List of research on how ME/CFS is spread (epidemiology)?

[joshualevy]

Is there a summary of ME/CFS epidemiology research somewhere? I don't mean how common it is; I'm interested in how it is spread. My memory is that when AIDS was first described, the first thing that was determined, was that it was a sexually transmitted disease, and that very much helped to narrow the search for the causative agent. Has similar work been done with ME/CFS? Has it been attempted?

Everyone complains that most research is "a shot in the dark", which is true. However, we can learn how it is spread without knowing anything about the exact cause. (This is the whole point of the book "The Ghost Map".) Once we know the general method of spread, it allows us to focus on a much smaller set of possible causes. Also, we can prevent new infections even if we can not cure existing ones (which certainly has a public health benefit). My memory is that for AIDS, they first figured out it was sexually transmitted (by tracking transmission), and then they figured out the size of the infectious particle (by filtering), and then they found the exact virus. By the time they were looking at specific viruses, they knew the basic size of the thing they were looking for.

Is that what "The Incline Village" study was trying to do? Is that study on line? Has anyone else tried to do something similar?

 

[minkeygirl]

There's a few other cluster groups. David Bell in Lynsonville New York and there was one in Florida even before Incline Village.

I don't think Nevada was a study. The CDC was called in to investigate this "thing" that was getting so many people sick but they mostly skiied.

You can probably find them by googling.

 

[Hip]

There are several pathogens associated with ME/CFS, and most of these are spread by the respiratory route, or by the oral-fecal route. That is to say, the pathogens exists in the respiratory secretions and feces, and so can be spread by normal social contact.

There is one rarer cause of ME/CFS that is spread by vectors: Ross River virus is spread by spread by mosquitoes.

 

[Woolie]

MECFS is a little different from AIDS. First, even though there is evidence for a viral trigger in many cases, only a small subset of infected persons will develop the full-blown illness. Second, there seem to be a number of pathogens that can result in a similar endpoint. There is still debate as to whether the full-blown illness is caused by ongoing pathogen activity, or whether it represents some form of immune dysfunction initiated by the initial infection (such as in some autoimmune diseases). The recent success of drugs such as rituximab has led some to more seriously consider the immune dysfunction idea.

The study below is the perhaps the closest thing to what you seek. Its a prospective study that examined people with acute viral infections, then followed up to see how many developed full-blown MECFS. They identified three specific viruses as being implicated in the development of MECFS, defined narrowly (EBV, Q fever and Ross River virus). But of course, there may be others they didn't test for (including possibly non-viral pathogens).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1569956/

From the discussion:

"These findings confirm that chronic fatigue syndrome is a relatively common sequel of several different infections—now documented to include Epstein-Barr virus, Ross River virus, and Q fever—but not minor upper respiratory tract or gastrointestinal infections. .... severity of the acute illness rather than the specific pathogen may be the major determinant of post-infective fatigue syndrome".

There is not a lot of research of this type, because most research activity up till recently has been focused on psychosomatic models (a bit like Type I diabetes in the 1970s, where psychosomatic models had a lot of sway). This is now slowly starting to change, though, so we might see more work of this kind in the future.

 

[barbc56]

I doesn't appear that most cases of me/cfs are contagious. The cluster outbreaks may be a different disease or a very small subset of me/cfs.

Research seems to be indicating that the susceptibility is some disfunction within the patient.

Not everyone who gets mono, or other illnesses ends up with me/cfs and that's telling.

Basically, its the hit and run theory.

It would definitely be interesting and possibly helpful to know the differences between the causes of clusters and individual cases of me/cfs. But with the lack of funding and the state of knowledge at this time about me/cfs, this line of inquiry is not a high priority.

Barb

 

[Woolie]

On a complete aside, if you're interested in psychosomatic models of Type I diabetes, this very influential book from the 1970s talks about how children with "psychosomatic diabetes" exacerbate their own symptoms with the unconscious aim of manipulating their parents:

Baker, L., Minuchin, S., Liebman, R., & Rosman, B. L. (1978). Psychosomatic Families: Anorexia Nervosa in Context. Harvard University Press.

It even presents some convincing data that support this hypothesis!

You probably think this idea is as ridiculous (and offensive) as I do, but if you're curious, take a look at Coyne et al's critical analysis of their idea:

http://deepblue.lib.umich.edu/bitst...606.1988.tb00726.x.pdf?sequence=1&isAllowed=y

Luckily, the psychosomatic theorists have now pretty much left the type I diabetes domain and moved on to other illness domains. Unluckily, MECFS was one of these, but we're not alone. Just about all poorly understood illnesses have been targets at one time or another (try googling "psychogenic movement disorders" or "psychogenic nonepileptic seizures", for other current targets).

