The role of low-grade inflammation in ME/CFS (Chronic Fatigue Syndrome) - associations with symptoms, 2019, Jonsjö et al

T

Tom Kindlon

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https://www.sciencedirect.com/science/article/abs/pii/S0306453019313198

Psychoneuroendocrinology
Available online 26 December 2019, 104578
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The role of low-grade inflammation in ME/CFS (Chronic Fatigue Syndrome) - associations with symptoms
Author links open overlay panelMartin AJonsjöabf
Gunnar LOlssonabRikard KWicksellcKjellAlvingdLindaHolmströmaeAnnaAndreassonfg
a
Behavior medicine, Karolinska University Hospital, Stockholm, Sweden
b
Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
c
Dept. of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
d
Dept. of Women's and Children's Health, Uppsala University, Uppsala, Sweden
e
Dept. of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden
f
Stress Research Institute, Stockholm University, Stockholm, Sweden
g
Dept. of Medicine Solna, Karolinska Institutet, Stockholm, Sweden
Received 5 July 2019, Revised 4 December 2019, Accepted 20 December 2019, Available online 26 December 2019.

https://doi.org/10.1016/j.psyneuen.2019.104578Get rights and content
Highlights
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Associations between inflammatory markers and common symptoms in ME/CFS.

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Higher levels of markers were significantly associated with higher levels of symptoms.

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Biological sex moderated several associations.

Abstract
Background
Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) often present with a range of flu-like symptoms resembling sickness behavior as well as widespread pain and concentration deficits. The aim of this study was to explore the association between inflammatory markers previously shown to be related to fatigue severity in ME/CFS and common ME/CFS symptoms post-exertional fatigue, impaired cognitive processing, musculoskeletal pain and recurrent flu-like symptoms, and the moderating effect of sex on these associations.

Methods
53 adult patients diagnosed with ME/CFS at a specialist clinic were included in the study. Fasting blood plasma was analyzed using the Olink Proseek Multiplex Inflammation panel (β-NGF, CCL11, CXCL1, CXCL10, IL-6, IL-7, IL-8, IL-10, IL-18, TGF-α, TGF-β-1 and SCF) and BioRad Human Cytokine Type 1 assay (TNF-α). Participants rated the average severity of symptoms (0-10) based on the 2011 International Consensus Criteria of ME/CFS during a structured clinical interview. Associations between inflammatory markers and symptom severity were analyzed using bivariate correlations and moderated regression analyses bootstrapped with 5000 repetitions.

Results and conclusions
Only β-NGF was associated with the fatigue severity measure. However, higher levels of CCL11, CXCL10, IL-7, TNF-α and TGF-β-1 were significantly associated with higher levels of impaired cognitive processing and musculoskeletal pain, and sex was a significant moderator for CXCL10, IL-7 and TGF-β-1. Future studies should investigate the relationship between inflammatory markers and key symptoms in ME/CFS in a longitudinal design in order to explore if and for whom low-grade inflammation may contribute to illness development.

Keywords
Myalgic Encephalomyelitis
Chronic Fatigue Syndrome
ME/CFS
cytokines
symptoms
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© 2019 Published by Elsevier Ltd.
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Easier to read abstract
Background
Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) often present with a range of flu-like symptoms resembling sickness behavior as well as widespread pain and concentration deficits. The aim of this study was to explore the association between inflammatory markers previously shown to be related to fatigue severity in ME/CFS and common ME/CFS symptoms post-exertional fatigue, impaired cognitive processing, musculoskeletal pain and recurrent flu-like symptoms, and the moderating effect of sex on these associations.

Methods
53 adult patients diagnosed with ME/CFS at a specialist clinic were included in the study. Fasting blood plasma was analyzed using the Olink Proseek Multiplex Inflammation panel (β-NGF, CCL11, CXCL1, CXCL10, IL-6, IL-7, IL-8, IL-10, IL-18, TGF-α, TGF-β-1 and SCF) and BioRad Human Cytokine Type 1 assay (TNF-α). Participants rated the average severity of symptoms (0-10) based on the 2011 International Consensus Criteria of ME/CFS during a structured clinical interview. Associations between inflammatory markers and symptom severity were analyzed using bivariate correlations and moderated regression analyses bootstrapped with 5000 repetitions.

Results and conclusions
Only β-NGF was associated with the fatigue severity measure. However, higher levels of CCL11, CXCL10, IL-7, TNF-α and TGF-β-1 were significantly associated with higher levels of impaired cognitive processing and musculoskeletal pain, and sex was a significant moderator for CXCL10, IL-7 and TGF-β-1. Future studies should investigate the relationship between inflammatory markers and key symptoms in ME/CFS in a longitudinal design in order to explore if and for whom low-grade inflammation may contribute to illness development.
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and Sci hub link, https://sci-hub.se/10.1016/j.psyneuen.2019.104578
 
Interesting
Funding

This work was supported by the research fund (Risk Hälsa) at Skandia Insurance Company, Ltd, Sweden. The funder had no role in study design, data collection, analysis, interpretation, decision to publish, or preparation of the manuscript. The funder has no financial interest, in Sweden or internationally, in classifying ME/CFS patients as psychiatric.
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mango said:
I believe this is part of their efforts to try and subgroup patients by combining psychological and biological data; an intent they have previously stated in, for example, research plans submitted to the Ethical Review Authority.

