Palmitic Acid and Mitochondrial Function

Wishful

Senior Member
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Alberta
I recently tried butter again, and found that it makes my ME symptoms worse. After a significant amount of butter (didn't weigh it), I'd start feeling very achey and sluggish-brained within a few hours. I usually didn't feel better until the next day.

The next test was to take the same amount of butter, but take some (1000 mg) L-carnitine with it. No increase in symptoms. I had the same response with meat fats before, though my sensitivity to them gradually reduced after months of taking carnitine with meat-meals. Based on the different fats I tried, I'm pretty sure that the culprit is palmitic acid.

Palmitic acid concentrations in tissues seems fairly tightly controlled, but maybe a big dietary dose temporarily raises it in the body. One aspect of palmitic acid is that it binds to cellular proteins via palmitoylation. It 'plays a key role in cell signaling, protein localization, trafficking, and stability, as well as protein–protein interactions'. It affects mitochondrial function, regulating metabolism.
Among it's many possible interactions, it may affect pyruvate production. See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2860959/ for more details.

Palmitic acid is also involved in sphingolipid production, something that has shown to be abnormal in ME.

I know that someone posted recently that butter reduced their ME symptoms. Has anyone else noticed any effects, positive or negative from fats rich in palmitic acid (beef, sheep, pork, butter, cocoa butter, palm oil)? Does anyone use palm oil regularly without noticing any negative effects?

If palmitic acid affects other PWME, it would be something to bring to the attention of researchers.
 

Richard7

Senior Member
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Australia
@Wishful, my impression is that a lot of pwme/cfs seem to benefit from taking carnitine. My preference is to take it as Acetyl L Carnitine (ALCAR).

My understanding (wikipedia) is that fats with 14 or more carbons (palmitate is c16) cannot be oxidised without carnitine.

If one accepts the metabolomic conclusions of Armstrong et al: pwme/cfs use lipids and aminos for energy, and probably can only use the energy provided by carbohydrates after first converting them into fats (the first of which would be palmitate). It would make sense that anyone with ME/CFS would be metabolising more fat and therefore need more carnitine that the rest of the population.

I normally take 2 - 2.5g/day in two doses, which seems sufficient but I have not experimented with larger doses.
 

Wishful

Senior Member
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Alberta
Carnitine doesn't do anything noticeable for me other than avoid worse symptoms from palmitic acid. I very much doubt that I'm processing carbs abnormally. Carnitine is required for transporting fatty acids across the mitochondrial membrane. What I'm trying to figure out is why an excess of dietary PA causes problems if it's not being transported across the membrane at an adequate rate. The paper I linked to offers some possibilities, with elevated PA in the cytoplasm mucking around with proteins. If there's adequate carnitine present in the cells, that should lower the PA level in the cytoplasm.

I posted it mainly for those people trying to figure out ME. Maybe thinking about PA and metabolism (and the immune system?) will trigger a connection with something else.
 

Wishful

Senior Member
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6,421
Location
Alberta
Well, I'm not obese, so it shouldn't be doing that to me. I'm pretty sure that the effect on me involves transport across mitochondrial membranes. I doubt that I'm going to figure it out myself, though I will keep looking for other factors involved.
 

bad1080

Senior Member
Messages
436
gonna add this here as well:

from the video here: https://forums.phoenixrising.me/thr...-get-out-of-the-dauer-state.61191/post-995231
i found that palmitic acids (which are in almost everything thanks to palm oil) are a major driver for CNS inflammation (it leads to glia cell activation) AND mitochondrial dysfunction.

The Neuroinflammatory and Neurotoxic Potential of Palmitic Acid Is Mitigated by Oleic Acid in Microglial Cells and Microglial-Neuronal Co-cultures
https://pubmed.ncbi.nlm.nih.gov/33604780/

Palmitic Acid, but Not Lauric Acid, Induces Metabolic Inflammation, Mitochondrial Fragmentation, and a Drop in Mitochondrial Membrane Potential in Human Primary Myotubes
https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2021.663838/full
 
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