But what is vitamin A toxicity? Do we all have full livers? No. 30% of us might have full livers.
Some of us have vitamin A dysregulation which is caused by poor metabolism (low NAD state) and/or effluxing vitamin A back into the blood due to high intracellular calcium (SSC activation of NMDA, EMF activation of calcium channels, Magnesium deficiency causes STRA6 to prefer to stay on and efflux vA out into blood). High blood vitamin A levels aren’t good for sure, but they are also a squeaking wheel for major metabolic issues.
If you have HIGH retinol and LOW uric acid you have a molybdenum cofactor deficiency, and this could merely be inadequate molybdenum intake. If you take molybdenum, but still have low uric acid and high retinol, then you are struggling with making MoCo. Come join the Moco Steal group. 
We need to be making MoCo to have back up enzymes for metabolizing retinol and retinaldehyde. It requires several cofactors to be made.
Does vitamin A, in the form of retinol, trigger us to make uric acid? No. I would say that retinol is associated with high uric acid first due to enzyme competition. If XOR family enzymes are busy dealing with other substrates on the left of the diagram below (caffeine, high dose niacin, purines, aldehydes, etc), then it can’t play back up for ALDH enzymes metabolizing retinol and retinaldehyde.
We need MoCo for SUOX which metabolizes sulfite. Sulfite destroys thiamine. Sulfite toxicity will cause the pentose phosphate shunt pathway to prefer to send RP5 towards uric acid. If sulfite toxicity is very high it will stop the pentose phosphate shunt pathway all together by inhibiting the first enzyme, glucose-6-phosphate dehydrogenase. Having low uric acid could mean severe sulfite toxicity and severe MoCo deficiency. Having high uric acid could mean low B1 status.
B1 Deficiency Causing Increase Purine Synthesis. Another possibility is that the underlying issue is excessive shuttling or RP5 towards purine synthesis in the setting of thiamine deficiency (needed for TKT activity) due to sulfite toxicity. This sulfite toxicity could have been originally caused by high dose vitamin A causing a MoCo Steal. Sulfite immediately destroys B1, but the body will do it’s best to mop up sulfite (binds to B12, betaine aldehyde, cysteine). However, B1 deficiency can be caused by other factors too including excessive caffeine intake, too much sushi, Lasix therapy, poor oral intake, etc. B1 deficiency causes more RP5 resulting in more PRPP and the production of more uric acid. This pulls XOR enzymes away from retinol and retinaldehyde metabolism.
Does a ZERO vitamin A diet solve the uric acid problem? No. In fact, it could make it worse. The adaptative immune system uses vitamin A in the form of retinoic acid (see diagram). We do need physiological levels of retinoic acid to prevent XOR dominance happening where the innate immune system attacks bacteria and viruses with H2O2 made using Xanthine Oxidase instead of recruiting additional immune cells.
Consuming 25-50% of the RDA of vitamin A plus adding a lower dose of niacin (35 mg) at those meals seems to help my family.
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I’m a dietitian, not a doctor. I am probably not your dietitian. Please consult with a personal healthcare provider prior to making changes to you diet, medications, supplements, or lifestyle. This is written only to inform, and not to diagnose or treat a condition. This blog does not replace an evaluation by a medical professional. – Meredith Arthur, MS, RD, LD