Low Toxin Diet Grant Genereux's Theory Of Vitamin A Toxicity

[Dr. B]

Choline.

interesting I thought choline is vitamin B8,
whereas b3 and b4 are both niacin, like b3 is niacin, but b4 is niacinamide or nicotinamide riboside
there is even PABA, which I think is considered b10 or b15... and some others like even inositol maybe considered a B...

"Unsaturated aldehydes are highly reactive towards cysteine residues which form adducts and inactivate several key mitochondrial enzymes such as glutathione S-transferase, glyceraldehydes 3-phosphate dehydrogenase, etc. and cytoskeletal proteins, energy metabolism proteins which cause cardiac contractile dysfunction (Bhatnagar 2006; LoPachin and Gavin 2014)."​

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- The retinoic acid receptor drives neuroinflammation and fine tunes the homeostasis of interleukin-17-producing T cells

- Generation of Retinaldehyde for Retinoic Acid Biosynthesis

is there any way to know how a given vitamin or mineral affects things like the catalase enzyme, glutathione levels, hydrogen peroxide levels? like iodine promotes peroxide, but im wondering how things like chromium or some of the b vitamins or zinc affect catalase and peroxide and glutathione.. or vitamin d, k, c, e, A, etc... i think you mentioned vitamin K stresses the glutathione system...

 

[Amazoniac]

- Vitamin A and Vitamin E: Will the Real Antioxidant Please Stand Up?

Vitamin A, acting through its metabolite, all-trans-retinoic acid, is a potent transcriptional regulator affecting expression levels of hundreds of genes through retinoic acid response elements present within these genes. However, the literature is replete with claims that consider vitamin A to be an antioxidant vitamin, like vitamins C and E. This apparent contradiction in the understanding of how vitamin A acts mechanistically within the body is a major focus of this review. Vitamin E, which is generally understood to act as a lipophilic antioxidant protecting polyunsaturated fatty acids present in membranes, is often proposed to be a transcriptional regulator. The evaluation of this claim is another focus of the review. We conclude that vitamin A is an indirect antioxidant, whose indirect function is to transcriptionally regulate a number of genes involved in mediating the body's canonical antioxidant responses. Vitamin E, in addition to being a direct antioxidant, enables the increase of peroxidized lipids that alter both metabolic pathways and gene expression profiles within tissues and cells. However, there is little compelling evidence that vitamin E has a direct transcriptional mechanism like that of vitamin A. Thus, we propose that the term antioxidant not be applied to vitamin A, and we discourage the use of the term transcriptional mediator when discussing vitamin E.

 

[Daniil]

@Vinero Have you tried adding vitamin C? You are also describing the symptoms of vitamin C deficiency.

 

[Vinero]

@Vinero Have you tried adding vitamin C? You are also describing the symptoms of vitamin C deficiency.

Yes I tried vitamin C but it didn't do anything. I tried lots of things to make the eye symptoms go away like adding fats like olive oil, coconut oil, nuts and seeds.
I also tried minerals like zinc, selenium, molybdenum, copper, magnesium, calcium but none of these did anything. B vitamins I tried too but no improvement. Butter made it all go away very rapidly. So I assume it's the vitamin A in butter that's having the good effect.

 

[InChristAlone]

Yes I tried vitamin C but it didn't do anything. I tried lots of things to make the eye symptoms go away like adding fats like olive oil, coconut oil, nuts and seeds.
I also tried minerals like zinc, selenium, molybdenum, copper, magnesium, calcium but none of these did anything. B vitamins I tried too but no improvement. Butter made it all go away very rapidly. So I assume it's the vitamin A in butter that's having the good effect.

It would have been amazing if you had used a vitamin A supplement to see if it really was the vitamin A. And even if it was we don't know how retinoic acid is affecting estrogen. Lots of things have affects on estrogen and other hormones which could cause the dry eyes. For instance after a yr on cyproheptadine I had bad dry eyes. A few months of low A is not enough to become deficient.

 

[Daniil]

Yes I tried vitamin C but it didn't do anything. I tried lots of things to make the eye symptoms go away like adding fats like olive oil, coconut oil, nuts and seeds.
I also tried minerals like zinc, selenium, molybdenum, copper, magnesium, calcium but none of these did anything. B vitamins I tried too but no improvement. Butter made it all go away very rapidly. So I assume it's the vitamin A in butter that's having the good effect.

