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Extinguishing the theory of Vitamin-A toxicity in the west - Depletion of retinol levels as an immune response in infectious diseases and vaccination
Quote from Jiří on July 2, 2025, 1:15 am@tobias-2 so how much kilos of liver a day are you eating to not end up dying from severe vitamin A depletion lol.
I don't think I will start eating liver or any vit A bomb again. I can compare decade on vit A HEAVY diet and 8 years on very low vit A diet. Btw all those years on low vit A were during covid. I had it confirmed once with test..
Moderate amounts. I will continue eating liver, ca 100-200 grams a month. It's the best source for an almost complete list of essential nutrients 🙂
Quote from Tobias on July 2, 2025, 1:03 amIt's an interesting topic for sure. The newer studies suggest a rapid depletion and if you read the studies regarding the occurance of unatural vaccine triggered serum retinol release to the point of accute toxicity that then drains the level storage the image becomes clear. Especially regarding the amount of infections the last 5 years, and the amount of injections.
I don't see a convincing study in your article. You cited this Mawson paper:
Multiple Vaccinations and the Enigma of Vaccine Injury
You might be referring to this quote:
Vaccination may reproduce, to a normally minor extent, the pathogenesis of many infectious diseases, such as flu-like signs and symptoms. Based on our hypothesis, this involves a mild degree of activation of retinoid pathways and generally mild acute “side-effects” that are manifestations of hypervitaminosis A; injury due to vaccines involves retinoid overaction and/or accumulation, liver damage, and the spillage of higher amounts of stored retinoids into the circulation.
First of all, this is a HYPOTHESIS. There is no experimental data cited.
Second, its applicability is to hypervitaminosis A:
Our model suggests that susceptibility to vaccine injury is increased in persons with high background stores of vA in the liver; that is, such stores may increase the risk of tissue damage via activation of the retinoid cascade within the liver.
They are talking about people with vitamin A overload, not deficient people.
Also, again, this is just a model. It's a guess, not an experiment.
Quote from whatisaging on July 2, 2025, 2:06 amQuote from Tobias on July 2, 2025, 1:03 amIt's an interesting topic for sure. The newer studies suggest a rapid depletion and if you read the studies regarding the occurance of unatural vaccine triggered serum retinol release to the point of accute toxicity that then drains the level storage the image becomes clear. Especially regarding the amount of infections the last 5 years, and the amount of injections.
I don't see a convincing study in your article. You cited this Mawson paper:
Multiple Vaccinations and the Enigma of Vaccine Injury
You might be referring to this quote:
Vaccination may reproduce, to a normally minor extent, the pathogenesis of many infectious diseases, such as flu-like signs and symptoms. Based on our hypothesis, this involves a mild degree of activation of retinoid pathways and generally mild acute “side-effects” that are manifestations of hypervitaminosis A; injury due to vaccines involves retinoid overaction and/or accumulation, liver damage, and the spillage of higher amounts of stored retinoids into the circulation.
First of all, this is a HYPOTHESIS. There is no experimental data cited.
Second, its applicability is to hypervitaminosis A:
Our model suggests that susceptibility to vaccine injury is increased in persons with high background stores of vA in the liver; that is, such stores may increase the risk of tissue damage via activation of the retinoid cascade within the liver.
They are talking about people with vitamin A overload, not deficient people.
Also, again, this is just a model. It's a guess, not an experiment.
"Second, its applicability is to hypervitaminosis A:
Our model suggests that susceptibility to vaccine injury is increased in persons with high background stores of vA in the liver; that is, such stores may increase the risk of tissue damage via activation of the retinoid cascade within the liver.
They are talking about people with vitamin A overload, not deficient people."
High background stores (not overload) - But this becomes semi-important if the reaction leads to vA deficiancy though-.
Quote from Tobias on July 2, 2025, 2:29 amHigh background stores (not overload) - But this becomes semi-important if the reaction leads to vA deficiancy though-.
There is simply no evidence that this hypothesized spillage of high stores leads to a liver deficiency. They don't even speculate on this happening.
High background stores are the entire context for this hypothesis. It's like tilting a cup which is full: it spills easily. If the cup is only half full, the tilt won't spill as much, or any, if it's low enough.
Our model suggests that susceptibility to vaccine injury is increased in persons with high background stores of vA in the liver; that is, such stores may increase the risk of tissue damage via activation of the retinoid cascade within the liver. [...] Based on this model, retinoid-induced liver damage related to multiple vaccinations leads to a transient form of cholestatic liver dysfunction in which stored retinoids enter the circulation, causing a broad range of adverse effects as manifestations of vA toxicity.
I also think you're underestimating how much vitamin A the blood can handle. In their hypothetical scenario, they assume the inability to produce retinol binding protein, so the dumped retinol would also be unbound and toxic. If all that liver's vitamin A went into the blood, we would be dead for sure.
