6 ms·

> doctors dismiss patients as crazy or "making it up." I don't think that's true, at least not in my experience anyway. People (myself included) are too quick

> doctors dismiss patients as crazy or "making it up." I don't think that's true, at least not in my experience anyway. People (myself included) are too quick to conflate "all in your head" with "making it up". Things "in your head" can and do have real, physical, life-limiting, effects. If it turns out that ME/CFS doesn't has a physical marker, then what? There may never be a way to verifiably test for it other than symptomatically. It's no less real for the people living with the effects, but there may be no pill to take, or injection to administer.

j_maffe 3y ago
Yes but recent studies have shown that it's neither of those, meaning that the symptoms are physiological. Not that I'm dismissing the importance of proper care of people with my psychiatric issues with fatigue or pain, it just doesn't apply to ME/CFS/LC anymore.
- cpncrunch 3y ago
  Which studies have been replicated?
krisoft 3y ago
> If it turns out that ME/CFS doesn't has a physical marker, then what? The problem is that ME/CFS is similar in presentation to other conditions such as for example certain kinds of depression. The difference is that exercise is thought to help with those conditions and exacerbates ME/CFS. Thus there are two different groups of people, one who you are helping by encouraging them to exercise and one who you are harming. If you can't tell them apart the system is bound to hurt someone.
- GordonS 3y ago
  PEM (post-exertional malaise) is a core symptom of ME/CFS, but I've never heard of it being a symptom of depression. IME it's more correct to say that depression can be a symptom of ME/CFS - having your life blow up can do that.
  - rocqua 3y ago
    The point was that for depression, exercise is a treatment. Whilst for ME/CFS, exercise is harmful. Hence it is important to make a distinction between the two, so you give proper treatment.
  - soudiere 3y ago
    Post-exertional malaise is a poor diagnostic indicator, the sensitivity and specificity are quite low. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988339/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988339/ First problem, I do not have ME/CFS, let's use the Maes et al (2012) scale. 0-5 scale, 5 being the worst. "1 means mild exacerbations of fatigue/pain/neurocognitive symptoms following exercise (either cognitive or physical)" Yep, after a longer, harder than normal bike ride I'm quite fatigued, in quite a bit of pain (bad back, knee, shoulder), and can't think particularly well. "2 means moderate exacerbations of symptoms following exercise; 3 means severe, incapacitating exacerbations lasting less than 24 hours;" Accurately describes what happens when I do HIIT style intervals that exceed my work capacity, or what it's extremely hot outside. Dreadfully exhausted, usually have to nap, or lay on the couch, every muscle hurts, extremely sore, difficult & painful to move for 24-72 hours. I'm not saying ME/CFS does not exist, this is just a terrible indicator. The worst part is making it so specific obscures the large body of existing research that would provide tools for treatment protocols here, eg work capacity in athletes.
    - GordonS 3y ago
      I'm not saying the existence of a symptom (PEM) is as good as a diagnostic test; rather, in the absence of diagnostic tests, they are "enough" to diagnose CFS. And PEM isn't the only common symptom, there are others, such as a constant lactic acid-like burning sensation in the limbs. I know you said you don't have CFS, but trust me - the fatigue we suffer after PEM is nothing like "normal" body fatigue after exercise. I think we'll find a diagnostic test eventually. At least, I hope we do.
- soudiere 3y ago
