ME associated with flu, but not vaccine

[Hip]

Do people with enteroviral triggers usually get tested early?

Not usually. The evidence for enteroviral association in ME/CFS comes from finding chronic enterovirus infections in ME/CFS patients.

 

[halcyon]

Do people with enteroviral triggers usually get tested early?

They were in this study.

 

[Vic]

I found this study which mentions the use of the Pandemrix H1N1 vaccine on 470,000 children and adolescents in Norway from October 2009 to January 2010. It was found this vaccine is linked to significantly increased risk for narcolepsy with cataplexy.

Pandemrix contains the adjuvant AS03 which consists of vitamin E, squalene and polysorbate 80.

Though I am not sure if Pandemrix was the only H1N1 vaccine used in the mass vaccination in Norway during the 2009 H1N1 pandemic.

But if it was, then I think can conclude that the AS03 adjuvant is not linked to triggering ME/CFS.

Why do you conclude that? What if ME/CFS is a type of narcolepsy?

 

[SOC]

I'm confused about this statement about no anecdotal statements linking the flu and ME/CFS. Don't a lot of patients say that they got the flu and it never went away (and then a lot of other symptoms get added on)?

I think the confusion arises because we often can't easily distinguish between the flu itself and a "flu-like illness" unless it develops into a severe acute infection. Symptoms of many viral illnesses are similar, so we say we had the flu, but we could have had any of a number of viral infections. It's rare that anyone is actually tested to identify the virus in the early stages (if at all).

So while there's a lot of report about people saying their ME/CFS was triggered by a flu-like illness (I'm one of them), we really don't know what the actual virus was.

 

[searcher]

I think the confusion arises because we often can't easily distinguish between the flu itself and "flu-like illnesses" unless it develops into a severe acute infection. Symptoms of many viral illnesses are similar, so we say we had the flu, but we could have had any of a number of viral infections. It's rare that anyone is actually tested to identify the virus in the early stages (if at all).

So while there's a lot of report about people saying their ME/CFS was triggered by a flu-like illness (I'm one of them), we really don't know what the actual virus was.

I totally agree. I just don't think it's fair to say that there isn't anecdotal evidence linking the flu with ME/CFS, since a flu-like illness is a very common trigger. Hip seemed surprised by the findings in this paper whereas it reflected my own experience, even though I don't know for sure what initial virus I had.

 

[Hip]

I just don't think it's fair to say that there isn't anecdotal evidence linking the flu with ME/CFS, since a flu-like illness is a very common trigger.

What you are saying is just too vague and imprecise to call evidence. Lots of viruses cause a flu-like illness, but we can't just then assume they are all linked to ME/CFS.

Why do you conclude that? What if ME/CFS is a type of narcolepsy?

If you want to massively blur the distinctions between diseases, you can conclude anything you like.

 

[Vic]

If you want to massively blur the distinctions between diseases, you can conclude anything you like.

But what if the distinction really is blurred? As I progressed through many stages of this... syndrome... one was indeed an odd type of narcolepsy. Aren't there studies that show it's like PWME are awake during sleep and asleep when awake?

Anyways I haven't looked into it much, but one part of the total fatigue contribution to CFS/ME is a type of sleepiness that can sometimes increase to the level of passing out or close. The mechanisms seem to be similar.

 

[acer2000]

As far as I am aware, thimerosal has not been linked to any diseases or health conditions. If it was, then eating a can of tuna fish would probably trigger the same diseases, since a calculation I did elsewhere showed you will get more mercury lodged in your brain after consuming a can of tuna fish than you will from a mercury-containing vaccine.

An accumulation of mercury in the body may increase the risk of autoimmune conditions, but high body burdens of mercury are going to come from regularly eating fish with high mercury content (such as tuna, or even worse, restaurant sushi), not really from vaccines.

Sure, and I don't want to open a debate about what effects (if any) Thimerosal has. Personally, I don't think putting mercury in anything that goes in the human body is a good idea. Especially when there are viable alternatives. And I don't eat tuna.

