I've seen this claim a lot in the media over the last 10 years by lazy journalists, the problem is that it simply isn't true. The medications predominantly prescribed to women have had trials that have had participants that are predominantly or entirely women and this has been true for decades...
Just wow, It's easily falsifiable too as people with LC have very diverse expectations and many of them had never even heard of ME/CFS when they first got COVID. Why do they (Garner et al.) not notice that it is them who keep projecting expectations and experiences onto others?
The recovery point creates an interesting opportunity - DecodeME *should* keep track of those who recover in the future and examine reported experiences of those people. DecodeME has a very large, relatively unbiased cohort that could be great for following people over time.
Remissions need to be tracked prospectively, eg enroll people with their details while they are still ill and then see who recovers over time. Everything else suffers from strong selection bias. Collect data when people report trying specific treatments and then collect data on remission...
Plants have evolved to have many specific innate 'immune' defenses because they don't have legs and can't just walk away from infectious diseases! I'm not sure what we can learn from that though.
I'm not sure how valuable plant gene knock out studies given that genes tend to be involved in so...
Besides deconditioning, and microvascular unit regulation failure (https://journals.physiology.org/doi/full/10.1152/ajpheart.00278.2003), there is another possibility for reduced skeletal muscle O2 diffusion.
Note that VO2Max occurs far below maximal motor unit usage.
The reduced skeletal...
That is a misunderstanding,
Forestglip posted a hypothesis:
I argued that we don't see any ***consistent*** patterns like that in brain imaging studies.
"selective excitation of a small proportion of neurons" in the brain isn't what we are talking about and I don't see how that would cause...
You are going to have to explain this to me because (a) we haven't seen it and (b) what are we supposed to see? "Fatigue" doesn't have to be "encoded" at all. We do know that feedback from peripheral afferents in muscles reduces the excitability of the motor cortex (this is central fatigue)...
We might not understand the patterns but there still necessarily will be a pattern. The brain can't be active in certain regions or have unique connectivity patterns as a causative factor without those showing up consistently across studies.
Note that there are brain/behavioural responses to fatigue which is most likely what they are measuring - the patterns they observe aren't necessarily the cause or sensory mechanisms of mental fatigue.
What I don't understand is why there would need to be such a top-down predictive mechanism in the first place. There are molecular feedback mechanisms in place - in the CNS we have neurovascular coupling. (and ventilatory responses to low oxygen).
I think too many people (especially doctors and...
The problem is no one has the foggiest idea of how this could possibly happen without actual brain damage. All the ideas about brain 'plasticity' are just vague and not demonstrated as to how this leads to such pathology.
Case control studies like this tell us nothing about epidemiological associations. You need population based studies for that.
The sample itself is heavily biased.
It is involved in peripheral signalling too. https://pmc.ncbi.nlm.nih.gov/articles/PMC11641455/ https://www.sciencedirect.com/science/article/abs/pii/S0163725824001797
GABA is also involved in central fatigue, part of how the motor cortex excitability is damped from muscle afferent feedback.
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