  All exercise excerbates ME/CFS? Only certain types? Cochrane systemic review, "exercise therapy for chronic fatigue syndrome", 8 studies, 1518 participants "Investigators compared exercise therapy with 'passive' control in eight trials, which enrolled 971 participants. Seven studies consistently showed a reduction in fatigue following exercise therapy at end of treatment, even though the fatigue scales used different scoring systems ... Serious adverse reactions were rare in both groups (RR 0.99, 95% CI 0.14 to 6.97; one study, 319 participants; moderate‐quality evidence)" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419524/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419524/ Fairly plausible, mitchondrial biogensis is an adaption to exercise, it may be impaired in ME/CFS patients, but not totally inhibited, and more mitochondria may lessen the severity of the pathogenesis of ME/CFS.
- hollerith 3y ago
  The only way a competent clinician can fail to distinguish CFS from depression is if the patient is outright lying. Most CFS patients for example have exercise intolerance, in which after the patient exercises more than his or her limit (which in severe cases could be walking on level ground for 10 minutes) everything proceeds like it does for a healthy person for 24 hours, then he or she becomes incapacitated for days. Eating lots of carbs, glutamine and creatine will tend to make the period of incapacitation shorter than they would otherwise be at least in non-severe cases of CFS. And this is consistently what happens after every exercise session that goes above the patient's individual exercise threshold. And if the threshold changes, it does so only gradually over a period of months. And if it changes, it changes for reasons other than how diligently or frequently the patient exercises. My experience (in California) has been that most doctors have been willing to assume I am being truthful, but a significant fraction seem to want to spend their time and energy only on conditions that the patient cannot be deceiving them about.
- quenched 3y ago
  > The difference is that exercise is thought to help with those conditions and exacerbates ME/CFS It's proven to be the case. A repeat cardiopulmonary exercise (2-day CPET) is currently the only widely replicated biomarker for ME/CFS. Only ME/CFS shows a reduction in performance and a lowering of ventilatory threshold on the second day. Anyone else (sedentary, cancer, heart or lung disease, MS, depression) will show an improvement. [1] A study this year showed a striking effect looking at the metabolites in urine after exercising female ME patients vs sedentary healthy controls. The ME patients just did not excrete metabolites as the healthy controls did. [2] "This indicates that ME/CFS patients have a general metabolic dysregulation that is part of their exercise intolerance and PEM in which altered metabolic excretion is a contributing factor." There's also a very simple clinical discriminator between ME/CFS and depression. If you ask a depressed person what they would do if they were suddenly cured, their answer will be "Not sure, I don't know, I can't think of anything, nothing really." If you ask someone with ME/CFS the same question, the response would be "Go to the shops, drive my car, walk on the beach, see my friends... etc". [1] https://www.mdpi.com/2227-9032/8/3/192 https://www.mdpi.com/2227-9032/8/3/192 [2] https://www.mdpi.com/1422-0067/24/4/3685 https://www.mdpi.com/1422-0067/24/4/3685
aestetix 3y ago
> If it turns out that ME/CFS doesn't has a physical marker, then what? There may never be a way to verifiably test for it other than symptomatically. It's no less real for the people living with the effects, but there may be no pill to take, or injection to administer. To me, this argument does not make sense. Consider the example of Physics Girl (I linked the video in another comment). The video shows her before COVID, and after COVID. It's obvious that her COVID infection did something to cause her to go from being an amateur astronaut to being bed-bound. There is clearly some kind of imbalance, somewhere. We use biomarkers like CRP levels to determine whether someone has an infection, others for cancer, or any other disease. Why would it be different for this? If we can identify some kind of biomarker... be it a protein, something in the blood, etc, and link it to COVID, then we can start testing treatments to see how they impact the biomarker.
