Discussion in 'Latest ME/CFS Research' started by Dolphin, Sep 13, 2015.
Given the sample sizes, those results shouldn't lead one to accept the null hypothesis.
It would be interesting to see what the effect sizes were to see how interesting or otherwise these particular findings are.
people who have problems with fatigue rest for longer periods and do less. they were actually taking grant money to prove the obvious.that money could of been better spent elsewhere.is this post just to wind people up.
I have to laugh (bitterly) when they say this. How can they have a well-characterized sample when we don't even have a single clear definition? They shouldn't be saying they have "a well-characterized sample", they should be telling us which definition they used so we know to which group the research might apply.
If they were going to do damaging testing (moderate intensity aerobic exercise and a demanding cognitive challenge ) then they might as well have used the 2-day CPET.
I know it's hard to do decent research without reasonable funding, but I'm not sure research with ill-defined cohorts and questionable conclusions does us any good. Better the money spent on these studies be pooled into a single substantive research study.
With luck, these researchers will learn more about ME/CFS and do more valuable research in the future.
Enough with the statistically sub-par studies. Sample sizes of 10-12?
Are they completely insane?
i have done 3 CPET so far since onset of my illness.
i can say for sure that post exertional relapse leads at least for me to poorer quality of sleep. And decreased cognitive and physical functioning. It works like a clock every single time.
Now if we could please have a homogenous cohort, large sample, quality measurement which includes EEG, imaging, and blood measurement, we could put this to rest for sure.
Stupid timing on the accelerometer use. By starting use immediately following exertion, and ending 24 hours later, they are looking at the OI/exercise intolerance period. PEM would've just been starting up at the same time that the accelerometers finished collecting data.
They sound like a bunch of people who have no idea what ME or PEM is. The lead author is a "chronic fatigue" researcher, which really says it all I suppose. It looks like they've done some intelligent stuff in the past, but they really need to learn about a disease before attempting to research it.
In the hope that they do read this:
Use a real ME definition. PEM is mandatory. It typically starts 24 hours after exertion, lasts for days or weeks, and features the exacerbation of neurological, immune, and muscular symptoms which have nothing to do with "fatigue". If you want ME patients, doctors, or researchers to take you seriously, use the Canadian Consensus Criteria or International Consensus Criteria to select patients. If your funding depends on using Fukuda or the Australian equivalent, you still need to select only patients who have PEM.
Use a big enough group to have some hope of producing relevant results. If you have 22 patients, put them all in the physical PEM group. Researchers seeking to disprove that ME is a biological disease like to use tiny samples of patients so that positive results are impossible and they can crow about having disproven some biological theory. Using tiny sample sizes looks very suspect, especially when the preliminary research has already demonstrated that PEM objectively exists and has been independently replicated by several groups.
Figure out what you're studying. If it's chronic fatigue, please leave ME, CFS, and ME/CFS out of it. These are entirely different illnesses. Pick one. You do not get to put CF patients in a study and claim it applies to CFS. And if you are studying chronic fatigue, then looking for exercise intolerance doesn't make any sense in the first place.
Here is what Dr LLoyd says about the 2 days CPET :
Okay, I was trying to be nice in my prior post and avoid the first adjectives which sprung to mind. But what a bleeping moron! I can understand someone not understanding how the CPET works, but how stupid do you have be to go spouting off on a subject of which you apparently have absolutely no understanding?
A maximal CPET has several ways built in to control for volition. If someone holds back, their Respiratory Exchange Rate (RER) will not exceed 1.1, heart rate won't hit predicted levels, etc, and then it's not a bloody maximal CPET at all.
I'm a lawyer with no background in medicine or biology, but apparently I know far more about maximal CPETs than a researcher and licensed MD who thinks he's an authority on the subject. Beyond pathetic. Probably just another psychobabbler who can't comprehend anything involving science.
These conference abstracts often lead to full papers so we may get some more information again.
You can also try a Google Site Search
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