Discussion in 'Detox: Methylation; B12; Glutathione; Chelation' started by Jimbo39, Aug 4, 2016.
Shoot! Has anyone been able to open this? All I have is an IPAD 2. I had my sister scan it and email it to me then I cut and pasted here. What am I doing wrong other than investing in a laptop?
Arrrrrrrrg. Sent to cloud and pasted. Still doesn't work
Try going to "upload a file" and see if that works.
@TigerLilea. OK I pushed "up load a file" downloaded the PDFs from cloud. They appear below the reply box. Let's see if this'll work.
Awesome. For me it says open in IBook which is kind of a hassle. I'm too brain fried to make the comments I wanted to. Maybe tomorrow or after my nap.
It worked - I can see all five pages.
@TigerLilea. Thank you
I'm going to start with OAs that are either really low or high. I'd appreciate any feedback if I'm making any wrong assumptions or if you could tell me how one OA could have a connection with another.
PHENYLALANINE: This was by far the most whacked out OA. 239 (ref 22-61). 4 times the high norm. Dr. Amy says "high P. can have a range of neurological consequences." That doesn't say very much. I found that: high levels of P can be a neurotoxin; P makes up 50% of aspartame; and P is the direct precursor to the neurotransmitter PEA. All my neurotransmitters are low to low normal but PEA is elevated. There's a disorder called PKU. If I remember right people who have it can't get rid of P. They take a med called Kuvar which is BH-4. So if I take this, should it lower my P levels? Or are there other supplements that would do the trick? Oh yeah, P (or is it aspartame?) is found in protein. So I'm going to have to change my diet big time.
PKU is a very serious but rare genetic disorder which manifests in the newborn - one of the inborn errors of metabolism. You wouldn't have survived to adulthood untreated if you had this.
It is the result of a defective enzyme, phenylalanine hydrolase (PH) which converts phenylalanine to tyrosine. In a small subset of PKU patients, the enzyme is ok but there are various defects in production of the cofactor for the enzyme, BH4. The result is the same, they can't make tyrosine, and thus can't make the neurotransmitters derived from tyrosine, viz dopamine, adrenaline and noradrenaline.
You can make tyrosine and these neurotransmitters.
Still phe is very elevated and it would be worth trying to get to the bottom of it.
Is there some concentrated source of phe in your diet? Read the PKU literature to look for hidden sources of phe.
There is a condition called hyperphenyalaninaemia , essentially PKU lite, which appears to result from low (but not absent) function of the PH enzyme.
I'd be asking for a plasma amino acid test to know what is really going on in blood rather than just urine. The urine result could be due to something else (though I can't think what at the moment).
If you have done 23 and me it could be worth researching SNPs on PH.
If not, and particularly if you find blood phe is high and tyr relatively low, it could be worth finding out about genetic testing for PH.
I wouldn't be rushing into a protein restricted diet until I knew a lot more.
@alicec Thank you that was really informative.
Ok from what I understand: BH2 (is this a type of folic acid?) + DHPR =BH4. I don't know where I'm going with this other than a possible folic deficiency. DHEA is made from tryptophan and aspartic acid. My levels are 45 (22-61) and 45 (22-88). Tyrosine is 58 (23-113).
So tyrosine=dopamine? And tryptophan =serotonin?
I don't know. This is my diet:
Lots of meat and fatty oils (coconut, fish)
Dark green vegetables ( kale, asparagus, green beans, broccoli)
Sweet potatoes, avocados, eggplants, tomatoes.
No nuts or legumes
Limited fruit- melons, figs, blueberries
I think I have this. Your link said people with phe levels over 120 mold/l o
Ok I'll do that
I really need to do this. I feel like I'm shooting in the dark.
Not quite. Folate and biopterin (the base structure of BH4/BH2) are related but not identical. Two enzymes are involved in regeneration of BH4, DHPR and DHFR (dihydrofolate reductase).
Here is a recent post I made on the subject.
Yes. Your test shows that you can do both of these conversions, though it's possible that one or more steps might be sluggish.
Doesn't sound like a problem - it was just a thought.
The value is for plasma and I think it is important to see what is happening in blood before making further decisions.
If you find high phe and lowish tyr this does suggest you have a problem with the PH enzyme.
If your problem is with the BH4 cofactor then you would also expect to see elevated tryptophan since BH4 is a cofactor for tryptophan hydrolase which converts trp to 5HTP (5 hydroxy trp) , the first step in serotonin synthesis.
I think a specific form of B6 is needed to metabolize Phe
This is getting complicated fast. Kinda exciting too. I couldn't follow everything but it seems the process is cyclical and not downstream. qBh2-BH2 w/DHFR-BH4-qBH2
My tyr (wait, is this tyrosine or tryptophan?) Anyway my tyrosine is 58 (28-113). Tryptophan is 45 (23-88)
This seems weird because my tryptophan seems normal but I've definitely a serotonin problem (the lowest of my neurotransmitters).
How is your thyroid? I can't get enough serotonin with low T3.
In the neurotransmitter synthesis pathways we have been discussing, BH4 is converted to qBH2 which is recycled back to BH4 by DHPR.
qBH2 can convert to BH2 (very similar but not identical) which is recycled back to BH4 by DHFR.
You don't really need to know those fine distinctions, just that the BH4 form is necessary for enzyme activity.
tyr tyrosine, trp tryptophan. Yes I noticed that in urine only the phe is abnormal. It may well be like this in plasma also but maybe not. I was just trying to cover various theoretical possibilities.
Wait till you get plasma results before speculating too much.
There could be many reasons for low serotonin, may be quite different from your phe problem.
Abstract— A phenylketonuria-like state was produced in the preweanling rat, and the metabolism of phenylalanine in the normal and phenylketonuric brain was compared. The effect of B6 vitamers on the disposition of phenylalanine was also investigated. Phenylalanine was metabolized mainly by transamination and to a lesser extent by decarboxylation in both the normal and phenylketonuric-like brain. Small amounts of amine were detected in all the brains throughout the experimental period. More than 95 percent of the metabolized amino acid appeared as aromatic acids, which steadily accumulated and remained in the brain for the duration of the experiment. No change in the metabolic pattern was produced by pyridoxol. In striking contrast, pyridoxamine prevented the accumulation of acidic metabolites in the brains of all animals tested. We suggest that pyridoxamine phosphate and/or pyridoxamine is actively associated with the removal of excess keto acids and aldehydes from the brain.
@Gondwanaland Huh? Now you're really making my head ache. I had to look up transamination, decarboxylation, aromatic acids and pyridoxol.
What really caught my eye concerning transamination was: amino acid +a-ketoglutarate -a-Keto acid+glutamate. My AKG is zilch (<dl). How does this fit into the equation? More glutamate? The second pathway: glutamate+oxaloaloate-AKG+aspartate. I've been supplementing with oxaloaceletate simply because I heard it was an efficient way to pump glutamate into the bloodstream. But am I inadvertently increasing aspartate? Kinda got off on a tangent.
So I'm guessing that pyridoxol is good. What kind b6 is this?
I'm waiting for my results. Everything's so intertwined and interconnected. Accordingly to my functional doc my adrenals are "shot" so I wouldn't be supprised if it were the case with my thyroid.
How does the thyroid produce serotonin?
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