Your post is saying that the physical effects the mental (p->m). I'm saying after a sustained period of p->m, then beliefs begin to formulate at a subconscious level resulting in m->p so then you get p<->m. The p<->m is the downward spiral that makes the condition appear progressive in nature.
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What is the biomechanics of the damage from overexertion
- Thread starter Aerose91
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SOC
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Yeah, yeah, yeah. Same old BPS crap in sheep's clothing. I'll start listening when people start providing solid, objective, unbiased, properly designed and interpreted scientific evidence of m->p on any substantive level. So far all they've got is a lot of hypotheses and badly designed and analyzed so-called research that wouldn't stand up in any hard science arena.
I fully disagree with the psychological theory. With overexertion, i will wake up in the middle of the night with burning pain, vomiting, fluish, too weak to stand and parts of my brain will go down all at the same time- and some of that is psychological? My brain infections and SPECT scan say otherwise. It doesn't fluctuate at all despite my moods or mindset. It's a 100% physical reaction of the disease.
I will hit you with this- it's physically impossible to die from a mental illness. Impossible (i mean due to physical causes not suicide). If so much of this can be mindset then why is there a death rate from it?
I think every psychosomatic hypothesis dreamt up thus far has been disproven in the context of ME/SEID. It's really time to move on.
I absolutely do not believe ME is psychosomatic any more than any other illness. That does not mean there are no psych effects - there are psych effects in cancer, AIDS, MS, RA, SLE, heart disease, Parkinson's, Alzheimer's, etc. i.e. Any serious illness has some effects on psychological function. Patient care does improve when psychological issues are addressed in diseases where there is no fast easy cure - even those that can be effectively managed medically and/or surgically.
The problem is not the idea that there is a psych component to our illness. It's that the more important physical illness has been ignored. I know my moods are not what they used to be. That tends to happen when one's life is turned upside down and one has to transition from health to illness at a young age. On top of that, perturbations in the immune system will obviously affect psych function.
The sad part is that as patients we must choose between ignoring psych aspects or ignoring physical - neither is the right course. Appropriate treatment would involve addressing every possible treatable aspect of disease - without stigma. That is true in any serious chronic disease. Unfortunately, an ME patient who becomes depressed then is promptly filed in the depression bin and the ME diagnosis is simply abandoned as the doc now has a label he/she can use.
The problem is not the idea that there is a psych component to our illness. It's that the more important physical illness has been ignored. I know my moods are not what they used to be. That tends to happen when one's life is turned upside down and one has to transition from health to illness at a young age. On top of that, perturbations in the immune system will obviously affect psych function.
The sad part is that as patients we must choose between ignoring psych aspects or ignoring physical - neither is the right course. Appropriate treatment would involve addressing every possible treatable aspect of disease - without stigma. That is true in any serious chronic disease. Unfortunately, an ME patient who becomes depressed then is promptly filed in the depression bin and the ME diagnosis is simply abandoned as the doc now has a label he/she can use.
The problem I have with that statement is that it assumes mind-body dualism - i.e. that psych and physical are entirely isolated concepts. They aren't. Most major diseases have physical and psych symptoms - they are all real, they are all biological/chemical in origin, and they are all important. e.g. If a person has antibodies to serotonin receptors, and as a result develops depression - is that a physical or psych disease? Both!
I don't think ME is a particularly mental disease, but in general, any disease that has more effects on the brain is more likely to show psych symptoms. Alzheimer's patients are often anhedonic, depressed, highly agitated, etc. Patients with CJD (a prion disease of the brain that rapidly leads to death) present often with psych symptoms, and most patients with Huntington's initially present with changes in mood. These diseases are all invariably fatal.
So ME isn't psych any more than any other organic brain disease - but it has components of psych just as any disease that affects the brain. You can't go screwing around in the brain and breaking things and not expect effects on mood and cognition (we almost all experience cognitive difficulties, at least intermitttently - i.e. brain fog).
SOC
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@Eeyore, I don't think anyone is arguing the physical to mental part of the psych argument. The objection is to the mental to physical theory that cmt12 drops into PR occasionally to push upon us. Cmt12 is calling it "m->p", but it's the same tired theory that we create and/or perpetuate our physical illness through pathological thought processes. Hence his bit about "makes the illness appear progressive" as if he has any evidence beyond personal belief that it is not actually progessive.
I'm not sure if the illness is progressive - I suspect like MS it varies from patient to patient. I don't think mine is progressive - it's more relapsing/remitting - but I wouldn't claim that is true for everyone. That's just my own experience - although I think it is not uncommon.
I don't subscribe to the theory that "illness belief" is the cause of ME. It's overly simplistic and not very original, and it really doesn't fit with the facts.
I don't subscribe to the theory that "illness belief" is the cause of ME. It's overly simplistic and not very original, and it really doesn't fit with the facts.
That's interesting @Mij - My cycling appears to be much longer than most people's. I might have a bad crash which takes years to recover from, then years of relatively good health, during which physical activity doesn't crash me again (or sometimes, only extreme physical activity).
My major crashes were about 1995 (onset), 2000, 2005, and 2014. After each, I experienced symptoms for years and years, slowly improving. I am not sure that I ever returned to normal, and I think I might come back to a lower baseline each time - although I'm not certain. Sometimes, the symptoms can be different - which I do not really understand.