- maxehmookau 3y ago
  > Consider the example of Physics Girl (I linked the video in another comment). The video shows her before COVID, and after COVID. It's obvious that her COVID infection did something to cause her to go from being an amateur astronaut to being bed-bound. I didn't really make an argument to "not make sense". Right now, ME/CFS may just be a collection of symptoms rather than a specific _thing_ that can be tracked, measures and cured. Or it may be a specific infection. We don't know. Sure, it's compelling. But the plural of anecdote isn't data. It may seem obvious, but so far we haven't found the biomarker yet and must surely keep an open mind that one may not exist. I'm not saying we should stop looking, but that the thing we're looking for may not appear.
  - aestetix 3y ago
    Ah, I see what you're saying. I think a more logical approach (for me) would be to say that there might be multiple biomarkers which could present ME/CFS type symptoms in different ways. Dr. Bhupesh Prusty has recently given some lectures on his discoveries related to Fibernectin, for example. That could be a massive breakthrough, but we need more studies on it. One other data point that might interest you: apparently a large percentage of ME/CFS patients are finding relief through valtrex. Apparently there is some relation to the herpes virus, although nobody understands how or why.
PaulKeeble 3y ago
The name ME comes from the observation in the 1950s that the brain stem was inflamed as shown on CT scans run in the Royal free hospital in London (what is now called St Thomas' hospital). In the 1980s they found numerous immune and metabolic dysfunctions in sufferers as well and the list of physiological things wrong has steady increased since. Yet mostly doctors have treated patients with psychology and tried to force them to exercise despite being intolerant to it and despite thousands of papers showing the biology of the disease. None of what medicine has done can be justified, it ignores all the science and evidence.
- darrenf 3y ago
  > the Royal free hospital in London (what is now called St Thomas' hospital) ??? The Royal Free is in Hampstead, and still exists. St Thomas’ is on the south bank of the Thames at Westminster bridge.
- maxehmookau 3y ago
  Your comment kinda casts doctors as the boogiemen though and I struggle to understand the motive for them to act in this way. Doctors, generally, want the best outcome for their patients. I find it hard to believe that they're doing something actively harmful that's against accepted best practices, informed by scientific literature, because... they hate their patients? If there truely were thousands of papers showing a specific biology for the disease that could be targeted and treated why would any doctor ignore that?
  - hotdogscout 3y ago
    Unwillingness to admit they don't know what's happening, memes, resentment of criticism after malpractices. Any illness with primarily neurological symptoms have a history of medical malpractice and gaslighting. As early as 1944, an author in the Journal of Nervous and Mental Disease remarked: "The history of prefrontal lobotomy has been brief and stormy. Its course has been dotted with both violent opposition and with slavish, unquestioning acceptance." The last recorded lobotomy in the United States was performed by Dr. Walter Freeman in 1967 and ended in the death of the person on whom it was performed. https://en.m.wikipedia.org/wiki/Lobotomy https://en.m.wikipedia.org/wiki/Lobotomy

