InChristAlone
Member
I wanted to share some really great quotes from this paper:
Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective
There is so much juicy info in this article I encourage everyone interested in learning about vitamin A and D to read it! I think this has many implications for avoiding viral disease especially for those who don't supplement vitamin D and live in the North, or even live in the South and have a desk job as lack of UV exposure is a risk factor for influenza. As an anecdote I moved to the South last yr where we get almost yr round vitamin D and this past winter no one in my family got sick. It does take making beach trips a priority even when it's not swimming weather. For those in the North I would recommend limiting vitamin A in the winter months or whenever you feel that you are getting colds/flu more often, but this paper does not make recommendations so as always perceive, think, act.
"This paper presents a new model of the etiopathogenesis of influenza, suggesting that host resistance and susceptibility to the disease depend importantly on the ratio of vitamin D to vitamin A; reduced exposure to sunlight and/or preexisting vitamin D deficiency simultaneously increase the accumulation, expression, and potential toxicity of endogenous retinoids, and the decreased vitamin D to vitamin A ratio triggers viral activation or increases susceptibility to novel strains of influenza virus. It is suggested that increased but normal physiological concentrations of retinoid effectively inhibit influenza pathogenesis whereas higher background concentrations (i.e., very low vitamin D : A ratios) worsen it and induce the severe complications of the disease."
"The symptoms of influenza are similar to those of retinoid toxicity; supplementary and/or pharmacological concentrations of retinoids induce influenza-like symptoms; viral activity is regulated in part by retinoids; and retinoids influence the mechanisms that both inhibit and contribute to influenza pathogenesis."
"Low concentrations of retinoic acid are essential growth factors for certain types of cells, but higher concentrations inhibit cell growth and are cytotoxic, mutagenic, and teratogenic. Exogenous vitamin A toxicity can occur due to excessive dietary consumption or from treatment with retinoids. Although vitamin A toxicity from provitamin A plant carotenoid sources has never been reported, the absorption and hepatic storage of preformed vitamin A from animal foods, fortified foods, and supplements in the form of retinyl esters can result in hypervitaminosis A. An endogenous form of retinoid intoxication can also occur naturally during cholestasis, when vitamin A metabolites are refluxed into the circulation from the liver in bile acids [75]. A variety of environmental factors can interact with endogenous sources of vitamin A to induce localized forms of retinoid toxicity or overexpression, as reviewed in this paper."
"An acute increase in the concentration of other retinoids, for example, retinoic acid, a 40-fold more potent teratogen than retinol [77] occurs after ingesting a large amount of vitamin A."
"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."
"A high intake of retinol also completely abolished the protective effect of vitamin D on distal colorectal adenoma, women in the highest quintile of vitamin D intake ingested about 10,000 IU/day of retinol, and there was a strong correlation overall between dietary intakes of vitamins A and D."
"Thus, rising temperatures and greater sunlight in the summer months could catabolize tissue concentrations of vitamin A to such a degree that it would prevent influenza viruses from making use of it to replicate. Conversely, the seasonal increase in influenza during the winter months may occur partly from the fact that vitamin A remains available for the virus to replicate in cooler temperatures."
"In an unusual case report, the symptoms of influenza A infection were described as being perfectly mimicked by the retinoic acid syndrome."
"Headache, a common symptom of influenza [117], is also a major feature of retinoid toxicity [118]. Conjunctivitis and photophobia are also common during acute seasonal influenza infection, especially in avian influenza A infections in humans [119]. An oculorespiratory syndrome (ORS) consisting of red eyes, photophobia, blurred vision, palpebral edema, ocular pain and itching, and conjunctival secretions is reported after influenza vaccination [120]. A similar pattern of ocular side effects has been described in diet-induced hypervitaminosis A and secondary to isotretinoin use."
