CFS/ME is associated with pandemic influenza infection, but not with an adjuvanted pandemic influenza vaccine, 2015, Magnus, Hornig, Lipkin et al

If I understand correctly, according to the description of methods, this data has no controls to assess diagnostic biases.

I think ME is underdiagnosed and diagnosis is suppressed by economic, political and professional pressures. From personal experience, getting my own diagnosis was like getting blood out of a stone.

So I take the view that ME diagnosis is subject to practitioner bias from the outset. It seems true that if a practitioner is diagnosing in the context of previous H1N1 diagnosis by consulting health records then this could change the risk of diagnosis, possibly making it higher if a patient has previously had H1N1 diagnosed.

Conversely, given the adverse outcomes regarding herd immunity due to the changes in parental immunisation strategies due to controversies over vaccine adjuvants, licensed medical practitioners are well aware of a political, economic and professional push to continue vaccination to ensure herd immunity and might be influenced by the context of a patients presentation in relation to vaccination records and reluctant to diagnose ME in that context.

This is not empirical data because, much as I treasure their overall beneficial influence on human existence, it depends on practitioner based diagnosis and medics are human beings, like us all, subject to bias.

 

They use the term "symptomatic" infection, but I don't imagine there was any attempt to quantify the symptom severity. It's probably unlikely that anyone one was tested for "asymptomatic" infection, either.

It would be very interesting if the severity of the influenza symptoms were linked to ME/CFS onset (as in the Dubbo study), but an objective measure of flu severity may not be easy to obtain for a large group, as everyone would need to be tested at a similar point in their illness.

There's at least one study that found mildly elevated spinal fluid protein in some ME patients (and in no controls), which might be a marker of a prior severe infection. That might be a sign of the "mild encephalitis" that is sometimes proposed as a cause for ME, or it might just be a sign of a severe infection that has done something else to initiate ME.

I'm not saying that only a severe infection can trigger ME, but it would be interesting if the probability of developing ME after an infection was on a curve related to the infection's objectively measured severity.

 

Though conversely, some people in Ireland might say that some doctors are in a rush to give a diagnosis of CFS to those who believe they (parents, etc.) have been damaged by the (HPV) vaccine.

 

In addition, only because their interesting result is consistent with the model of "symptomatic" infection, this result would not strengthen this model anyway as the model is unlikely to explain gradual onsets (where no infection is known, and no symptoms from any infection are apparent).

In my case, BTW, it started on a low level in late summer after at least two ticks, and I doubt that this was due to a normal symptomatic reaction against the infect borrelia. It ever stayed on a low level until a very symptomatic EBV infection.

I seems that not every infectious agent is able to cause ME, so a question could be: "What are the properties of some infectious agents that makes them able to trigger ME (as well as some chemicals)?" In respect of influenza I personally would search here: https://www.ncbi.nlm.nih.gov/pubmed/19194459 ("... is strongly activated by manganese ions ...).

 

Yes, interesting point, I dont have an axe to grind either way over adjuvants myself but notice it is becoming a hot topic again considering the recent pre-proof by Sepúlveda et al which was published here, discussing HPV and ME. Just when you thought ME research couldn't get any more controversial, I wonder what Nancy Klimas has to say about it, considering her work on GWS.

Obviously its best for everyone if we can prove whatever the truth is so we can vaccinate with confidence in best practice but to that end it felt appropriate to point out that medical diagnosis of ME is not currently an empirical measurement and is subject to bias. I hope that will change and we will get a lab test to assist diagnosis, which could then provide empirical data and that would provide more accurate and convincing information.

 

A notable result of this study is that despite the influenza strain being associated with increased ME/CFS cases, immunisation to this strain did not reduce the risk - and it is important to note that the sample size of this study is the population of Norway.
Table 2: Adjusted HR of 0.97 (95% CI: 0.91–1.04) compared to the unvaccinated reference of 1.0.


Would the immunisation make a difference in a country like the USA with over 50 times the population? Perhaps, but we cannot say for sure.

I recently read a paper comparing the risk of Guillain Barre Syndrome (autoimmune syndrome caused by anti-ganglioside antibodies) from different influenza strains, that noted that differences in induction of the syndrome could be due to differences in structure of hemagglutinin over time, namely increased sialic acid binding sites, or altered neuraminidase function (leading to reduced sialic acid - (or hypothetically, ganglioside) removal from hemagglutinin complexes. Since the vaccine relies on these surface proteins, theoretically the rate of induction of the syndrome by the vaccine would also change.

