentially providing clues to the biology of Long Covid."

 

the article seems slightly different now [i only skimmed but e.g. no section headers].

in any case here is my slight reworking of the dilemma spoken of in the quote [forgive any slight inexactness]:

1. horn 1: study the problem and try to find out something useful. thie also presents opportunity to demonstrate transparency and unbiasedness incidentally possibly increasing v uptake. show that you are doing everything you can to ensure v safety. find side effect prevention and treatment, subgroups who should not have v, etc. this will incidentally possibly prevent said subgroups from having to point out that their reaction to the v is not being studied, etc.

2. horn 2: don't study the problem, because somebody claims that doing science will make the think they will get sick.

 

In the context of research there would have to be a definition of what is meant by "trigger". The common meaning is something which has causal impact, rather than simply meaning x preceding y. Defining trigger in ME/CFS is challenging because we don't know what any of the underlying mechanisms are so there's no way to connect a pre illness event with becoming ill no matter how closely the chronology matches. The 'common sense' approach of seeing x preceding y and drawing a conclusion does not give us a scientific standard unless there is supporting evidence.

Whether 'x' is a medical treatment, an infection or something else doesn't matter, because we can't identify the trigger unless we far better understand the 'y'.

This something I wrote in another thread, for infection substitute 'vaccine':

....... [we might also need to question] the assumption that a single recognisable infection is foundational and causative in ME. As noted in the first post in this thread, a majority of patients report that they become long term ill after (in their recollection) a virus like infection, however these remembered events may not link actual pathology.

Self reports of a link between onset and permanent decline in health provide a further instance of absence of evidence, there being no established link between any given virus that is demonstrable in any definable percentage of the patient population. The symptomology of ME resembles many post infection syndromes but correlation isn’t causation, and symptoms are not underlying pathology.

This is not to say that infection, viral or otherwise, has no role in ME/CFS, nor that some patients may accurately identify a pivot point between long term health and long term illness but we should not confuse patient recall of events with underlying pathology that may be hidden and slowly progressing months or years in advance of what otherwise may seem to be a causative infection.

This of course is counter to the history of defining works on ME by Ramsay and subsequently Acheson, where outbreaks of viral illness were identified as causative. It is quite painful for many of us ‘old hands’ to think that Ramsay may have been wrong in his conception of ME as specifically a post acute infection condition, but as the identified patient population has grown in the last 7 decades, so the certainty that ME is foundationally and causatively a result of identifiable infection, has receded.

Prushty in https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-018-1644-y states: In the majority of ME/CFS cases, there is no conclusive evidence for chronic viral infection, but it is plausible that viruses could act via a “hit and run” mechanism; this theory proposes that viruses trigger the disease, cause immune abnormalities and leave a dysfunctional immune system and/or autoimmunity.

A hit and run mechanism does not require an identifiable infection, for example an endemic virus may not cause any noticeable illness, it is also the case that the viruses that Prushty has noted are of interest, many challenge the human immune system in infancy long before the onset of ME/CFS in most patients. Re-activation of dormant virus could cause illness later in life and be a hit and run initiator of ME/CFS at that point, but it may equally be the case that the hit and run is initiated in infancy but that the effect only becomes evident much later in life.

Where does this leave us ? As a patient I don’t have an answer, but I do think that patients and researchers should adopt scepticism about both the idea that persistent infection is a cause of ME/CFS pathology, and about the idea that identifiable infections which seems to occur at the pivot point between long term good health and long term bad health for ME patients, is uniquely an indicator of the commencement of underlying pathology.

 

I agree and others, who know much more about this than I do, have suggested immune dysregulation. Perhaps the GWAS study (Chris Ponting) will provide evidence of the underlying cause.

 

> In the context of research there would have to be a definition of what is meant by "trigger". The common meaning is something which has causal impact, rather than simply meaning x preceding y. Defining trigger in ME/CFS is challenging because we don't know what any of the underlying mechanisms are so there's no way to connect a pre illness event with becoming ill no matter how closely the chronology matches. The 'common sense' approach of seeing x preceding y and drawing a conclusion does not give us a scientific standard unless there is supporting evidence.

take as good a sample of pwme as reasonable, note poss confounds, do same for a bunch of controls and dysauto/sle/whatever, get their health status. v some with informed consent. do [stfu .. ltfu). would that work? [this is just off the cuff.]

i am pretty sure i would find that useful even if philosophers say we still don't /know/ causation. and there might be weaknesses in such a study.

to me there is no legitimate reason to not study us.

