Crashes - what does science tell us for practical use?

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Yes, this does make sense to me and I've considered it, but I don't really understand the exact pathways and processes by which the brain burns energy. It also resonates with my experience with CFS through mild and moderate - the 'lactic acid buildup in muscles' never made as much sense to me because going to the gym might not crash me, but a long day of running errands might do so.
I can't explain the pathomechanism of a crash. But brain cells have mitochondria as well as muscle cells. I think we have a systemic problem with energy delivery/production and not one that is solely focused on muscles. The lactic acid is more the consequence of a crash than the cause I think.
 

Pyrrhus

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For me there is a connection to the gut for mental PEM. Any mental exertion or concentration will lead to very bad acid reflux - that's the most noticeable symptom.
Because the lower Esophageal sphincter cant close due to Lack of Energy from PEM?!

Possibly relevant:
In case anyone is interested, there are actually three different types of reflux, each associated with three different valves (sphincters) in the digestive system.

  1. Gastro-esophageal reflux is when the lower esophageal sphincter fails to close, allowing the contents of the stomach, such as acidic enzymes, to flow back up into the esophagus. This often results in heartburn.
  2. Laryngo-pharyngeal reflux is when the upper esophageal sphincter fails to close, allowing contents in the esophagus to flow back up into the back of the throat and then back down into the lungs. This often results in coughing fits and a feeling of "nasal drip" on the back of the throat.
  3. Duodeno-gastric reflux is when the pyloric sphincter fails to close, allowing contents in the small intestine, such as bile, to flow back up into the stomach and allowing stomach acid to continuously leak into the duodenum. Symptoms may include pain, nausea or vomiting. Vomit may have the dark brown color of bile. One patient describes it here: https://forums.phoenixrising.me/thr...y-disorder-duodenum-and-gaping-pylorus.79344/

It is apparently common to have multiple types of reflux at the same time. All three valves (sphincters) in the upper digestive system are controlled by the autonomic nervous system.
 

ljimbo423

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If I can connect the gut w/ mental PEM, then everything I've researched in ME/CFS will finally come together.
If ME/CFS researcher Jarred Younger is right about primed or sensitized microglia in the brain causing inflammation and symptoms.

It could be from the increase in LPS from a leaky gut found in a few studies, causing increased immune system activity in the body. ME/CFS researcher Micheal Vanelzakker said recently in a new video that the vagus nerve can pickup signals from gut dysbiosis, and activate microglia directly, causing primed microglia and symptoms of ME/CFS too.

One or both of these processes could be causing primed microglia in the brain. Therefore activating the sickness response and causing symptoms.

The reverse might also be true. Stress from even simple things, is causing the sensitized/primed microglia in the brain to activate, and again cause the sickness response and PEM, which causes more stress, and messes up the gut.. Which might then, set the whole process in motion again.

The research I've done, says stress alone, can cause primed microglia and weaken the Blood Brain Barrier. However, I don't believe stress alone could or would cause and sustain ME/CFS.
 
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Irat

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If ME/CFS researcher Jarred Younger is right about primed or sensitized microglia in the brain causing inflammation and symptoms.

It could be from the increase in LPS from a leaky gut found in a few studies, is causing increased immune system activity in the body. Micheal Vanelzakker said recently in a new video that the vagus nerve can pickup signals from gut dysbiosis, and activate microglia directly, causing primed microglia too.

One or both of these processes could be causing primed microglia in the brain. Therefore activating the sickness response and causing symptoms.

The reverse might also be true. Stress from even simple things, is causing the sensitized/primed microglia in the brain, to activate and again cause the sickness response, which causes more stress and messes up the gut.. Which might then, set the whole process in motion again.

The research I've done, says stress alone, can cause primed microglia and weaken the Blood Brain Barrier. However, I don't believe stress alone could or would cause and sustain ME/CFS.
Yes the primed microglia and also the limbic system keeps the sickness going.the tiniest stress for me causes severe crashes.so question is what caused the priming in the first place,this I would say is for everyone different and can,as already discussed here,go back to childhood for some....priming is basically kindling of stressors in life ...thats how I would describe it,but also one single huge event can cause it.
 

ljimbo423

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priming is basically kindling of stressors in life ...thats how I would describe it,but also one single huge event can cause it.
I agree. It could be that is what happens when some of us get an EBV infection that triggers ME/CFS. The infection is the straw that breaks the camels back so to speak. Causing microglia to become sensitized, which is causing symptoms and PEM.
 

hapl808

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The reason why I don't totally buy the stress hypothesis is that a really enjoyable hour long phone conversation will crash me worse than a thirty minute stressful phone call, and maybe even worse than an hour long stressful phone call. Which really sucks because it means I have to limit my enjoyable interactions, even on the phone.
 

