The Research Council of Norway invites ME-patients to propose research projects

[Jonathan Edwards]

We're a bit OT but why would this suggest CNS/ANS stuff rather than immune stuff?

I cannot think of any regulatory principle in the immune system that would pop up in adolescence and again at 35. There might be two separate high risk points - there are immunological diseases that go for either adolescence (Reiter's) or 35 (MS) but for the same illness to be influenced by both time points is weird in immune terms. I am not sure I can think of a better explanation in CNS terms but the CNS is an order of magnitude more complicated again.

 

[Jonathan Edwards]

I tend not get too excited by epidemiological ME/CFS research as the diagnosis is often based on questionnaires so is not very solid.

When there are good cheap diagnostic tests, I will get more excited by epidemiological studies.

And if one just goes by people with (existing) confirmed diagnoses, one will normally only get a small percentage of the total ME/CFS population so likely a biased sample.

I think that is fair enough but the Norwegian study that shows two clear peaks in both sexes needs some sort of explanation. Ascertainment bias might do it by it is hard to see why.

 

[Jonathan Edwards]

Do you know why adolescence seems to trigger the illness? Or other illnesses. The usual answer is hormonal changes, but what is it about those that causes such big problems for some? There must be more.

No idea why adolescence shows a rapid rise in incidence around 12, going on going up in girls but not boys. The only adolescent rheumatological disease that seems to have an explanation is ankylosing spondylitis. That affects ligament insertions and seems to target them at the point when they stop growing. Reiter's is not really adolescence because it occurs with new infections, some sexually transmitted, when young people meet new environmental factors around 18-22. Lupus starts in adolescence in girls with menarche but goes on getting commoner as the twenties.

 

[Jonathan Edwards]

The anecdotes do seem to keep coming in. If there is genuinely a re-dip in health in those with teen onset at 35 I think that may tell us something really important. We know very little about the way brainstem functional regulation shifts with age for instance. The other factor I find intriguing is that the 35 peak is the same as for MS, which affects the whole CNS. But once one has some data it is easier to tease out the options.

 

[Dolphin]

I tend not get too excited by epidemiological ME/CFS research as the diagnosis is often based on questionnaires so is not very solid.

When there are good cheap diagnostic tests, I will get more excited by epidemiological studies.

And if one just goes by people with (existing) confirmed diagnoses, one will normally only get a small percentage of the total ME/CFS population so likely a biased sample.

Probably the majority of ME/CFS epidemiological research has been run by psychiatrists and psychologists, so people should keep that in mind if they are thinking of asking for it.


A lot of people think that knowing the exact number of patients would make a lot of difference. However it is very difficult to do at the moment as easy reliable testing methods are not available for large studies.

Just knowing many people are affected doesn't guarantee extra funding: it is recognised that fibromyalgia affects a lot more people than ME/CFS but there is still relatively little biomedical research into fibromyalgia.

So I'd recommend asking for "safer" research than epidemiological studies: by safer I mean ones that won't lead to dubious conclusions.

 

[Amaya2014]

I'd recommend more specific testing for functional disability. I've had nuerospych evals and a functional capacity examination. The tests are given individually by different specialties and aren't compared to each other.

From what I've seen, even the CPET doesn't show the marked impairment that results from someone with CFS trying to walk, talk, follow instructions, remember details, and any of the other myriad multi-tasking demands of real life.

Instead of patients continually forced to keep relating symptoms (hoping someone will believe us) why not develop testing for ME/CFS with a combination of physical and cognitive challenges?

 

[Jonathan Edwards]

Probably the majority of ME/CFS epidemiological research has been run by psychiatrists and psychologists, so people should keep that in mind if they are thinking of asking for it.

A lot of people think that knowing the exact number of patients would make a lot of difference. However it is very difficult to do at the moment as easy reliable testing methods are not available for large studies.

Just knowing many people are affected doesn't guarantee extra funding: it is recognised that fibromyalgia affects a lot more people than ME/CFS but there is still relatively little biomedical research into fibromyalgia.

So I'd recommend asking for "safer" research than epidemiological studies: by safer I mean ones that won't lead to dubious conclusions.

I can see where you are coming from, Dolphin. On the other hand it was the epidemiology of RA that got us to the point of understanding mechanism. The incidence pattern is that of cumulative stochastic internal events. And that is the mechanism, I am pretty sure. And the epidemiology came principally from Scandinavia - where they seem to have a rather obsessive tendency for recording everything. The attraction of a longitudinal study would be that it could establish fairly easily whether the teen peak and the 35 peak are part of the same process - whatever that might be. One might argue that a lot of them do not really have ME, but then there is a question as to what they do have. Underreporting would not be a problem if it was uniform. There has to be some sort of explanation for the rather unique profile of Norwegian ME onset. If it is an ascertainment bias problem I would expect a longitudinal study to reveal that.

The ascertainment issue could also be mitigated by the sort of technique Nacul used, where multiple criteria are applied so that you can get and idea of how much noise you have. You need to trawl at a primary care level, but that is what Scandinavians are good at.

 

[Justin30]

Is someone going too collectively gather the info from the PR thread and send it to the Research Council of Norway?

Or can someone please send an email address as to where requests should be send?

I personally would like to see subgroups defined or stage.

• I feel that true ME as defined is Neuro Immune which highlights my experience and many others
• Translated into research into CNS and Immune connection
• Treatment for reel ME (for the ones that are stuck in Bed or limited to the their homes)
• Defining the trigger and the process that ensues

Thanks

 

[5150]

1.) We need to be able to "know the difference" between different cohorts. What treatment(s) work on each cohort, because it seems there are definite variations.

