Awesome info. Thanks. And a note that might be useful for some, or in the very least amusing for others: It's possible to JUICE raw potatoes to extract most of the protein while leaving behind most of the starch (at least, it seems to me in theory that ought to be the result). The potato juice can then be fried like scrambled eggs, or added to soups. It has a pleasant wholesome potato-y flavor, although the texture can be odd and kinda slimey.
What would mitoswab results showing complexes 2+3 functioning at 7% mean? Could that indicate succinate dehydrogenase deficiency? Even if complex 2 on its own is functioning over 100 percent? Also on lab data, succinate is relatively high in relation to other lab values. Could this strongly indicate succinate dehydrogenase deficiency? Can that suggest severe amino acid deficiency? I have symptoms of severe glutamate deficiency.
If inborn errors of metabolism includes the citric acid cycle. I am very confused with it. I don’t know why i still dont understand it.. it is only 8 steps. My mitoswab results don't make any sense to me. I think people with defects in the citric acid cycle are deficient in glutamate and aspartate, lets say if it is succinate dehydrogenase that is the issue, which causes amino acid derangement. Do you think s lot of people with weak collagen and poor healing have this issue?
I found myself re-reading this a year after it was published and I can't wrap my head around this bit.
"the removal of the glutamine nitrogen will encourage oxaloacetate to leave the citric acid cycle to enter the urea cycle as aspartate, which will then maximize the amount of complex II-feeding FADH2 that is generated at the level of succinate dehydrogenase compared to the activity of the NADH-generating reactions of the cycle."
After aspartate enters the urea cycle it is converted to arginino-succinate which is then converted to arginine and fumarate. Fumarate enters the citric acid cycle and is converted to malate which is converted to oxaloacetate, generating NADH.
In this case, I'm confused as to how glutamine maximizes FADH2. Is this an example of the citric acid cycle operating in reverse?
It's going to depend on the ultimate fate, and the relative demands for various products, such as NADH, FADH2, ATP, citrate, and so on. I think it's best to conceive of a theoretical end product of the carbon skeleton. If you are depositing extra carbons into the citric acid cycle beyond what is needed to run it, they are destined to exit. To simplify I would think of citrate (--> fat) or oxaloacetate (--> glucose) as the end products, then calculate. Using OAA makes more sense if you are isocalorically replacing carbohydrate with glutamine. Using citrate makes more sense if you are adding glutamine calories and keeping everything else constant. Lots of in between gray areas.
Then the question is what are you comparing it to. So if you are replacing carbohydrate with glutamine that question is easy -- compare it to glucose -- if adding glutamine calories the choice is more subjective.
Happy birthday!
Awesome info. Thanks. And a note that might be useful for some, or in the very least amusing for others: It's possible to JUICE raw potatoes to extract most of the protein while leaving behind most of the starch (at least, it seems to me in theory that ought to be the result). The potato juice can then be fried like scrambled eggs, or added to soups. It has a pleasant wholesome potato-y flavor, although the texture can be odd and kinda slimey.
Happy bday! Thank you for all you do--I am learning so much from you!
Happy Birthday. My wife’s also. Have a great week since birthdays after xmas so soon isn’t a big celebration.
Happy birthday!
Happy birthday and thank you for your invaluable contributions!!
Happy Birthday!
Fascinating article.
Happy Birthday, Sir Masterjohn! You have proven yourself a true gift to the world over the years 🎉🙌🏼🎉
Happy Birthday
Happy birthday, Chris!
Happy birthday!
Happy Birthday
Does supplementing with L-Glutamine help with leaky gut ?
It can.
What would mitoswab results showing complexes 2+3 functioning at 7% mean? Could that indicate succinate dehydrogenase deficiency? Even if complex 2 on its own is functioning over 100 percent? Also on lab data, succinate is relatively high in relation to other lab values. Could this strongly indicate succinate dehydrogenase deficiency? Can that suggest severe amino acid deficiency? I have symptoms of severe glutamate deficiency.
I replied to this comment in the other place you left it.
Happy birthday!!
Can you please do a video on the citric acid cycle, and what genetic defects with it can cause amino acid deficiency and weak collagen? Thanks 😊
The energy metabolism course has a lot on the citric acid cycle. I should do a whole course on inborn errors of metabolism.
If inborn errors of metabolism includes the citric acid cycle. I am very confused with it. I don’t know why i still dont understand it.. it is only 8 steps. My mitoswab results don't make any sense to me. I think people with defects in the citric acid cycle are deficient in glutamate and aspartate, lets say if it is succinate dehydrogenase that is the issue, which causes amino acid derangement. Do you think s lot of people with weak collagen and poor healing have this issue?
Weak collagen could be a collagen-specific problem like an EDS variant or it could be a respiratory chain problem.
Mitoswab tests the respiratory chain, not the citric acid cycle.
Happy birthday!
I found myself re-reading this a year after it was published and I can't wrap my head around this bit.
"the removal of the glutamine nitrogen will encourage oxaloacetate to leave the citric acid cycle to enter the urea cycle as aspartate, which will then maximize the amount of complex II-feeding FADH2 that is generated at the level of succinate dehydrogenase compared to the activity of the NADH-generating reactions of the cycle."
After aspartate enters the urea cycle it is converted to arginino-succinate which is then converted to arginine and fumarate. Fumarate enters the citric acid cycle and is converted to malate which is converted to oxaloacetate, generating NADH.
In this case, I'm confused as to how glutamine maximizes FADH2. Is this an example of the citric acid cycle operating in reverse?
Thanks!
It's going to depend on the ultimate fate, and the relative demands for various products, such as NADH, FADH2, ATP, citrate, and so on. I think it's best to conceive of a theoretical end product of the carbon skeleton. If you are depositing extra carbons into the citric acid cycle beyond what is needed to run it, they are destined to exit. To simplify I would think of citrate (--> fat) or oxaloacetate (--> glucose) as the end products, then calculate. Using OAA makes more sense if you are isocalorically replacing carbohydrate with glutamine. Using citrate makes more sense if you are adding glutamine calories and keeping everything else constant. Lots of in between gray areas.
Then the question is what are you comparing it to. So if you are replacing carbohydrate with glutamine that question is easy -- compare it to glucose -- if adding glutamine calories the choice is more subjective.
It's going to take me a while to wrap my head around this.
Thank you.