Mitochondria and Immunity in Chronic Fatigue Syndrome, 2020, Anderson & Maes

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Preprint

https://www.researchgate.net/public...dria_and_Immunity_in_Chronic_Fatigue_Syndrome
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Mitochondria and Immunity in Chronic Fatigue Syndrome

• March 2020

• George Anderson
• Michael Maes

Description

It is widely accepted that the pathophysiology and treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) could be considerably improved.

The heterogeneity of ME/CFS and the confusion over its classification have undoubtedly contributed to this, although this would seem a consequence of the complexity of the array of ME/CFS presentations and high levels of diverse comorbidities.

This article reviews the biological underpinnings of ME/CFS presentations, including the interacting roles of the gut microbiome/permeability, endogenous opioidergic system, immune cell mitochondria, autonomic nervous system, microRNA-155, viral infection/re-awakening and leptin as well as melatonin and the circadian rhythm.

This details not only relevant pathophysiological processes and treatment options, but also highlights future research directions.

Due to the complexity of interacting systems in ME/CFS pathophysiology, clarification as to its biological underpinnings is likely to considerably contribute to the understanding and treatment of other complex and poorly managed conditions, including fibromyalgia, depression, migraine, and dementia.

The gut and immune cell mitochondria are proposed to be two important hubs that interact with the circadian rhythm in driving ME/CFS pathophysiology.

 

[alktipping]

I do not know where he got the figure of 75% of m e patients having a major depressive disorder from . but I think its grossly inflated . otherwise it comes across as a review of many papers published in the last decade .and of course a wish for better/more research which is always needed.

 

[Dolphin]

Here's the journal link
https://www.sciencedirect.com/science/article/abs/pii/S027858462030292X

Progress in Neuro-Psychopharmacology and Biological Psychiatry
Available online 26 May 2020, 109976

Mitochondria and immunity in chronic fatigue syndrome
Author links open overlay panelG.AndersonaM.Maesbcd
https://doi.org/10.1016/j.pnpbp.2020.109976Get rights and content

Abstract
It is widely accepted that the pathophysiology and treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) could be considerably improved. The heterogeneity of ME/CFS and the confusion over its classification have undoubtedly contributed to this, although this would seem a consequence of the complexity of the array of ME/CFS presentations and high levels of diverse comorbidities. This article reviews the biological underpinnings of ME/CFS presentations, including the interacting roles of the gut microbiome/permeability, endogenous opioidergic system, immune cell mitochondria, autonomic nervous system, microRNA-155, viral infection/re-awakening and leptin as well as melatonin and the circadian rhythm. This details not only relevant pathophysiological processes and treatment options, but also highlights future research directions. Due to the complexity of interacting systems in ME/CFS pathophysiology, clarification as to its biological underpinnings is likely to considerably contribute to the understanding and treatment of other complex and poorly managed conditions, including fibromyalgia, depression, migraine, and dementia. The gut and immune cell mitochondria are proposed to be two important hubs that interact with the circadian rhythm in driving ME/CFS pathophysiology.

Keywords
Chronic fatigue syndrome
Pathophysiology
Treatment
Mitochondria
Gut microbiome
Immune
Viral re-awakening
Circadian
Endogenous opioidergic system
Vagus nerve
Abbreviations
α7nAChR
alpha 7 nicotinic acetylcholine receptor
AANAT
aralkylamine N-acetyltransferase
AMPK
AMP-activated protein kinase
aSMase
acidic sphingomyelinase
ATRA
all-trans retinoic acid
BBB
blood-brain barrier
CIRS
compensatory immune regulatory system
EBV
Epstein-Barr virus
HDAC
histone deacetylase
HMGB
high mobility group box
HuR
human antigen receptor
IBS
irritable bowel syndrome
Ig
immunoglobulin
IL
interleukin
IRS
immune-inflammatory response system
LDH
lactate dehydrogenase
LPS
lipopolysaccharide
MDD
major depressive disorder
ME/CFS
myalgic encephalomyelitis/chronic fatigue syndrome
miR
microRNA
mTOR
mechanistic target of rapamycin
NK
natural killer
NLRP
NACHT, LRR and PYD domains-containing protein
O&NS
oxidative and nitrosative stress
OXPHOS
oxidative phosphorylation
PDC
pyruvate dehydrogenase complex
PGC-1α
peroxisome proliferator-activated receptor gamma coactivator 1-alpha
PI3K
phosphatidylinositol 3-kinase
PPAR
peroxisome proliferator activated receptor
RBP
RNA binding protein
ROS
reactive oxygen species
TCA
tricarboxylic acid
TGF
transforming growth factor
Th
t-helper
TLR
toll-like receptor
Tregs
regulatory T cells
TTP
tristetraprolin

 

[Joan Crawford]

I do not know where he got the figure of 75% of m e patients having a major depressive disorder from . but I think its grossly inflated . otherwise it comes across as a review of many papers published in the last decade .and of course a wish for better/more research which is always needed.

Most pwME are frustrated, fed up and pissed off. Not clinically depressed (and that as a construct is pretty shaky).

If patients are given questionnaires rather than clinican administered structured clinical interview with time enough to distill out what is going on, then MDD will be over inflated.

Being pee'd off and struggling with multiple losses including lack of money, loss of job, status, relationships, being unable to do activities and fun stuff people valued makes it understandable that people will experience periods of low mood. But, that's an understandable reaction to a major life changing event. With help, support, medical care and understanding most people are remarkably resilient.