Meredith Arthur

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/articles/PMC40…

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

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/molybdenum-and…

@DrSteveGoeddeke @DrSteveGoeddeke no worries! 😀

@MeredithWTS sorry didn't notice there was a video link! I'll check it out.

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

@DrSteveGoeddeke @DrSteveGoeddeke sorry it's a graphic, but there is a link to a video above the graphic. If you don't have time for a video, the theory that MoCo is shifted to other enzymes besides sulfite oxidase depending on what's happening in the body or consumed leading to sulfite toxicity.

@MeredithWTS That graphic doesn't allow anyone to actually understand the problem being proposed. I'm interested, but can't make any sense of this, and I had physiology / biochem / organic chem in school.

@nullbotto @TradMaldOwl @nullbotto I think so, too. Calpain protease activation from High intracellular calcium could be caused by SSC or Glutamate. Here's an article about Calpain and Parkinson's. PubMed share.google/ipLtx9BwBRCOdo… My daughter has Autism from MBD5 deletion but sulfite worsens her symptoms

@MeredithWTS @TradMaldOwl I think this is very relevant for most Autism, ADHD and Parkinson's.

@KatBoniface @JennyJones64 and I were chatting about your post on ceruloplasmin protecting against kainate/glutamate toxicity. I had read that SSC only weakly activates kainate receptors. Maybe this issue is that SSC can high Ca, activates gephyrin, causes losses of glycine and GABA synapses

Appropriate copper metabolism protects against Kainate dependent glutamate excitotoxicity- so disregulation lowers the threshold for excitotoxic events. pubmed.ncbi.nlm.nih.gov/25843655/

Headline is a bit water is wet, but the findings have interesting connections & confirmations. Like: “Disturbances in copper-dependent antioxidant pathways, which can promote oxidative stress, promote inflammation, and contribute to tissue injury.”

@KatBoniface Thanks for that! I'll share in the group by taking a screenshot. And post the article.

@MeredithWTS Naltrexone is typically studied alongside other drugs, which is frustrating but also provides clues. Like this w/ Ket, it lowered rapid release of glutamate- not well replicated in other circumstances so it may be a modulator (good) rather than inhibitor. nature.com/articles/s4159…

Well there seems to be quite an explosion in discussion on glutamate! I’ll thread some resources here. In the meantime, AMA 🤷‍♀️

@KatBoniface This is fascinating. I love it when people come from different areas and have similar ideas. Posted your slide about glutamate hypometabolism in the MoCo steal group on Facebook. One person was wondering if LDN is good or bad for glutamate metabolism.

@MeredithWTS Folks I know with heavy sulfur sensitivity (genetic, microbiome, or metabolic) typically have a much harder time adjusting glutamate!

@KatBoniface Interesting!!

Here is a quick and dirty overview of glutamate hypometabolism, which appears to be a major underlying driver of excitotoxicity as well as clogging critical energy systems.

@KatBoniface Our group sees glutamate dysfunction from altered sulfite metabolism. Here is a diagram I made for the group.

I want to emphasize this. I've yet to see someone with ME/CFS who didn't have signs of glutamate disfunction. But what type is not universal. x.com/KatBoniface/st…

@TheDogofDestiny @AndrewDBaird1 I wonder why my roosters aren't dying off super fast? They don't lay eggs so can't detox. Also, sometimes they'll eat the eggs if one happens to have cracked. They continue to live.

Nutrition Defective has unkindly declared it will end badly for those eating 10-20 gram cubes of cheese and 1-2 eggs a day and doing the otherwise low vitamin A diet. If you have such massive faith in the benefits of reducing vitamin A why would the vitamin A in these foods matter ? 51 mcgs of retinol in 20 grams of cheese and 160 mcgs in 2 eggs. This is about 703 IUs. That's at least a tenfold reduction in my previous Vitamin A consumption. Any risk of excess Vitamin A might begin at 3,000 IUs for some being generous. Again, I'd say clown world has lost perspective. In clown world Vitamin A metabolism is ignored. In clown world because of their restrictive diet some seem incapable of metabolising any Vitamin A and some have food intolerances. I guess it's already ended badly for some of them. 7 years following someone still trying to figure it out and realising you need some calcium.

@AndrewDBaird1 Learning from people's negative experiences to something you suggest, telling them you are sorry that something you suggested didn't work well, and then adjusting your recommendations is the best "going back to school" that exists. <3

The problem with censorship during an experiment is that desperate people running out of solutions will start eating eggs, dairy or calcium for example and never reveal or report back what they are doing. And there's so many now that you've no idea if your successes and failures are taking censored alternatives or not. Censorship takes away opportunity to learn why phosphatidylcholine helps cell membranes, bile flow and supports methylation. It also stops your network learning the outcomes of those you censored and your outcomes are corrupted by non-disclosure. Shame on you.

@stag________ @mcclure_kerr @Elijahkrings That's a great summary of what Jenny and I hypothesize. We definitely don't want the H2S producing bacteria providing hydrogen sulfide to us in excess.

From my understanding Sulfite Paradox Hypothesis posits SRB overgrowth as compensatory for H2S production, not sulfate production or sulfite toxicity. I suspect but have not verified that the body’s endogenous enzymatic H2S production requirements are much lower than the H2S provided by SRB overgrowth, thus still making the overgrowth “unjustified.” But it’s at least physiologically plausible. She still recognizes SUOX as endgame.

There is no correct diet for H2S sibo. There are no safe foods. You’re backed into a corner. Pick the minimum amount of the most benign calories possible and supp your way out of it. It’s a fight with a lower life form and you’re outnumbered. By a lot. Reach for the big guns.

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? 🤔

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.

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/proposed-alter… doi:10.1007/s10545-011-9279-7

@tamararivc @patientled @JanetDafoe @tamararivc watching your video now. 🤯 I notice struggles with Phe metabolism and urinary losses of biopterin. Sulfite binds to qBH2 causing loss of recycling of BH2 to BH4. Acquired SUOX/MoCo deficiency could contribute to ME3. doi:10.1007/s10545-011-9279-7  (pg 8)

After 2 years of work, here's a video and preprint of my #MECFS #LongCOVID Hypothesis of Insulin Mediated Noradrenergic Neuron Dysfunction! youtube.com/watch?v=psALpJ… This builds upon a hypothesis published in the @patientled Hypothesis Journal ⬇️ @JanetDafoe 1/22

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/articles/PMC25…