J.G

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For me there is a connection to the gut for mental PEM. Any mental exertion or concentration will lead to very bad acid reflux - that's the most noticeable symptom. Otherwise I don't get reflux, so it seems clearly related to PEM although I'm not sure why.
Oh wow, first time I've seen anyone describe this specific PEM-reflux connection! Applies to me as well. When I was at my worst (ie. in a state of continuous PEM), I had to very consciously double-stack my pillows to elevate my head or deal with acid coming up the esophagus 24/7. Very unpleasant. It's less of an issue now that my health is somewhat more stable, but I still double-stack, and when I inevitably overdo it, the acid returns with a vengeance.
 
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Irat

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The reason why I don't totally buy the stress hypothesis is that a really enjoyable hour long phone conversation will crash me worse than a thirty minute stressful phone call, and maybe even worse than an hour long stressful phone call. Which really sucks because it means I have to limit my enjoyable interactions, even on the phone.
Both good (eustress) and bad stress(distress) result in your body releasing hormones, such as adrenaline and cortisol, that trigger common signs of stress: butterflies in the stomach, racing heart and sweaty palms. Ultimately, what distinguishes good stress from bad is how you react or feel about the experience.so when we are sick even laughing can be too much for us and can cause a crash or wired feeling.
 

hapl808

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Both good (eustress) and bad stress(distress) result in your body releasing hormones, such as adrenaline and cortisol, that trigger common signs of stress: butterflies in the stomach, racing heart and sweaty palms.
I think possibly more neurotransmitter related than hormone, although it's obviously all connected and part of the same system. For me, a pleasant phone call is unlikely to trigger a high HR or sweaty palms or anything like that. I'm not describing an 'exciting' call, just a pleasant but long conversation.

I wear a Garmin to log HR and I've noticed no correlation to HR or 'stress' level and the following day PEM. However, stress level (HRV) during the average day often does correlate with my general fatigue as my baseline HR is much higher than it should be and HRV is lower.
 

Irat

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I think possibly more neurotransmitter related than hormone, although it's obviously all connected and part of the same system. For me, a pleasant phone call is unlikely to trigger a high HR or sweaty palms or anything like that. I'm not describing an 'exciting' call, just a pleasant but long conversation.

I wear a Garmin to log HR and I've noticed no correlation to HR or 'stress' level and the following day PEM. However, stress level (HRV) during the average day often does correlate with my general fatigue as my baseline HR is much higher than it should be and HRV is lower.
I don t know,I crash from any phone call.,or conversation with my neighbour ,pleasant or not well first I get wired then I crash .
 

seamyb

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ROSs are mediators and modulators of the immune system as well as used by the immune system to attack stuff. While it's attacking stuff (under the chronic infection model) the immune system is spitting out ROSs and using the level of ROSs to decide what to do. Exercising just tells your immune system you're not on board with what it's trying to do by confounding its signalling molecules with added ROSs and so it decides to punish you. Given the immune system has no Coldplay CDs, it makes you ill instead.

Even if you ignore the personification of the immune system, this may be 100% bullshit. But it's a theory. Immune system is confused by ROS.
 
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For me, a pleasant phone call is unlikely to trigger a high HR or sweaty palms or anything like that.
For me the activity can be as pleasant as it wants to be if I do too much I crash. That's why I don't think that anything psychological is involved.

If I read through all the symptoms and trajectories of all the PR folks I cant believe anymore that we all have the same illness. I think that's why most studies on cytokines and infections etc are inconsistent and some treatments work for some and don't work for others.

I think we are only united by PEM/PENE and I think it's a cluster of illnesses that are abandoned in the medical/research field bc of the psychobabble.
 

Viala

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If I read through all the symptoms and trajectories of all the PR folks I cant believe anymore that we all have the same illness. I think that's why most studies on cytokines and infections etc are inconsistent and some treatments work for some and don't work for others.

I think we are only united by PEM/PENE and I think it's a cluster of illnesses that are abandoned in the medical/research field bc of the psychobabble.
I still think we have the same illness, but each one of us is affected in a different way. Our bodies are not the same and we have our own weak links. It can be one culprit, only manifested differently, something that we missed. So what could it be?

I was thinking today about CFS outbreaks and how CFS is not infectious. So what have we missed, do these outbreaks still happen? What do they have in common? What we have in common with people that suffered from these outbreaks?
 
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Sometimes I am thinking that there are subgroups and sometimes I think there are different starting points but they lead sooner or later to the same track of reaction in the body.

