Humble nutrition researcher exploring altered Vitamin A metabolism and a little known by product of vitamin A metabolism, anhydroretinol.

Joined May 2024
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Meredith Arthur retweeted
There was a study on Ghanaian women where a retinol molecule was recycled 37 times to plasma. Whilst toxins can be recycled in the body what is particularly interesting is that a group led by Michael Green has also studied live neonatal rats. Adult rats recycle retinol 10-12 times and neonatal rats born to low Vitamin A mothers fed a low vitamin A intake recycled retinol molecules 144 times before irreversible loss. Vitamin A-retinoic acid supplementation reduced this to 100 times. This shows lower effective stores/status correlate with more extensive recycling to conserve vitamin A. This places great doubt on it being a toxin and that the body is recycling to get rid of it. It's not a poison. It's essential. pmc.ncbi.nlm.nih.gov/article…
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Sulfur intolerance feels like toxicity. Is this from sulfite oxidase/MoCo deficiency, from an excessive neutrophil response, or H2S-producing bacteria in the gut fueling neutrophil production of sulfite, or all of these? Do we take high-dose molybdenum? 🤔youtu.be/gve_oNlF87s
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Oxalate dumping. It's a real issue, and it also happens as we recover our ability to metabolize sulfite to sulfate. It can lead to low ionized calcium levels due to oxalate binding to calcium in the blood. Video: youtu.be/rzBwNDAyrys Blog: weakthereforestrong.com/moly…
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The MoCo Steal is Jenny Jones, PhD's hypothesis, which she shared with me when my daughter was having worsening neurological function. It ended up being sulfite, SSC, and glutamate toxicity. High serum A was just a symptom of this dysfunction. youtu.be/zFRSgr58BcE
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Facts. <3 In addition to aldehyde oxidase, xanthine dehydrogenase also metabolizes excess niacin metabolites. Both are backups for vit. metabolism. They use FAD and NADH. We need less burden on backups for ALDH1A1. Some niacin - yes! Too much - No. What is too much? 🤔
Molybdenum is not involved in the aldehyde dehydrogenase enzyme. It helps the aldehyde oxidase enzyme which plays a role in regulating hepatic Vitamin A homeostasis. ALDH1A1 being the high-affinity, low-capacity enzyme and AOX being the low-affinity, high-capacity enzyme. Aldehyde dehydrogenase uses NAD or NADP as co-factors. Magnesium may assist in its function, depending on the specific class of aldehyde dehydrogenase. Aldehyde oxidase is also helped by FAD and iron-sulfur clusters. pmc.ncbi.nlm.nih.gov/article… pmc.ncbi.nlm.nih.gov/article…
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I've got the flu. New video! 8 min. youtu.be/SxPFSvmA4T8 It's my shortest video ever! Nothing like a modern-day lion to make me tired?! 🤯 2 months ago, when I wasn't working on SUOX, I would have never made a short video. It would have been an hour-long insomniac event.
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I've noticed people with MoCo/SUOX deficiency are struggling with Phe/Tyr metabolism and urinary losses of biopterin (my daughter included). Sulfite binds to BH2.weakthereforestrong.com/prop… doi:10.1007/s10545-011-9279-7
19 Sep 2024
Replying to @tamararivc
In Subtype 3 (ME3) There is a deficiency of norepinephrine synthesis, worsened by mental & physical exertion. Causes could be BH4 deficiency, reduced tyrosine hydroxylase activity or other factors. @BinitaKane @amibanerjee1 @WesElyMD @zalaly @TeamSRRaj @doctor_zeest 3/22
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Anhydrodretinol, a natural metabolite of retinol in the body, causes T-cell death. Alcohol acid retinol = AR. If NAD is low and back up SULT1A1 doesn't have sulfate to buffer alcohol, T-cells die. How will we clear COVID in a high AR state? pmc.ncbi.nlm.nih.gov/article…
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Anhydrodretinol, a natural metabolite of retinol in the body, causes T-cell death. Alcohol acid retinol = AR. If NAD is low and back up SULT1A1 doesn't have sulfate to buffer alcohol, the conditions are ripe for T-cell death. How will we clear COVID in a high AR state?
Replying to @MeredithWTS
Lack of retinoic acid (and excess) could cause mitochondrial dysfunction and lead to excessive activation of NMDA receptors. People doing very low vitamin A could be making this problem worse. pmc.ncbi.nlm.nih.gov/article…
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Is S-sulfocysteine (SSC), a sneaky NMDA ligand, causing chronic damage to peripheral organs? doi.org/10.1007/s42399-020-0… Instead of sulfite binding to cystine to make SSC, perhaps mop it up with something else. docs.google.com/document/d/1…
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Here is an updated diagram of the sulfite paradox including "Modern Day Lions", B2 deficiency, BH2 binding to sulfite, and increasing glutamate levels.
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Tweaking the diagram a bit more. B1 deficiency caused by sulfite can lead to activation of HIF-1alpha. Thiamine deficiency induces HIF-1alpha. faseb.onlinelibrary.wiley.co… econtent.hogrefe.com/doi/10.… HIF-1alpha inhibits PDHC. pubmed.ncbi.nlm.nih.gov/1651…
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Daily we come to the crossroads of the HIF-1alpha pathway and Transsulfuration. Will your flight from the modern-day lion end in sulfate or sulfite? Could the amount of SSC or free sulfite you make daily determine your long-term health struggles? weakthereforestrong.com/786-…
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Cod liver oil as therapy by which to kill measles-infected lymphocytes. Cod liver oil contains anhydroretinol which destroys lymphocytes. Too much daily though could cause problems! pubmed.ncbi.nlm.nih.gov/8340… asm.org/Articles/2019/May/Me… cidrap.umn.edu/measles/measl… pubmed.ncbi.nlm.nih.gov/8340…
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This was fun! Here is a google doc link for better viewing with additional thoughts on mosaic OAT markers shown in the diagram. docs.google.com/document/d/1…
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In a low NAD state (due to sulfite causing a functional B6 deficiency) alcohol can be metabolized by SULT. If SULT (needs sulfate) can't metabolize alcohol this makes the conditions right to make ANHYDRORETINOL. No vitamin A in the liver of alcoholics, right? Makers of AR?
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I love explaining experiences with maps! High SSC can cause hypertension, hyperchloremia, and cerebral edema, but some people have hypotension when in a high sulfite and thiosulfate state due to loss of sodium. Some people fluctuate between the two states. (see my other post).
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Another update. CSA can activate NMDA. It's not thought to be a major contributor to neurodegenerative disease. Even in SUOX deficiency, GOT1 still works, while CBS and CSE are slow. Cells become cysteine deficient & sulfite toxic. pmc.ncbi.nlm.nih.gov/article… link.springer.com/referencew…
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Why would uric acid and retinol both be high in the blood? If the body is busy with purine metabolism, it loses its backup enzymes for retinol and retinaldehyde metabolism. Check B1 status as this could be altering the pentose phosphate shunt. See comments.
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Updated Sulfite Paradox Map to delineate the difference between cysteine SULFENIC acid vs Cysteine SULFINIC acid.
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