In their ACT research plan (2015) it says that the aim of evaluating symptoms in relation to psychological, neuroimmunological and endocrinological factors is to define what patient groups wiil have the best effect of ACT.
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Sly Saint said:
founded in BPS, so need to be a bit wary.
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I agree.

mango said:
About the Stress Research Institute in English:

https://www.stressforskning.su.se/english/

Here's what they say about psychoneuroimmunology:

https://www.stressforskning.su.se/english/research/psychoneuroimmunology
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Stressforskning said:
In psychoneuroimmunology, aspects of behaviour is studied in relation to the interplay between the brain, the endocrine and the immune system.

Within this framework, we study factors such as stress and sleep in relation to immune function.

We also study how immune defence influences measures of brain function, subjective (self-rated) health, pain regulation and social interaction as part of a so called sickness response.
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From the article, my bolding:

"The interaction between the immune system and the brain might contribute to the understanding of symptom variation in ME/CFS. In short, when the immune system is activated, inflammatory cytokines are released and soon the afflicted person will present with sickness behavior such as fatigue, malaise, anxiety, anhedonia, worsened mood, reduced social interaction and increased pain sensitivity (10). The sickness behavior response has been considered a key mechanism in the recovery from acute illness, while persistent sickness behavior may contribute to the debilitating symptoms in some patients with ME/CFS. To date, the relationships between low-grade inflammation and the commonly reported postexertional, flu-like, musculoskeletal and neurocognitive symptoms in ME/CFS are still unclear."
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"Specifically, we wanted to investigate (a) the association between sickness behavior-related inflammatory markers and recurrent flu-like symptoms in ME/CFS, and (b) the associations between inflammatory markers previously shown to be related to fatigue severity in ME/CFS and common ME/CFS symptoms post-exertional fatigue, impaired cognitive processing and musculoskeletal pain, and (c) the moderating effect of biological sex on these associations, as there is a lack of studies in ME/CFS research exploring sex differences."
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"This is consistent with previous studies in the sickness behavior literature, for example in experimental studies where elevations of pro-inflammatory cytokines and sickness symptoms after stimulation of the immune system are repeatedly demonstrated "
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Isn't using the term sickness behavior and theorizing that persistent sickness behavior is causing symptoms in ME patients characteristic of the BPS cabal?

Edit:Just to clarify, the question is rhetorical since these researchers are part of the BPS cabal.

Edit2: The question is apparently not rhetorical. These researchers have however only produced BPS-research in the past, and while it might not be obvious by reading just this particular paper, if one reads their complete body of work, I think it is fair to say they are part of the BPS cabal. One of the researchers involved, Gunnar Olsson, is personally responsible for many Swedish ME patients having lost large parts of their life during the past decade, due to deterioration after following his activity increasing advice.
I for one do not trust them a bit.
 
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Anna H said:
Isn't using the term sickness behavior and theorizing that persistent sickness behavior is causing symptoms in ME patients characteristic of the BPS cabal?
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My understanding is that they are saying that sickness behaviours 'contribute' to ME symptoms. I tend to agree in my particular case because I experience both in almost 30 yrs.
 
Anna H said:
Isn't using the term sickness behavior and theorizing that persistent sickness behavior is causing symptoms in ME patients characteristic of the BPS cabal?
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No, rest assured that sickness behavior perspectives of ME/CFS come from the biomedical camp, not the biopsychosocial camp. Sickness behavior is the set of symptoms you get from an infection, hence it implies some sort of infectious or inflammatory process behind it.

Michael Maes looked at whether sickness behavior might be involved in ME/CFS in one of his papers, and Michael VanElzakker's vagus nerve infection hypothesis of ME/CFS involves sickness behavior also.
 
Anna H said:
Isn't using the term sickness behavior and theorizing that persistent sickness behavior is causing symptoms in ME patients characteristic of the BPS cabal?
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Technically no. It's the proper clinical term. In chemotherapy patients, this would include nausea and fatigue.

But that's the problem with behavioral models that overrule medicine, it's impossible to tell whether they are using the proper term or using it with deceitful intent to mean something else entirely.

Were the BPS model an honest and legitimate effort, they would take great pains to clear up ambiguity. But they do the opposite, exploit the confusion deliberately, because the deceit is itself part of the model.

So then it becomes about whether they are real scientists or believe in the BPS nonsense. It appears to be the latter, so here they probably use the incorrect meaning, but using the terminology itself isn't necessarily characteristic. It just creates so much unnecessary confusion, but without it the BPS model can't even pretend to have substance.
 
@Hip @rvallee
OK, thanks for explaining. I stand corrected.
But when the suggested treatment for said sickness behavior, eg symptoms, is to ignore it and pursue activities regardless, because sickness behavior is not considered to be part of or reflect a severe illness, as is suggested by this research team in other studies, like the ACT study, then it is clearly BPS, right?
Because that is what they do, and how they use the term. I do not think Michael VanElzakker would argue that sickness behavior implicates ME is not a severe disease and that PEM should not be taken seriously.

You are right @rvallee, they really do create a lot of confusion while trying to achieve medical credibility.

I wish tough, that people would view this paper in a larger context, considering all the work that has been produced by this research team, of which this particular paper is just a small part. This research team have been active in Sweden for many years and represent a large part of the (bio) psychosocial research being done here.
 
There's an alternative name sometimes used: sickness response. I think that's a better term than sickness behaviour.

I also think some clinicians see a link and therefore assume the sickness response causes, or is, ME. But it could be the other way around too: ME causes a prolonged sickness response.
 
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