"Vitamin A supplementation has not been shown to improve recovery during acute pneumonia in most human clinical trials. In a double-blind, placebo-controlled trial of vitamin A supplementation on childhood morbidity in Haiti, 11,124 children ages 6–83 months were sequentially assigned by household units to receive either a capsule containing 200,000 IU of vitamin A and 40.6 mg vitamin E or a capsule containing only 40.6 mg vitamin E (placebo) every 4 months. Indicators of childhood morbidity were studied 2–8 weeks after each administration of vitamin A and placebo capsules. At 2 weeks after supplementation the vitamin A group had an increased prevalence of all symptoms and signs of childhood morbidity, including diarrhea, rhinitis, cold/flu symptoms, cough, and rapid breathing. The risk of morbidity was highest 8–17 weeks after receiving the megadose of vitamin A. The study showed an increased 2-week prevalence of diarrhoea and the symptoms of respiratory infections after vitamin A supplementation, although mortality rates of the 2 groups were similar [123]. A meta-analysis of vitamin A supplementation trials concluded that when given alone, vitamin A slightly increased the incidence of respiratory tract infections [124]."
"Production of RA during EBV infection may enhance viral replication by promoting keratinocyte differentiation."
"It is suggested that influenza-induced liver involvement worsens the outcome of infection via the hepatic release of unbound retinyl esters and retinoic acids which are transported to and damage the lung as well as other organs, thereby contributing to the development of pneumonia, heart and kidney failure, and sepsis."
"Given the toxicity of retinoids and the fact that retinoid stores in the liver are sufficient to last the average adult for about two years [79], the presumably high quantity of retinoids spilled into the circulation in cholestatic conditions, including influenza, has the potential to cause considerable tissue damage.
(4) The mechanisms of tissue damage following the release of retinoids from the liver in influenza infection also could be due to the hepatic release of the enzyme xanthine oxidase (XO), which affects vitamin A metabolism."
"Reduced but not necessarily deficient background retinoid concentrations (i.e., a high vitamin D : A ratio) could have the opposite effect of reducing disease susceptibility, lowering disease severity, and improving disease outcomes. These hypotheses have implications for the prevention and treatment of influenza virus infections."
"Retinoid receptor overexpression may thus contribute to the pathogenesis of influenza and related viral infections, causing an endogenous form of hypervitaminosis A that manifests itself in the symptoms of the disease."
Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective
There is so much juicy info in this article I encourage everyone interested in learning about vitamin A and D to read it! I think this has many implications for avoiding viral disease especially for those who don't supplement vitamin D and live in the North, or even live in the South and have a desk job as lack of UV exposure is a risk factor for influenza. As an anecdote I moved to the South last yr where we get almost yr round vitamin D and this past winter no one in my family got sick. It does take making beach trips a priority even when it's not swimming weather. For those in the North I would recommend limiting vitamin A in the winter months or whenever you feel that you are getting colds/flu more often, but this paper does not make recommendations so as always perceive, think, act.
"This paper presents a new model of the etiopathogenesis of influenza, suggesting that host resistance and susceptibility to the disease depend importantly on the ratio of vitamin D to vitamin A; reduced exposure to sunlight and/or preexisting vitamin D deficiency simultaneously increase the accumulation, expression, and potential toxicity of endogenous retinoids, and the decreased vitamin D to vitamin A ratio triggers viral activation or increases susceptibility to novel strains of influenza virus. It is suggested that increased but normal physiological concentrations of retinoid effectively inhibit influenza pathogenesis whereas higher background concentrations (i.e., very low vitamin D : A ratios) worsen it and induce the severe complications of the disease."
"The symptoms of influenza are similar to those of retinoid toxicity; supplementary and/or pharmacological concentrations of retinoids induce influenza-like symptoms; viral activity is regulated in part by retinoids; and retinoids influence the mechanisms that both inhibit and contribute to influenza pathogenesis."
"Low concentrations of retinoic acid are essential growth factors for certain types of cells, but higher concentrations inhibit cell growth and are cytotoxic, mutagenic, and teratogenic. Exogenous vitamin A toxicity can occur due to excessive dietary consumption or from treatment with retinoids. Although vitamin A toxicity from provitamin A plant carotenoid sources has never been reported, the absorption and hepatic storage of preformed vitamin A from animal foods, fortified foods, and supplements in the form of retinyl esters can result in hypervitaminosis A. An endogenous form of retinoid intoxication can also occur naturally during cholestasis, when vitamin A metabolites are refluxed into the circulation from the liver in bile acids [75]. A variety of environmental factors can interact with endogenous sources of vitamin A to induce localized forms of retinoid toxicity or overexpression, as reviewed in this paper."
