Protein folding will happen regardless of the protein you eat.
https://en.wikipedia.org/wiki/Protein_folding
(on why I would never take any supplemental amino acids or any thing that is a product of an enzymatic reaction.)
I will give you my favorite examples; treatment of Parkinson's with L-Dopa (a protein).
One of the first line treatments for PD is L-Dopa. Does it cure PD? Nope. Does it help some symptoms with PD? Yes. Does it make the disease progress faster? Evidence points to yes:
http://www.nejm.org/doi/pdf/10.1056/NEJMoa033447
This is what I see happening in PD. First, a chart.
Amine Pathway
View attachment 12347
(I am not going to riddle this with links to the research. If you want to check, check, if you cannot find the research ask me. Also, I am using B2 as shorthand for FAD which is the cofactor and a reduced form of B2. Increasing B2 will increase FAD in the body)
So they know there is problem with Dopamine neurons in PD so they give l-dopa to make more dopamine. As you can see in the chart l-dopa is turned into dopamine by DDC (AAAD in the chart) which uses B6 as a cofactor. So they also have PD patients supplement with B6. (Hey, look at that! Doctors using cofactors to speed up enzymatic reactions!) But while this helps with symptoms it does not cure the disease. Why is this? Here is my theory.
People with PD also seem to have high activity MAO and COMT enyzmes, meaning the break down dopamine more quickly than the average person. As we can see, MAO uses B2 as a cofactor and COMT uses magnesium. Since these enzymes work fast they will use more B2 and Magnesium, thus making it more likely they will have deficiencies in these vitamins (and they do have these deficiencies). The deficiencies will be higher with the more protein they eat.
Now, when MAO breaks down dopamine it creates oxidative stress, this is what causes the dopamagenic nerve degeneration in PD. (COMT does not increase oxidative stress but puts more pressure on the MAO enzyme)
So, by giving L-DOPA to PD patents they are actually causing more oxidative damage even though some symptoms go away!
Now, lets look at B2 as a cofactor for MAO. It is obvious that increasing B2 would also be bad since this would also speed up MAO and causing oxidative stress. Yet, they find ribolavin deficiency highly prevalent in PD patients. But they find riboflavin helps PD when not on L-Dopa and on was on a low protein diet!
http://www.scielo.br/scielo.php?pid=S0100-879X2003001000019&script=sci_arttext
So, why does this work?
Well, they also find alteration in glutathione metabolism in PD. Looking at the glutathione pathway we see:
View attachment 12348
Hey, look at that, a B2 deficiency will also slow glutathione recycling! What do they find in PD patients? Lower levels of reduced glutathione! So, any OTHER genes as well that might reduce the raw materials for glutathione must be examined as well, like CBS.
However, people with fast MAO and COMT genes should lower protein intake FIRST. They should not take riboflavin unless they have bad Glutathione Reductase genes. Once people have Parkinson's they should lower protein AND take B2 until glutathione levels are restored. And once symptoms are resolved they should stop the B2.
Once the nerve damage is done it might be too late, but this will prevent those with these genes from getting PD and it will stop the progression of the disease.
So we see,by treating with a product (l dopa) we will create imbalance by using up cofactors that might be needed for other enzymes (B2). This leads to the common cycle of first it works, then it does not. Since I started taking only cofactors I have not had this issues. I take them till I feel better then I stop. When I feel symptoms coming back I take them again.