Have you tried natural products with vitamin C? Lemons were considered a classic cure for scurvy. Synthetic vitamin C can be different and it may lack cofactors.

 

[Daniil]

It would have been amazing if you had used a vitamin A supplement to see if it really was the vitamin A. And even if it was we don't know how retinoic acid is affecting estrogen. Lots of things have affects on estrogen and other hormones which could cause the dry eyes. For instance after a yr on cyproheptadine I had bad dry eyes. A few months of low A is not enough to become deficient.

+1

 

[Lollipop2]

sounds crazy and worrisome mate... ive been using 10000 IU daily for like a year or more, and prior to that ive been using 5000IU daily for 5 years...

I think developing Parkinson’s from Vit D 8,000 is beyond rare and most likely some other comorbidity was going on. A lot of fear mongering going on with Vit D, Vit A, and Vit K. Do your research.

 

[Lollipop2]

So I assume it's the vitamin A in butter that's having the good effect.

I believe it. Vit A supplementation could be problematic but naturally occurring Vit A in butter and milk have all the cofactors that promote good absorption and health in your system. @Mr.Bollox.

 

[Dr. B]

I think developing Parkinson’s from Vit D 8,000 is beyond rare and most likely some other comorbidity was going on. A lot of fear mongering going on with Vit D, Vit A, and Vit K. Do your research.

the vitamin K supplements have reports of hair shedding, vitamin A also does but in higher amounts. vitamin K seems to stress the glutathione system, I think Amazoniac posted that. that could explain the hair shedding and other effects people are getting with larger doses. you basically need to use something else to boost up your glutathione if using vitamin k.

Yes I tried vitamin C but it didn't do anything. I tried lots of things to make the eye symptoms go away like adding fats like olive oil, coconut oil, nuts and seeds.
I also tried minerals like zinc, selenium, molybdenum, copper, magnesium, calcium but none of these did anything. B vitamins I tried too but no improvement. Butter made it all go away very rapidly. So I assume it's the vitamin A in butter that's having the good effect.

did you try milk or cheese? could it be the unique fatty acids in butter?

 

[Dr. B]

I believe it. Vit A supplementation could be problematic but naturally occurring Vit A in butter and milk have all the cofactors that promote good absorption and health in your system. @Mr.Bollox.

why was I tagged?

 

[Amazoniac]

- Anti-Peat - Grant Genereux's Theory Of Vitamin A Toxicity

- Anti-Fibrotic Potential of All Trans Retinoic Acid in Inflammatory Bowel Disease

Spoiler

"Besides the observations of Bai and colleagues already discussed, additional insight into ATRA effects comes from human tissue studies by Sanders and colleagues, working at the London School of Medicine and Dentistry in 2014 [17]. They investigated potential sources of ATRA in gut tissues from healthy subjects and Crohn’s disease (CD) patients. Ileal and colonic tissues were collected from ten CD patients undergoing endoscopy or surgery and compared with similar tissues from healthy subjects. Cell fractions were harvested from these tissue samples and antigen presenting cells (APC) isolated by flow cytometry to assess their RALDH activity. The group first characterized APCs by population markers into myeloid, CD103+, and CD103-dendritic cells. Analysis revealed that the RALDH activity was doubled and tripled within CD103+ and CD103-myeloid dendritic cells (respectively) extracted from CD samples as compared to healthy controls. Although ATRA levels were not measured and the CD sample size was small, the findings indicate that the capacity to generate ATRA is common to multiple APC populations in the human intestine. The upregulation of ATRA generating capacity in CD patients may reflect a compensatory mechanism like the alternate ATRA source found in TNFΔ ARE mice in the context of chronic intestinal inflammation. Again, despite positive effects on toleragenic CD103+ dendritic cells, RALDH activity appeared insufficient to attenuate disease, or may have even provided ATRA for the differentiation of pro-inflammatory gut macrophages that might have increased intestinal inflammation."