Which makes me wonder whether drift in the surface protein structures of influenza has let to altered rates of induction of ME/CFS (for a given infection rate) over time?

 

This study has been discussed perviously on ME/CFS forums. I will copy and paste what I wrote in 2015 in this post, to stimulate discussion:




The authors found a twofold increase in the risk of developing ME/CFS in those who were diagnosed with H1N1 swine flu. I assume this increase in risk is relative to the general population (who were not diagnosed with H1N1 influenza).

But note that the number of people who caught the H1N1 virus will be higher than the number of people actually diagnosed with having H1N1 influenza (because the majority of people catching the virus would have only had minor symptoms, or have been asymptomatic, so were not diagnosed).

Studies show that just after the 2009 pandemic, around 24% of the general population, and 50% of school-age children were seropositive for H1N1, meaning they had caught the virus at some point.

So, people actually diagnosed with H1N1 influenza in general must have been hit much harder by the H1N1 virus, because presumably these were the people whose symptoms were so bad on contracting H1N1 that they had to go to their doctor.

Thus what this study may be measuring is how severely someone's body or immune system may be reacting to the H1N1 virus. By focusing on those who were actually diagnosed with H1N1 influenza, rather than focusing on the larger set of people those who are seropositive for H1N1, this study may merely be selecting people whose immune system reacts more strongly to a H1N1 viral infection.

Now people who naturally mount a strong inflammatory response to viral infection might conceivably be much more likely to develop ME/CFS, given that ME/CFS is often viewed as a chronic inflammatory condition driven by viral infection. So this might explain why people from the group diagnosed with H1N1 influenza were found to be at higher risk for later developing ME/CFS.



Thus I can see two ways we can interpret the results of this study:

(1) The first interpretation is that H1N1 influenza virus does not trigger ME/CFS, but those who get major influenza symptoms on catching from H1N1 may simply be more immunologically disposed to developing ME/CFS (but only when they catch the usual ME/CFS-triggering viruses like enterovirus or EBV).

(2) The second interpretation is that H1N1 influenza virus does sometimes trigger ME/CFS.



Possibly one way to work out when the first or second interpretation might be correct is to look at the timing of the onset of ME/CFS after coming down with H1N1 influenza. We know with the usual ME/CFS-triggering viruses, you tend to get either rapid-onset ME/CFS (the disease appearing within days of contracting the triggering virus), or you get gradual-onset ME/CFS (the disease appearing within a few months of contracting the triggering virus).

So if we looked at the average time of onset of ME/CFS during the 39 months that the cohort was tracked, if there are a lot of cases of ME/CFS appearing withins days of coming down with their H1N1 influenza, or within a few months of their H1N1 influenza, then that suggests the H1N1 virus is actually triggering ME/CFS.

But if the typical onset time of ME/CFS is found at random times during the 39 month observation period, that suggests the H1N1 virus is not triggering ME/CFS.

Perhaps we will find some info on the onset time of ME/CFS in the full paper.



There is also a third possibility:

(3) The third interpretation is that H1N1 influenza virus does not trigger ME/CFS as such, but after coming down with a major case of H1N1 influenza, the body becomes more vulnerable to later developing ME/CFS (when catching one of the usual ME/CFS triggering viruses like enterovirus or EBV).

 

I wonder what the data on narcolepsy is in the same population, particularly in relation to ME. My thinking being that if narcolpesy is autoimmune disease and ME is caused (hypothetically) by suppressing autoimmune reactions then the people with ME ought not to be the ones with narcolepsy and vice versa.

Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy
https://www.pnas.org/content/115/52/E12323

Personally I have dark suspicions about H1N1, since around that time 2009, I contracted a fluey virus which stayed with me for many years causing recurring bouts of upper respiratory tract infection whenever I got even the slightest bit cold. After much trial and misery and many bouts of this virus I discovered the threshold temperature to trigger virus activity was 27°C and I had to keep my ambient temperature at this level to avoid recurrences of viral activity. In fact its only in the last year I have begun to find myself able to be without a fleece hat on indoors 24/7 without getting symptoms of recurrence, though I still keep my mobile thermostat at 27°C and am very careful not to let my head get cold and keep a snood-hoody (tubular fleece neck warmer with integral hood) close by at all times.