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

[Vinero]

Hello
I have no time to read this 374 page topic
But u have read a lot of positive experience about people that are following a low vit a diet and i want to give it a shot.
One problem, everybody talk about low vit a intake but nobody talk about exact numbers.
So my question is: when you talk about low, what is the limit intake then?

I try to stay below 100 IU per meal. So if I eat three meals a day it means 300 IU is the upper limit for me. But to be fair, I have no idea how much vitamin A my beef contains. I have no idea how much vitamin A is in my apples. Some apples might contain only 50 IU per apple. Other apples might contain 300 IU per apple. You have to look at the color of the flesh. If it's white there's no carotenoids. The more yellow or orange it is the higher the carotenoid content. Only choose apples that are white-flesh after you peel them. Don't eat apples that seem yellowish. The same rules apply for potatoes. Only buy varieties of potato that are white-flesh.. No yellow-flesh potatoes. Purple-flesh potatoes and fruit are fine since the purple color is caused by anthocyanins not carotenoids. Anthocyanins are anti-oxidants so they may be helpful to inhibit excessive retinoic acid production. Also try to avoid fatty cuts of meat were the fat seems yellowish/orange.
We never know exactly how much vitamin A is in foods. All we can do is eat those foods that in theory are lowest in vitamin A, and that don't make us feel worse after eating them. For me this includes things like rice (white or brown), potatoes (white or purple flesh), white bread, apples, lean beef, turkey breast, almonds, macadamia nuts, mushrooms, black beans, and white beans.
I have also experimented with whole grains like oats, barley, whole wheat, spelt, buckwheat, rye, and also lentils. If you look up these foods they seem safe since they are low in vitamin A. But I get dry eyes and my energy levels get lower when I eat those foods on a daily basis. I don't think whole grains are appropriate for the low vitamin A diet, except brown rice.

 

[AK18]

I try to stay below 100 IU per meal. So if I eat three meals a day it means 300 IU is the upper limit for me. But to be fair, I have no idea how much vitamin A my beef contains. I have no idea how much vitamin A is in my apples. Some apples might contain only 50 IU per apple. Other apples might contain 300 IU per apple. You have to look at the color of the flesh. If it's white there's no carotenoids. The more yellow or orange it is the higher the carotenoid content. Only choose apples that are white-flesh after you peel them. Don't eat apples that seem yellowish. The same rules apply for potatoes. Only buy varieties of potato that are white-flesh.. No yellow-flesh potatoes. Purple-flesh potatoes and fruit are fine since the purple color is caused by anthocyanins not carotenoids. Anthocyanins are anti-oxidants so they may be helpful to inhibit excessive retinoic acid production. Also try to avoid fatty cuts of meat were the fat seems yellowish/orange.
We never know exactly how much vitamin A is in foods. All we can do is eat those foods that in theory are lowest in vitamin A, and that don't make us feel worse after eating them. For me this includes things like rice (white or brown), potatoes (white or purple flesh), white bread, apples, lean beef, turkey breast, almonds, macadamia nuts, mushrooms, black beans, and white beans.
I have also experimented with whole grains like oats, barley, whole wheat, spelt, buckwheat, rye, and also lentils. If you look up these foods they seem safe since they are low in vitamin A. But I get dry eyes and my energy levels get lower when I eat those foods on a daily basis. I don't think whole grains are appropriate for the low vitamin A diet, except brown rice.

How many weeks did it take you to improve?

 

[ursidae]

However many for the dairy allergy to subside

 

[saraleah]

It took a few weeks nearly zero A until things improved, things got worse before they got better. After a few weeks there were improvements in my vision that have been completely consistent. I had never in my life experienced sustained, clear, non blurry vision before. That was the first improvement. I still see clearly after 18 months.
My autoimmune condition improved somewhat the same time, greatly improved after 8 months, but occasionally flared up. So frustrating and I almost gave up. Decided to drop the grains, potatoes, black beans( oxalate) to see what happens. That was in month 13.
For 153 days now I have experimented with these lower carb, low A foods. No grains, yes beans but not lentils or black beans, no potato (oxalate) little fruit- berries, pumpki, sunflower seeds., macadamias. This has helped a lot, the only flare up I traced to lentils as a carb. Leutein? A cup of fat free Greek yogurt sometimes. Carbs 30-70 a day, which is not Keto.
This has resulted in the biggest improvements all around, there have been too many to list, including far less hair shedding.

