Discussion in 'Health News and Research unrelated to ME/CFS' started by Andy, Jan 10, 2021.
Open access, https://bmjopen.bmj.com/content/11/1/e040730
These studies demonstrate just how worthless this entire line of research is.
Total idiocy. Maybe these women have unexplained illness because the idea that women are hysterical has prevented the explanations from being found. Maybe they don't move much because they are ill. Maybe they are anxious because they know they have a problem and instead of getting help, see their doctor fleeing into the FSS fantasy world. Maybe they keep going to doctors because they have a real disease that requires treatment, not because they are serial somatizers with no insight.
The lack of association between neuroticism, stressful life events and FSS will cause a moment of surprise, then they'll keep trying to make this idea work somehow. Not because it's true but because the healthcare system doesn't want to take responsibility or admit uncertainty for these patients so some justification has to be made up.
I don't seem to be able to find my surprised face.
The strongest predictor of consultations was probably frustration in patients that fundamental human needs weren't able to be met as a result of illness.
This is as absurd as researching what features of cooking affect the outcome without considering heat at all.
This entire field of research needs to be shut down, has absolutely nothing to contribute.
So, if you are old, fat, and female don't bother seeing a doctor?
Well at least they couldn’t spin that result....
At least they published it. If neither neuroticism nor trauma (as a subset of stressful life events) can predict their definition of psychosomatism, what else can? When there are no predictors, how can they assume that causality exists? For CFS, predictors exist.
I don't know - I'd have expected 'neuroticism' would be associated with a tendency to answer the sorts of questionnaires used to diagnose FSS more negatively. I guess alternative/exclusionary MH diagnoses may affect who gets an FSS diagnosis?
Only read the abstract.
He must be referring to infection.
I wonder if there is a correlation between seeing a psychiatrist and an FSS diagnosis? Maybe the answer is to fire all psychiatrists? There, no more FSS! Not that I am being satirical or sarcastic or anything . . .
We need to know if treating FSS results in substantive numbers of improvements in patients as shown by objective markers. Like days worked and actual income restoration. Or how active people are using, for example, actometers. I am guessing, in advance of that evidence, that its both a bogus diagnosis and failed treatment for that bogus diagnosis.
Regarding predictors, you first have to differentiate if you want to predict a diagnosis disregarding the imperative and preceding causality or if you want to make the assumption that causality must exist preceding the diagnostic event, and therefore, take into account an initial event. If you disregard causality, your predictor might be completely confounded by pre-CFS but post-causal factors. Thus, study designs would have to delimit their selection method to a certain assumed subgroup of the disease. Infection certainly seems to be the most adequate subgroup. Since initial EBV-associated mononucleosis happens during childhood for the most time, children are suited as participants.
In 2014, a study has analyzed exactly this question (10.1080/21642850.2013.869176). I recommend reading it yourself, especially the discussion. Stress did not show to have predictive value at all. The study has limitations, though. The first limitation that they point out, though, I don't see critically. If they tracked stress during mononucleosis, you could only associate it with mononucleosis and not recognize it as a predictive factor for the reason mentioned above since EBV could also induce stress via its pathology. Since durational infection severity basically could predict CFS, this would then even contribute to the observational bias in their self-assessed questionary.
Typically for CFS, the sample size is small. The study only covered 6-months while CFS often is only diagnosed after at least 6 months. But the 6 month period seems rather arbitrary to me, just to improve specificity because the medical systems are very slow with co-diagnoses due to patient overload. And even if co-diagnoses are found, this is no exclusion of CFS, especially within the subsequent period of an EBV infection.
Their discussion also takes position on another study on psychological stress predicting CFS, which was conducted on a subgroup of children who were referred to psychologists. Clearly, this must be a confounding factor. How can you expect not to find psychological stress to predict CFS outcome when you only look at predisposed cases? It's just another study trying to push a narrative by design. You can associate fatigue with the psyche within any disease group if you look at predisposed cases only.
Overall, there is sufficient data that EBV and mononucleosis are associated with CFS. This study also shows that disease severity is most likely predicting post-infectious CFS. This makes infection a very likely causality of CFS and not the psyche.
Regarding the question of why certain cases are more severe than others, I believe that HLA genotypes will be determined in the UK DecodeME study to also show predictive value. I believe so because genotypes have been found for almost any other reactive autoimmunity, and infection susceptibility, especially for long-haulers and latent infections such as COVID-19 and antibiotics-resistant Lyme Borreliosis, which is HLA-DR4/DRB1-associated.
Some studies still might keep following the psyche narrative. Even if they find something, I'm convinced that it might only come down to long-term cortisol levels as the driving factor, which contributes to EBV and COVID-19 disease severity and duration. Yes, an association could be made between the psyche and CFS, but cortisol levels are mostly due to environmental factors such as lifestyle and workload and not due to any kind of trauma. Of course, diseases that are associated with cortisol levels, such as PTSD, will represent themselves with greater saturation in the overall population. But without an infection, they might very well never develop CFS.
This is just the nature of modern psychiatry. Everyone must have a psychological disorder and if they show none, a psychiatric disease must be involved. You probably know different anecdotes.
this entire field is about laziness .doctors who do not want to put time and effort into diagnoses or helping patients with treatment aimed at symptoms use this nonsense to negate their responsibility to that patient . this has been common practice forever if you can be bothered to read any of the many papers that disseminate the ridiculous ideas about the benefits of being sick or disabled . the entire language of the medical profession seems to other patients like we are just an inferior species .
Exactly. That they even reduce us to our costs to the health care system. That they even mention this in their motivational argument shows where they are heading and which mindset drives them. They think we are overburdening the system even though we do not deserve the same share of attention as any other severe or chronic patient who would also cause a lot of costs.
@mat, of course we all know infections are the commonest precipitating factor for ME.
I assumed you meant predisposing factors, in other words something inherent in the person or their environment that makes them more likely to get ME following an infection.
That could be genetic - as yet unproven in large enough studies, and, as you say, DecodeME should sort that out, and psychological, behavioural and environmental factors, none of which, as far as I know, predispose to ME.
Does anyone know if DecodeME also has a questionary regarding pre-CFS infection? I really hope that they will try to differentiate subgroups. I can not participate, this is why I'm asking.
Maybe check out the FAQs on the DecodeME website
It would be more useful to look at how the GP reacts to the first patient consultation to see if there is a pattern. Which blood tests are done? What advice is given? What referrals are made?
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