"Intestinal fibrosis remains one of the most serious complications of Crohn’s disease, and to a lesser extent, UC. Marked by an excessive deposition of extracellular matrix (ECM) by activated mesenchymal cells, it was thought to be an irreversible, inevitable consequence of chronic inflammation, that, all too often, leads to bowel obstruction and subsequent stricture resection. Because of its alarming contribution to the morbidity and mortality of IBD, intestinal fibrosis has commanded significant attention. Progress on understanding mechanisms, clinical management and potential treatments for IBD fibrosis has been chronicled over the last 20 years in two review articles from the same group, the first published in 2008 and second, more recently in 2017 [32, 33]. Looking back over the last few decades, the group noted that while potent anti-inflammatory biologic therapies have revolutionized IBD treatment, they have made little impact on fibrosis. This not only underscores the urgent unmet medical need for novel therapies, but also challenges the view of inflammation as the sole driver of gut fibrosis and suggests underlying, inflammation-independent self-perpetuating, fibrostenotic processes. Deeper mechanistic understanding should reveal novel targets for therapies specific to type and degree of intestinal fibrosis in IBD."

"While no report establishes the ability of ATRA to treat IBD fibrosis specifically, there is a wide, suggestive literature based on the ability of ATRA to limit fibrosis in various other tissues. However, a small number of reports also suggest that ATRA might enhance ECM production and exacerbate fibrosis both in vitro and in vivo. In 2013, this controversial point was reviewed in detail by Zhou and colleagues [34]. Along with efforts to elucidate mechanism, that body of work strongly suggests that exogenous ATRA treatments could be effective at reducing IBD fibrosis."

"The 70-plus publications reviewed by Zhou from the last 30 years focused on the role of ATRA in liver, lung and kidney fibrosis. In the liver, nine different publications reporting thirteen separate in vivo and in vitro effects of ATRA on fibrotic processes were summarized. Of these, eleven indicated a protective role for ATRA against liver fibrosis/extracellular matrix accumulation while just two, from the same group, suggested a negative role involving the accumulation of ECM in the liver. In lung tissue, five different publications reporting seven separate in vivo or in vitro effects of ATRA on fibrotic processes were summarized, where all seven indicated a protective role for ATRA against pulmonary fibrosis and/or extracellular matrix accumulation. And finally, in kidney tissue, sixteen different publications reporting eighteen separate in vivo or in vitro effects of ATRA on fibrotic processes were summarized, with seventeen indicating a protective role for ATRA against pulmonary fibrosis/extracellular matrix accumulation and only one, a negative role. A summary of mechanistic observations showed that ATRA not only effectively inhibits the expression of various collagens (III, 1A1, Procollagen I) and other pro inflammatory pro-fibrinogenic bio molecules (e.g., α-SMA, TNF-α, and IL-6 etc), but also fibrosis overall."

"While the anti-inflammatory activity of ATRA in IBD may depend on its ability to attenuate Microbiota induced Th17 driven inflammation via a CD103+ dendritic cell driven expansion of gut regulatory T cells, a body of evidence also suggests the presence of an inflammation-independent, anti-fibrotic activity [35]. Gut fibrotic mechanisms are based on the same mechanisms of exaggerated expansion and activation of mesenchymal cells, (fibroblasts, myofibroblasts, and smooth muscle cells) with subsequent accumulation of collagen-rich ECM seen in other organs [33, 36]. Leakage of enteric flora and other luminal components, immune and non-immune cell products and processes (e.g., proliferation, epithelial and endothelial to mesenchymal and stellate cell transition, migration of bone marrow derived stem cells) combine to drive fibroblast and myofibroblast expansion and activation in parallel with activation of the immune response. Normally, these mechanisms combine to promote a healing response to injury, but in the context of chronic IBD, they drive intestinal fibrosis.

Several studies examining effects of ATRA on the cell types mentioned above support a potential protective effect of ATRA on gut fibrosis. The ability of ATRA to reverse radiation induced fibroblast proliferation in the lung and to limit proliferation and collagen secretion in cardiac fibroblasts was described in 2006 [37, 38]. While an older report from 1991 suggested that under inflammatory conditions, ATRA could augment synovial fibroblast proliferation, a recent publication by Shimizu and colleagues reported that ATRA played a key role in reducing liver stellate cell activation [39]. Several additional reports buttress this observation, documenting anti-fibrotic effects on pancreatic stellate cell differentiation and activation [40-43]. Finally, a pair of reports from the early 2000’s describes ATRA as a potent inhibitor of both proliferation and migration of human vascular smooth muscle cells and a regulator of ECM turnover [44, 45]. Overall, the activity of ATRA on cells responsible for gut fibrosis would appear to be protective."

