Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

Energizer

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wow dude got lost into mysticism

You say that like it's a bad thing to be interested in the occult. His very first profile picture I remember on Peatarian in 2012 was of William Blake, the most famous English mystic himself. I think he has been into mysticism and the occult for quite some time. I wonder why he disappeared from the internet though, I enjoy his articles.
 

Potato

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You say that like it's a bad thing to be interested in the occult. His very first profile picture I remember on Peatarian in 2012 was of William Blake, the most famous English mystic himself. I think he has been into mysticism and the occult for quite some time. I wonder why he disappeared from the internet though, I enjoy his articles.
He got too close to the truth, that's what happened to me too and now I'm a potato!
 

tim333

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Enlightened potatoes are usually toxic as, too much solanine.
 

Tarmander

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You say that like it's a bad thing to be interested in the occult. His very first profile picture I remember on Peatarian in 2012 was of William Blake, the most famous English mystic himself. I think he has been into mysticism and the occult for quite some time. I wonder why he disappeared from the internet though, I enjoy his articles.
only a bad thing if you want to keep your feet on the ground
 
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Haters gonna hate, potatoes gonna potate.
giphy (9).gif
 

saraleah

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Not before unfortunately but twice after eating pretty close to no vitamin A and they were still well within the normal range FWIW. My D levels were up to 95 last November without supplements and only sun and sunlamps since the year before. I will have to find the reports and post them. My cholesterol and blood pressure also normalized fairly quickly.
That's great news, Blossom!
 

Mito

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2020 Aug 4;21(15):E5570. doi: 10.3390/ijms21155570.

Consequences of Vitamin A Deficiency: Immunoglobulin Dysregulation, Squamous Cell Metaplasia, Infectious Disease, and Death


Abstract
Vitamin A is an important regulator of immune protection, but it is often overlooked in studies of infectious disease. Vitamin A binds an array of nuclear receptors (e.g., retinoic acid receptor, peroxisome proliferator-activated receptor, retinoid X receptor) and influences the barrier and immune cells responsible for pathogen control. Children and adults in developed and developing countries are often vitamin A-deficient or insufficient, characteristics associated with poor health outcomes. To gain a better understanding of the protective mechanisms influenced by vitamin A, we examined immune factors and epithelial barriers in vitamin A deficient (VAD) mice, vitamin D deficient (VDD) mice, double deficient (VAD+VDD) mice, and mice on a vitamin-replete diet (controls). Some mice received insults, including intraperitoneal injections with complete and incomplete Freund's adjuvant (emulsified with PBS alone or with DNA + Fus-1 peptide) or intranasal inoculations with Sendai virus (SeV). Both before and after insults, the VAD and VAD+VDD mice exhibited abnormal serum immunoglobulin isotypes (e.g., elevated IgG2b levels, particularly in males) and cytokine/chemokine patterns (e.g., elevated eotaxin). Even without insult, when the VAD and VAD+VDD mice reached 3-6 months of age, they frequently exhibited opportunistic ascending bacterial urinary tract infections. There were high frequencies of nephropathy (squamous cell hyperplasia of the renal urothelium, renal scarring, and ascending pyelonephritis) and death in the VAD and VAD+VDD mice. When younger VAD mice were infected with SeV, the predominant lesion was squamous cell metaplasia of respiratory epithelium in lungs and bronchioles. Results highlight a critical role for vitamin A in the maintenance of healthy immune responses, epithelial cell integrity, and pathogen control.
Consequences of Vitamin A Deficiency: Immunoglobulin Dysregulation, Squamous Cell Metaplasia, Infectious Disease, and Death - PubMed
 

Blossom

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My latest results after eating 20-50% of my RDI several days per week over the last 5 months.
 

LLight

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Beta-toxinoid is not on my menu until I am below 30 mcg/dL of Zyklon A. When I can easily monitor my Zyklon A levels why would I ingest more poison and beta-toxinoid than necessary? I will never touch death-organ again, it makes no sense to have elevated Zyklonic acids in my bloodstream for 10 hours after intoxication.

Retinoic acid is a nutrient? lol, no, it's a hormone and lower yet still ELEVATED amounts are indeed TOXIC. This is not up for debate, this is a well established scientific fact.

