Oxalate is a Potent Inhibitor of LDH resulting in decrease NAD recycling and impaired vitamin A metabolism

OXALATE from plants or made from VITAMIN C or GLYCINE or Miralax (PEG) in the body can impair Vitamin A metabolism

Oxalate is a component of plants that is impossible for the body to completely break down. It is a poison.  We absorb it at variable rates, but some of us make it in our bodies from vitamin C and glycine.  Excess vitamin C becomes oxalate through direct breakdown and without enzymes. Usually this occurs in vitamin C over 2000 mg, but it can happen at lower doses as well. Never take vitamin C to “bowel tolerance” as this is likely actually death of the intestinal cells due to oxalate poisoning.  Glycine is metabolized to oxalate in a B6 and thiamine deficient state, but when there is adequate B6 and Thiamine, it does not become oxalate.

When oxalate is high it impairs an enzyme called Lactate Dehydrogenase (LDH).  We have to make some lactate to keep energy metabolism going. When the body is producing lactate, it also produces NAD+ which is what drives vitamin A (retinol and retinal) metabolism forward. What I found through a deep dive into literature is that Oxalate doesn’t directly inhibit alcohol dehydrogenase or retinol dehydrogenase or aldehyde dehydrogenase which was what I was searching for.  Oxalate actually impairs lactate dehydrogenase (LDH) which lower NAD+ levels.  I hypothesize that oxalate takes away the “energy” needed to drive those reactions forward by impairing LDH. 

LDH is actually the last enzyme involved in the formation of oxalates. I believe that oxalate being able to have a feedback inhibition on LDH is a safety mechanism built into our human biology, but that it backfires and wreaks metabolic havoc on vitamin A metabolism and also energy metabolism.

Oxalate impairs LDH activity via NAD dependent pathway




Oxalate Pathogenic In Autism (Perhaps this is the connection! If oxalate impairs LDH, resulting in low NAD, then retinal levels increase. These complex with ethanolamine causing A2E and microglial activation resulting in neurological decline. Read this post for more information.)


Lactate and pyruvate act as redox buffer to balance NADH/NAD


Jenny Jones, PhD, pointed the article below out to me as supporting evidence for the connection between need for normal LDH reaction to restore NAD levels. She is the oracle to my batman!


The article bleow is an excellent article! This gives the big picture of NAD production, recycling, and salvage pathways. Amazing! LDH, which is inhibited by oxalate, plays a pivotal role in NAD recycling.

NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential



1. Low oxalate diet 

2. Avoid excess  vitamin C in excess (variable per person, but most kids don’t need more than 500 mg per day)

3. Ensure adequate levels of B6 and thiamine  (Seizure meds tend to deplete B6 – ask doctor about 50 mg of P5P, active form of B6) – ask doctor before starting supplements – CAUTION!!! I believe that supplementation of any form of B6 in a low NAD state will cause B6 toxicity. Read this post for that hypothesis.

4. Avoid glycine supplements and also collagen powders as these are high in glycine

5. Avoid Miralax or any PEG product (macrogol is another name for PEG) – see below

MIRALAX can become OXALATE and also can tie up alcohol dehydrogenase and dehydrogenase that are needed for Vitamin A metabolism

Approximately 3.7% of PEG based laxatives are absorbed. This can be metabolized by the body to glyoxylate and then to oxalate especially in a B6, Thiamine, or Niacin deficient state. This will impair LDH, subsequently lower NAD, and thus impair vitamin A metabolism, but also overall metabolism.  In addition the first two steps of PEG metabolism involve alcohol dehydrogenase and aldehyde dehydrogenase. They are enzymes used in vitamin A metabolism. So Miralax may tie up these enzymes for an unknown period of time. This would be an interesting study in a rat lab.

So many people with Autism take PEG (Miralax). PEG can also cause gut dysbiosis (see below for info on bacterial steal of NAD+) Perhaps many have A2E complexes of the essential ether lipid ethanolamine due to increasing retinal levels (this is a hypothesis). 

PEG with weights greater than 4000 aren’t absorbed (1960 studies), but somewhere along the way a manufacturer changed it out for PEG 3500, probably due to cost, and the researchers felt absorbing 200 ml out of 5400 ml was no big deal.

I propose that 3.7% absorbed of the PEG laxative are causing a big deal. And the unabsorbed product is causing gut dysbiosis.

Ever notice that the label says not for use in children? Also to not use more than a week?





1. Ask your doctor if you can stop Miralax

2. Ask your doctor for alternatives such as magnesium, senna, glycerin suppositories, etc.

This is not written to diagnose or treat a condition, but only for informative purposes. Please consult your doctor before stopping or starting medications or supplements, and before making dietary or lifestyle changes based on the information provided. –  Meredith Arthur, MS, RD, LD 

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