DePaul: NIH funds Chicago-based study of chronic fatigue syndrome and mono in college age students

“We need to know what causes one of the most debilitating health conditions, which is ME/CFS. The best way to figure this out is to identify healthy individuals and then observe what occurs when they are infected with something that might be triggering the disease, such as a virus, like Epstein-Barr virus, the cause of infectious mononucleosis, then to see who recovers and who does not and why,” said Jason, a principal investigator of a new five-year, $2.8 million study funded by the National Institute of Neurological Disorders and Stroke, one of the National Institutes of Health.

https://resources.depaul.edu/newsro...2rH-Tcq3d1lEhx6oFhOcYsMZmn9qHQIjIr2mC6irLcqR4

 

“Psychological, autonomic, and biological risk factors predispose people to developing ME/CFS following IM. We will determine which of these factors, if any, is also important for maintaining ME/CFS over time,” noted Jason, director of the Center for Community Research in DePaul’s College of Science and Health.

My bold. I didn't know that was considered as something given..

 

Considering that careful competent research would obviously show (and has already shown) that psychological factors are irrelevant, I have no problem with that. Though of course the framing here is misleading in that it is widely believed that it is the case, not that it actually is.

The field of ME is actually in need of competent clinical psychology, it would invalidate the psychosomatic model entirely. Problem is so far most of the funding for clinical psychology research in ME has been with the specific intent of proving, even manufacturing, the relation, not of finding out whether there is any.

The same could be said of the objective (null) impact of cognitive therapies and health-related quality of life. We already know the answers to that but the studies have been too small to compare to the massive funding the BPS-ME model has had. In the end the whole power of PACE is just that: the big price tag and accompanying sunk cost.

Bonus point that it makes the whole thought-terminating cliché of anti-psychology ridiculous, not that it isn't already but whatever.

 

It's not exactly clear what the sample size is but the number 4,500 is mentioned. If this is the sample size we might only expect ~10 to ever develop ME/CFS, and not necessarily after (confirmed) mono.

 

Jason is a professor of psychology - and he was diagnosed with CFS in 1990 - so perhaps including the psychological angle was important to getting support from the psychology department of which he is a part. As @rvallee said, seeking psychological risk factors may well be just a way to demonstrate that there are none.

The one psychological factor I can think of worth investigating would be "chronic stress" of the kind that college students might be subject to. "Chronic stress" might have some kind of effect on the immune system - but that may be largely due to the behavioral consequences of "chronic stress," like poor diet, insufficient sleep, altered sleep patterns, poor hygiene, insufficient attention to other medical issues, etc... i.e., "chronic stress" leading to pre-existing biological stresses that might make a case of IM much worse once you got infected.

 

It is not clear to me from the information provided how they propose to test the autonomic and biological factors involved for such a large cohort.

 

Someone knows the head author? Looking at the wrong variables.

Students that develop CFS will have more vaccines by quantity and less sex partners and as a result have higher humoral immunity at baseline - just in this cohort.

Are vaccines responsible? No (yes), as it could be just a function of socioeconomic status which would prevent early microbial exposure.

If you are not playing outside with soil bacteria (even less with girls these days) and not hooking up when you are young, you will not have any herpesvirus immunity.
Mono is going to fry your brain in college - it is a serious immune challenge in a time of stress.

 

Surely vaccines don't affect immunity to mono, because there is no vaccine for mono.

Whether or not someone gets mono in college is related to whether or not they were previously seroconverted. When seroconversion happens during childhood, this is usually due to exchange of saliva e.g. sharing utensils or popsicles etc.

I don't think it has anything to do with playing in dirt, because the viruses that cause mono are obligate human pathogens - they can't survive in soil.

The higher risk of getting mono in college is associated with improved living/hygiene standards in which children are less likely to exchange saliva with each other, and with young people who have not seroconverted before going to college living in close proximity with each other where they are more likely to share drinks, kiss, have sex, etc.

Vaccines and soil, as far as I am aware, don't have anything to do with it.

Somebody correct me if I am wrong.

 

This is nonsense. We are all exposed to herpesviruses simply by mixing with other people.
The "hygiene hypothesis" is also completely in empirical evidence, given the abundance of bacteria in our living spaces (gut microbiome differences could just as easily be explained by food differences). Regardless of how clean you try to live, how carefully you wash your hands, your skin is always coated in bacteria (and this is normal and healthy).

 

Saliva in cans is what I mean by dirt, but to be esoteric the diffusion of children into reduced points of contact from their neighbors creating an isolated environment - instead I said dirt.

In the 1970s the average age of seroconversion to mono was 3 years old and now it’s 17. In the 80s it shifted upward to the spike in CFS. This is from chapter 53 of The Epidemiology of Infectious Disease but it’s really an amalgamation if many sources.

