Onset patterns and course of myalgic encephalomyelitis/ chronic fatigue syndrome, 2019, Chu et al

Mij said:
Based on your symptoms, do you feel that your cognitive function is declining over time? Do you have periods where you feel 'normal' again?
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I don't ever have periods where I feel normal again.

Despite the damage, I feel I 'worked around' it. I don't think in precisely the same manner I used to. I've spoken to people who've known me all my life, and they agree. It's enough to imply a re-mapping process, at least to me.

I don't think I'm incurring any further damage (much).

I will say that a lot of our symptoms are very situational and I can easily go from minor to moderate over two or three days if I stop taking any of the OTC meds I use. I think untreated ME could very well lead to further damage, though all I have to go by are the fact of my white matter hyperintensities and that they were clustered around the areas responsible for language. My word-finding was so poor I was off-and-on aphasic at my worst.

It's still possible that's a coincidence.
 
Merged thread

MEA Summary Review: US study of onset patterns and course of illness in ME/CFS

https://www.meassociation.org.uk/20...-course-of-illness-in-me-cfs-29-january-2019/

29 January 2019

Charlotte Stephens, Research Correspondent, ME Association

Epidemiology studies are few and far between in the field of ME/CFS.

They are important as they can tell us how many people in a given population are likely to have the disease or are likely to develop it.

They can help to identify patterns which may give useful clues for studying the cause of ME/CFS and could help with diagnosis and treatment.

Their findings can also be used to help shape policy decisions in evidence-based practice (for example, the NICE clinical guideline) and demonstrate the impact of a disease to other official bodies and organisations.

This new epidemiology study from Dr Lily Chu (with help from Prof. Jose Montoya), describes the results from 150 respondents to a survey who met the Fukuda criteria for ME/CFS…
 
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I haven't read the whole thing in detail, but when they say that 43% of their subjects reported a professional diagnosis of depression, seasonal affective disorder, or dysthymia compared to 7% of the US population, it's not clear to me if they distinguished whether such a diagnosis was made before or after onset.
 
Some interesting comments in this paper. It's full of interesting observations that closely align with my own thoughts.

By prospectively following adolescents stricken by Epstein-Barr mononucleosis, Katz et al. (99) have already demonstrated that autonomic dysfunction is predictive of ME/CFS several months later.
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This is interesting because I suspect that the subtle tension and increased heart that for me appears to precede crashes is due to autonomic nervous system activity.

Alternatively, peri-onset stressful events might act as the “straw that broke the camel's back,” accelerating a pathological process which was already underway.
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Since I had a prodromal phase before the onset, I suspect that the illness was indeed already present in some form.

Conversely, when the sympathetic nervous system involved in reacting to stress should be dampened, for example, during nighttime to facilitate sleep, its activity is instead elevated, possibly leading to another major ME/CFS symptoms, unrefreshing sleep (56, 94).
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Consistent with my observations.

Ideas about acuity and its link to infection should also be re-examined. Some past case definitions have included onset within a few hours or days as part of their criteria (100–102). In contrast, for the majority of our subjects, the first intimation of illness to full-blown ME/CFS often occurred over months if not years (Table 3). This is congruent with empirical data: while a few studies reported that around 60% and up to 91% of subjects disclose an “acute” onset (42, 52, 72), the majority of subjects (between 59 and 77%) in many studies describe a “gradual” onset. (37–39, 41, 103).
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My story was prodromal phase, definite onset of relatively mild severity with worsening over the next few years, and then stabilization and continued disability.

Also, the patients with gradual onset may be underdiagnosed.

The high rate of unemployment we observed (47%) is in line with the 40–81% rate noted in other studies (7, 16, 21, 23, 24, 39, 41–43, 133). Commencement of ME/CFS decimated the pre-illness employment rate by at least 40% in Japan (43), Australia (41), and the United Kingdom (133). Moreover, surveys rarely asked those still employed if they were able to retain their prior hours, duties, position, salary, or even field: in the Japanese study, only 2% of respondents did not have to modify their occupation whereas both Tiersky (20) and Kingdon (133) found much reduced work hours.
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New information to me.
 
ME/CFS has also been shown to be present in second- and third-degree relatives (33, 35) in a dose-response matter, i.e., the more genetic distance between the ME/CFS patient and a relative, the lower the risk. Since second- and third-degree relatives are less likely to share the same household or lifestyle factors as FDRs, this pattern strengthens the argument that there might be a shared genetic rather than environmental factor increasing the risk of disease. Astonishingly, hardly any studies have examined families where multiple members are sick with ME/CFS. More than 2 decades ago, Levine (156) showed a gradient of natural killer cell activity with family members affected by ME/CFS having the lowest values, followed by those unaffected but related, and finally, un-related friends of the family having the highest and normal values. By evaluating such family pedigrees, especially in conjunction with genetic or other biomarkers, we might better comprehend the risk factors behind and the mechanisms of ME/CFS.
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The Open Medicine Foundation is doing that at the moment, in their multi omics study.
 