These observations led us to propose that exposure to multiple vaccinations, possibly with additional chemical insults of a liver-damaging nature, plausibly explains GWI and its observed chronicity [52]. Based on this hypothesis, the suggested pathogenesis is a chemically induced impaired liver function involving activation of the retinoid cascade in the liver. This inhibits the secretion of retinol-binding protein 4 (RBP4), thereby lowering serum retinol concentrations, but simultaneously increases the accumulation and expression of retinoids in the liver, leading to apoptotic hepatocellular damage and the entry of retinyl esters and retinoic acid into the circulation in toxic concentrations. The result is an endogenous chronic form of hypervitaminosis A.
Quote from whatisaging on July 2, 2025, 2:58 am
Quote from Tobias on July 2, 2025, 2:29 amHigh background stores (not overload) - But this becomes semi-important if the reaction leads to vA deficiancy though-.
There is simply no evidence that this hypothesized spillage of high stores leads to a liver deficiency. They don't even speculate on this happening.
High background stores are the entire context for this hypothesis. It's like tilting a cup which is full: it spills easily. If the cup is only half full, the tilt won't spill as much, or any, if it's low enough.
Our model suggests that susceptibility to vaccine injury is increased in persons with high background stores of vA in the liver; that is, such stores may increase the risk of tissue damage via activation of the retinoid cascade within the liver. [...] Based on this model, retinoid-induced liver damage related to multiple vaccinations leads to a transient form of cholestatic liver dysfunction in which stored retinoids enter the circulation, causing a broad range of adverse effects as manifestations of vA toxicity.
I also think you're underestimating how much vitamin A the blood can handle. In their hypothetical scenario, they assume the inability to produce retinol binding protein, so the dumped retinol would also be unbound and toxic. If all that liver's vitamin A went into the blood, we would be dead for sure.
These observations led us to propose that exposure to multiple vaccinations, possibly with additional chemical insults of a liver-damaging nature, plausibly explains GWI and its observed chronicity [52]. Based on this hypothesis, the suggested pathogenesis is a chemically induced impaired liver function involving activation of the retinoid cascade in the liver. This inhibits the secretion of retinol-binding protein 4 (RBP4), thereby lowering serum retinol concentrations, but simultaneously increases the accumulation and expression of retinoids in the liver, leading to apoptotic hepatocellular damage and the entry of retinyl esters and retinoic acid into the circulation in toxic concentrations. The result is an endogenous chronic form of hypervitaminosis A.
You have to look at the broader picture, the one I explain in the article.
"The large amount of viral RNA and consequent overwhelming immune stimulation will cause increased RA consumption, and with the time, depletion of retinol reserves in the body [20], [21]. " https://www.sciencedirect.com/science/article/pii/S0898656821002102?via%3Dihub
It is a combination of accute toxicity due to unatural triggers because of vaccines that trigger multiple infections (spike proteins) ultimately depleting the retinol reserves that lead to deficiancy.
We know that retinol is used to fight infections, the vaccines disrupts the retinoid singaling causing cytokain storms that leads to Toxicity, but not chronic. As multiple infections caused by the cytokain storms i.e the immunesystem attacking the body cells leads to a depletion.
When breaking this down you have to take all the information - in the different studies into consideration.
This raises the question of vaccines being the number 1 culprit - not Vitamin A
There is overwhelming evidence that vaccines distrupts the retinoic acid signaling pathways causing toxicity that lead to autoimmune disease.
"The distribution of retinoid receptor proteins in the adult nervous system is different from that seen during development. and suggests that retinoid signaling likely has a physiological role in the adult cortex, amygdala, hypothalamus, hippocampus, striatum, and associated brain regions. A number of neuronal specific genes contain recognition sequences for the retinoid receptor proteins and can be regulated directly by retinoids. Disruption of retinoid signaling pathways in rodent models indicates their involvement in the regulation of synaptic plasticity and associated learning and memory behaviors. Retinoid signaling pathways have also been implicated in the pathophysiology of Alzheimer's disease, schizophrenia, and depression. "
Role of retinoid signalling in the adult brain https://pubmed.ncbi.nlm.nih.gov/15882777/
And the the childhood vaccines are to blame for a dysfunctional signaling system in children - not vitamin a
I’m unclear how you have gone from the release of retinyl esters from the liver, creating retinoids overabundance in the blood, a toxic effect in the cells , depletion of stores to ‘retinoid deficiency’.
Why would you need more of something that is toxic to your cells? Can you please explain why more is better? Are you saying that we need more vitamin a / retinoids to fight the disease? Even if that was the case, we don’t take eg 100 paracetamols/ 100 cups of lemon and ginger when we get a pain. I may be misunderstanding the argument so it would be great if you could explain further. Thank you
I make it clear in the article and in the posts above discussing with whatisaging.