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- All-trans Retinoic Acid Induction of Sulfotransferases

Spoiler

"Regulation of sulfotransferase expression by endogenous molecules (specifically hormones) is relatively well documented (Klaassen et al. 1998; Runge-Morris 1998; Dunn & Klaassen 2000). The biochemical consequences of these regulations are of importance in relation to their physiological processes. There are few reports, however, studying drug or xenobiotic induction of sulfotransferases in either animal tissues or cultured human cells (Runge-Morris et al. 1998; Maiti & Chen 2003a & b). In the present investigation, we found that retinoic acid can increase sulfotransferase expression and activity in rat tissues and cultured human cells. This induction was seen at the gene expression level."

"Retinoic acid induction of rat sulfotransferases is tissue type-dependent, and the effect of retinoic acid on intestinal sulfotransferases is, in general, greater than liver sulfotransferases (fig. 1 and 2). This is in agreement with our previously published sulfotransferase inductions in rat liver and intestine by methotrexate (Maiti & Chen 2003a) and tamoxifen (Maiti & Chen 2003b). Tissue type-dependence was also seen with retinoic acid induction of (human)sulfotransferase1E1 in human colon Caco-2 cells but not in human liver Hep G2 cells (fig. 3 and 6). These results suggest that intestine is one of the important organs for xenobiotic detoxification."

"Retinoic acid induction of rat sulfotransferases is also sex-dependent. This is demonstrated for both liver and intestinal sulfotransferases at the protein level by enzyme activity (fig. 1 and 2) and Western blot (fig. 4), and at the mRNA expression level by RT-PCR (fig. 7). In general, sex dimorphism in the expression of several rodent sulfotransferase genes is primarily mediated via the gender specific profile of pituitary growth hormone secretion (Klaassen et al. 1998; Delesque-Touchard et al. 2000). Retinoic acid metabolism in human and rat tissues are also gender-dependent (Klein-Szanto et al. 1980; Stephensen & Gildengorin 2000). Endogenous substrates for sulfotransferases are primarily hormones. The sex dependent regulation of sulfotransferases suggests an important role of sulfotransferases in the regulation of sex hormones."

"Retinoic acid mediated induction of sulfotransferases can increase xenobiotic detoxification through sulfation. This induction can also increase endogenous concentrations of sulfated hormones (usually biologically inactive) and decrease active hormone concentrations leading to changes in physiology. The induction of (human)sulfotransferase2A1 by retinoic acid could also lead to changes in other enzyme levels through peroxisome proliferator-activated receptor. It has been reported that dehydroepiandrosterone sulfate can induce CYP4A via peroxisome proliferator-activated receptor (Ram & Waxman 1994)."

"In the present investigation, Western blot results are in basic agreement with enzyme activity results. This suggests that the effect of retinoic acid on sulfotransferase activities is caused by increasing quantities of sulfotransferase protein rather than by modification of sulfotransferase proteins or other factors. RT-PCR results are also in agreement with enzyme activity and Western blot results. This suggests that retinoic acid induction of sulfotransferases is at the mRNA expression level in both rats and human cell lines."

"Retinoic acid induced transcriptional regulation of sulfotransferase genes suggests a probable nuclear receptor mediated induction process. Induction of drug metabolizing enzymes is primarily through nuclear receptors. Some receptors have been shown to be responsible for xenobiotic induction of cytochrome P-450 families 1, 2, 3, and 4 (Akiyama & Gonzalez 2003; Pascussi et al. 2003). Most of these receptors form heterodimers with retinoid X receptor a before binding to the responsive elements in the promoter regions of these drug metabolizing enzyme genes (Abu-Abed et al. 1998). Retinoic acid exerts its molecular actions mainly through retinoic acid receptor and retinoic X receptor nuclear receptors (Marill et al. 2003). Retinoic acid has a high affinity for retinoic acid receptors. It also binds to retinoic X receptor a. Sulfotransferase induction mechanisms by xenobiotics are not well known. Retinoic acid induction of sulfotransferases supports the hypothesis that xenobiotic induction of sulfotransferases is also mediated through nuclear receptors, and these receptors may form heterodimers with retinoic X receptor a or retinoic acid receptors."

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1 ng/ml is about 0.003 µM; after meals values might get higher.