 

[jyb]

I just had my blood retinol levels tested for the first time.

I did low/no vitamin A for a year or so 2019-2020, then low vitamin A 2020-21 (no large vitamin A sources, but butter daily, as well as eating out occasionally)

View attachment 21044
So uhh...really don't imagine I will be needing any vitamin A in my diet for years to come.

Isn't it expected, though? It seems that you are eating a "reasonable" diet considering butter, so you get a value in the "reference interval". The reference interval is probably what you expect for a typical healthy person, so not values you'd get by eating stuff like liver - it's very rare in a diet, I know people who never ate liver once in their entire life. Butter or other dairy product may be one the most common ways people get their retinol, and most people don't eat a lot of butter. So you might expect if you eat butter that you don't get deficient in retinol in just a year or two.

Sorry if this is irrelevant, I didn't read the whole thread so reacting out of context.

 

[Tarmander]

Isn't it expected, though? It seems that you are eating a "reasonable" diet considering butter, so you get a value in the "reference interval". The reference interval is probably what you expect for a typical healthy person, so not values you'd get by eating stuff like liver - it's very rare in a diet, I know people who never ate liver once in their entire life. Butter or other dairy product may be one the most common ways people get their retinol, and most people don't eat a lot of butter. So you might expect if you eat butter that you don't get deficient in retinol in just a year or two.

Sorry if this is irrelevant, I didn't read the whole thread so reacting out of context.

Somewhere in range is definitely what I would expect, but that high was surprising. I did literally zero vitamin A in my diet for a year. Butter has 350 IU per tablespoon. Say I am doing a couple tablespoons per day or less...that really is not much vitamin A. Considering how long I ate liver for, it makes sense, but still seemed shocking.

 

[Amazoniac]

- Advanced Nutrition and Human Metabolism (978-1-337-11555-1)

"The mechanism by which carotenoids function is linked in part to their structure, more specifically their extended system (often nine or more) of conjugated double bonds that make them soluble in lipids and capable of quenching singlet oxygen (¹O2) and free radicals (atoms or molecules with one or more unpaired electrons)."

"Quenching is a process by which electronically excited molecules or atoms, such as singlet oxygen, are inactivated. Singlet oxygen possesses higher energy and is more reactive than ground state molecular oxygen, which typically exists in triplet (³O2) rather than singlet (¹O2) form. Singlet oxygen is generated from lipid peroxidation of membranes; transfer of energy from light (photochemical reactions); the respiratory, also called oxidative, burst occurring in some phagocytic cells (enzymatic reactions); and the dismutation of superoxides (spontaneous reaction). Singlet oxygen, like free radicals, readily reacts with organic molecules such as protein, lipids, and DNA and thus can damage cellular components unless removed. Carotenoids can react with (quench) singlet oxygen, and it is the conjugated double-bond systems within the carotenoids that permit the quenching. The singlet oxygen (¹O2) transfers its excitation energy and returns to the ground state (³O2), and the carotenoid receiving the energy enters an excited state. Resonance states in the excited carotenoid allow some stabilization. Carotenoids then release the energy in the form of heat and thus do not need to be regenerated like some other antioxidants (e.g., vitamins C and E).