"An acute increase in the concentration of other retinoids, for example, retinoic acid, a 40-fold more potent teratogen than retinol [77] occurs after ingesting a large amount of vitamin A."
"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."
"A high intake of retinol also completely abolished the protective effect of vitamin D on distal colorectal adenoma, women in the highest quintile of vitamin D intake ingested about 10,000 IU/day of retinol, and there was a strong correlation overall between dietary intakes of vitamins A and D."
"Thus, rising temperatures and greater sunlight in the summer months could catabolize tissue concentrations of vitamin A to such a degree that it would prevent influenza viruses from making use of it to replicate. Conversely, the seasonal increase in influenza during the winter months may occur partly from the fact that vitamin A remains available for the virus to replicate in cooler temperatures."
"In an unusual case report, the symptoms of influenza A infection were described as being perfectly mimicked by the retinoic acid syndrome."
"Headache, a common symptom of influenza [117], is also a major feature of retinoid toxicity [118]. Conjunctivitis and photophobia are also common during acute seasonal influenza infection, especially in avian influenza A infections in humans [119]. An oculorespiratory syndrome (ORS) consisting of red eyes, photophobia, blurred vision, palpebral edema, ocular pain and itching, and conjunctival secretions is reported after influenza vaccination [120]. A similar pattern of ocular side effects has been described in diet-induced hypervitaminosis A and secondary to isotretinoin use."
"Vitamin A supplementation has not been shown to improve recovery during acute pneumonia in most human clinical trials. In a double-blind, placebo-controlled trial of vitamin A supplementation on childhood morbidity in Haiti, 11,124 children ages 6–83 months were sequentially assigned by household units to receive either a capsule containing 200,000 IU of vitamin A and 40.6 mg vitamin E or a capsule containing only 40.6 mg vitamin E (placebo) every 4 months. Indicators of childhood morbidity were studied 2–8 weeks after each administration of vitamin A and placebo capsules. At 2 weeks after supplementation the vitamin A group had an increased prevalence of all symptoms and signs of childhood morbidity, including diarrhea, rhinitis, cold/flu symptoms, cough, and rapid breathing. The risk of morbidity was highest 8–17 weeks after receiving the megadose of vitamin A. The study showed an increased 2-week prevalence of diarrhoea and the symptoms of respiratory infections after vitamin A supplementation, although mortality rates of the 2 groups were similar [123]. A meta-analysis of vitamin A supplementation trials concluded that when given alone, vitamin A slightly increased the incidence of respiratory tract infections [124]."
"Production of RA during EBV infection may enhance viral replication by promoting keratinocyte differentiation."
"It is suggested that influenza-induced liver involvement worsens the outcome of infection via the hepatic release of unbound retinyl esters and retinoic acids which are transported to and damage the lung as well as other organs, thereby contributing to the development of pneumonia, heart and kidney failure, and sepsis."
"Given the toxicity of retinoids and the fact that retinoid stores in the liver are sufficient to last the average adult for about two years [79], the presumably high quantity of retinoids spilled into the circulation in cholestatic conditions, including influenza, has the potential to cause considerable tissue damage.
(4) The mechanisms of tissue damage following the release of retinoids from the liver in influenza infection also could be due to the hepatic release of the enzyme xanthine oxidase (XO), which affects vitamin A metabolism."
"Reduced but not necessarily deficient background retinoid concentrations (i.e., a high vitamin D : A ratio) could have the opposite effect of reducing disease susceptibility, lowering disease severity, and improving disease outcomes. These hypotheses have implications for the prevention and treatment of influenza virus infections."
"Retinoid receptor overexpression may thus contribute to the pathogenesis of influenza and related viral infections, causing an endogenous form of hypervitaminosis A that manifests itself in the symptoms of the disease."