 

[Amazoniac]

- Nuclear Hormone Receptors and Gene Expression

- Triorganotin compounds - ligands for “rexinoid” inducible transcription factors: Biological effects

Spoiler

- Structural Determinants of Allosteric Ligand Activation in RXR Heterodimers

Spoiler

- 9-Cis-13,14-dihydroretinoic acid, a new endogenous mammalian ligand of retinoid X receptor and the active ligand of a potential new vitamin A category: vitamin A5

- Alternative retinoid X receptor (RXR) ligands

- Activation of Retinoic Acid Receptors by Dihydroretinoids
- Retinol Saturase: More than the Name Suggests
- Natural ligands of RXR receptors (I thought that it was posted here, but couldn't locate it)

- Vitamin A5/X, a New Food to Lipid Hormone Concept for a Nutritional Ligand to Control RXR-Mediated Signaling

Spoiler

"Recently, 9-cis-13,14-dihydroretinoic acid (9CDHRA) has been identified as an endogenous retinoid and an RXR ligand with physiological relevance in mice [10] opening thus the possibility of dynamic, ligand-dependent control of RXR-related functions and pathologies. In mice, reduced available levels of 9CDHRA have been associated with spatial working memory deficits, shown previously to be highly sensitive to ligand-dependent functions of RXR [11]. Accordingly, pharmacological treatment with 9CDHRA displayed memory-enhancing effects in delayed spatial tasks in mice. Such findings point to the possibility that limited availability of 9CDHRA is most likely related to nutritional intake of its precursor(s) or dysfunction of precursor metabolism. This may compromise ligand-dependent functions of RXRs and lead to some of the RXR-related pathologies, which span beyond mnemonic deficits [14,15,16,17]. Critical for addressing such a hypothesis is knowledge of the precursor(s) and metabolic pathway(s) involved in generation of 9CDHRA, which remain virtually unexplored. Whereas a previous study indicated an involvement of retinol binding protein, Rbp1, as an important component of the metabolic pathway for 9CDHRA synthesis [11], the biologically-relevant precursors are not known, but have been conceptualized [12⇈]. Thus, specific isomerization of the 9-cis-double bond (reviewed in [10,12]) and selective saturation of the C13,C14-double bond [18,19,20] have been proposed as potential direct and indirect pathways for the conversion of all-trans-retinol (ATROL), known as vitamin A1, to dihydroretinoids including 9CDHRA."

"Indeed, ATROL and all-trans-β,β-carotene (ATBC) could be considered as the most likely precursors of 9CDHRA. If such a hypothesis were validated, 9CDHRA could be considered as a new active metabolite of ATROL and a member of the vitamin A1 cluster. Otherwise, 9CDHRA should be considered as a member of a new class of vitamin or at least a new class of the vitamin A family. In this study we focused on the identification of physiologically- and nutritionally-relevant precursor(s) of the RXR-ligand, 9CDHRA."

"9CDHROL is distinct from ATROL (vitamin A1-alcohol) in several aspects. Most importantly 9CDHROL, but not ATROL, is efficiently metabolized to 9CDHRA, which was recently identified as an RXR ligand with physiological relevance, which may directly mediate RXR-specific pro-mnemonic activities. Despite such differences, we cannot exclude minor indirect metabolic links between vitamin A1 and A5/X pathways. In mice using moderate to high supplementation doses of either retinoid (ATROL or 9CDHROL), such a conversion was not observed in the three representative compartments of the organism analyzed in this study. However, oligodendrocytes cultured in vitro displayed weak, but significant, conversion of ATROL to 9CDHROL following treatment with a high concentration of ATROL, likely due to an optimal 9-cis specific metabolic environment for direct enabling of RXRγ-mediated signaling shown previously to be important for remyelination process [35]. Finally, in contrast with the high homeostatic regulation of vitamin A1 at various levels [32,33,34], vitamin A5/X bioavailability in the organism seems to be regulated more in a food intake and specific nutrient-dependent switch to enable RXR-mediated signaling."

"We also show that the new carotenoid 9CDHBC acts as an efficient provitamin A5/X compound, is also found in the food matrix of plant origin, shown here as an example in peach extracts, and may act as a proximate intermediate in the biosynthesis of 9CDHRA (Figure 5). Whereas ATBC acts as an efficient provitamin A1 source, it is not metabolized in vivo (mice) and in vitro (oligodendrocytes) to 9CDHROL or 9CBC, and further to 9CDHRA. Instead, 9CBC is present in humans with preferred accumulation in organs, while less abundant in the serum [36] and moderately abundant in the human food chain, and may represent the nutritionally-relevant provitamin A5/X (present data and [37,38,39]). 9CBC originates mainly from plant-based metabolism [40] or from food processing of ATBC [38,41]. As mice are not an optimal model to study nutri-kinetics of carotenoids [42], we speculate a more likely scenario of 9CBC obtaining an important nutritional-relevant precursor function in humans. This more important nutritional relevance to humans can additionally be speculated due to its weak-moderate precursor potential for 9CDHBC in directly exposed in vitro cultured oligodendrocytes."

