Any metabolomic experts- especially serine?

vision blue

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I've had a big change in my amino acid results - suddenly huge amount of serine.
Edit- looks like no takers, so have edited out the gory details. If anyone interested in discussing/comparing, pleaes let me know. Thanks.
 
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vision blue

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Ooh. Yes. Will try to PM you this week.
(If by chance youve already gotten it accepted for publication, the ref woukd be awesome)

Look forward to it. Thanks much for posting

What i remember of my original serine post, i was able to also tell the increase was due to an increase in the serine synthesis pathway. My understanding is tbus is usually tightly regulated snd usually not used- but does increase in cancer. But perhaps whenever tissue repair or growth is needed?
 

vision blue

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OK, @LINE and I are having an interesting private conversation, so thought I would repost my original post on serine to see if anyone else wants to chime in.

"
I've had a big change in my amino acid results - suddenly huge amount of serine. have taken AA tests for past ten years so i have lots of past data to compare to.



My phophotoserine also high, so i suspect increase in serine is that that is being converted. (at least this shows i have plenty of magneisum finally! otherwise i dont' think it can covert- something i've expereinced in the past)



And now i'm forgeting the steps, but so far suggest this is all from a greatly increased glycolosis.



Will get an OAT to try to see if that's true.



So first i was thinking this may well be cancer. I don't have sepsis and was thinking my serine and glycolosisi is upregulating serine to feed the tumor.



BUT, there's somethig else to condier. i was just reading that when resources are in abundance, there is actually an increae in glycolosis. And that this is actually the preferred method for normal cells not just cancer cells - the fact that not as much ATP is produced doesn't matter of resources are abundant apparently. And its only when resources are scarce that the method producing the most ATP (krebs) is used in order to conserve energy.



curious to know if people know about this. And if they have any evidence, papers, etc etc to suggest this is rong. This become relevent because basically i went right before the AA test from a state of starvation the last few years to a state of resource excess. I suddenly did a bunch of things- doubled protein intake, started taking mujltivitamin again, started eating tons of a breakfast cereal that contains way too much by way of vitamins. (i was able to do this in part because i've been able to tolerate more foods in part from gut healing after a couple of years)



wonder- is it possible that that made my body switch over to gycolosis in attempt to do what it needs to do to get out of my wasting away state- build musle , repiar tissues etc.?



in a way, if that's true, its exciting. But on the other hand, so much lysine can also fuel cancer growth. presumably won't cause it, but if i got a little cancer somewhere (quite likely)- this will make it grow. (and some cancer treatements basically take away folic acid and even lyisine in some models to keep cancer cells from using lysine and glycolosiss). So much lysine can also be toxic to brain, though some is good- very good in some peoples models. btw, it think it binds adreniline (proably not "bind" techincally but makes adreneline less avaialble) - that would be good for me since i have way too much of it.



anyway, maybe though it was too much too fast? i aslo see now why calorie restriction and putting body in starvation mode can keep canders from growing.



I dont' think i can cut down on my glucose/carb consumption as my body does not seem to handle fats well and in addition i have other food intolerances (big ones) that greatly limit what proteins i can eat.



Also now don't know what to do. Let my glycolosis do what it wants and risk growth not just of (needed!) muscle but also cancer? or mabye alternate days (like some CR folk advocate).



(In terns of ME/CFS specifically, to pick up where another thread has been discussing, CFS folk do have normal glycolosis but then can't use the pyruvate to make the Co-A think needed for the krebs cycle. STill thinking about this part)



(I should also add in case it means anything to anyone that recently tested my hemoglobin a1c and while in the normal range, is flagged as higher than ideal and perhaps suggesting an oncoming insulin resistence. in addition, my ratio of hdl to triglycericdes (I think thats the ratio of interst) is not as high as it should be,)"
 

LINE

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I do know from my countless trials and research that pathways can be tricky, but ultimately, there is a missing co-factor being a specific vitamin, then I look for mineral balance and then other aminos. The link I shared discusses some common vitamins that are involved.


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vision blue
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Hi. Thanks for sharing your literature search. My perspective was different.
O e of the pieces was “- Mildly elevated serine can be a sign of vitamin B6 insufficiency or pyridoxal 5-phosphate coenzyme dysfunction.
- High levels of serine when accompanied by low threonine, indicates glucogenic compensation and catabolism.
Supplement threonine and BCAAs”

And “Serine can be used as an energy source. Formed from threonineand phosphoserine (requiring B6, manganese, and magnesium), serine is necessary for the biosynthesis of acetylcholine, a neurotransmitter used in memory function.”
Need to see if I can find the original message that I posted on the list in my notes on it all before I ended up deleting it.