2.)Related to separate variants, we must know "what causal pathogen(s) for that variant, and its' method of transmission... i.e., what is infectious to others and How?

For each "strata" or variant, it is important to know : its source, what treatment it responds to, and is it contagious & if so, by what means is it contagious?

Thanks for the opportunity to ask these questions.
Go Norway!

 

[Forbin]

Just some speculation:

In order to have a relapse, you first have to get well, and that seems to be what sets adolescent onset apart - i.e., a higher recovery rate. So, the effect that's seen may simply result from the fact that "recovered" adolescent cases have the "opportunity" to relapse, whereas those with later, unremitting onset don't have that "opportunity."

Why mid 30's? Perhaps if you've "recovered" in adolescence, you've gone on to have a family. By your mid-30's you may be more likely to have school-age children in the house and thus you (and/or your friends and associates of similar age) are more likely to pick up any of the viruses that are running rampant in the local school district. Perhaps other factors increase your exposure to viruses in your mid-30's, as well. Whatever the origin, fighting a virus (any virus) might tip your precariously "recovered" immune system into a relapse.

 

[user9876]

I can see where you are coming from, Dolphin. On the other hand it was the epidemiology of RA that got us to the point of understanding mechanism. The incidence pattern is that of cumulative stochastic internal events. And that is the mechanism, I am pretty sure. And the epidemiology came principally from Scandinavia - where they seem to have a rather obsessive tendency for recording everything. The attraction of a longitudinal study would be that it could establish fairly easily whether the teen peak and the 35 peak are part of the same process - whatever that might be. One might argue that a lot of them do not really have ME, but then there is a question as to what they do have. Underreporting would not be a problem if it was uniform. There has to be some sort of explanation for the rather unique profile of Norwegian ME onset. If it is an ascertainment bias problem I would expect a longitudinal study to reveal that.

The ascertainment issue could also be mitigated by the sort of technique Nacul used, where multiple criteria are applied so that you can get and idea of how much noise you have. You need to trawl at a primary care level, but that is what Scandinavians are good at.

I'm assuming you are proposing some type of study where time lines are generated (when disease is diagnosed, seems better, gets severe, gets milder, re-diagnosed, etc) for a lot of patients to try to understand the temporal process. Rather than looking at incident rates in the overall population?

I think such a project sounds like it could be interesting although I wonder if a problem would be if there are a large number of patients who simply give up on doctors for a time rather that the disease changing.

 

[actup]

I am also quite curious re: this question. My son, aged 30, and my sister's son, aged 33, both had been low energy and needed more sleep than their friends during adolescence. They became much more ill after viral infections( tonsillitis and mono respectively) in their mid twenties and were both diagnosed with post viral ME/CFS soon after. My thirteen year old granddaughter has been exhibiting flu-like symptoms and PEM since she took up competitive soccer last year(her parents reject my concerns). My sister, her two daughters and I were diagnosed with ME/CFS at the end of peri menopause. My parents and in-laws lived healthy long lives.

I have many questions but to my knowledge no one has done research on multi generational families with CFS. I'm anxious to give the the younger ones some hope.

 

[justy]

I had 'something' going on, after glandular fever at age 13, which by the time I was early 20's was full blown ME. Then I appeared to recover until I was 38, when I then became very ill and have never recovered.

 

[Scarecrow]

Another double peak anecdote here but I'm a little offset from the epidemiological peaks.

Onset following IBS at 15 (I assume the IBS was relevant) but disease progress was very gradual until infectious trigger at 21.

90 - 95% "recovered" at 24 and remained so until 38 when another gradual decline started. Final trigger was at 42.

 

[sarah darwins]

So is there anything someone in the "at risk" group for a 30-something relapse might do to mitigate the risk?

 

[Sasha]

I had the opposite trend - viral trigger mid-20s, very sick to mid-30s, 95% "recovered" in late 30s, relapse mid-40s.

This is why we need some proper epidemiology! We're a bunch of anecdotes.

 

[msf]

No idea why adolescence shows a rapid rise in incidence around 12, going on going up in girls but not boys. The only adolescent rheumatological disease that seems to have an explanation is ankylosing spondylitis. That affects ligament insertions and seems to target them at the point when they stop growing. Reiter's is not really adolescence because it occurs with new infections, some sexually transmitted, when young people meet new environmental factors around 18-22. Lupus starts in adolescence in girls with menarche but goes on getting commoner as the twenties.

Hormones? Of course, the question then is, how do hormones influence whether or not you get ME?

 

[Gemini]

This is why we need some proper epidemiology! We're a bunch of anecdotes.

Add me to the bunch-

Infectious trigger at 20, very ill, bedridden/homebound... " recovery"... relapse at 45...

 

[Tuha]

I would like to know what is causing muscle fatigue, accumulation of lactate, possible oxigen distribution in our bodies.
I think these problems are significant in lmost each patient. I think this is the reason why we are so exhausted. I can live quite good with other symptomps but what kills me is that horrible exhaustion.
I think that muscle exhaustion is a significant part why we are so exhausted. Maybe a research in this area could move us significantly and give us a treatement soon

 

[A.B.]

I want to know why we tend to tolerate chemicals poorly (food additives, sensitivity to medication, being bothered by the smell of chemicals that others seem to tolerate just fine). Maybe this is even related to the metabolic abnormalities mentioned by Tuha.

It could tell us a lot about where in the body the biochemistry is messed up.