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More recent scientific studies suggesting a role for Vitamin A
Control by the brain of vitamin A homeostasis
Summary
Vitamin A is a micronutrient essential for vertebrate animals maintained in homeostatic balance in the body; however, little is known about the control of this balance. This study investigated whether the hypothalamus, a key integrative brain region, regulates vitamin A levels in the liver and circulation. Vitamin A in the form of retinol or retinoic acid was stereotactically injected into the 3rd ventricle of the rat brain. Alternatively, retinoids in the mouse hypothalamus were altered through retinol-binding protein 4 (Rbp4) gene knockdown. This led to rapid change in the liver proteins controlling vitamin A homeostasis as well as vitamin A itself in liver and the circulation. Prolonged disruption of Rbp4 in the region of the arcuate nucleus of the mouse hypothalamus altered retinol levels in the liver. This supports the concept that the brain may sense retinoids and influence whole-body vitamin A homeostasis with a possible “vitaminostatic” role.
Control by the brain of vitamin A homeostasis - PMC (nih.gov)
Further back:
Control of oxidative phosphorylation by vitamin A illuminates a fundamental role in mitochondrial energy homoeostasis
Summary
The physiology of two metabolites of vitamin A is understood in substantial detail: retinaldehyde functions as the universal chromophore in the vertebrate and invertebrate eye; retinoic acid regulates a set of vertebrate transcription factors, the retinoic acid receptor superfamily. The third member of this retinoid triumvirate is retinol. While functioning as the precursor of retinaldehyde and retinoic acid, a growing body of evidence suggests a far more fundamental role for retinol in signal transduction. Here we show that retinol is essential for the metabolic fitness of mitochondria. When cells were deprived of retinol, respiration and ATP synthesis defaulted to basal levels. They recovered to significantly higher energy output as soon as retinol was restored to physiological concentration, without the need for metabolic conversion to other retinoids. Retinol emerged as an essential cofactor of protein kinase Cδ (PKCδ), without which this enzyme failed to be activated in mitochondria. Furthermore, retinol needed to physically bind PKCδ, because mutation of the retinol binding site rendered PKCδ unresponsive to Rol, while retaining responsiveness to phorbol ester. The PKCδ/retinol complex signaled the pyruvate dehydrogenase complex for enhanced flux of pyruvate into the Krebs cycle. The baseline response was reduced in vitamin A-deficient lecithin:retinol acyl transferase-knockout mice, but this was corrected within 3 h by intraperitoneal injection of vitamin A; this suggests that vitamin A is physiologically important. These results illuminate a hitherto unsuspected role of vitamin A in mitochondrial bioenergetics of mammals, acting as a nutritional sensor. As such, retinol is of fundamental importance for energy homeostasis. The data provide a mechanistic explanation to the nearly 100-yr-old question of why vitamin A deficiency causes so many pathologies that are independent of retinoic acid action.—Acin-Perez, T., Hoyos, B., Zhao, F., Vinogradov, V., Fischman, D. A., Harris, R. A., Leitges, M., Wongsiriroj, N., Blaner, W. S., Manfredi, G., Hammerling, U. Control of oxidative phosphorylation by vitamin A illuminates a fundamental role in mitochondrial energy homoeostasis.
Quote from Andrew B on August 14, 2024, 7:59 amControl by the brain of vitamin A homeostasis
Summary
Vitamin A is a micronutrient essential for vertebrate animals maintained in homeostatic balance in the body; however, little is known about the control of this balance. This study investigated whether the hypothalamus, a key integrative brain region, regulates vitamin A levels in the liver and circulation. Vitamin A in the form of retinol or retinoic acid was stereotactically injected into the 3rd ventricle of the rat brain. Alternatively, retinoids in the mouse hypothalamus were altered through retinol-binding protein 4 (Rbp4) gene knockdown. This led to rapid change in the liver proteins controlling vitamin A homeostasis as well as vitamin A itself in liver and the circulation. Prolonged disruption of Rbp4 in the region of the arcuate nucleus of the mouse hypothalamus altered retinol levels in the liver. This supports the concept that the brain may sense retinoids and influence whole-body vitamin A homeostasis with a possible “vitaminostatic” role.