Repeated vaccination (or stress) would reduce the available reservoir of IFN and TNF Alfa to attack neuroviruses specifically by negative feedback on the cytotoxic T cells.

If only the board had a world renowned immunologist to verify that. Not that I’m correct about vaccines necessarily but that it could weaken NK response. He’s not even a firm believer in Th0 divisions.

 

Symptomatic presentation increases by age as I mentioned earlier and since initial severity dictates permanent illness, the time matters.

 

I think it's important to recognise that not all bacteria and viruses are the same. Many are harmless, some are pathogenic, some we get exposed to at an early age and develop natural immunity, others live on a percentage of us (e.g. meningococcus, staphylococcus) causing no harm but if they invade our bodies can be fatal...

Many viruses are usually pretty harmless (e.g. rhinovirus), the viruses that cause mono often cause no illness when people are exposed to them at a young age, and they live inside many people in latent form without causing disease for the person's entire life.

But in some cases when people are exposed e.g. to EBV at an older age, they develop mono and sometimes recover without problems, happily live their lives with the latent infection, while others will develop ME, others MS, and others Lymphoma.

In some countries, exposure at an early age can lead to Lymphoma.

So the interactions between pathogens and hosts are dependent on many factors: the specific species and strain of pathogen, time of exposure, environmental factors, available treatments, immune system factors, epigenetics...

So we can't just lump things like exposure to 'bacteria', 'vaccines', or 'viruses' into one pot.

The factors leading to a person getting mono, and then getting ME as a result, are likely to be multifactorial but also quite specific in my view.

I don't know about the evidence for vaccines reducing the ability of the immune system to fight off e.g. EBV. I haven't looked into this and don't know whether or not there is specific evidence of this so I won't comment.

I personally think genetic factors which affect immune system or cellular function might be more important in conversion from mono to ME than how many vaccines a person has had.

Since most people are vaccinated nowadays, and most people don't get ME, I think it's probably not vaccines, and probably a combination of viral, host genetics, and environmental factors such as age of EBV exposure, stress levels at time of exposure, etc.

Just like why some people get MS or lymphoma after EBV exposure, but not ME. Most of these people will be vaccinated too. And so will most of the people who stay well.

I think we probably have to look in more detail at the intracellular and intercellular virus-host interactions to understand what the causal mechanisms are in post-mono ME, and why these are different from the interactions that happen in people who don't get ME after mono. I.e. I think we have to focus on the biochemical and molecular specifics of this interaction, and work back from there.

 

There is a serious risk about blurring correlation vs causation when talking about predisposition.

Random example. Hypermobility can lead to people requiring orthotics. Orthotics are not a predisposition or comorbidity of ME. Most would say it is the hypermobility. In fact, I would suggest the hypermobility is not even the comorbidity per se - because hypermobility is merely a symptom of some collagen anomalies, which could also manifest themselves cardiacly, the cornea or in the gut perhaps. With physiological, and sometimes surgical and then antibiotic, implications for some of these. The gut issues maybe even then having a psych effect, but I defer to others on that.

Biological features or conditions, which are entirely physiological nature, might have a higher comorbidity with psych issues, sure. But where there is any evidence to suggest the psych issues are caused by the biological condition, either physiologically or even behaviorally, that's causation of the psych by the phsyiological issue or maybe even just correlation. But it is definitely not causation of the physical by psych methinks.

Therefore, the predisposition and correlation of ME would be with the biological feature in this example, not the psych collateral impact.

Christmas cards don't cause Christmas. That difference between causation and correlation needs to be made very clear and not just cut through, particularly with the dangerous history of ME.

 

Another important analogy.

Autism spectrum disorder is is correlated with hypermobility, as I understand it (potential role of the gut). And being on the spectrum clearly has an implication psychologically, in terms of how one deals with the world and the additional cognitive load, let alone stress, that can result.

But again there is a massive distinction to be made between correlation and causation. Even if the causative mechanisms are not 100% clear, the distinction must be made. Children are born autistic or hypermobile and with any caused predispositions, not with psych issues off the bat.

 

The burden to caveat is substantial.

Distinct words like predisposition, correlation and even comorbidity will too often end up being interpreted as causation. My memory of the behavioural research is that it's a common behavioural failing to mix these when interpreting, even in technically skilled people. I think it's that same phenomenon that makes some articles be insufficiently clear about what they are NOT saying. And insufficiently break down what they are saying. Psychology is a hugely important profession, but does inherently allow for a philosophical lack of rigour more akin to social science. They have to break down and tie down more thoroughly.

Heavy caveating is needed in the specific light of the history and sociological of many conditions, even in terms of the sociology of the medical profession... ME is a textbook example of where it is needed.

 

Corrected logic in original post...