 

Searching again for papers that explore whether vaccination may be a precipitating factor for ME/CFS, and or cause worsening.

found:

'Precipitating factors for the chronic fatigue syndrome', Irving E Salit, 1997, Journal of Psychiatric Research.
https://doi.org/10.1016/S0022-3956(96)00050-7
"Immunization was not a significant precipitant."

 

Just found this thread (had been searching for vaccination rather than immunisation).

Which lists articles /letters to editors, anecdotal content not research papers.

https://www.s4me.info/threads/medsc...d-to-functional-neurological-disorders.22042/

 

Enhanced Gene Expression Following Vaccination in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis
Ekua W. Brenu et al
https://www.scirp.org/pdf/_2013032814255107.pdf
International Journal of Clinical Medicine > Vol.4 No.3, March 2013
10.4236/ijcm.2013.43029

 

NZ context

2006 statement from IMAC on 'Chronic Fatigue Syndrome (CFS) and immunisation"
"It was concluded that evidence linking CFS to HBV vaccination largely consists of data generated from publicity. " Ugh.
https://www.immune.org.nz/sites/default/files/ConcernChronicFatigueImac2006V02Final.pdf

 

The Effects of Influenza Vaccination on Immune Function in Patients with Chronic Fatigue Syndrome /Myalgic Encephalomyelitis

https://file.scirp.org/pdf/IJCM20120600017_29918208.pdf

International Journal of Clinical Medicine, 2012, 3, 544-551

http://dx.doi.org/10.4236/ijcm.2012.36098 Team from Griffith Health Institute, Queensland


Abstract “... In this pilot study immunization with influenza vaccine is accompanied by a degree of immune dysregulation in CFS/ME patients compared with controls. While vaccination may protect CFS/ME patients against influenza, it has the ability to increase cytotoxic activity and pro-inflammatory reactions post vaccination. The role of Tregs in promoting a toxic effect at 28 days post-vaccination in our patient group cannot be ruled out. The benefits of influenza vaccine still likely outweigh the risks CFS/ME patients experience following vaccination. “

 

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated with pandemic influenza infection, but not with an adjuvanted pandemic influenza vaccine, 2015, Magnus et al

This was about the 2009 H1N1 pandemic in Norway.

This is the thread we have on it.

 

@RoseE

With the title do you mean vax as trigger for initial ME onset or as trigger for ME crash or both?

The papers listed here so far suggest you're looking for both?

 

Yes, I guess it has morphed into looking for both.

 

He wrote at some point that Hep B vaccine caused issues in 19/20 patients investigated, but I do not recall details.

 

I think it just got left hanging the way so many things have been left in ME research.

I will say though that 19 from 20 sounds very high but then people who thought they had been harmed by a vaccine are more likely to respond to the questionnaire. Everyone in my husband's department were vaccinated against hep B, three injections each, and none of them (more than 50 I think) had any problem even his friend who had ME. (He managed to stay in employment with support and lots of rest outside work)

 

MEA page = We’re collecting information on hepatitis B vaccination and ME/CFS – can you help? | 13 January 2016

which links to the Chief Medical Officer's report: https://meassociation.org.uk/wp-content/uploads/CMO-Report-2002.pdf

and which says:

"Immunisations – A few case reports have suggested that CFS/ME has occurred after immunisations, though intercurrent events, including infection, might have played a part in the disease process. It is biologically plausible that some processes seen after infections could also occur after immunisations, but this has yet to be confirmed by a good quality cohort study in the case of CFS/ME. Current advice to avoid immunisations during infections is designed to avoid such triggering."

A 2010 MEA survey which gives 338 out of 591 responses attributing ME to a vaccination trigger of any kind to HepB, is published at the bottom of that MEA page.

As in my earlier post in this thread I remain sceptical about what 'trigger' means in the context of ME/CFS. Correlation does not necessarily indicate causation and we need more careful terminology when dealing with temporal associations with apparent ME/CFS onset, if discussions with the potential to influence research directions are not to be mired in misdirection.