"Future studies of this cluster of compounds should contribute to understanding the pleiotropic activities of RXRs, and especially the physiological function of the RXR-ligand and its nutritional precursors. RXR-mediated signaling, which coordinates signaling pathways with several heterodimer binding partner nuclear receptors like PPARs, LXR and NR4A as permissive and RARs and vitamin D receptor (VDR) as non-permissive partners [4,43], is selectively augmented in various neurological diseases: obesity, diabetes and further diseases of the cardiovascular system such as atherosclerosis [1,2,5]. Further studies should focus on details of the metabolic pathway of these food derived compounds like provitamin A5/X (9CBC / 9CDHBC) involving BCO1/2-mediated cleavage pathways [44,45,46,47], as well as starting from the food precursor vitamin A5/X (9CDHROL / 9CDHROL-ES) towards the bioactive RXR-ligand 9CDHRA via a further ALDH1A-oxidation [48,49,50,51]."

"We anticipate that enhancement/modulation of general vitamin A deficiency syndromes in humans by selectively modulating the vitamin A5/X signaling pathway instead of vitamin A1 signaling pathways via treatment with vitamin A5/X cluster derivatives may be selectively beneficial for the treatment of dysfunctions with a major RXR-involvement and RXR-dysfunctionality as determined in RXR-mediated signaling dependent diseases and various neurological diseases such as psychotic diseases, dysfunctional myelination diseases and neurodegenerative diseases as well as cancer, atherosclerosis, allergies and obesity/diabetes [1,2,5]."

Spoiler: Figure 5. Metabolic pathway of the novel vitamin A5/X / provitamin A5/X pathway

@Jorge, check these out, it might be possible to make Poisonil* more harmful.

*Killcirol should be toxic regardless of conditions.​

 

[maillol]

Good paper on the interaction of Vitamin A with Vitamin D

Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective

Reduced exposure to solar radiation, leading to a deficiency of vitamin D and hence impaired innate immunity, has been suggested as a trigger for influenza viral replication and as an explanation of seasonal influenza. Although this hypothesis accounts for many unexplained facts about the...

www.hindawi.com

Some highlights:

"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."

"the symptoms of influenza are similar to those of retinoid toxicity"

"Vitamins A and D are inversely associated in that vitamin A can inhibit the actions of vitamin D and vice versa."

"In humans, concomitant supplementation with vitamin D greatly increases the dose of vitamin A required to cause toxicity; for instance, Myhre et al. [98] found that the median dose for inducing vitamin A toxicity was >2,300 IU/kg of body weight per day higher when vitamin D was added to the diet. For a hypothetical 75 kg person representing the median, vitamin D supplementation would have allowed an additional 175,000 IU vitamin A/day before toxicity symptoms were likely to be reported."

"solar radiation has opposite effects on vitamins A and D, catabolizing vitamin A but increasing the concentration of vitamin D"

"Tang et al. [85] investigated the effect of sunlight on retinyl esters and retinol in human skin, blood, and cultured keratinocytes. Sunlight irradiation led to a significant reduction in epidermal retinyl esters in Caucasian skin in both summer and winter, whereas epidermal and dermal retinol and dermal retinyl esters were affected to a lesser extent. When serum from volunteers who had taken a large dose of retinyl palmitate to elevate serum retinyl esters was exposed to sunlight, the serum retinyl esters disappeared after 10 minutes of exposure."

 

[LauriePartridge]

Good paper on the interaction of Vitamin A with Vitamin D

Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective

Reduced exposure to solar radiation, leading to a deficiency of vitamin D and hence impaired innate immunity, has been suggested as a trigger for influenza viral replication and as an explanation of seasonal influenza. Although this hypothesis accounts for many unexplained facts about the...

www.hindawi.com

Some highlights:

"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."

"the symptoms of influenza are similar to those of retinoid toxicity"

"Vitamins A and D are inversely associated in that vitamin A can inhibit the actions of vitamin D and vice versa."