Thirty-five percent of subjects also described at least one FDR afflicted by an autoimmune disorder.
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I found this curious.

The risk of autoimmune diseases in first degree relatives is discussed here:
https://genetics.emory.edu/documents/resources/Emory_Human_Genetics_Autoimmune_Disorders.pdf

Two out of my three siblings have autoimmune diseases (Type 1 Diabetes, autoimmune Thrombocytopenic Pupura), so I found this association curious. My intial onset was not associated with an infection, but instead associated with an acute autoimmune syndrome.
 
I found it interesting in that it discusses the effect of the female reproductive system on ME.

Despite the highest prevalence of ME/CFS being recorded in the 40–50 age range (124, 129), no other study has asked about the impact of menopause on symptoms.
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Considering that ~75% of people affected are women (16, 40, 41, 43, 104, 124–126) and that onset often occurs during their reproductive years, i.e., between the ages of 10–40 (16, 23, 39–42), exceptionally few studies have evaluated the impact of female reproductive events on ME/CFS.
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My orthostatic symptoms have worsened during menopause, but it may just be coincidence. I have wondered if stopping the POP affected my fluid retention but GP was dismissive.

Not seen a any studies on ME, osteoporosis and bisphosphonates, but this must be of interest to a significant proportion of lake, men and women.
 
This is a paper trying to fill a major gap in research, looking at factors preceding ME and at the evolution of symptoms over time, something that just has to contain valuable clues.
But it's a paper of two distinct parts, one good and one disappointing.

The first part, the actual survey of patients, leaves a lot to be desired. Questionnaires about symptoms years after the event. Selection by Fukuda. The authors themselves estimate that about 30% of participants didn't meet any stricter criteria. Then there's the huge number of comorbidities, many of them psychological. Of course it's important to recognise that many patients do have comorbidities but it does mess with data. The authors explain some of the practical reasons behind their choices but still, it looks like a great big fat missed opportunity.
In the section Strength and Limitations they write "Our results also contribute to the paucity of data on the evolution of symptoms longitudinally". I suspect that wasn't exactly what they meant to say but in a way that's what they did by adding more low quality data.

By contrast, the second part, the discussion and review of their own and others' studies is nuanced and thoughtful, especially given the paucity of good data to analyse. Though some points could have been made clearer. For example, they observe that patients report significantly fewer postexertional symptoms later in the illness than at the beginning, and that patients explain this as due to 'treatment', by which they primarily mean pacing. That's fine as far as it goes but it's not made clear that the underlying condition hasn't changed. Readers not already thoroughly familiar with ME are unlikely to understand this correctly. More likely they would assume a reduction in reported symptoms due to a treatment is like somebody reporting reduced hayfever when taking antihistamines: treatment reduces symptoms and patient returns to normal activity. That last bit just doesn't happen very often in ME.

I do like their expression "stuttering onset" in addition to the usual either acute or gradual.
 
Seems to me there is a lot of murkiness still in how the study was accomplished.
It makes me want to scream "will no one rid us of this meddlesome Fukuda.

I'd like to see a study with some nice clean data. And then replicate it. Given that I know nothing about science I have the audacity to say I won't get excited until then. <sigh> I really want to get excited about some data. :grumpy:

ETA:sp
 
Most common co-morbid medical and psychiatric conditions reported by our subjects with ME/CFS compared to the general United States population and previously published prevalence among ME/CFS subjects
fped-07-00012-t006.jpg
 
Comment from the lead author, Dr Lily Chu, shared with permission:
Some people have asked why we used the Fukuda criteria: the data were collected from subjects recruited between 2010-2012, before the NAM criteria and ME-ICC were published. Studies take time and it would have taken years to start/ finish a study with different recruitment criteria. Often times, in research, you have to work with what is available, recognizing both the strengths of weaknesses.

We believe our results are useful. In our 2017 Fatigue paper https://www.tandfonline.com/doi/abs/10.1080/21641846.2017.1299079 -- which covers the same group -- we found that 70% of this group fit ME-ICC and CCC criteria. Also, 90%-99% of our subjects endorsed PEM: the 90% figure when we asked for more details post-exertion and the 98% when we merely asked if they suffered from "PEM".This is covered in the 2018 PLOS One paper https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0197811 concerning PEM.

Visit the Stanford ME/CFS Initiative website https://med.stanford.edu/chronicfatiguesyndrome.html to learn about our other projects and how you can help.
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