I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
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 grapes on July 3, 2025, 8:28 am@tobias-2 why coming here with a theory which contradicts the purpose of the discussion board? Your views on vitamin A seem to be mainstream, so you'd probably would have found more support any other place than here. Have you tried that?
In my opinion your "science" arguments don't look convincing at all. I could believe that some stored retinol could be used to fight infections, but that would not cause a widespread deficiency. And if vaccine injury were to be linked to retinol, that would rather be from releasing too much and thus causing harm by itself, not from provoking deficiency.
Did you not catch the part about vaccines distrupting the retonic acid signaling systems? - This could indeed cause a widespread deficiency. This is the main thesis in the article and it seems to me you didn't read it properly - the first response is a release cascade which overloads the system causing hypervitaminosis A - then comes the retinol depletion. It is all explained in the article.
Quote from Tobias on July 3, 2025, 3:42 amQuote from whatisaging on July 2, 2025, 11:58 amQuote from Tobias on July 2, 2025, 3:21 amYou 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.
Once again, I don't see any evidence. The paper you cite is another opinion piece:
A novel HYPOTHESIS for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder
The full texts of references [20] and [21] don't even contain the word retinol! How is this evidence of retinol depletion?
Here are reference [20] and [21]'s abstracts. They are biochemistry papers which study retinoic acid pathways. They are not papers which demonstrate retinol depletion.
[20]: Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs) constitute distinct families of pattern-recognition receptors that sense nucleic acids derived from viruses and trigger antiviral innate immune responses. TLR3, TLR7, and TLR9 are membrane proteins localized to the endosome that recognize viral double-stranded RNA, single-stranded RNA, and DNA, respectively, while RLRs, including RIG-I, Mda5, and LGP2, are cytoplasmic proteins that recognize viral RNA. Upon recognition of these nucleic acid species, TLRs and RLRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in activation of NF-κB, MAP kinases, and IRFs that control the transcription of genes encoding type I interferon and other inflammatory cytokines, which are important for eliminating viruses. Here, we review recent insights into the signaling pathways initiated by TLR and RLR and their roles in innate and adaptive immune responses.
[21]: Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns via pattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulated via various posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus–host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.
If you're using AI to find literature, that's fine, but you need to actually read the papers. AI hallucinates.
There you go they explain why retinol depletion happens right there (20,21)
"Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade..."
It's distrupting the signaling system, releasing the storages. I am confident the authors of the paper know what they are talkIing about, in their own words:
"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"
I cited another paper because you have to look at it from a broader perspective - all the information I gathered. Which I told you.
If you want to put effort in debunking my article, you have to debunk the science in which I'm refering to.
Thank you.
Are you trolling? You can literally read my analysis of this opinion piece's sentence in your quote. You deleted its references to [20] and [21]. I already showed these have no evidence of retinol depletion, they are just biochemical studies. They don't even contain the word retinol.
I can't believe you are doubling on down this opinion piece nonsense instead of putting in the work to look for a decent reference.
Quote from Tobias on July 3, 2025, 4:04 amQuote from whatisaging on July 2, 2025, 11:58 amQuote from Tobias on July 2, 2025, 3:21 amYou 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.
Once again, I don't see any evidence. The paper you cite is another opinion piece:
A novel HYPOTHESIS for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder
The full texts of references [20] and [21] don't even contain the word retinol! How is this evidence of retinol depletion?
Here are reference [20] and [21]'s abstracts. They are biochemistry papers which study retinoic acid pathways. They are not papers which demonstrate retinol depletion.
[20]: Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs) constitute distinct families of pattern-recognition receptors that sense nucleic acids derived from viruses and trigger antiviral innate immune responses. TLR3, TLR7, and TLR9 are membrane proteins localized to the endosome that recognize viral double-stranded RNA, single-stranded RNA, and DNA, respectively, while RLRs, including RIG-I, Mda5, and LGP2, are cytoplasmic proteins that recognize viral RNA. Upon recognition of these nucleic acid species, TLRs and RLRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in activation of NF-κB, MAP kinases, and IRFs that control the transcription of genes encoding type I interferon and other inflammatory cytokines, which are important for eliminating viruses. Here, we review recent insights into the signaling pathways initiated by TLR and RLR and their roles in innate and adaptive immune responses.
[21]: Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns via pattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulated via various posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus–host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.
If you're using AI to find literature, that's fine, but you need to actually read the papers. AI hallucinates.
There you go they explain why retinol depletion happens right there (20,21)
"Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade..."
It's distrupting the signaling system, releasing the storages. I am confident the authors of the paper know what they are talkIing about, in their own words:
"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"
I cited another paper because you have to look at it from a broader perspective - all the information I gathered. Which I told you.
If you want to put effort in debunking my article, you have to debunk the science in which I'm refering to. The reference to retinol depletion is linked in my article. I don't know what you are talking about mate. But it seems you got it mixed up.
I got it mixed up, huh? You've got me laughing, so maybe this is just trolling.
Quote from Tobias on July 3, 2025, 8:21 amQuote from lil chick on July 3, 2025, 5:26 amQuote from Tobias on July 3, 2025, 4:47 amQuote from lil chick on July 3, 2025, 4:23 amAll the science and theories and big words in the world don't mean squat if people reduce their load of VA and feel better.
You are right. We're different. Some have overload, others have deficiency.
However, that doesn't justify attacking the messenger because of cognitive dissonance.
Gosh I'm sorry if my word choices made you feel attacked. It was not my intent. Your topic title actually is pretty darn aggressive haha.
The question of whether VA has real usages is one that worries me, but I have no doubt that VA overload is a real thing, and that most people, by the time they are older, are experiencing some of it. When young people get diseases of old age, or anyone gets mysterious diseases that respond to nothing else... they might want to consider it.
There are plenty of nutrients that get overloaded when ingested to excess. No one argues that people become iron-overloaded, for instance. Yet we need iron.
I was refering to whatisaging (Y)
I'm attacking the messenger now? What a joke. You're claiming that opinion pieces with insufficient references constitute scientific evidence of retinol depletion, and are now doubling down.
Quote from Tobias on July 3, 2025, 9:38 am
Did you not catch the part about vaccines distrupting the retonic acid signaling systems? - This could indeed cause a widespread deficiency. This is the main thesis in the article and it seems to me you didn't read it properly - the first response is a release cascade which overloads the system causing hypervitaminosis A - then comes the retinol depletion. It is all explained in the article.
I'm not sure I believe in the existence of "retinoic acid signalling system", used for anything other than retinoids metabolism. A body using a toxic molecule for signalling seems like a logical fallacy. I might be wrong on that.
So we kind of agree on the first part - temporary toxicity after releasing too much of retinol, but not on the second part - induced deficiency causing harm.
@grapes When I compare my high vit A days and "deficient" days(because after 8 years of no high or even moderate vit A foods I have to be deficient in eyes of mainstream medical system) I will pick "deficiency" every day of the week. 😀
Quote from whatisaging on July 3, 2025, 9:58 amQuote from Tobias on July 3, 2025, 3:42 amQuote from whatisaging on July 2, 2025, 11:58 amQuote from Tobias on July 2, 2025, 3:21 amYou 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.
Once again, I don't see any evidence. The paper you cite is another opinion piece:
A novel HYPOTHESIS for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder
The full texts of references [20] and [21] don't even contain the word retinol! How is this evidence of retinol depletion?
Here are reference [20] and [21]'s abstracts. They are biochemistry papers which study retinoic acid pathways. They are not papers which demonstrate retinol depletion.
[20]: Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs) constitute distinct families of pattern-recognition receptors that sense nucleic acids derived from viruses and trigger antiviral innate immune responses. TLR3, TLR7, and TLR9 are membrane proteins localized to the endosome that recognize viral double-stranded RNA, single-stranded RNA, and DNA, respectively, while RLRs, including RIG-I, Mda5, and LGP2, are cytoplasmic proteins that recognize viral RNA. Upon recognition of these nucleic acid species, TLRs and RLRs recruit specific intracellular adaptor proteins to initiate signaling pathways culminating in activation of NF-κB, MAP kinases, and IRFs that control the transcription of genes encoding type I interferon and other inflammatory cytokines, which are important for eliminating viruses. Here, we review recent insights into the signaling pathways initiated by TLR and RLR and their roles in innate and adaptive immune responses.
[21]: Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patterns via pattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulated via various posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus–host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.
If you're using AI to find literature, that's fine, but you need to actually read the papers. AI hallucinates.
There you go they explain why retinol depletion happens right there (20,21)
"Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade..."
It's distrupting the signaling system, releasing the storages. I am confident the authors of the paper know what they are talkIing about, in their own words:
"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"
I cited another paper because you have to look at it from a broader perspective - all the information I gathered. Which I told you.
If you want to put effort in debunking my article, you have to debunk the science in which I'm refering to.
Thank you.
"Are you trolling? You can literally read my analysis of this opinion piece's sentence in your quote. You deleted its references to [20] and [21]. I already showed these have no evidence of retinol depletion, they are just biochemical studies. They don't even contain the word retinol."
You're not just understanding what the reference actually says. I explained it. They are explaining the mechanisms causing a signaling cascade. You have to read it again.-
There you go they explain why retinol depletion happens right there (20,21)
"Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade..."
It's distrupting the signaling system, releasing the storages. I am confident the authors of the paper know what they are talkIing about, in their own words:
"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"
I cited another paper because you have to look at it from a broader perspective - all the information I gathered. Which I told you.
If you want to put effort in debunking my article, you have to debunk the science in which I'm refering to.
Thank you.
Are you trolling? You can literally read my analysis of this opinion piece's sentence in your quote. You deleted its references to [20] and [21]. I already showed these have no evidence of retinol depletion, they are just biochemical studies. They don't even contain the word retinol.
I can't believe you are doubling on down this opinion piece nonsense instead of putting in the work to look for a decent reference.
"Are you trolling? You can literally read my analysis of this opinion piece's sentence in your quote. You deleted its references to [20] and [21]. I already showed these have no evidence of retinol depletion, they are just biochemical studies. They don't even contain the word retinol."
You're not just understanding what the reference actually says. I explained it. They are explaining the mechanisms causing a signaling cascade. You have to read it again.-
Quote from Tobias on July 4, 2025, 12:46 am
There you go they explain why retinol depletion happens right there (20,21)
"Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade..."
It's distrupting the signaling system, releasing the storages. I am confident the authors of the paper know what they are talkIing about, in their own words:
"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"
I cited another paper because you have to look at it from a broader perspective - all the information I gathered. Which I told you.
If you want to put effort in debunking my article, you have to debunk the science in which I'm refering to.
Thank you.
Are you trolling? You can literally read my analysis of this opinion piece's sentence in your quote. You deleted its references to [20] and [21]. I already showed these have no evidence of retinol depletion, they are just biochemical studies. They don't even contain the word retinol.
I can't believe you are doubling on down this opinion piece nonsense instead of putting in the work to look for a decent reference.
"Are you trolling? You can literally read my analysis of this opinion piece's sentence in your quote. You deleted its references to [20] and [21]. I already showed these have no evidence of retinol depletion, they are just biochemical studies. They don't even contain the word retinol."
You're not just understanding what the reference actually says. I explained it. They are explaining the mechanisms causing a signaling cascade. You have to read it again.-
You are not understanding the problem. An explanation of a mechanism is not evidence that it caused retinol depletion in real life people.
I just had a discussion with my husband about how the linen storage under the eaves is musty and that I can't store linens there. He told me how theoretically it should not be a musty area. But all the theories in the world don't matter if then linens get musty there.
I love to theorize and my favorite question is WHY? But models are only as good as their ability to predict real life.