Discussion in 'Latest ME/CFS Research' started by Firestormm, Sep 13, 2013.
This is a Benjamin Natelson study. It seems like they only looked at Cykotine markers to see if there was any change post stress.
Why is the results so different than all the other studies???
Haven't read the article yet but lots of reasons could explain difference:
1) If they selected subjects using Fukuda, did they make sure they had PEM/ sore throat/ enlarged lymph nodes as one of the criteria subjects had? Remember you can fit Fukuda without having any signs/ symptoms of immune dsyfunction. If no immune symptoms, perhaps that's why no cytokine changes seen.
2) What type of exercise did they employ?
3) Which cytokines did they look at and what were the techniques used to test for cytokines? Cytokines fluctuate naturally even in healthy people and the assay technique can affect results.
4) When did they take the cytokine samples and how frequently did they do it? Some people get PEM immediately after an activity, others have more delayed response - like a day or two - before it is felt. Remember, we don't have good studies about the timing and duration of PEM. I've not seen one study where they asked people about PEM AND also drew cytokines at the same time -- which would seem like a pretty simple thing researchers should consider.
5) Did the subjects have any other illnesses? Remember in the Utah Lights' study, people with FM had a different gene profile than people with only CFS or CFS+FM. Often times, I wonder if some FM patients are being classified as having CFS because they qualify due to fatigue and non-immune Fukuda symptoms. If that's the case, these subjects might not have changes with activity; some FM patients get much better with exercise unlike CFS patients.
(I know two people who are related - one has CFS, the other FM; the latter can take aerobics classes and feel good afterwards, the former crashes.)
The results of this must be compared to those of healthy individuals.
A study of men attending a military training course who underwent strenuous exercise, calorie deficiency and sleep deprivation.
There was an increase in neutrophils, but a general suppression of the immune system.
I'm not really sure what the 'expected' result of the Natelson study would have been.
They used three different techniques,
They did make a series of interesting observations and they noted differences between the CFS&FM group vs the CFS group.
I actually believe the conclusion is quite sound, that changes in symptoms are not caused by stress-induced cytokine changes in serum.
edit: that is not to say that changes in spinal fluid might not be important.
This was a previous study by many of the same authors from 2010:
This is bias on my part but I would take those Natelson studies with a grain of salt because he has said publicly before that he thinks the cause of CFS is the brain and not in the immune system. So if his studies confirm what he believes, I'm not surprised.
As most people know already anyway, the literature on cytokines has been inconsistent in the past.
My bias of course is the opposite. Part of this is I feel sick each and every day, like I have the flu.And I have the data to back it up in myself -- I have extremely elevated cytokines taken at different time points by my immunologist. In some case, 10X normal range.
But also because I think it's too premature to conclude brain or immune system -- I think it's probably both and the way they interact. In addition, it appears to date that the people who do get substantially better do so because of medications that affect the immune system -- antivirals, IVIG, rituximab, etanercept, etc.I've not heard of brain-directed meds that have substantially improve CFS for people; some drugs like Provigil may help with alertness but others report it gives them perception of (rather than true) energy only to crash later.
The effects of exercise on the immune system can vary a lot depending on duration/ intensity etc. I did a little reading on this in the past and it seems like a "moderate" degree of exercise is best. Too little and the immune system doesn't get stimulated enough (e.g. "practice" for when the bugs invade); too much and it can become suppressed (e.g. triatheletes, some of whom regularly get mild colds). In fact these "practice" sessions are one theory why moderate exercise can decrease colds and flus in people.
What would be the point of a sleep deprivation night on subjects who may have circadian rhythm problems?
I may be wrong about this and need to read the full paper of course. If they deprived subjects of sleep for one night and these are people who get their best sleep during the day (like I do) then I'd question that as a choice of ordeal.
Also there was another thread on this forum for people who felt better after not sleeping. I'm one of these odd ones who feels as if some sort of "switch" turns if I sleep from say midnight to 8am. I awake feeling wretched.
I just read this paper quickly. Unfortunately I don't have the supplemental tables - they showed the nonsignificant results which might have helped give context. There were plenty of examples of different patterns within any one analytic method e.g. a statistical significant result within either the controls or the patients before/after exercise or sleep, and with the other group even going in the opposite direction, but this didn't reach significance.
I think a big problem is the sample sizes: when there are big variances, it seems likely a lot of these samples would be underpowered.
Also the point Hope123 brings up could be relevant: people not having exertion-related CFS but just satisfying four of the other 7 minor Fukuda criteria.
Also, looking at Table 3 ["VAS scores before and after the nights"], for sleepiness, pain, blue, anxiety & fatigue, it's far from clear to me that the patients were "hit" hard enough to find effects
I recall that one of the Dubbo studies found very large numerical differences (e.g. 10 vs 140 - a vague impression from one scale that comes to mind) but because they weren't statistically significant (as large variances and very small sample sizes e.g. less than 10 I think) they said no evidence for immune dysfunction/similar. That seemed very premature and so does this, although to a lesser extent (the differences here weren't as big the Dubbo study I had in mind, as I recall).
It is interesting, I had highly raised cytokines across the board (one of them I think 100's times the norm). After treatment with nexavir and antibiotics, they all normalized...but I did not feel any different.
You can also try a Google Site Search
Separate names with a comma.