"Mitochondria Trifunctional Protein"

So yesterday we spoke about SIDS and that the deficiency of a specific "enzyme" called "Mitochondrial Trifunctional Protein" (MTFP), seems to be the cause.
In a previous Health tip, I spoke about strengthening our immune system by correcting our "mitochondria". This "mitochondria" is a function that orchestrates immunity in our immune cells.
The main function of our "mitochondria" is to "metabolize" or break down carbohydrates and "fatty acids" in order to generate energy. It's the "structures" within our cells.
So to finish this topic to yesterday's conversation . . . "mitochondria" are found in all our cells at "any" age and the cells that have the most in them are the "muscle" and "fat". And yesterday we spoke about how MTFP affects the heart which is a muscle and fatty acids of newborns.
An important feature of this function, is that it can regulate activation, differentiation, and "survival of immune cells". Mitochondria uses oxygen available within the cells to convert chemical energy from food we eat into cell energy in a form usable to the host cell. That us!
So I did a little more research on this topic.
Now . . . MTFP deficiency "prevents" this conversion. In this case . . . it prevents the body from converting certain fats to energy particularly during periods without food (fasting when we sleep). Allowing a build up, having a toxic effect.
So, what can cause this "mitochondria" malfunction??
Mitochondrial diseases are caused by abnormal genes that lead to "flawed proteins" or other molecules in the mitochondria.
When the mitochondria are defective . . . the cells do not have enough energy. The used oxygen and fuel molecules then build up in the cells and cause damage . . . as with SIDS and the heart.
Now . . . The genetics of "mitochondrial trifunctional protein" deficiency is based on mutations in the HADHA, which is the protein coding gene, and HADHB, which is the encoding gene. Meaning . . . HADHA codes a protein gene and HADHB allows HADHA to be able to code that gene. So you can't have one without the other.
And . . . this mutation of one and/or both causes this disorder of "mitochondrial trifunctional protein". Which causes fat to NOT metabolize and break down. This allows this long-chain fatty acid to build up and damage the liver, heart and muscles.
Okay . . . so I could find any elements that cure this disorder of "mitochondrial trifunctional protein" directly. However . . . is did find some elements that protect the mitochondria and neurotransmitter signaling???
And that would be . . . antioxidants, B family vitamins and most importantly "magnesium". The reason for this is that if magnesium levels are inadequate in the body . . . the ability to boost mitochondrial function lessens, thus compromising their performance.
I'll continue researching to find answers.
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