j_maffe 3y ago

Yes but recent studies have shown that it's neither of those, meaning that the symptoms are physiological. Not that I'm dismissing the importance of proper care of people with my psychiatric issues with fatigue or pain, it just doesn't apply to ME/CFS/LC anymore.

cpncrunch 3y ago
Which studies have been replicated?

krisoft 3y ago

> If it turns out that ME/CFS doesn't has a physical marker, then what? The problem is that ME/CFS is similar in presentation to other conditions such as for example certain kinds of depression. The difference is that exercise is thought to help with those conditions and exacerbates ME/CFS. Thus there are two different groups of people, one who you are helping by encouraging them to exercise and one who you are harming. If you can't tell them apart the system is bound to hurt someone.

GordonS 3y ago
PEM (post-exertional malaise) is a core symptom of ME/CFS, but I've never heard of it being a symptom of depression. IME it's more correct to say that depression can be a symptom of ME/CFS - having your life blow up can do that.
- rocqua 3y ago
  The point was that for depression, exercise is a treatment. Whilst for ME/CFS, exercise is harmful. Hence it is important to make a distinction between the two, so you give proper treatment.
- soudiere 3y ago
  Post-exertional malaise is a poor diagnostic indicator, the sensitivity and specificity are quite low. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988339/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7988339/ First problem, I do not have ME/CFS, let's use the Maes et al (2012) scale. 0-5 scale, 5 being the worst. "1 means mild exacerbations of fatigue/pain/neurocognitive symptoms following exercise (either cognitive or physical)" Yep, after a longer, harder than normal bike ride I'm quite fatigued, in quite a bit of pain (bad back, knee, shoulder), and can't think particularly well. "2 means moderate exacerbations of symptoms following exercise; 3 means severe, incapacitating exacerbations lasting less than 24 hours;" Accurately describes what happens when I do HIIT style intervals that exceed my work capacity, or what it's extremely hot outside. Dreadfully exhausted, usually have to nap, or lay on the couch, every muscle hurts, extremely sore, difficult & painful to move for 24-72 hours. I'm not saying ME/CFS does not exist, this is just a terrible indicator. The worst part is making it so specific obscures the large body of existing research that would provide tools for treatment protocols here, eg work capacity in athletes.
  - GordonS 3y ago
    I'm not saying the existence of a symptom (PEM) is as good as a diagnostic test; rather, in the absence of diagnostic tests, they are "enough" to diagnose CFS. And PEM isn't the only common symptom, there are others, such as a constant lactic acid-like burning sensation in the limbs. I know you said you don't have CFS, but trust me - the fatigue we suffer after PEM is nothing like "normal" body fatigue after exercise. I think we'll find a diagnostic test eventually. At least, I hope we do.
soudiere 3y ago
All exercise excerbates ME/CFS? Only certain types? Cochrane systemic review, "exercise therapy for chronic fatigue syndrome", 8 studies, 1518 participants "Investigators compared exercise therapy with 'passive' control in eight trials, which enrolled 971 participants. Seven studies consistently showed a reduction in fatigue following exercise therapy at end of treatment, even though the fatigue scales used different scoring systems ... Serious adverse reactions were rare in both groups (RR 0.99, 95% CI 0.14 to 6.97; one study, 319 participants; moderate‐quality evidence)" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419524/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419524/ Fairly plausible, mitchondrial biogensis is an adaption to exercise, it may be impaired in ME/CFS patients, but not totally inhibited, and more mitochondria may lessen the severity of the pathogenesis of ME/CFS.
hollerith 3y ago
The only way a competent clinician can fail to distinguish CFS from depression is if the patient is outright lying. Most CFS patients for example have exercise intolerance, in which after the patient exercises more than his or her limit (which in severe cases could be walking on level ground for 10 minutes) everything proceeds like it does for a healthy person for 24 hours, then he or she becomes incapacitated for days. Eating lots of carbs, glutamine and creatine will tend to make the period of incapacitation shorter than they would otherwise be at least in non-severe cases of CFS. And this is consistently what happens after every exercise session that goes above the patient's individual exercise threshold. And if the threshold changes, it does so only gradually over a period of months. And if it changes, it changes for reasons other than how diligently or frequently the patient exercises. My experience (in California) has been that most doctors have been willing to assume I am being truthful, but a significant fraction seem to want to spend their time and energy only on conditions that the patient cannot be deceiving them about.
quenched 3y ago
> The difference is that exercise is thought to help with those conditions and exacerbates ME/CFS It's proven to be the case. A repeat cardiopulmonary exercise (2-day CPET) is currently the only widely replicated biomarker for ME/CFS. Only ME/CFS shows a reduction in performance and a lowering of ventilatory threshold on the second day. Anyone else (sedentary, cancer, heart or lung disease, MS, depression) will show an improvement. [1] A study this year showed a striking effect looking at the metabolites in urine after exercising female ME patients vs sedentary healthy controls. The ME patients just did not excrete metabolites as the healthy controls did. [2] "This indicates that ME/CFS patients have a general metabolic dysregulation that is part of their exercise intolerance and PEM in which altered metabolic excretion is a contributing factor." There's also a very simple clinical discriminator between ME/CFS and depression. If you ask a depressed person what they would do if they were suddenly cured, their answer will be "Not sure, I don't know, I can't think of anything, nothing really." If you ask someone with ME/CFS the same question, the response would be "Go to the shops, drive my car, walk on the beach, see my friends... etc". [1] https://www.mdpi.com/2227-9032/8/3/192 https://www.mdpi.com/2227-9032/8/3/192 [2] https://www.mdpi.com/1422-0067/24/4/3685 https://www.mdpi.com/1422-0067/24/4/3685