My recollection is reading with there were a couple of different ways in which serine could be elevated, and one was bby way of the Serine Synthesis Pathway (SSP).
I Was able to determine from my other amino acids that this appeared to be the Source of my elevation. Further reading then suggested that this was a bad thing Since it is only used in drastic circumstances pretty much. So either desperate need for energy or is used by cancer cells to grow. Then I also remember concluding that it’s possible I was prediabetic but that could be a cause to but I no longer remember why I came to this conclusion. I will try to find my notes on it



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LINE
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Thanks for that information. I do not know where you are with this CFS process but I can say that there are many endocrine/immune/neuro shifts that occur.

Obviously with immune activation, there are profound changes that occur since the immune system is the strongest force in the body. It requests the endocrine system to help fight the primary problem and with these endocrine shifts then cell function is altered.

Alteration of cells then begins to morph the responses of the body. One part of the endocrine responses includes adrenal function which turns on to support the immune response. The adrenals produce many hormones that change cell behavior but also use nutrients at high levels.

One nutrient that comes to mind is magnesium, I pick up on this with your statement of "pre diabetic" since magnesium is a good possibility. Of course, there could be many other possibilities. I wonder if you had any mineral testing done.


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Yesterday at 6:36 PM
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vision blue
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HI. I found my original post to the group on serine. I've pasted back into the thread and very curious to know if you have any comments and if that meshes with what you've unconvered or if you've just been wokring on serine things unrelated to these issues.
in answer to your question here, Depends which minerals? I was able to identify a magnesium deficiency based on amino acid test results and blood test was also right at the cutoff of normal, which of course means we know its likely not in the cells. but that was several years ago. As you'll see in the post, i was able to fix that though have back slid a bit. Based on all things considered, a magnesium defieiceny does not seem to be the casue of my increase in urinary serine. And if anythign, as you'll see in the post, since magesium is needed to covert phosphserine into serine , if anything, repleting magnesium is what allowed the serine increase to manifest.
Maybe if we discuss stuff on the thread, others will chime in? Not sure. alot of people probably don't realize how important this all is to CFS because of its role in glycolosis which is all screwed up along with krebs in CFS.


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LINE

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With metabolic pathways, I hack by using trial and error methods. In other words, I have all my supplements and start dosing and observe, it is not the most ideal way but it works after a number of tries. I usually start with b vitamins and either do a general b complex or individual.

Serum (blood) testing is not an ideal way to measure mineral status (with a few exceptions such as sodium, potassium). Magnesium testing via serum is unreliable (this comes from many hours of research), people can have normal serum levels but still be deficient. The body will prioritize the serum levels so the body will always pull minerals from storage sites to make sure the blood levels are normal.

Best thing to do is test mineral status, I use tissue analysis from Trace Elements which is the best (doing this for 30 years). OAT testing?
 

vision blue

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Yes, have done OAT testing. and hair mineral analysis, and amino acid testing, and stool testing, and urine testing for calcium and magnesium.

Was hoping you'd bring the discussion back specifically to serine and as I mentioned my upregulation of the SSP. Sure, magnesium involved in near everytying but I have not data suggesting that a defiiciency causes increase in SSP and serine. Plus, if anything my magesium status was better than has been in past when there was no serine issue. (I thought i had mentioned that I was not using serum magnesium as an indicator of stores, but the best data came from the amino acid test showing quite a few pathways blocked, all traceable to low magnesium levels. The serum value was just a bonus- for it to be that low, even if technically normal, is consistent with the low levels the AA urine test pointed to. Since magesium in blood is so tightly regulated, fact it went down even a little was significant). Anyway this is all besides the point, has nothing to do with the serine issue, but am responding to your comments about it. ) And yeah, trial and error and the vague sense of connection of metabolic pathways all true, but not the specificity I was hoping for.

I read through your word document (mostly a collection of abstracts from published studies). I think that's talking about somethign else entirely- how D-serine formed in brain from S-serine, also formed in brain. I'm not sure if those brain- formed serines talks to these other processes getting measured through urine serine. Your document also dealt with what deficiences of brain serine can do to people (the abstracts of studies) - again dosn't seem relevent.

oh well, thanks for the interst, maybe the thread will be of interest to someone else eventually and we can explore the nitty gritty