5 ms·

Increasing the count and efficiency of mitochondria is gonna be a big deal. ME/CFS is caused by these organelles not working as they should.

by emsign 1y ago

rogerkirkness 1y ago
Highly recommend red light therapy for this. There's a spreadsheet that contains [1] all the scientific research does on effect on mitochondria. [1]: https://docs.google.com/spreadsheets/u/1/d/1ZKl5Me4XwPj4YgJCBes3VSCJjiVO4XI0tIR0rbMBj08/edit#gid=0 https://docs.google.com/spreadsheets/u/1/d/1ZKl5Me4XwPj4YgJC...
- azinman2 1y ago
  That’s a long list. Not all research is good research, or shows the effect you’re looking for. Where did this come from? Do you use red light therapy? For what? How often? Where do you focus it? I did manage to get some red light masks although I find it hard to fit into my routine
  - ulf-77723 1y ago
    Would also be interested in a routine that makes sense. People use habit stacking or habit chaining to get it into their routines - helps me tremendously to make new things a daily habit. But this depends on how often red light therapy might be actually helpful.
- francisofascii 1y ago
  Isn’t simply getting enough outdoor sunlight just as good as red light therapy.
  - rogerkirkness 1y ago
    Yes, assuming you get exactly the right amount and somehow also never too much of the bad UV light. It's a finicky thing to get right, but bottom line yes.
azinman2 1y ago
It’s not clear to me CFS is really a thing. To me it’s a catch all BS diagnosis that basically says “we don’t know what this is, so we’re calling it CFS”.
- emsign 1y ago
  It is definitely a thing. It all fits with the mitochondria theory: after physical or mental exhaustion (increased metabolic turnover provided by mitochondria) the recovery time (sleep) for ME/CFS patients is increased to such a degree that normal daily tasks gets them into a energy low they can't recover from anymore.
  - cpncrunch 1y ago
    Except there isn't any evidence of mitochondria problems in ME/CFS, even though a lot of studies have looked at them.
    - Lazare 1y ago
      I don't think that's quite right? There's been a fair amount of evidence pointing at possible issues, but there's no clear answer due to poor (or just different) study design, small sample sizes, different criteria across studies, different sample groups, etc. So eg https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02452-3 https://translational-medicine.biomedcentral.com/articles/10... reviewed 19 studies, many of which did find "evidence of mitochondria problems", but concluded: > ...it is difficult to establish the role of mitochondria in the pathomechanisms of ME/CFS/SEID due to inconsistencies across the studies. Future well-designed studies using the same ME/CFS/SEID diagnostic criteria and analysis methods are required to determine possible mitochondrial involvement in the pathomechanisms of ME/CFS/SEID. [...] There is consistent genomic research suggesting that ME/CFS/SEID is not a primary mitochondrial disorder, however, mitochondrial decline might occur due to secondary effects of other disrupted pathways. [...] As population samples were small, these results should be interpreted cautiously. I wouldn't summarise that as "no evidence". It's more like "ME/CFS doesn't seem to be a genetic disorder causing defective mitochondria, and the mitochondria look the same, but they seem to function differently for some reason even if we lack enough data to figure out why yet". Note that, eg, of the 19 studies reviews, 5 tried to check for differences in mitochondrial respiration between ME/CFS patients and healthy controls, and 4 of the 5 found notable differences; one study was able to reliably detect if a cell sample came from a ME/CFS patient or a healthy control based on measuring mitochondrial respiration. I don't know that's enough to fully reject the null hypothesis just yet, but it's certainly not clear we can accept it either.
kridsdale1 1y ago
I’m already getting a lot of (subjective) benefit from doing what I can with supplements that target each phase of the Krebs cycle’s bottlenecks, and glutathione production to delay ROS damage (which this paper finger-points at). My mental endurance to do things like program and handle corporate politics lasts hours longer on days when I do this. Next I need to get a lot better cardio endurance but I have some pulmonary problems to deal with.
gavinray 1y ago
Anyone interested in this should look up "MOTS-C" and "SS-31". They're readily available online. Both of them are peptides that enhance mitochondrial function. MOTS-C in particular is very fascinating. I have a vial of 20mg I've yet to use.
robwwilliams 1y ago
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Increasing the count and efficiency of mitochondria is gonna be a big deal. ME/CFS is caused by these organelles not working as they should.