¹O2 + β-carotene → ³O2 + excited β-carotene → β-carotene + heat​

In addition to quenching singlet oxygen, β-carotene and other carotenoids have the ability to react directly with free radicals (radical scavenge), especially peroxyl radicals (ROO•), which cause lipid peroxidation. Such actions by carotenoids decrease circulating peroxide concentrations and reduce lipid peroxidation (thus helping to minimize damage to cells). Radical scavenging by carotenoids involves the donation of a hydrogen atom or an electron and results in the formation of a carotenoid radical. Electron delocalization over the carotenoid’s conjugated double bond system stabilizes the carotenoid."​

- Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

- Fungistatic activity of all-trans retinoic acid against Aspergillus fumigatus and Candida albicans

 

[LLight]

Interesting article, thanks. Only quick glance right now, reads more like retinol defiency

Seems like with this new data:

Retinol Depletion in Severe COVID-19

Background and Purpose Vitamin A is depleted during infections. Vitamin A has been used successfully in measles, RSV and AIDS patients and is an effective vaccine adjuvant. In this study, low retinol levels were found in patients with severe COVID-19. Retinoid signaling impairment in COVID-19...

www.medrxiv.org

 

[LeeLemonoil]

Seems like with this new data:

Retinol Depletion in Severe COVID-19

Background and Purpose Vitamin A is depleted during infections. Vitamin A has been used successfully in measles, RSV and AIDS patients and is an effective vaccine adjuvant. In this study, low retinol levels were found in patients with severe COVID-19. Retinoid signaling impairment in COVID-19...

www.medrxiv.org

K

Thanks a lot again @LLight, you bring up valuable articles as usual.


It’s clear to me that both Vitamin A and D and their derivates are crucial modulators of immunity by „sitting“ comfortably in between the major steroids - reacting and modulating to/their action. They can, to an extent, also compensate for either „too much“ or „not enough“ androgen or estrogen signaling.
Crude terms. They influence the steroid signaling homeostaticaly and especially the immunity actions of the steroids.

In acne that is well described by a bunch of articles, I’ll seek them out FYI

 

[Ihor]

I want to testify that after taking 15 mg of hydrocortisone per day, my body aches from vitamin A products, which I had for a long time have noticeably decreased, now like dairy products or oranges, there are almost no negative effects. Perhaps this is due to excessive inflammation, which is not controlled when cortisol is low.

 

[somuch4food]

I want to testify that after taking 15 mg of hydrocortisone per day, my body aches from vitamin A products, which I had for a long time have noticeably decreased, now like dairy products or oranges, there are almost no negative effects. Perhaps this is due to excessive inflammation, which is not controlled when cortisol is low.

This study I found describes retinoic acid (vit A) as pro inflammatory in presence of chronic inflammation: Retinoic Acid Is Elevated in the Mucosa of Patients With Active Ulcerative Colitis and Displays a Proinflammatory Role by Augmenting IL-17 and IFNγ Production - PubMed

 

[tim333]

Seems like with this new data:

Retinol Depletion in Severe COVID-19

Background and Purpose Vitamin A is depleted during infections. Vitamin A has been used successfully in measles, RSV and AIDS patients and is an effective vaccine adjuvant. In this study, low retinol levels were found in patients with severe COVID-19. Retinoid signaling impairment in COVID-19...

www.medrxiv.org

Ok lets break down the abstract:

Abstract
Background and Purpose:

Vitamin A is depleted during infections.

Yeah so what does that tell us? If vitamin A is being depleted there will be a lot of retinoic acid leaving the liver... creating a toxic situation... and that is exactly what is happening during an infection. The more vitamin A is in the liver the more retinoic acid will be released.

Vitamin A has been used successfully in measles, RSV, and AIDS patients and is an effective vaccine adjuvant.

What an outrageous non sequitur. Massive amounts of retinoic acid are intoxicating the body during an infection how can administering vitamin A ever be a good idea?

In this study, low retinol levels were found in patients with severe COVID-19.

Yep. So?

Retinoid signaling impairment in COVID-19 disrupts Type-I interferon synthesis. Material and Method: Two groups were formed in the study. The patient group consisted of 27 (Group 1) severe COVID-19 patients hospitalized in the intensive care unit with respiratory failure, and the control group consisted of 23 (Group 2) patients without COVID-19 symptoms. Serum retinol levels were analyzed by ELIZA and HPLC in both groups. Findings: Retinol levels were found to be significantly lower in the patient group (P <0.001). There was no difference in retinol between two different age groups in the patient group (P> 0.05). There was no significant difference in retinol between men and women (P> 0.05). Comorbidity did not affect serum retinol levels (P >0.05). Conclusion: Serum retinol levels were low in patients with severe COVID-19. Drugs preventing retinol excretion were not stopped in the patient group. Some patients took vitamin A externally. Despite this, retinol was low in COVID-19 patients. Retinol depletion impairs Type-I interferon synthesis by impairing retinoid signaling. Retinoid signaling may be the main pathogenetic disorder in COVID-19. This pathogenesis can serve as a guide for adjuvants, drug targets, and candidate drugs. Retinol, retinoic acid derivatives, and some CYP450 inhibitors may work on COVID-19.

