Lessons From Heat Stroke for Understanding Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, 2021, Stanculescu, Bergquist et al.

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Lessons From Heat Stroke for Understanding Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome

Dominic Stanculescu, Nuno Sepúlveda, Chin Leong Lim and Jonas Bergquist

Abstract

We here provide an overview of the pathophysiological mechanisms during heat stroke and describe similar mechanisms found in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Both conditions are characterized by disturbed homeostasis in which inflammatory pathways play a central role. Splanchnic vasoconstriction, increased gut permeability, gut-related endotoxemia, systemic inflammatory response, central nervous system dysfunction, blood coagulation disorder, endothelial-cell injury, and mitochondrial dysfunction underlie heat stroke. These mechanisms have also been documented in ME/CFS. Moreover, initial transcriptomic studies suggest that similar gene expressions are altered in both heat stroke and ME/CFS.

Finally, some predisposing factors for heat stroke, such as pre-existing inflammation or infection, overlap with those for ME/CFS. Notwithstanding important differences - and despite heat stroke being an acute condition - the overlaps between heat stroke and ME/CFS suggest common pathways in the physiological responses to very different forms of stressors, which are manifested in different clinical outcomes. The human studies and animal models of heat stroke provide an explanation for the self-perpetuation of homeostatic imbalance centered around intestinal wall injury, which could also inform the understanding of ME/CFS.

Moreover, the studies of novel therapeutics for heat stroke might provide new avenues for the treatment of ME/CFS. Future research should be conducted to investigate the similarities between heat stroke and ME/CFS to help identify the potential treatments for ME/CFS.
 
I was recently going down rabbit holes looking at similarities between long term effects of heat stroke or serious heat "exhaustion", which I gather can be much more serious than it sounds but also not necessarily dramatic and sudden enough to raise the serious alarm. I had most of the symptoms of heat exhaustion and some of the symptoms of heat stroke when my first recognizable symptoms started (during and after crossfit) so I've always wondered if there was a link.

After the 'onset' I went to the GP, who said try going for a walk instead of gym, and offered anxiety medication.
 
my illness began with a fever that lasted for the best part of 14 days so from my point of view some parts of the mechanisms of heatstroke may well overlap in m e . just to add i guess it was a pretty high fever because i have very little memory regarding those 14 days with Beijing flue .
 
I was recently going down rabbit holes looking at similarities between long term effects of heat stroke or serious heat "exhaustion", which I gather can be much more serious than it sounds but also not necessarily dramatic and sudden enough to raise the serious alarm. I had most of the symptoms of heat exhaustion and some of the symptoms of heat stroke when my first recognizable symptoms started (during and after crossfit) so I've always wondered if there was a link.

After the 'onset' I went to the GP, who said try going for a walk instead of gym, and offered anxiety medication.
Ahh, I remember it well...
The hot summer of 2018. I worked a physical 12 hour day in sweltering conditions. That night I thought I had heat stroke, but it was pem, my first time.
We've been together ever since
 
Splanchnic vasoconstriction, increased gut permeability, gut-related endotoxemia, systemic inflammatory response, central nervous system dysfunction, blood coagulation disorder, endothelial-cell injury, and mitochondrial dysfunction underlie heat stroke.

No, heat underlies heat stroke.

These mechanisms have also been documented in ME/CFS.

Not that I am aware of.


Time to stop making things up as you go along, guys. There are real live patients out there.
 
They say hot weather reduces exercise performance but mine incrased dramatically after an initial period of adjustment. Instead of interfering it seemed to normalize things.
 
I can't say specifically much about any concept like - and especially in this paper - the leaky gut problems (which seems to be a crushingly important health issue in the occasional paper and then never show up again, surely we can determine if we're all walking around poisoned by LPS bacteria?) but the methods used to link the two conditions could be stretched and applied to pretty much any condition. I appreciate this is probably a thought experiment but if it were a BPS paper it would be tore to shreds. The gene transcription part seems awfully stretched thin. The mitochondrial sectional seems to suggest a completely two unrelated processes, if there is even enough information to be said which probably there is not.

So the conclusions seem doubly stretched.

We suggest that the research on heat stroke might provide important lessons for understanding and treating ME/CFS. First, the findings from heat stroke confirm the possibility of systemic inflammation that is not associated with an exogenous pathogen (but rather with endogenous toxins). Heat stroke is primarily an inflammatory response following an external stressor (i.e., an increase in ambient temperature or over-exertion during exercise). This insight is likely important for the broader acceptance of ME/CFS as a disease that does not necessarily result from an exogenous pathogen.

Second, the findings from heat stroke describe a sequence and causality between physiological disturbances in various body systems, including the cardiovascular, gastro-intestinal, immune, and central nervous systems.

Third, heat stroke provides a model for disease perpetuation. The heat stroke literature describes a “vicious cycle” centered around intestinal injury involving the release of nitric oxide, the leakage of endotoxins, and the increased production of inflammatory cytokines. This model may also be relevant for understanding the perpetuation of disease state in ME/CFS,
 
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