by emsign 1y ago

Increasing the count and efficiency of mitochondria is gonna be a big deal. ME/CFS is caused by these organelles not working as they should.

rogerkirkness 1y ago

Highly recommend red light therapy for this. There's a spreadsheet that contains [1] all the scientific research does on effect on mitochondria. [1]: https://docs.google.com/spreadsheets/u/1/d/1ZKl5Me4XwPj4YgJCBes3VSCJjiVO4XI0tIR0rbMBj08/edit#gid=0 https://docs.google.com/spreadsheets/u/1/d/1ZKl5Me4XwPj4YgJC...

azinman2 1y ago
That’s a long list. Not all research is good research, or shows the effect you’re looking for. Where did this come from? Do you use red light therapy? For what? How often? Where do you focus it? I did manage to get some red light masks although I find it hard to fit into my routine
- ulf-77723 1y ago
  Would also be interested in a routine that makes sense. People use habit stacking or habit chaining to get it into their routines - helps me tremendously to make new things a daily habit. But this depends on how often red light therapy might be actually helpful.
francisofascii 1y ago
Isn’t simply getting enough outdoor sunlight just as good as red light therapy.
- rogerkirkness 1y ago
  Yes, assuming you get exactly the right amount and somehow also never too much of the bad UV light. It's a finicky thing to get right, but bottom line yes.

azinman2 1y ago

It’s not clear to me CFS is really a thing. To me it’s a catch all BS diagnosis that basically says “we don’t know what this is, so we’re calling it CFS”.

emsign 1y ago
It is definitely a thing. It all fits with the mitochondria theory: after physical or mental exhaustion (increased metabolic turnover provided by mitochondria) the recovery time (sleep) for ME/CFS patients is increased to such a degree that normal daily tasks gets them into a energy low they can't recover from anymore.
- cpncrunch 1y ago
  Except there isn't any evidence of mitochondria problems in ME/CFS, even though a lot of studies have looked at them.
  - Lazare 1y ago
    I don't think that's quite right? There's been a fair amount of evidence pointing at possible issues, but there's no clear answer due to poor (or just different) study design, small sample sizes, different criteria across studies, different sample groups, etc. So eg https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-020-02452-3 https://translational-medicine.biomedcentral.com/articles/10... reviewed 19 studies, many of which did find "evidence of mitochondria problems", but concluded: > ...it is difficult to establish the role of mitochondria in the pathomechanisms of ME/CFS/SEID due to inconsistencies across the studies. Future well-designed studies using the same ME/CFS/SEID diagnostic criteria and analysis methods are required to determine possible mitochondrial involvement in the pathomechanisms of ME/CFS/SEID. [...] There is consistent genomic research suggesting that ME/CFS/SEID is not a primary mitochondrial disorder, however, mitochondrial decline might occur due to secondary effects of other disrupted pathways. [...] As population samples were small, these results should be interpreted cautiously. I wouldn't summarise that as "no evidence". It's more like "ME/CFS doesn't seem to be a genetic disorder causing defective mitochondria, and the mitochondria look the same, but they seem to function differently for some reason even if we lack enough data to figure out why yet". Note that, eg, of the 19 studies reviews, 5 tried to check for differences in mitochondrial respiration between ME/CFS patients and healthy controls, and 4 of the 5 found notable differences; one study was able to reliably detect if a cell sample came from a ME/CFS patient or a healthy control based on measuring mitochondrial respiration. I don't know that's enough to fully reject the null hypothesis just yet, but it's certainly not clear we can accept it either.

kridsdale1 1y ago

I’m already getting a lot of (subjective) benefit from doing what I can with supplements that target each phase of the Krebs cycle’s bottlenecks, and glutathione production to delay ROS damage (which this paper finger-points at). My mental endurance to do things like program and handle corporate politics lasts hours longer on days when I do this. Next I need to get a lot better cardio endurance but I have some pulmonary problems to deal with.

gavinray 1y ago

Anyone interested in this should look up "MOTS-C" and "SS-31". They're readily available online. Both of them are peptides that enhance mitochondrial function. MOTS-C in particular is very fascinating. I have a vial of 20mg I've yet to use.

robwwilliams 1y ago

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome