Discussion in 'Latest ME/CFS Research' started by Denise, Jun 19, 2017.
(I have not read it yet)
One of the better descriptions of the symptoms I've seen:
And a polite "bugger off" to the psychobabblers:
A good description of the severity of ME/CFS:
Recovery/remission data does look much better than it is for adults:
A very strong endorsement of pacing:
And the opposite of the rationing of medical care we've seen in some quackier documents:
Some interesting data regarding family prevalence rates:
They're very dismissive of Fukuda, with more enthusiasm for CCC:
But they've proposed their own criteria, due to CCC being a bit complicated for clinical use:
I've started reading it, and so far it looks excellent.
I hope Esther Crawley reads and digests every word and feels ashamed of herself. A few retracted papers would be appreciated too, Esther.
Diagnostic form, including evaluation of severity:
Lab testing to rule out other diseases:
Additional tests as indicated:
Differential and exclusionary diagnoses to consider:
Differences in symptoms compared to anxiety or depression:
Differences compared to Munchausen's by Proxy:
Explicit instructions for what a doctor can do for a child with ME:
There are several nice charts of possible treatments for various symptoms. Sleep:
Personally I disagree with PEM starting immediately after exertion. That can happen with a different form of exercise intolerance which we also probably often have:
Good info regarding GET:
I doubt this ever actually happens. It's just a "maybe" situation we get from quacks pushing exercise:
I don't think there's any scientific support for the claim that exercise programs improve outcomes for people who are already in remission:
I'm a bit nervous about phrases like "remaining as active as possible." I think it distracts from putting the emphasis on avoiding excessive activity:
I wish they'd stopped at pacing:
They seem to be advocating symptom-based GET, which isn't as likely to be physically harmful, but still distracts from avoidance of excess exertion. It also creates expectations that exercise can improve symptoms or the ME itself, which is not supported by any evidence:
But again, a good caveat:
Some of the recommendations for dealing with OI do not take the underlying ME into account. Walking around, flexing muscles, etc, can trigger PEM in moderate and severe patients. I'd be a lot happier if they included a warning about that.
Possible medications for OI treatment:
I think they're underestimating the prevalence of homebound patients:
The sections on very severe (bedridden) ME are generally very good. One quibble I have is with the phrasing of the warning that staff might try to force rehabilitation too rapidly. They shouldn't be forcing rehabilitation at all.
Again, CBT/GET is getting much more credit than it's due. It hasn't been shown to be of any value in mild or moderate patients either:
Apparently they haven't read the studies showing abnormal immune response corresponding with increased symptoms lasting at least a month after getting the flu vaccine:
@Valentijn Thanks for running through that. I've read most of it and had similar reactions.Overall, I think its good and will be helpful but that statement about CBT/GET in mild isn't supported by evidence except oxford. And i was surprised by the vaccine recommendation and the estimates of severely ill.
The school based material looks useful and is much needed
I don't get PEM immediately after exertion, but my symptoms do worsen and stay worse so I understand the confusion.
The percent severally ill/recovery rates don't make sense at all to me. I think part of it is, its easier to stay in school than it is to work/cook/commute/manage a household so that may classify you as "less severe" when your still as sick. That was the case for me. Or CFS may be more present in young people than in adults. Or over-diagnosed or there may be normal periods of fatigue in youth that get counted as CFS. Because 88% recovery rates don't jive with 5-8% of adults. Those numbers just can't be the same condition, they can't even be the same waste basket.
I thought it was excellent. It made me a bit sad actually. No need to elaborate, I'm sure.
Or they are counting 'in temporary remission' as 'recovered'.
From ~13-16 I was tutored at home due to CFS.
At ~20, I 'recovered' and was able to attend university. I now realise that I was deploying numerous coping strategies to reduce the load to what I could manage, and justifying them as 'just being lazy'.
I then crashed badly, as the workload increased.
If you can't run a marathon, and get utterly exhausted (nomatter your time, or if you in fact complete it), and then do the same time or better in two weeks - you are not over CFS.
I've heard now from multiple people that they were sick in their teens, found coping mechanisms in their 20s (or actually improved), and by their late 20s/early 30s were sick again. Though they cite the Norwegian study here that shows increased prevalence at these times, longitudinal studies need to be performed to find out if this is true in the same individuals.
But that is the definition of PEM. So now you confused me.
Yes at anecdotal level this is definitely a thing, needs studying. It was (relatively) easy to improve in my twenties but I now feel stuck. Is there some metabolic change in your twenties which could be artificially replicated in your late thirties?
Yes, there probably is. I have theories, but no evidence.
This is the best explanation I have come across to date. It probably wont be the last no doubt.
I pretty much would've said the same. Except I'd like to see some real diagrams that show what hormones dip in late 20s / early 30s rather than a general statement about the stress of baby-raising. Many of us never got that opportunity (!) so I want something more solid.
I went looking for evidence of this, but it's too general a thing to say ("big hormone shifts in yer 30s") and so I kept coming across pop science articles.
Stages of Reproductive Aging Workshop system is a way of describing lifetime changes for women
Are the ME peaks -5 and -3a (i.e. Reproductive stage, but not the stable, regular bit)? This diagram (probably deliberately) doesn't include typical ages.
Activin isn't mentioned on that diagram. Does activin vary over lifetime like inhibin B? @JaimeS
Activin and inhibin are two closely related proteincomplexes that have almost directly opposite biological effects. Identified in 1986,activin enhances FSHbiosynthesis and secretion, and participates in the regulation of the menstrual cycle. Many other functions have been found to be exerted by activin, including roles in cell proliferation, differentiation, apoptosis,metabolism, homeostasis, immune response, wound repair, and endocrinefunction. Conversely, inhibin downregulates FSH synthesis and inhibits FSH secretion."
Thinking of https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-017-1161-4
"Elevated activin B levels together with normal activin A levels identified patients with the diagnostic symptoms of CFS/ME, thus providing a novel serum based test. The activins have multiple physiological roles and capture the diverse array of symptoms experienced by CFS/ME patients."
Found this, but the two age groups aren't split according to what we want to know. Does indicate Activin changes over lifetime though:
Follicular inhibin B was reduced in older versus younger women (504 +/-82 versus 748+/-72 total pg). Luteal inhibin A was reduced in older versus younger women (668 +/-72 versus 1152+/-216 total pg). Activin A was elevated throughout the cycle of older versus younger women, without within-cycle fluctuations (21+/-2 versus 11+/-1 total ng).
Lack of restraint by inhibin A and inhibin B contributes to the FSH rise associated with reproductive aging. This loss of restraint occurs in a tandem fashion, with inhibin B reduction before ovulation and inhibin A reduction after ovulation. Activin A may also play an endocrine role in maintaining elevated FSH in older reproductive-aged women."
Mind you I'm not sure how this explains a peak late thirties and then a reduction with menopause. Could activin and inhibin change through the menopause at different rates so you get a just-before peri menopause imbalance?
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