InChristAlone
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Anthony Mawson PhD, president of Chalfont Research Institute is doing some good research on vitamin A:
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]"
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."
...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.
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."
https://www.researchgate.net/public...ng_Hypothesis_for_a_Continuing_Health_Problem
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]"
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. "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."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.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."
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.
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."
https://www.researchgate.net/public...ng_Hypothesis_for_a_Continuing_Health_Problem