Control by the brain of vitamin A homeostasis - PMC (nih.gov)
Sir, if a five-minute skim of a paper has become the holy grail of scientific validation for you, then I must commend Grant’s brain for surviving this long without turning into scrambled eggs.
I truly can't fathom your fascination here. You're quick to dismiss a decade-long experiment where someone meticulously tracked their vitamin A levels with blood tests and image scans, as if skepticism is your middle name. Yet, you have no problem swallowing every tidbit of online wisdom as if it’s been handed down from the gods themselves.
Respectfully , I think your attempt to farm new clients for your online health service by being "innovative" isnt working .
Retinoic Acid and Its Role in Modulating Intestinal Innate Immunity
Abstract
Vitamin A (VA) is amongst the most well characterized food-derived nutrients with diverse immune modulatory roles. Deficiency in dietary VA has not only been associated with immune dysfunctions in the gut, but also with several systemic immune disorders. In particular, VA metabolite all-trans retinoic acid (atRA) has been shown to be crucial in inducing gut tropism in lymphocytes and modulating T helper differentiation. In addition to the widely recognized role in adaptive immunity, increasing evidence identifies atRA as an important modulator of innate immune cells, such as tolerogenic dendritic cells (DCs) and innate lymphoid cells (ILCs). Here, we focus on the role of retinoic acid in differentiation, trafficking and the functions of innate immune cells in health and inflammation associated disorders. Lastly, we discuss the potential involvement of atRA during the plausible crosstalk between DCs and ILCs.
Retinoic Acid and Its Role in Modulating Intestinal Innate Immunity - PMC (nih.gov)
Quote from Andrew B on August 14, 2024, 8:24 amRetinoic Acid and Its Role in Modulating Intestinal Innate Immunity
Abstract
Vitamin A (VA) is amongst the most well characterized food-derived nutrients with diverse immune modulatory roles. Deficiency in dietary VA has not only been associated with immune dysfunctions in the gut, but also with several systemic immune disorders. In particular, VA metabolite all-trans retinoic acid (atRA) has been shown to be crucial in inducing gut tropism in lymphocytes and modulating T helper differentiation. In addition to the widely recognized role in adaptive immunity, increasing evidence identifies atRA as an important modulator of innate immune cells, such as tolerogenic dendritic cells (DCs) and innate lymphoid cells (ILCs). Here, we focus on the role of retinoic acid in differentiation, trafficking and the functions of innate immune cells in health and inflammation associated disorders. Lastly, we discuss the potential involvement of atRA during the plausible crosstalk between DCs and ILCs.
Retinoic Acid and Its Role in Modulating Intestinal Innate Immunity - PMC (nih.gov)
Alright, let's get straight to the point. Here's where your logic crumbles and your methods fall apart. It's the same kind of deliberate mistake made by those who rely solely on "scientific research" to push whatever propaganda they blindly follow.
You posted that research paper, barely skimming the heading and summary, then copy-pasting it here without a second thought. This is what I call "intellectual trickery." You can use this garbage to "prove" anything, but anyone with half a brain won't fall for it!
If you'd bothered to actually read the paper you posted about intestinal immunity, you'd have noticed the following:
- Page 5: The document mentions that atRA has a "rather unorthodox pro-inflammatory role" in dendritic cells. In the presence of IL-15, atRA acts as an adjuvant, promoting the secretion of pro-inflammatory cytokines IL-12 and IL-23 by dendritic cells.
- Page 9: atRA, in concert with IL-23 and IL-1β, accelerates the conversion of ILC1 to ILC3, increasing IL-22 production, which contributes to colonic inflammation.
The author clearly states that Vitamin A can contribute to gut inflammation. You're making a fool of yourself by blindly regurgitating research, thinking everyone will just swallow it without question.
First off, that paper is just a summary of a bunch of other research done on mice, all claiming the benefits of vitamin A. If we scrutinize all those papers, we'd likely find dubious claims, just like the misleading heading of this one. Last I checked, we're not mice. And if you know anything about dextran sulfate sodium (DSS)-induced colitis in mice, you'd realize it's not the same as autoimmune colitis in humans—it's a fake injury mimicking colitis, substantially different from the human condition.
