Dysregulated provisions of oxidisable substrates to the mitochondria in ME/CFS lymphoblasts (Missailidis et al., 2021)

[Learner1]

@Learner1 thanks very much. I am unsure at this point what kind of balance of amino acids I need.
@godlovesatrier I'm not sure why whey isolate doesn't agree with me anymore. It did at one time but last time I bought the stuff that used to work well and the nausea came. I gave it away.

I found that my needs differ greatly from the traditional body building-oriented powders and the happy vegan ones, so I could use one, but I still needed to supplement the ones I'm shortest of.

 

[godlovesatrier]

Yep and also trytophan and I think tyrosine can cause spikes in serotonin or dopamine which down regulated all other aminos used for hormone balance in the brain. That's 3 months of dark depression from down regulation you do not want trust me.

Taking it with co factors or an amino acid complex is very important.

 

[Pyrrhus]

Related discussion:

Research Interview: Daniel Missailidis
https://forums.phoenixrising.me/threads/research-interview-daniel-missailidis.83713/

 

[Learner1]

Related discussion:

Research Interview: Daniel Missailidis
https://forums.phoenixrising.me/threads/research-interview-daniel-missailidis.83713/

I followed the link but it was not clear to me what he has found. My testing indicates I am overusing glycolysis and using large amounts of amino acids, have hyperactive complex IV, huge oxidative stress, and GDF15, mentioned above is very high.

And I've been to multiple mito specialists who have concluded that I don't have a genetic mito disease, but I do seem to have mito problems, but don't know what to do to help. The last one I talked to was upset about my suppressed TSH of all things and advised me to stop all my thyroid meds and I'd be cured... I have Hashimoto's, thyroid nodules and low T3, so that seemed highly inappropriate.

So, how does one apply Daniel's findings or even figure out if they're a match?

 

[Oliver3]

The takaway:
The results suggest that ME/CFS metabolism is dysregulated such that alternatives to glycolysis are more heavily utilised than in controls to provide the mitochondria with oxidisable substrates.

Is this a form on insulin resistance?