"CYP3A4 is most likely the enzyme that is responsible for the increased clearance and decreased circulating at-RA concentrations in adults undergoing chronic treatment with the enzyme inducing antiepileptic drugs phenytoin and carbamazepine [99]. In infants and children treated with phenytoin, phenobarbital, carbamazepine and ethosuximide, the plasma concentrations of at-RA were more than 70% lower than in untreated children, suggesting that these drugs significantly induce at-RA metabolism [100]." (The role of CYP26 enzymes in retinoic acid clearance)

Hypertonicity Regulation of Cytochrome P450 CYP3A
"intervention with prolonged dehydration involving alternating between 24-hour cycles of water-deprivation and water ad lib for 1 week (cyclic water-deprivation; four 24-hour water-deprivation and three 24-hour water ad lib periods), increased expression of NFAT5 target genes" [...]
"CYP3A4 mRNA levels were noted to be elevated in the liver and kidney (11.8 ± 4.8-fold over water ad lib, n = 14, p = 0.04 and 2.2 ± 0.4-fold, n = 9, p = 0.02, respectively), with concurrent CYP3A protein and activity increase."

And CYP3A4 is not the only enzyme that could catabolize RA and could be under the influence of fluid intake. Same thing regarding CYP26B1 and CYP2E1.

I don't know how much these epileptic drugs elevate the CYP3A4 enzyme but this seems rather significant.

Moreover:
"Retinoic acid (RA), which also regulates cell growth and development, and ABA are both carotenoid derivatives with shared structural features and signaling mechanisms."
Abscisic acid: new perspectives on an ancient universal stress signaling molecule - ScienceDirect

"Abscisic acid (ABA) is the most important regulator of the dehydration response in plants and the ABA and MAPK perception and signaling pathways are involved in any abiotic stress that involves decrease of turgor pressure and water loss (Danquash et al., 2014)."
Abscisic Acid - an overview | ScienceDirect Topics
Maybe just a coincidence and I'm just mad :D
 
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tallglass13

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View attachment 18914 My latest results after eating 20-50% of my RDI several days per week over the last 5 months.
Wow that's incredible blossom thank you for the update. Everything looks good and you are now at the very bottom range of vitamin A. Could you please share what your diet is these days you probably have it in other post, but 20% VA RDA and you went lower in your vitamin A blood work which is incredible!
And your cholesterol is between 150 and 170 these days coming down from a whopping 270, is that correct?
 
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Amazoniac

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Got this from a previous publication that showed how circulating levels of 13-cis poisonoic acid are normally equal or higher than the all-trans variant:

- 13-cis Retinoic Acid Exerts its Specific Activity on Human Sebocytes through Selective Intracellular Isomerization to All-trans Retinoic Acid and Binding to Retinoid Acid Receptors
Abstract said:
Despite its potent biologic effect on human sebocytes, 13-cis retinoic acid exhibits low binding affinity for cellular retinoic acid binding proteins and nuclear retinoid receptors. Hence, 13-cis retinoic acid may represent a pro-drug possibly acting through all-trans isomerization. In this study, marked isomerization of 13-cis retinoic acid has been confirmed in cultured SZ95 sebocytes showing 2- to 15-fold higher levels of all-trans retinoic acid at 12–72 h, as measured by high performance liquid chromatography. In contrast, only low amounts of all-trans retinoic acid were converted intracellularly to its 13-cis isoform. 9-cis retinoic acid was not detected after either 13-cis retinoic acid or all-trans retinoic acid treatment. The rapid isomerization of 13-cis retinoic acid to high levels of all-trans retinoic acid was a sebocyte-specific event, as no significant isomerization of 13-cis retinoic acid to all-trans retinoic acid occurred in HaCaT keratinocytes. De novo mRNA expression of cytochrome P450 1A1, a major xenobiotic metabolizing enzyme, in SZ95 sebocytes was induced by all-trans retinoic acid, but not by 13-cis retinoic acid. In addition, mRNA levels of cellular retinoic acid-binding protein II, which is supposed to regulate the concentration of intracellular all-trans retinoic acid, rapidly increased under all-trans retinoic acid treatment (30 min-6 h), whereas the 13-cis retinoic acid effect was markedly weaker and delayed. Both 13-cis retinoic acid and all-trans retinoic acid suppressed mRNA expression of cytochrome P450 1A2. In parallel experiments, 13-cis retinoic acid significantly reduced SZ95 sebocyte proliferation at 10-7 M, showing 30–40% inhibition after 9 d. All-trans retinoic acid and 9-cis retinoic acid exhibited similar anti-proliferative effects. AGN 193109, a pan-antagonist of the retinoic acid receptors, antagonized the anti-proliferative activity of all retinoic acid isomers tested in a concentration-dependent manner with complete abolishment at ratios of 1:10 13-cis retinoic acid and 1:1 all-trans retinoic acid. Coincubation of SZ95 sebocytes with 13-cis retinoic acid and AGN 193109 did not alter the intracellular concentration of 13-cis retinoic acid and its isomerization profile. In contrast, the retinoid X receptor antagonist CD 3507 did not affect the inhibition of SZ95 sebocyte proliferation induced by retinoic acids. Our findings indicate: (i) a selective 13-cis retinoic acid isomerization to all-trans retinoic acid in the intracellular compartment of SZ95 sebocytes; (ii) a reduced all-trans retinoic acid inactivation process after 13-cis retinoic acid treatment as compared with treatment with all-trans retinoic acid; and (iii) a retinoic acid receptor-mediated inhibition of SZ95 sebocyte proliferation. These data explain the sebocyte-specific activity of 13-cis retinoic acid and support a pro-drug/drug relation between 13-cis retinoic acid and all-trans retinoic acid.