By the way, I have colitis, and it was caused by ingesting huge amounts of vitamin A. Check out my post here:
: https://ggenereux.blog/discussion/topic/idb-ulcerative-colitis-and-chrons-is-caused-by-vitamin-a-toxicity/ . I think I know a bit more about colitus than somebody searching pubmed
Moreover, one of the few quality research studies I've read on colitis/IBD/Crohn's that used human experimental models is this one: :
https://pubmed.ncbi.nlm.nih.gov/32469071/
This study found that people in remission had lower amounts of RA. Those with active disease (in a flare) had more RA in their gut compared to those in remission or without the condition. This research was done at All India Institute Of Medical Sciences Delhi, India—the top medical university in India.
Another research paper, albeit done on a murine model (which you take as gospel), is
: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10536456/
The study used WIN 18,446, an ALDH1A inhibitor, to reduce RA synthesis in chronic IBD mouse models. Treatment initiated before inflammation onset reduced colitis severity.
This means they're developing a drug that blocks Vitamin A in the body to induce remission for colitis. So much for your so-called evidence.
Above post really highlights the kind of trickery Andrew, Meri, and their entourage use to deceive people—just Googling and pasting without verifying any claims. It's intellectual laziness at best, and deliberate misinformation at worst.
Shhhh… "This diet could actually heal people and make us a fortune! But first, we've got to wean folks off Grant's method. How? Simple—we’ll dazzle them with some 'scientific' sleight of hand. Just toss around fancy terms and cherry-pick a few studies. People love that stuff. We'll have them eating out of our hands (and our wallets) in no time!"
But still the answer they come out with is "its a metabolic issue" but we dont know a dime about it 😀
But seriously, isn't it hilarious how they think a little 'scientific juggling' can pull the wool over everyone's eyes? Spoiler alert: it doesn't work on those who actually read the research!
Even though I don’t put much faith in those papers myself, I firmly believe in "do it and see for yourself." That’s how you find the truth, not by blindly trusting manipulated research.
Quote from r on August 14, 2024, 2:03 pmQuote from Andrew B on August 14, 2024, 8:24 amRetinoic Acid and Its Role in Modulating Intestinal Innate Immunity
Abstract
Vitamin A (VA) is amongst the most well characterized food-derived nutrients with diverse immune modulatory roles. Deficiency in dietary VA has not only been associated with immune dysfunctions in the gut, but also with several systemic immune disorders. In particular, VA metabolite all-trans retinoic acid (atRA) has been shown to be crucial in inducing gut tropism in lymphocytes and modulating T helper differentiation. In addition to the widely recognized role in adaptive immunity, increasing evidence identifies atRA as an important modulator of innate immune cells, such as tolerogenic dendritic cells (DCs) and innate lymphoid cells (ILCs). Here, we focus on the role of retinoic acid in differentiation, trafficking and the functions of innate immune cells in health and inflammation associated disorders. Lastly, we discuss the potential involvement of atRA during the plausible crosstalk between DCs and ILCs.
Retinoic Acid and Its Role in Modulating Intestinal Innate Immunity - PMC (nih.gov)
Alright, let's get straight to the point. Here's where your logic crumbles and your methods fall apart. It's the same kind of deliberate mistake made by those who rely solely on "scientific research" to push whatever propaganda they blindly follow.
You posted that research paper, barely skimming the heading and summary, then copy-pasting it here without a second thought. This is what I call "intellectual trickery." You can use this garbage to "prove" anything, but anyone with half a brain won't fall for it!
If you'd bothered to actually read the paper you posted about intestinal immunity, you'd have noticed the following:
- Page 5: The document mentions that atRA has a "rather unorthodox pro-inflammatory role" in dendritic cells. In the presence of IL-15, atRA acts as an adjuvant, promoting the secretion of pro-inflammatory cytokines IL-12 and IL-23 by dendritic cells.
- Page 9: atRA, in concert with IL-23 and IL-1β, accelerates the conversion of ILC1 to ILC3, increasing IL-22 production, which contributes to colonic inflammation.
The author clearly states that Vitamin A can contribute to gut inflammation. You're making a fool of yourself by blindly regurgitating research, thinking everyone will just swallow it without question.
First off, that paper is just a summary of a bunch of other research done on mice, all claiming the benefits of vitamin A. If we scrutinize all those papers, we'd likely find dubious claims, just like the misleading heading of this one. Last I checked, we're not mice. And if you know anything about dextran sulfate sodium (DSS)-induced colitis in mice, you'd realize it's not the same as autoimmune colitis in humans—it's a fake injury mimicking colitis, substantially different from the human condition.
By the way, I have colitis, and it was caused by ingesting huge amounts of vitamin A. Check out my post here:
: https://ggenereux.blog/discussion/topic/idb-ulcerative-colitis-and-chrons-is-caused-by-vitamin-a-toxicity/ . I think I know a bit more about colitus than somebody searching pubmed
Moreover, one of the few quality research studies I've read on colitis/IBD/Crohn's that used human experimental models is this one: :
https://pubmed.ncbi.nlm.nih.gov/32469071/This study found that people in remission had lower amounts of RA. Those with active disease (in a flare) had more RA in their gut compared to those in remission or without the condition. This research was done at All India Institute Of Medical Sciences Delhi, India—the top medical university in India.
Another research paper, albeit done on a murine model (which you take as gospel), is
: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10536456/
The study used WIN 18,446, an ALDH1A inhibitor, to reduce RA synthesis in chronic IBD mouse models. Treatment initiated before inflammation onset reduced colitis severity.
This means they're developing a drug that blocks Vitamin A in the body to induce remission for colitis. So much for your so-called evidence.
Would you care to answer this? It’s downright dishonest of you to mislead people by posting a summary of a paper without even bothering to read it. If this is how you and your entourage conduct "research" and then treat your clients based on that, you’re nothing short of a fraud. This is incredibly dangerous. You blatantly claimed that Vitamin A is good for the gut, and based on your reckless suggestion, someone could start taking this harmful substance and ruin their life permanently. Show some accountability instead of relying on lazy Google searches. A person’s health shouldn’t be subjected to such careless misinformation from you.
Ladies and gentlemen, behold the cutting-edge research methodology of Andrew B and Meri Arthur: Google > skim the heading and conclusion, and voila, instant expertise! Ahaha, who needs the nitty-gritty details when you can just wing it, right? The proof is in the pudding, folks—just don’t ask what’s in it, because they sure didn’t bother to check!
Quote from r on August 21, 2024, 11:00 pmQuote from Jessica2 on August 20, 2024, 3:26 pm@r-2 literally everybody here has PubMed at their disposal and uses it. Unless you are a research scientist conducting your own studies that's what we have available. Meri Arthur forms her own theories based on many hours of going through these studies. You posted many. Are you the only one qualified to read the studies correctly and post them?
Sure, I'm not opposed to using studies, but this guy clearly didn't even bother to read them—just skimmed the headlines and expects us to take his word like he's some kind of 'big pharma' zealot.
The fact that he got caught with his pants down and still hasn't responded to me just proves that Andrew is a complete fraud.
I'd love to see what happens to anyone foolish enough to trust their health to his Google-search 'expertise'.
Another study on how Vitamin A can help the gut microbiome but in more simpler terms. Although I guess there is not really much point in replying to you, as you clearly have already made up your mind vitamin A is a toxin so you will deny anything that contradicts that
https://www.sciencedirect.com/science/article/pii/S0271531721000580#:~:text=1.1.-,1.,barrier%20function%20of%20the%20intestines.
"1.1.1. Vitamin A effects on the gut microbiome
Retinoids have functions in every cell of the body, with mucin production, cell growth and cell differentiation most important in the gut as these factors maintain the normal barrier function of the intestines. Dysfunction of the intestinal mucosa alters the permeability of the intestinal epithelium and modifies the production of biochemical factors that interact with gut microbes. Therefore, vitamin A status may affect the gut microbiome via changes to the intestinal mucosal barrier.
Several interventional studies have investigated the direct effects of vitamin A supplementation on the fecal microbiome composition in humans, as summarized in Table 1. A study in 306 infants in Bangladesh randomized to receive a single high dose of vitamin A or placebo within 48 hour of birth showed that boys receiving vitamin A had a higher abundance of fecal Bifidobacterium than boys receiving placebo, however, this difference was not seen in girls. For girls in late infancy, a positive association of plasma retinol with Actinobacteria (the phylum containing Bifidobacterium) and the commensal Akkermansia was found. However, there were no differences seen in the study population overall for Bifidobacterium and Proteobacteria [36]. In a single-blind, non-controlled pilot study, children with autism spectrum disorders completed a vitamin A intervention consisting of a single high dose (intended to prevent deficiency over a period of 4 to 6 months in young children), including gut microbe analyses at baseline and after 6 months in a subset of 20 participants [37]. At follow-up, there were a number of changes, including an increase in Bacteroidales order, Bacteroidia class, and Bacteroidetes phylum, and decrease in Proteobacteria, Actinobacteria, Enterobacter, Escherichia-Shigella, Clostridium, and Bifidobacterium compared to baseline. Although these findings are from an uncontrolled study, they suggest potential roles of vitamin A in modulating the gut microbiota in children with autism spectrum disorders [3"
Vitamin A is also important for the intestinal immune response to pathogens and tolerance to food-derived antigens [16]. Moreover, vitamin A regulates the gene expression of anti-microbial peptides [60]. In a study in children aged 5-15 months from Mexico, vitamin A supplementation increased the duration of enteropathogenic Escherichia coli infections, possibly by decreasing interleukin-8 and monocyte chemoattractant protein-1 concentrations. On the other hand, vitamin A supplemented children showed shorter enterotoxigenic Escherichia coli infections in association with fecal tumor necrosis factor-alpha and interleukin-6 concentrations [61]. Although not fully conclusive, together these findings corroborate that impairment of helper T cell-2 response when vitamin A is deficient (while favoring the helper T cell-1 profile) may harm the response against extracellular bacterial infections [56]."
You can find a ton of evidence that vitamin A is GOOD. Does that mean it is all factual information? Hardly. Science is so hijacked. You can manipulate findings easily. What is more interesting are papers revealing the HARM because those scientists are not going to get front page of any science journal.
Anthony Mawson is one such scientist
Malaria, Epstein-Barr virus, vitamin A, and Burkitt’s lymphoma: Response to Joob and Wiwanitkit
"We hypothesized that an endogenous form of retinoid toxicity related to malaria infection may be the common factor linking frequent malaria, Epstein-Barr virus (EBV) and Burkitt’s lymphoma (BL). Based in part on the observation that Plasmodium falciparum selectively absorbs vitamin A from the liver,[3] the main storage organ for the vitamin, it was proposed that the merozoite-stage parasites emerging from the liver use the ingested vitamin A as a cell membrane destabilizer to enter and reproduce in the red blood cells (RBCs). It was further suggested that the subsequent release of vitamin A from the RBCs into the circulation triggers an endogenous form of hypervitaminosis A, recognized as the signs and symptoms of malaria.[4] Repeated episodes of malaria would be expected to expose affected individuals to multiple toxic doses of vitamin A, particularly fatty tissues such as the brain and lymphatics. Latent EBV is also activated by the presence of excess retinoid, which in turn activates retinoid-responsive genes, thereby enhancing expression of the molecular mechanisms of BL.
...we note that low serum retinol concentrations do not necessarily indicate vitamin A deficiency, nor do they rule out vitamin A toxicity. In fact, low serum retinol may be accompanied by a high ratio of RE to total vitamin A (retinol plus esters), and the latter defines a state of toxicity when >10%.[8]"
https://sci-hub.hkvisa.net/10.1002/ijc.31122
A Role for the Liver in Parturition and Preterm Birth
"While essential in low concentration for multiple biological functions, vitamin A in higher concentration can be pro-oxidant, mutagenic, teratogenic and cytotoxic, acting as a highly surface-active, membrane-seeking and destabilizing compound. "
https://www.researchgate.net/publication/304002797_A_Role_for_the_Liver_in_Parturition_and_Preterm_Birt
Retinoid Expression in Onchocercal Skin Disease: Pilot Study
"Second, the common clinical features of onchocerciasis (eg,pruritus, musculoskeletal pain, bone changes, lethargy, and growth arrest in children) are similarly reported following excessive intakes of vitamin A or after prolonged treatment with retinoids. Hallmarks of onchocerciasis are severe visual impairment and skin DSM. Ocular reactions to prolonged use of systemic retinoid therapy likewise include corneal opacities, disorders of refraction, and alterations in retina and optic nerve. The manifestations of DSM (depigmentation) in onchocerciasis include areas of complete pigment loss (ie, vitiligo) with islands of normal skin pigment (“leopard skin”). Consistent with the hypothesis, mice homozygous for the vitiligo (Mitf-vit) mutation experience progressive degeneration of the retina as well as uneven pigmentation of the retinal pigment epithelium (RPE), associated with significantly increased retinyl ester concentrations in eyes and liver. Retinyl palmitate is increased 5-fold in the eyes of affected mice at 10 weeks postnatally and increased 3-fold at 22 weeks of age, whereas plasma retinol levels remain in the normal range. In the mutant RPE, retinyl ester levels are significantly elevated 4-fold by postnatal week 8. By 10 weeks of age, retinaldehyde dehydrogenase and RA are significantly elevated in the neural retina of Mitf-vit mice relative to controls. The suggestion that increased RA could contribute to the retinal degeneration of Mitf-vit mice by inducing apoptosis is supported by other observations indicating that retinoids can induce apoptosis. All-trans-RA also causes moderate to complete DSM (depigmentation) of Yucatan swine skin. The appearance of skin DSM (depigmentation) and severe visual impairment in these animals, in association with increased retinyl ester and RA concentrations in skin and eyes, suggests that similar processes may be occurring in onchocerciasis."
https://www.researchgate.net/publication/319941869_Retinoid_Expression_in_Onchocercal_Skin_Disease_Pilot_Study
Prostate Cancer in Mississippi: Epidemiology, risk factors, and prevention International Journal of Current Research
"One of the largest studies on the relationship between circulating retinol concentration and prostate cancer risk, based on a randomized, double-blind, placebo-controlled trial, reported a positive association between blood retinol level and the risk of prostate cancer. According to this study, the risk of both total and aggressive prostate cancer was increased by 20% in men with high circulating retinol levels.
https://www.researchgate.net/publication/365442121_Prostate_Cancer_in_Mississippi_Epidemiology_risk_factors_and_prevention_International_Journal_of_Current_Research_Sep_30_2022
Liver Damage and Exposure to Toxic Concentrations of Endogenous Retinoids in the Pathogenesis of COVID-19 Disease: Hypothesis
"Review of the literature reveals that COVID-19 disease closely resembles an endogenous form of hypervitaminosis A. We propose that SARS-CoV-2 virus-induced liver damage causes retinoic acid and stored retinyl esters to be released into the circulation in toxic concentrations, unbound to protein, with resulting damage to organs including the lungs, heart, blood vessels, and skin. Several lines of evidence support this model of disease causation. Subject to testing, strategies for the effective treatment and prevention of COVID-19 could include targeting the action and accumulation of retinoids."
https://www.researchgate.net/publication/351569124_Liver_Damage_and_Exposure_to_Toxic_Concentrations_of_Endogenous_Retinoids_in_the_Pathogenesis_of_COVID-19_Disease_Hypothesis
Rubella Virus Infection, the Congenital Rubella Syndrome, and the Link to Autism
"Evidence is reviewed here suggesting that the signs and symptoms of rubella may be due to alterations in the hepatic metabolism of vitamin A (retinoids), precipitated by the acute phase of the infection. The infection causes mild liver dysfunction and the spillage of stored vitamin A compounds into the circulation, resulting in an endogenous form of hypervitaminosis A. Given that vitamin A is a known teratogen, it is suggested that rubella infection occurring in the early weeks of pregnancy causes CRS through maternal liver dysfunction and exposure of the developing fetus to excessive vitamin A. On this view, the multiple manifestations of CRS and associated autism represent endogenous forms of hypervitaminosis A. It is further proposed that regressive autism results primarily from post-natal influences of a liver-damaging nature and exposure to excess vitamin A, inducing CRS-like features as a function of vitamin A toxicity, but without the associated dysmorphogenesis.
...vitamin A can be very toxic if released into the circulation unbound to protein, i.e., as retinyl esters (REs) rather than as RBP. Retinoid toxicity can occur due to excessive dietary intake, supplements, and vitamin A medications. Vitamin A intake only marginally above the recommended amount is associated with embryopathy, reduced bone mineral density in the neonate, and increased risk for hip fracture. REs destroy cell membranes and are a major source of vitamin A toxicity. Retinoid toxicity can also occur in cholestatic liver disease due to the spillage of RA into the circulation in bile and the leakage of REs into the circulation from damaged hepatocytes.
https://www.researchgate.net/publication/335978779_Rubella_Virus_Infection_the_Congenital_Rubella_Syndrome_and_the_Link_to_Autism
Gulf War Illness: Unifying Hypothesis for a Continuing Health Problem
"The features of GWI also overlap with those of fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity, in all of which liver dysfunction has been documented, suggesting a unifying hypothesis. It is proposed that multiple vaccinations, with concurrent or subsequent exposure to PB or additional chemical insults of a liver-damaging nature, plausibly explain the pathogenesis and the observed chronicity of GWI. The suggested mechanism for GWI is thus a chemically-induced impaired liver function, with the spillage of stored vitamin A compounds (“retinoids”) into the circulation in toxic concentrations, resulting in an endogenous chronic form of hypervitaminosis A."
Anthony Mawson created a patent for diagnosing gestational diabetes, preeclampsia, and fetal growth restriction using a blood sample to identify and measure the concentrations of retinol (vitamin A alcohol), retinyl esters and retinoic acid.
"Given that an accepted standard of hypervitaminosis A is percentage of retinyl esters >10%, the increased level found in this experiment (23.96% vs. 11.25% in the controls) supports the hypothesis that preeclampsia, gestational diabetes and FGR are expressions of an endogenous form of retinoid toxicity associated with impaired liver function, as indicated by increased liver enzymes. The model suggests that reducing liver and/or circulating levels of retinyl esters and retinoic acid could prevent and reverse these pregnancy-related conditions as well as FGR.
The results thus support the hypothesis that STZ induces hepatic dysfunction which in turn initiates the sequence of adverse events leading to GDM-PREEC-FGR and SGA via alterations in retinoid metabolism and exposure to toxic retinoid compounds released into the maternal and fetal circulation from the cholestatic liver. "
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis (SJS/TEN): Could Retinoids Play a Causative Role?
"This paper reviews evidence suggesting that the different medications implicated in SJS/TEN have the common property of interacting and synergizing with endogenous retinoids (vitamin A and its congeners), in many instances causing the latter to accumulate in and damage the liver, the main storage organ for vitamin A. It is hypothesized that liver damage leads to the spillage of toxic retinoid compounds into the circulation, resulting in an endogenous form of hypervitaminosis A and cytotoxicity with widespread apoptosis, mediated by granulysin and recognized as SJS/TEN. Subject to testing, the model suggests that symptom worsening could be arrested at onset by lowering the concentration of circulating retinoids and/or granulysin via phlebotomy or plasmapheresis or by pharmacological measures to limit their expression."
Another Anthony Mawson paper on brain tumors:
"The use of retinoids (vitamin A and its congeners) in the treatment of certain tumors was originally based on the assumption that these conditions were associated with an underlying deficiency of vitamin A and that supplementation with pharmacological doses would correct the deficiency. Yet the results of retinoid treatment have been only modestly beneficial and usually short-lived. Studies also indicate that vitamin A excess and supplementation have pro-oxidant effects and are associated with increased risks of mortality from cancer and other diseases."
Serum retinol concentrations (normally 1–3 μmol/L) do not reflect hepatic vitamin A concentrations over a wide range of liver values,since the secreted RBP is under homeostatic control. Similarly, serum retinol concentrations vary little despite major alterations in vitamin A intake. Case reports of hypervitaminosis A often show serum retinol concentrations within normal limits, indicating that serum retinol is not a valid measure of vitamin A status during toxicity (Olson, 2001)."
Possible role of endogenous retinoid (Vitamin A) toxicity in the pathophysiology of primary biliary cirrhosis
In conjunction with high liver levels of retinoids, plasma retinol-binding protein and serum retinol levels are decreased in PBC (Moore, 1957; Kaplan et al., 1988). These decreased serum levels in the face of high liver levels of retinoids are not due to malabsorption or retinoid deficiency but due to decreased mobilization of retinoids from the liver (Mezey, 1982). Decreased mobilization may be due in part to the known inhibitory effect of increased retinoic acid levels on the hepatic secretion of RBP (Keilson et al., 1979; Barua et al., 1997). The initial accumulation of vitamin A in the liver may be associated with a change in estrogen levels.
...since the great majority of patients are adult women, and the disease can present at any age, even during pregnancy, hyperestrogenemia with associated increased sensitivity may be a more likely scenario. The estrogen component of the oral contraceptive pill is either ethinyl estradiol or mestranol (which is demethylated to ethinyl estradiol) (Lundberg, 1992), and estradiol is a known cholestatic agent. PBC-prone persons may have an unusual sensitivity to estrogen, which may increase the potential for cholestasis (Myers et al., 1981) and possibly PBC. Women who develop cholestasis during pregnancy or with oral contraceptives, may likewise have an increased sensitivity to estrogen (Reyes, 1982)
Retinoid metabolites are also present in the bile and include retinoyl beta-glucuronide, retinoic acid, retinotaurine, and other unidentified metabolites of vitamin A (Frolik, 1984, pp.189}190; Olson, 1996). Similar to the pathway outlined above, our hypothesis proposes that the increased amounts of retinoids found in the liver in PBC also accumulate in the bile and cause local cytotoxic effects and are spilled into the circulation to cause some of the signs and symptoms seen in PBC.
Based on our hypothesis, elevated retinol esters and/or retinoic acid levels may cause some of these effects in PBC. Similarities with respect to the musculoskeletal system include arthritis, osteoporosis, bone pain and spontaneous fractures. Effects that are not similar include osteomalacia, which is found in only a small number of patients with PBC, and calcification of soft tissues, which is found in some patients with retinoid toxicity. Interestingly, two of the most common presenting symptoms of PBC are often quoted as side effects of retinoid toxicity: fatigue and pruritus. Other manifestations common to both conditions are keratoconjunctivitis sicca (dry eyes), xerostomia (dry mouth) and xanthomas (likely caused by the hyperlipidemia found in each condition). Retinoid intoxication is also associated with dry skin and alopecia which, however, are not seen typically in PBC. Splenomegaly and hepatomegaly are also found in both conditions as well as hepatic fibrosis and cirrhosis. The following features are common to end-stage liver disease associated with both conditions: portal hypertension, palmar erythema, spider angiomas, and ascites. Other symptoms that are found in retinoid toxicity but are not typically seen in PBC are muscle pain, increased cerebrospinal fluid pressure, and many neurologic symptoms associated with the latter, including headache, nausea, ataxia, confusion, irritability, weight loss, and anorexia.
If the model is correct, patients with PBC should have higher tissue concentrations of retinoids than controls, and a higher ratio of serum retinyl esters to retinol. Moreover, dietary retinoid restriction should prevent and/or ameliorate the disease.
https://pubmed.ncbi.nlm.nih.gov/10968936/
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Quote from Janelle525 on August 28, 2024, 11:46 amYou can find a ton of evidence that vitamin A is GOOD. Does that mean it is all factual information? Hardly. Science is so hijacked. You can manipulate findings easily. What is more interesting are papers revealing the HARM because those scientists are not going to get front page of any science journal.
I mean yeah clearly too much is bad doesn't mean we don't need it though, from doing the mineral balancing stuff it is clear to me that it is needed, just people aren't metabolising it correctly due to various factors or they do have actual toxicity in Vitamin A.