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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 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.
Quote 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.
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.
Quote 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.
Quote 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.
All the science and theories and big words in the world don't mean squat if people reduce their load of VA and feel better.
Quote 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.
Quote 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.
Quote 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.
Quote 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.
Quote from Janelle525 on July 3, 2025, 6:48 amI've been on a very low vit A diet for 1.5 yrs and low for 7 yrs. My serum retinol didn't start going down until I was on a very low vit A diet. And it's still at what they consider 'optimal'!!! I know this isn't a good measure of liver stores, I tend to think having some level of vitamin A in the bloodstream means the liver is able to utilize it. But I won't go back to eating liver. Haven't been sick in 2 yrs despite stress and lack of sleep. I do live in the south so that helps. And I beans 2-3 times a day. I think that's essential to get rid of fat soluble toxins.
I've been on a very low vit A diet for 1.5 yrs and low for 7 yrs. My serum retinol didn't start going down until I was on a very low vit A diet. And it's still at what they consider 'optimal'!!! I know this isn't a good measure of liver stores, I tend to think having some level of vitamin A in the bloodstream means the liver is able to utilize it. But I won't go back to eating liver. Haven't been sick in 2 yrs despite stress and lack of sleep. I do live in the south so that helps. And I beans 2-3 times a day. I think that's essential to get rid of fat soluble toxins.
Quote from Jiří on July 3, 2025, 7:07 am@janelle525 that's interesting having "optimal" vit A serum after almost a decade of low vit A diet.. I think it shows that you are not running critically low and you can keep going.. Can I ask you what was your diet during very low times and what you added now?
@lil-chick especially when you consider that vit A is eliminated mainly with bile not urine like in carnivore animals etc.. So with that in mind how many people have sluggish bile flow/gallbladder issues? Especially in older age? Like 50% of people and like mostly all females? I have no doubt that people will end up with excess rather than deficiency. Exactly the same case for copper and iron.. Basically beef liver loaded with vit A, iron and copper is the ultimate poison food for most older people.. It has exactly the stuff that gets deposited in their liver which is not surprising. It is liver after all LOL...
@janelle525 that's interesting having "optimal" vit A serum after almost a decade of low vit A diet.. I think it shows that you are not running critically low and you can keep going.. Can I ask you what was your diet during very low times and what you added now?
@lil-chick especially when you consider that vit A is eliminated mainly with bile not urine like in carnivore animals etc.. So with that in mind how many people have sluggish bile flow/gallbladder issues? Especially in older age? Like 50% of people and like mostly all females? I have no doubt that people will end up with excess rather than deficiency. Exactly the same case for copper and iron.. Basically beef liver loaded with vit A, iron and copper is the ultimate poison food for most older people.. It has exactly the stuff that gets deposited in their liver which is not surprising. It is liver after all LOL...
Quote from Janelle525 on July 3, 2025, 7:23 am@jiri
My diet during very low times is 10% fat ground beef or chicken breast, white rice, white pasta, black beans, olive oil. I did still eat tomatoes and chili spice at times because my husband likes chili. I have been more lenient lately, I will eat cheese whenever I'm craving it. I'm not super strict on junk food, I eat potato and tortilla chips from time to time.
My diet during very low times is 10% fat ground beef or chicken breast, white rice, white pasta, black beans, olive oil. I did still eat tomatoes and chili spice at times because my husband likes chili. I have been more lenient lately, I will eat cheese whenever I'm craving it. I'm not super strict on junk food, I eat potato and tortilla chips from time to time.
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)
Quote 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)
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.
@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.