"In humans, concomitant supplementation with vitamin D greatly increases the dose of vitamin A required to cause toxicity; for instance, Myhre et al. [98] found that the median dose for inducing vitamin A toxicity was >2,300 IU/kg of body weight per day higher when vitamin D was added to the diet. For a hypothetical 75 kg person representing the median, vitamin D supplementation would have allowed an additional 175,000 IU vitamin A/day before toxicity symptoms were likely to be reported."

"solar radiation has opposite effects on vitamins A and D, catabolizing vitamin A but increasing the concentration of vitamin D"

"Tang et al. [85] investigated the effect of sunlight on retinyl esters and retinol in human skin, blood, and cultured keratinocytes. Sunlight irradiation led to a significant reduction in epidermal retinyl esters in Caucasian skin in both summer and winter, whereas epidermal and dermal retinol and dermal retinyl esters were affected to a lesser extent. When serum from volunteers who had taken a large dose of retinyl palmitate to elevate serum retinyl esters was exposed to sunlight, the serum retinyl esters disappeared after 10 minutes of exposure."

This is super helpful information. Thanks for posting. That explains why I got a bout of the flu in January after I stopped all D supplementation and increased my A in November/December.

 

[Dr. B]

Good paper on the interaction of Vitamin A with Vitamin D

Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective

Reduced exposure to solar radiation, leading to a deficiency of vitamin D and hence impaired innate immunity, has been suggested as a trigger for influenza viral replication and as an explanation of seasonal influenza. Although this hypothesis accounts for many unexplained facts about the...

www.hindawi.com

Some highlights:

"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."

"the symptoms of influenza are similar to those of retinoid toxicity"

"Vitamins A and D are inversely associated in that vitamin A can inhibit the actions of vitamin D and vice versa."

"In humans, concomitant supplementation with vitamin D greatly increases the dose of vitamin A required to cause toxicity; for instance, Myhre et al. [98] found that the median dose for inducing vitamin A toxicity was >2,300 IU/kg of body weight per day higher when vitamin D was added to the diet. For a hypothetical 75 kg person representing the median, vitamin D supplementation would have allowed an additional 175,000 IU vitamin A/day before toxicity symptoms were likely to be reported."

"solar radiation has opposite effects on vitamins A and D, catabolizing vitamin A but increasing the concentration of vitamin D"

"Tang et al. [85] investigated the effect of sunlight on retinyl esters and retinol in human skin, blood, and cultured keratinocytes. Sunlight irradiation led to a significant reduction in epidermal retinyl esters in Caucasian skin in both summer and winter, whereas epidermal and dermal retinol and dermal retinyl esters were affected to a lesser extent. When serum from volunteers who had taken a large dose of retinyl palmitate to elevate serum retinyl esters was exposed to sunlight, the serum retinyl esters disappeared after 10 minutes of exposure."

useful stuff mate so we can add vitamin D to the diet instead of lowering vitamin A?
what dosage of vitamin d3 was needed in order to allow additional 175000IU vitamin A usage per day i imagine its dose dependent...?

 

[maillol]

useful stuff mate so we can add vitamin D to the diet instead of lowering vitamin A?
what dosage of vitamin d3 was needed in order to allow additional 175000IU vitamin A usage per day i imagine its dose dependent...?

I tried to find out but the study they reference is a meta analysis so it's a mixture of different studies. It just says whether vitamin D was involved or not. They're all human case studies so I would imagine this means a relatively normal dose is probably effective.

This is the reference

Water-miscible, emulsified, and solid forms of retinol supplements are more toxic than oil-based preparations

ABSTRACT. Background: It is well established that an excessive intake of retinol (vitamin A) is toxic; however, it has been > 25 y since the last extensive t

academic.oup.com

 

[Daniil]

useful stuff mate so we can add vitamin D to the diet instead of lowering vitamin A?
what dosage of vitamin d3 was needed in order to allow additional 175000IU vitamin A usage per day i imagine its dose dependent...?

Sun exposure, possible, but not vitamin D supplements. If this worked, then vitamin D supplements would treat dandruff, acne, hair loss, etc. I haven't seen anything like this.

 

[Daniil]

Perhaps this is the reason why the Maasai are healthy with a large consumption of milk. But you should minimize carotenoids and unsaturated fat to minimize the oxidation processes on the skin. Personally, I would rather stick to a low-VA diet.

 

[Dr. B]

Sun exposure, possible, but not vitamin D supplements. If this worked, then vitamin D supplements would treat dandruff, acne, hair loss, etc. I haven't seen anything like this.

i thought vitamn d does treat those things theres anecdotes of it treating hair loss