 

[Snowdrop]

On the basis of having skimmed dozens of these psychogenic hypothesis studies I propose that the studies actually reveal more about the researchers and their 'fixation' on a dysfunctional family dynamic. Now why oh why are they constantly focussed on blame and then punishment (via psychological treatment)?

This paper should be resurrected. OK . . .back to the thread topic.

 

[duncan]

It might be interesting to see how ME/CFS maps vs MS. The supposed latitude tie to autoimmune disorders...

 

[user9876]

I doesn't appear that most cases of me/cfs are contagious. The cluster outbreaks may be a different disease or a very small subset of me/cfs.

Research seems to be indicating that the susceptibility is some disfunction within the patient.

Not everyone who gets mono, or other illnesses ends up with me/cfs and that's telling.

Basically, its the hit and run theory.

It would definitely be interesting and possibly helpful to know the differences between the causes of clusters and individual cases of me/cfs. But with the lack of funding and the state of knowledge at this time about me/cfs, this line of inquiry is not a high priority.

Barb

I've wondered that if ME has a viral trigger even say with some additional preconditioning of the immune system producing bad antibodies wouldn't we expect to see some clustering?

It seems to me the kind of thing a mathematical model could look at using virus spread models, and different susceptibility criteria. Then simply by having a viral trigger would some clusters be expected to appear?

 

[user9876]

It might be interesting to see how ME/CFS maps vs MS. The supposed latitude tie to autoimmune disorders...

I've seen suggestions relating to vit D deficiency and MS based on the latitude theory and perhaps also relating to other neurological conditions. So it would be interesting to see if ME follows a similar mapping,

 

[barbc56]

@user9876

I think I've also heard that. Is it an increased percentage? People in the northern latitudes have more vitamin deficiencies.

I'll have to see if I can find this. If anyone else knows, please post this.

As an aside is it northern latitudes or longitudes? I keep going back and forth which terminology fits, even when looking at a drawing. Could it be both?:thumbdown:

Barb

 

[Scarecrow]

As an aside is it northern latitudes or longitudes? I keep going back and forth which terminology fits, even when looking at a drawing. Could it be both?:thumbdown:

Latitude, definitely.

It's funny that everyone thinks the 'thumbs down' smiley is a head scratch. Makes me laugh every time - but it does look like a head scratch.

 

[barbc56]

What is it? ​

 

[ahmo]

@barbc56

 

[alex3619]

There was a global map made by patients some years ago, showing patient location. I do not think, based on what we know now, that the MS distribution is similar, but then we have not had a proper epidemiological study. Anthony Komarof tried to get an epidemiological study funded a few times in the 80s, but funding was denied.

It is not clear that its even valid to speak of CFS or ME spreading. Its not like a contagious illness as we normally understand it. Only the cluster outbreaks have a clear timeline, and possible incubation periods, which often match enteroviral incubation times. These are mostly anecdotal footnotes from doctors over the years. There is no large study looking at epidemiological factors, though I am not sure about some of the large studies that are in progress. This is complicated by there being different triggers, sporadic and cluster outbreaks (there have no formally recognized clusters in a long time now). I do think that many clusters are being redefined as other things, such as post Q fever.

 

[SOC]

I've wondered that if ME has a viral trigger even say with some additional preconditioning of the immune system producing bad antibodies wouldn't we expect to see some clustering?

It seems to me the kind of thing a mathematical model could look at using virus spread models, and different susceptibility criteria. Then simply by having a viral trigger would some clusters be expected to appear?

I expect this kind of study would be very valuable, but we have the major problem of not having a definitive diagnostic criteria. As long as we have a shit-load of people diagnosed with CFS who do not have neuroimmune illness, I suspect any epidemiology study is going to show nothing. A mathematical model is only as good as the data that does into it. GIGO

Once we're fairly confident the patient group doesn't include people with only untreated thyroid problems, only OI (for reasons other than ME), burnout, MDD, and a host of other fatiguing conditions, the patterns of transmission and geographical clusters may become quite clear. Until then, there's far too much noise in the input data to develop a useful pattern. This is why we keep hearing (mostly from the BPS idiots these days) that there's no clear patterns in this illness. Well yeah, when you take a near-random sample of people, you're not going to find any patterns... you idiots. Try taking a science class or two. (Whoops did I say that out loud? )