- All-trans Retinoic Acid Induction of Sulfotransferases
Abstract said:
All-trans retinoic acid is the bioactive form of vitamin A (retinol). Retinoids have been used clinically as therapeutic agents against a number of cancers. Retinoids have been reported to induce the phase I drug metabolizing enzymes, cytochrome P-450s. In contrast, effects of retinoids on sulfotransferases have not been as well studied. The present investigation evaluates the role of retinoic acid on the expression of aryl sulfotransferase IV and hydroxysteroid sulfotransferase a in male and female Sprague-Dawley rat liver and intestine. Cultured human hepatic carcinoma cells (Hep G2) and intestinal carcinoma cells (Caco-2) were also used to study retinoic acid's effect on simple phenol sulfating sulfotransferase, dehydroepiandrosterone sulfotransferase and oestrogen sulfotransferase. Enzyme assay and Western blot were used to determine sulfotransferase protein expression. Retinoic acid induced aryl sulfotransferase IV in liver of female rats and sulfotransferase a in liver of male rats. Intestinal rat aryl sulfotransferase IV and sulfotransferase a in male rats and intestinal aryl sulfotransferase IV in female rats were also induced after retinoic acid treatment. In Hep G2 and Caco-2 cells, retinoic acid differentially induced the three human sulfotransferase isoforms. In general, intestinal sulfotransferases were found to be more responsive than hepatic sulfotransferases to retinoic acid treatment. mRNA expressions were investigated using reverse transcription polymerase chain reaction with gene specific primers. Reverse transcription polymerase chain reaction results are in good agreement with enzyme activity and Western blot results. This suggests that retinoic acid induction of sulfotransferases is at the transcriptional level.

- Microbiota metabolite short chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43
Abstract said:
Intestinal IgA, which is regulated by gut microbiota, plays a crucial role in maintenance of intestinal homeostasis and in protecting the intestines from inflammation. However, the means by which microbiota promotes intestinal IgA responses remain unclear. Emerging evidence suggests that the host can sense gut bacterial metabolites in addition to pathogen-associated molecular patterns and that recognition of these small molecules influences host immune response in the intestines and beyond. We reported here that microbiota metabolite short-chain fatty acid acetate promoted intestinal IgA responses, which was mediated by “metabolite-sensing” GPR43. GPR43−/− mice demonstrated lower levels of intestinal IgA and IgA+ gut bacteria compared to those in WT mice. Feeding WT but not GPR43−/− mice acetate but not butyrate promoted intestinal IgA response independent of T cells. Acetate promoted B cell IgA class switching and IgA production in vitro in the presence of WT but not GPR43−/− dendritic cells (DC). Mechanistically, acetate induced DC expression of Aldh1a2, which converts Vitamin A into its metabolite retinoic acid (RA). Moreover, blockade of RA signaling inhibited the acetate induction of B cell IgA production. Our studies thus identified a new pathway by which microbiota promotes intestinal IgA response through its metabolites.

- Retinyl retinoate (poisonol joined with poisonoic acid: a nightmare)
 
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Blossom

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Wow that's incredible blossom thank you for the update. Everything looks good and you are now at the very bottom range of vitamin A. Could you please share what your diet is these days you probably have it in other post, but 20% VA RDA and you went lower in your vitamin A blood work which is incredible!
And your cholesterol is between 150 and 170 these days coming down from a whopping 270, is that correct?
Thank you. My A actually went up slightly from 32 last fall. I’ve been eating mostly meat with some butter, eggs, cheese, honey, mushrooms, cucumber, onions and pickles.
At the peak of Covid when I was working a lot at the hospital I stopped being as strict and I think that’s what made it go up.
My total cholesterol is holding steady in the 170’s from a prior 265 and the best news is that my recent liver panel was perfect. It’s surprising to me that just moderate amounts of butter and eggs caused my A it to rise. I feel really good these days and I’m getting pretty fit because I’m more active due to better energy. I’m also no longer taking any meds which I’m happy about and my high blood pressure returned to normal and has stayed normal since starting low A. I’m just going to keep an eye on my labs for now and eat how I enjoy and feel good eating.
 

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