Because of the conversation here in this thread I was reminded of the TRP receptor family especially the TRPV and TRPA1.
They can be activated by different triggers like temperature, chemicals, LPS from bacteria. So we have different starting points but they result in the activation of these receptors and from there to pain and inflammation, which play a role in some of us

There is a good article about the role of TRPs and bacterial toxins by Brett Booner et al. 2018
TRP Channels as Sensors of Bacterial Endotoxins

In addition to the canonical pathway of LPS detection mediated by TLR4, TRP channel-mediated pathways endow sensory neurons and airway epithelial cells with the ability to detect and react to bacterial endotoxins. While several TRP channels present in sensory neurons: TRPA1, TRPV1, TRPM3 and TRPM8, detect LPS, TRPV1 and TRPA1 can account for the majority of the LPS induced neuronal activation.
For example:
2.1. TRPA1
TRPA1 is a Ca2+-permeable non-selective cation channel with reported values of PCa2+/PNa+ between 0.8 and 7.9 [45,46,47]. This channel is activated by a large number of irritants found in plants, food, cosmetics and pollutants [48]. Several TRPA1 agonists are highly reactive electrophiles with a shared ability to modify covalently cysteine and lysine residues in the N-terminus of the channel [49,50]. Examples of electrophilic activators are allyl isothiocyanate (found in wasabi and mustard), cinnamaldehyde (in cinnamon), nicotine (in formulations of smoking cessation therapies), and acrolein (in exhaust gasses) [51,52,53,54]. TRPA1 functions as a chemosensor in sensory tissues involved in innate defence mechanisms, thereby contributing to the organism’s integrity [55,56]. Activation of TRPA1 in sensory neurons produces acute pain [52], thermal and mechanical hyperalgesia, and more general, inflammatory pain [51]. As such, TRPA1 is involved in various molecular pathways leading to inflammatory pain.
TRPA1 is expressed in numerous tissues throughout the body. Sensory neurons of the vagal, nodose, trigeminal and dorsal root ganglia express TRPA1 in unmyelinated C-fibers and myelinated Aδ-fibers, both in peptidergic and non-peptidergic neurons. TRPA1 expression was also reported in non-excitable cells, such as epithelial cells, fibroblasts [57], pancreatic islet cells, several cell types in the gastrointestinal tract [58,59,60], vascular endothelial cells [61] and several cell types in the respiratory tract [62,63]. This heterogeneous distribution of TRPA1 suggests its potential implications in physiological functions and pathological conditions, within and beyond the nervous system.
Take a look at figure 2:
Effects of the activation of TRP channels in sensory neurons by LPS

I will look if there is a connection to virus, too
 
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TRPA1 - mitochondria

Sensory Nerve Terminal Mitochondrial Dysfunction Activates Airway Sensory Nerves via Transient Receptor Potential (TRP) Channels
by Lika Nesuashvili et al. 2013

Our finding that mitochondrial dysfunction is sufficient to evoke airway sensory nerve activation is likely to be relevant for other sensory nerve types. Mitochondrial dysfunction and subsequent ROS production occurs in diseases such as type II diabetes, irritable bowel syndrome, and cardiovascular disease (Hall and Wiley, 1998; Rocha et al., 2010; Chowdhury et al., 2013). As such, we predict that mitochondrial-TRPA1 interactions may contribute to nociceptor activation in these pathologies
The question is, if TRPA1 plays a role in us, too.
 

sometexan84

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If ME/CFS researcher Jarred Younger is right about primed or sensitized microglia in the brain causing inflammation and symptoms.

It could be from the increase in LPS from a leaky gut found in a few studies, causing increased immune system activity in the body. ME/CFS researcher Micheal Vanelzakker said recently in a new video that the vagus nerve can pickup signals from gut dysbiosis, and activate microglia directly, causing primed microglia and symptoms of ME/CFS too.

One or both of these processes could be causing primed microglia in the brain. Therefore activating the sickness response and causing symptoms.

The reverse might also be true. Stress from even simple things, is causing the sensitized/primed microglia in the brain, to activate and again cause the sickness response, which causes more stress and messes up the gut.. Which might then, set the whole process in motion again.
:star::trophy: I like this ^^^^^
 
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Agree this is a core aspect of what many of us deal with.

We can possibly assume a viral event in genetically predisposed individuals, can gradually weaken the intestinal barrier and BB barrier.

in my case-

born
food allergies 1 year old
roll over car accident 18months (no injury in theory)
spinal defects 3 years old (evident)
sick with everything at 5
IBS around 7
Strep all the time
EBV at 10.
repeat X 60 more years.
 

ljimbo423

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We can possibly assume a viral event in genetically predisposed individuals, can gradually weaken the intestinal barrier and BB barrier.
I think those are very real possibilities. In addition to that, it could be possible that an EBV infection, Covid infection, or an acute stress, etc, also actually cause the microglia to become sensitized, (as ME/CFS researcher Jarred Younger thinks) in those of us that are predisposed to developing sensitized microglia, for various reasons.

Therefore causing symptoms and PEM virtually overnight.
 

sometexan84

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