However, I wanted to point out that the formulation of the particular vaccine might make a difference. It could well be that something other than the active ingredient can cause an adverse reaction and that this differs between countries and even manufacturers of vaccines for the same illness.

 

[acer2000]

Also "flu like illness" is pretty vague. Lots of things can cause "flu like illness" that aren't actually the flu, or even viruses. You can get flu like symptoms from chemical/environmental exposure for example.

I think as array based testing becomes better and cheaper it will become easier to characterize outbreaks of illness so doctors won't be guessing "whats going around". In fact last winter I had a wicked sore throat and cough. When I started to have a fever, I went to the urgent care. In addition to rapid flu tests (which are quite common now) I was given a respiratory virus panel swab. This checked for dozens of viruses and it came back that I had "Coronavirus 63". So then my doctor didn't prescribe antibiotics and I knew what to expect. They also entered my case into their community system so they knew to keep an eye out for other patients with the same.

 

[Hip]

I think as array based testing becomes better and cheaper it will become easier to characterize outbreaks of illness so doctors won't be guessing "whats going around".

Indeed. If patients coming down with infections were routinely tested in the future with a new cheap and effective pathogen gene sequencing technology, we would not be still arguing whether for example enterovirus can trigger ME/CFS.

When such a technology is widespread in future, we will have thousands of recorded cases where ME/CFS was seen to appear days after an acute infection, and we will have a full record of the pathogen that triggered it (including the full genome of the pathogen, so that we would even know which strain of the pathogen we were dealing with).

 

[BurnA]

I think the confusion arises because we often can't easily distinguish between the flu itself and a "flu-like illness" unless it develops into a severe acute infection. Symptoms of many viral illnesses are similar, so we say we had the flu, but we could have had any of a number of viral infections. It's rare that anyone is actually tested to identify the virus in the early stages (if at all).

So while there's a lot of report about people saying their ME/CFS was triggered by a flu-like illness (I'm one of them), we really don't know what the actual virus was.

It's true. I had a flu like illness although it wasn't the flu - I didn't have a fever but I did have sore throat and nasal blockage mucous etc. With fatigue. It's been discussed elsewhere but if this is autoimmune it probably doesn't matter what type of virus triggers ME/CFS , all that might be needed is something to activate an immune response . Is there conclusive evidence that one type of virus does or doesn't trigger this disease ?

 

[Mij]

However, I wanted to point out that the formulation of the particular vaccine might make a difference. It could well be that something other than the active ingredient can cause an adverse reaction and that this differs between countries and even manufacturers of vaccines for the same illness.

Dr.Hyde found that some pts that developed M.E were given contaminated vaccines.

 

[SOC]

Is there conclusive evidence that one type of virus does or doesn't trigger this disease ?

I don't think so, but there is talk that the intiating infection needs to be able to create an unusual immune response. That suggests either pathogens that have a special inpact on, or ways to evade, the immune system; or particularly virulent forms of more common viruses. For example, the 1918 influenza was able to cause a huge immune cascade -- a cytokine storm -- which is what made it much more dangerous than other flu strains. In that case, however, the extreme nature of the immune impact meant very many people who caught the virus has a very bad response, In our case, there has to be an explanation why we get very sick from the pathogen and most people don't, so it's not just that the pathogens in question create an unusual immune response.

 

[Dolphin]

Interesting. Both daughter and I got much worse after getting H1N1 in the 2009 pandemic. We already had ME, so it wasn't the root cause, but H1N1 made it much worse.

That's potentially interesting: given most people aren't diagnosed, the infection could lead to more people getting diagnosed and thus the infection might appear to be the initial cause but not actually be the initial cause.

