In looking upstream, the Tomas et al paper suggests "The lack of differences in PBMCs may suggest that the abnormalities found in whole cells shown previously is not due to abnormalities in the mitochondrial respiratory chain complexes but rather at different points of the respiration pathway such as movement of glucose into cells, AMPK abnormalities, or altered functioning of other mitochondrial enzymes (Tomas et al., 2017)."
It depends on the foods in the Keto diet. RBC deformability is improved by high polyunsaturated fat diets, and made worse by high saturated fat diets. Of course this presumes the polyunsaturated fats are not trans fats. Trans fats are even worse than saturated fats.
I would imagine that depends on the cause of the RBC abnormalities or deformabilty-disability to begin with.
That will modify it, but the flexibility of a membrane is due in a large part to its fat composition. Now in the case of oxidative and nitrosative stress, where those fats get damaged, polyunsaturated fats will have decreased benefit. This is particularly the case if they become trans fats.
I think the RBC deformability might need to be considered separately, as the “there’s something in the blood” theory still applies where plasma alone has been added to healthy cells, and found to diminish their ability to utilise oxygen.
Really appreciate your knowledge on this. I keep trying to get a local consultant with a background in CPET to read the research. Will let you know if I'm ever successful
Could you please explain this more fully for idiots like me?
I think the jury is out on whether a ketogenic diet is useful. I think glucose is still by far the most efficient energy source available to us and what the human body has adopted ..the brain uses about 70% of the glucose we normally consume. Whether our energy production is dysfunctional doesn’t necessarily equate to it being completely broken and so going extreme with a less efficient energy production does seem counterintuitive.
Don’t we have to break down the fats we eat first though to create the membrane phospholipids? I thought circulating fats are no larger than medium chain triglycerides and mostly fatty acids? So whether it’s poly when you eat it ..it mainly becomes fatty acids in the end anyway before it gets near to being part of a membrane. You also need saturated fatty acids for membrane production I think (although I am a bit hazy on that). I always thought the benefit of a diet higher in polyunsaturated fat than saturated fat was to reduce the amount of circulating cholesterol in the bloodstream and provide a source of omega fatty acids rather than anything to do with cell membranes?