My major crashes were about 1995 (onset), 2000, 2005, and 2014. After each, I experienced symptoms for years and years, slowly improving. I am not sure that I ever returned to normal, and I think I might come back to a lower baseline each time - although I'm not certain. Sometimes, the symptoms can be different - which I do not really understand.
I'm surprised to hear people say that you cannot die of a psych illness. Many illnesses currently classified as psychiatric, whatever that means, can be fatal. Although with modern treatment mortality rates are far lower than they used to be, untreated catatonia for instance has a very high mortality rate. Untreated severe depression can be ultimately fatal due to physical deterioration secondary to malnutrition and dehydration. Mania can be fatal due to exhaustion. Anorexia nervosa often kills people and only a minority of those deaths are due to suicide. Just goes to show you how utterly bogus and dangerous the mind-body dichotomy is. Obviously everything is biological on some level.
Wouldn't that suggest an underlying progression of the disease process despite remissions?
@Eeyore
I became ill in 1901 and kept a journal for many years, I can go back for referencing and I'm surprised at how much more I could do back then despite feeling 'sicker during the first 6yrs'. I'm no longer that 'sick' except for a viral reactivation(?) once a year that can put me out. This is particularly evident with my mental stamina, I used to read a book every 2 weeks, but now the mental stamina is just not there. This declined after too much overdoing physically.
I became ill in 1901 and kept a journal for many years, I can go back for referencing and I'm surprised at how much more I could do back then despite feeling 'sicker during the first 6yrs'. I'm no longer that 'sick' except for a viral reactivation(?) once a year that can put me out. This is particularly evident with my mental stamina, I used to read a book every 2 weeks, but now the mental stamina is just not there. This declined after too much overdoing physically.
If true - but I'm not sure it is true. I do not believe I've ever returned to normal baseline. I am not sure if each exacerbation leaves residual damage or not. it's not really obvious to me, and seems to be small relative to the variation that occurs over shorter time frames.
Also, I'm getting older - most healthy people lose physical function from their prime as they age anyways - it's hard to know what is what.
my brain didn't see the typo lol it's dead.
Acta Neuropathol. 1991;83(1):61-5.
Mitochondrial abnormalities in the postviral fatigue syndrome.
Behan WM1, More IA, Behan PO.
Author information
Abstract
We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.
Mitochondrial abnormalities in the postviral fatigue syndrome.
Behan WM1, More IA, Behan PO.
Author information
Abstract
We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection.
Neurosci Lett. 1996 Apr 19;208(2):117-20.
Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.
Vecchiet L1, Montanari G, Pizzigallo E, Iezzi S, de Bigontina P, Dragani L, Vecchiet J, Giamberardino MA.
Author information
Abstract
Patients with chronic fatigue syndrome (CFS) mainly complain of symptoms in the musculoskeletal domain (myalgias, fatigue). In 21 CFS patients the deep (muscle) versus superficial (skin, subcutis) sensitivity to pain was explored by measuring pain thresholds to electrical stimulation unilaterally in the deltoid, trapezius and quadriceps and overlying skin and subcutis in comparison with normal subjects. Thresholds in patients were normal in skin and subcutis but significantly lower than normal (hyperalgesia) in muscles (P < 0.001) in all sites. The selective muscle hypersensitivity corresponded also to fiber abnormalities at muscle biopsy (quadriceps) performed in nine patients which were absent in normal subjects (four cases): morphostructural alterations of the sarchomere, fatty degeneration and fibrous regeneration, inversion of the cytochrome oxidase/succinate dehydrogenase ratio, pleio/polymorphism and monstruosity of mitochondria, reduction of some mitochondrial enzymatic activities and increments of common deletion of 4977 bp of mitochondrial DNA 150-3000 times the normal values. By showing both sensory (diffuse hyperalgesia) and anatomical (degenerative picture) changes at muscle level, the results suggest a role played by peripberal mechanisms in the genesis of CFS symptoms. They would exclude the heightened perception of physiological signals from all districts hypothesized by some authors, especially as the hyperalgesia is absent in skin/subcutis.
Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.
Vecchiet L1, Montanari G, Pizzigallo E, Iezzi S, de Bigontina P, Dragani L, Vecchiet J, Giamberardino MA.
Author information
Abstract
Patients with chronic fatigue syndrome (CFS) mainly complain of symptoms in the musculoskeletal domain (myalgias, fatigue). In 21 CFS patients the deep (muscle) versus superficial (skin, subcutis) sensitivity to pain was explored by measuring pain thresholds to electrical stimulation unilaterally in the deltoid, trapezius and quadriceps and overlying skin and subcutis in comparison with normal subjects. Thresholds in patients were normal in skin and subcutis but significantly lower than normal (hyperalgesia) in muscles (P < 0.001) in all sites. The selective muscle hypersensitivity corresponded also to fiber abnormalities at muscle biopsy (quadriceps) performed in nine patients which were absent in normal subjects (four cases): morphostructural alterations of the sarchomere, fatty degeneration and fibrous regeneration, inversion of the cytochrome oxidase/succinate dehydrogenase ratio, pleio/polymorphism and monstruosity of mitochondria, reduction of some mitochondrial enzymatic activities and increments of common deletion of 4977 bp of mitochondrial DNA 150-3000 times the normal values. By showing both sensory (diffuse hyperalgesia) and anatomical (degenerative picture) changes at muscle level, the results suggest a role played by peripberal mechanisms in the genesis of CFS symptoms. They would exclude the heightened perception of physiological signals from all districts hypothesized by some authors, especially as the hyperalgesia is absent in skin/subcutis.