 

[Dolphin]

One possibility the authors raise:

However, many patients with influenza symptoms will not seek medical care during an influenza season. Only 2.4% of the study population received a physician diagnosis of influenza during the peak pandemic period. Presumably, patients with more severe symptoms seek medical care. The proportion of the population with clinical influenza infection during the pandemic has been estimated to be 20–30% [33,34], implying that a substantial number of the subjects categorized as uninfected in this study, actually were infected and therefore misclassified. Non-differential misclassification of exposures and end-points in a prospective study usually leads to underestimation of the effect of the exposure on the outcome, in this case influenza infection on later CFS/ME occurrence, suggesting that the true relative risk may be higher than estimated by us

 

[Dolphin]

Thinking about this study a bit more:

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.

It's an interesting point.

As I just posted, the authors do say that a lot (in the region of 90%, very approximately) of people who got ill with H1N1 never went to the doctor but they don't point out your (first) interpretation of the data:

However, many patients with influenza symptoms will not seek medical care during an influenza season. Only 2.4% of the study population received a physician diagnosis of influenza during the peak pandemic period. Presumably, patients with more severe symptoms seek medical care. The proportion of the population with clinical influenza infection during the pandemic has been estimated to be 20–30% [33,34], implying that a substantial number of the subjects categorized as uninfected in this study, actually were infected and therefore misclassified. Non-differential misclassification of exposures and end-points in a prospective study usually leads to underestimation of the effect of the exposure on the outcome, in this case influenza infection on later CFS/ME occurrence, suggesting that the true relative risk may be higher than estimated by us

 

[Dolphin]

That is a great question.

Unless influenza was the predomnant/most common trigger for this illness (study suggests the virus is a trigger for ~4% of cases), this study lacks the statistical power to demonstrate a reduction in risk. Side note: the hazard ratios were calculated using the Not infected/not vaccinated group as the baseline.

Here is the data, I hope this makes things a little clearer:

Just to post the following quote again as it is relevant to the bold part:

However, many patients with influenza symptoms will not seek medical care during an influenza season. Only 2.4% of the study population received a physician diagnosis of influenza during the peak pandemic period. Presumably, patients with more severe symptoms seek medical care. The proportion of the population with clinical influenza infection during the pandemic has been estimated to be 20–30% [33,34], implying that a substantial number of the subjects categorized as uninfected in this study, actually were infected and therefore misclassified. Non-differential misclassification of exposures and end-points in a prospective study usually leads to underestimation of the effect of the exposure on the outcome, in this case influenza infection on later CFS/ME occurrence, suggesting that the true relative risk may be higher than estimated by us

i.e. we can't be definite that H1N1 only triggered ~4% of cases, it could be a much larger figure.
(I suppose we can't be definite about lots of things. But I thought I'd point out this one issue when it was in my head).

 

[Snow Leopard]

Just to post the follow quote again as it is relevant to the bold part:

i.e. we can't be definite that H1N1 only triggered ~4% of cases, it could be a much larger figure.
(I suppose we can't be definite about lots of things. But I thought I'd point out this one issue when it was in my head).

It could also be less since the 4% figure was based on diagnosis of a "Influenza like illness".
But you are right, this is an inherent uncertainty of population cohort based (rather than clinic based) studies.

 

[SOC]

That's potentially interesting: given most people aren't diagnosed, the infection could lead to more people getting diagnosed and thus the infection might appear to be the initial cause but not actually be the initial cause.

I suspect this may true of more of us than we currently realize. We may have had ME for years (maybe all our lives), but it wasn't recognized until something sufficiently damaging knocked us over the edge into disability.

I often think about the history of HIV and some of the similarities to our history. For years the thinking was that the disease was AIDS, which was recognized when patients developed serious infections from pathogens ordinarily controlled by the human immune system. All AIDS patients were very, very ill people. Once they discovered the cause, HIV, they realized that the majority of patients with the disease were not those severe AIDS patients, but people who appear healthy or nearly so. The AIDS patients were just the easily-identified severe tip of the iceberg.

The same could be true for us. What we see as "real ME" with PEM, neuroimmune manifestations, and disability (50% reduction in activity level) may be only the severe tip of the iceberg. The illness itself may exist in people who currently don't have the symptom set we think of as ME. They may be walking timebombs, just waiting to encounter the wrong trigger -- a pathogen, a vaccine, who knows? -- that sets off the cascade that spirals down into ME. Or maybe it's just a matter of time for some people as their body systems degrade slowly from the disease without the need for the straw-that-broke-the-camel's-back single pathogen.