aestetix 3y ago

> If it turns out that ME/CFS doesn't has a physical marker, then what? There may never be a way to verifiably test for it other than symptomatically. It's no less real for the people living with the effects, but there may be no pill to take, or injection to administer. To me, this argument does not make sense. Consider the example of Physics Girl (I linked the video in another comment). The video shows her before COVID, and after COVID. It's obvious that her COVID infection did something to cause her to go from being an amateur astronaut to being bed-bound. There is clearly some kind of imbalance, somewhere. We use biomarkers like CRP levels to determine whether someone has an infection, others for cancer, or any other disease. Why would it be different for this? If we can identify some kind of biomarker... be it a protein, something in the blood, etc, and link it to COVID, then we can start testing treatments to see how they impact the biomarker.

maxehmookau 3y ago
> Consider the example of Physics Girl (I linked the video in another comment). The video shows her before COVID, and after COVID. It's obvious that her COVID infection did something to cause her to go from being an amateur astronaut to being bed-bound. I didn't really make an argument to "not make sense". Right now, ME/CFS may just be a collection of symptoms rather than a specific _thing_ that can be tracked, measures and cured. Or it may be a specific infection. We don't know. Sure, it's compelling. But the plural of anecdote isn't data. It may seem obvious, but so far we haven't found the biomarker yet and must surely keep an open mind that one may not exist. I'm not saying we should stop looking, but that the thing we're looking for may not appear.
- aestetix 3y ago
  Ah, I see what you're saying. I think a more logical approach (for me) would be to say that there might be multiple biomarkers which could present ME/CFS type symptoms in different ways. Dr. Bhupesh Prusty has recently given some lectures on his discoveries related to Fibernectin, for example. That could be a massive breakthrough, but we need more studies on it. One other data point that might interest you: apparently a large percentage of ME/CFS patients are finding relief through valtrex. Apparently there is some relation to the herpes virus, although nobody understands how or why.

PaulKeeble 3y ago

The name ME comes from the observation in the 1950s that the brain stem was inflamed as shown on CT scans run in the Royal free hospital in London (what is now called St Thomas' hospital). In the 1980s they found numerous immune and metabolic dysfunctions in sufferers as well and the list of physiological things wrong has steady increased since. Yet mostly doctors have treated patients with psychology and tried to force them to exercise despite being intolerant to it and despite thousands of papers showing the biology of the disease. None of what medicine has done can be justified, it ignores all the science and evidence.

darrenf 3y ago
> the Royal free hospital in London (what is now called St Thomas' hospital) ??? The Royal Free is in Hampstead, and still exists. St Thomas’ is on the south bank of the Thames at Westminster bridge.
maxehmookau 3y ago
Your comment kinda casts doctors as the boogiemen though and I struggle to understand the motive for them to act in this way. Doctors, generally, want the best outcome for their patients. I find it hard to believe that they're doing something actively harmful that's against accepted best practices, informed by scientific literature, because... they hate their patients? If there truely were thousands of papers showing a specific biology for the disease that could be targeted and treated why would any doctor ignore that?
- hotdogscout 3y ago
  Unwillingness to admit they don't know what's happening, memes, resentment of criticism after malpractices. Any illness with primarily neurological symptoms have a history of medical malpractice and gaslighting. As early as 1944, an author in the Journal of Nervous and Mental Disease remarked: "The history of prefrontal lobotomy has been brief and stormy. Its course has been dotted with both violent opposition and with slavish, unquestioning acceptance." The last recorded lobotomy in the United States was performed by Dr. Walter Freeman in 1967 and ended in the death of the person on whom it was performed. https://en.m.wikipedia.org/wiki/Lobotomy https://en.m.wikipedia.org/wiki/Lobotomy