One idea I have is that our illness may be at bottom an immune disorder that's been in place a long time, either as a genetic abnormality or an unknown pathogen (like HIV was) that has been in our bodies a long time. The multiple pathogens identified in PWME, none of them with enough frequency to be considered the cause of the illness, could be secondary infections. As in HIV, those secondary infections would be highly problematic, but not causal. They may be what's causing most of our symptoms (which is why our symptoms differ somewhat-- different secondary infections) so treatment is critical, but that doesn't get at the root cause of the illness. Again, like HIV.

My daughter had multiple hits before she finally went down for the count, so to speak. If we hadn't been aware of ME after the first one (because unlike her, I didn't mostly recover from that one), we might have claimed any of those hits as The Cause of her ME -- the weird extremely sudden-onset flu-like illness we both had, the pre-college vaccine boosters that dramaticly increased her ME symptoms, or the H1N1 that left her unable to finish the semester. My guess is that none of them is actually the root cause of her ME, they just moved her condition from apparently healthy to clearly very ill.

Of course, I could be completely wrong. This is just one of a number of my random speculations about ME.

 

[Dolphin]

I suspect this may true of more of us than we currently realize. We may have had ME for years (maybe all our lives), but it wasn't recognized until something sufficiently damaging knocked us over the edge into disability.

I often think about the history of HIV and some of the similarities to our history. For years the thinking was that the disease was AIDS, which was recognized when patients developed serious infections from pathogens ordinarily controlled by the human immune system. All AIDS patients were very, very ill people. Once they discovered the cause, HIV, they realized that the majority of patients with the disease were not those severe AIDS patients, but people who appear healthy or nearly so. The AIDS patients were just the easily-identified severe tip of the iceberg.

The same could be true for us. What we see as "real ME" with PEM, neuroimmune manifestations, and disability (50% reduction in activity level) may be only the severe tip of the iceberg. The illness itself may exist in people who currently don't have the symptom set we think of as ME. They may be walking timebombs, just waiting to encounter the wrong trigger -- a pathogen, a vaccine, who knows? -- that sets off the cascade that spirals down into ME. Or maybe it's just a matter of time for some people as their body systems degrade slowly from the disease without the need for the straw-that-broke-the-camel's-back single pathogen.

One idea I have is that our illness may be at bottom an immune disorder that's been in place a long time, either as a genetic abnormality or an unknown pathogen (like HIV was) that has been in our bodies a long time. The multiple pathogens identified in PWME, none of them with enough frequency to be considered the cause of the illness, could be secondary infections. As in HIV, those secondary infections would be highly problematic, but not causal. They may be what's causing most of our symptoms (which is why our symptoms differ somewhat-- different secondary infections) so treatment is critical, but that doesn't get at the root cause of the illness. Again, like HIV.

My daughter had multiple hits before she finally went down for the count, so to speak. If we hadn't been aware of ME after the first one (because unlike her, I didn't mostly recover from that one), we might have claimed any of those hits as The Cause of her ME -- the weird extremely sudden-onset flu-like illness we both had, the pre-college vaccine boosters that dramaticly increased her ME symptoms, or the H1N1 that left her unable to finish the semester. My guess is that none of them is actually the root cause of her ME, they just moved her condition from apparently healthy to clearly very ill.

Of course, I could be completely wrong. This is just one of a number of my random speculations about ME.

Yes, I have thought of this before. For example, I have wondered do anaesthetics really cause it or do they just bring out the syndrome which existed there already.

In my own case, I was a high functioning multi-sport athlete before I got an infection when 16 so think it was the infection that was the trigger.

Though a couple of years earlier I did start to feel tired by around 9pm at night: nothing like ME but did go to the doctor once about feeling tired. That may be nothing but I do always wonder if I had pulled back a little on my busy lifestyle, whether I might have prevented myself getting M.E.