Facepalm.

So the conclusion is that retinol and retinoic acid are good for COVID because vitamin A is depleted? No. It's the exact opposite! Most COVID symptoms are caused or exacerbated by elevated levels of retinoic acid!

Mawson on vitamin A and influenza:

According to the model proposed here, influenza-induced increased RAR activation inhibits the production and secretion of retinol binding-protein (RBP) via a process of feedback inhibition [185], thereby lowering serum retinol concentrations and simultaneously increasing the accumulation and expression of retinoids in the liver. These changes induce inflammation and tissue damage, consistent with the known role of excessive vitamin A in inducing liver damage [186] and apoptosis [187].

More Mawson:

A low vitamin D : A ratio has been postulated to increase the severity of influenza infection. The risk of severe illness may be further exacerbated by the effect of illness on the liver and its stored contents of vitamin A. On this model, activation of the retinoid cascade causes liver damage and the spillage of retinoic acid and unbound retinyl esters into the circulation. It is hypothesized that this induces lung damage, multiorgan 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.

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

 

[LLight]

@tim333 , you are right that this study does not prove causality between reduced vitamin A level and severe outcome of COVID19.

I have in mind the publication you linked but Covid is not influenza.

COVID is thought to be an issue of hypercoagulation while this (in vitro) publication seems to imply that vitamin A/RA inhibits coagulation. Well, we can always imagine a situation where an even greater concentration could have the opposite effect on coagulation.

Although there have been reports which have mentioned the in vivo inhibition of platelet aggregation and the enhancement of fibrinolytic activity by retinoic acid, the work presented in this manuscript describes for the first time the inhibition of thrombin (both Sigma and plasma) and in vitro platelet aggregation by vitamin A (retinol) and its derivatives – retinoic acid and retinaldehyde.

Inhibition of thrombin, an unexplored function of retinoic acid

Retinoic acid, a derivative of vitamin A, is known to possess in vivo anti-inflammatory, anti-platelet and fibrinolytic activities. We have investigated the in vitro thrombin and platelet aggregation inhibitory activities of vitamin A (retinol) and its ...

www.ncbi.nlm.nih.gov

 

[tim333]

@LLight

Elevated retinoic acid levels are common to a range of viral infections so I don't see a problem with bringing influenza into the discussion however I may have overstated retinoic acid's role in COVID symptoms, we don't really know. One thing that I'm confident about though is that retinoic acid during COVID is likely too high rather than too low.

 

[LeeLemonoil]

Ok lets break down the abstract:

Abstract
Background and Purpose:

Vitamin A is depleted during infections.

Yeah so what does that tell us? If vitamin A is being depleted there will be a lot of retinoic acid leaving the liver... creating a toxic situation... and that is exactly what is happening during an infection. The more vitamin A is in the liver the more retinoic acid will be released.

Vitamin A has been used successfully in measles, RSV, and AIDS patients and is an effective vaccine adjuvant.

What an outrageous non sequitur. Massive amounts of retinoic acid are intoxicating the body during an infection how can administering vitamin A ever be a good idea?

In this study, low retinol levels were found in patients with severe COVID-19.

Yep. So?

Retinoid signaling impairment in COVID-19 disrupts Type-I interferon synthesis. Material and Method: Two groups were formed in the study. The patient group consisted of 27 (Group 1) severe COVID-19 patients hospitalized in the intensive care unit with respiratory failure, and the control group consisted of 23 (Group 2) patients without COVID-19 symptoms. Serum retinol levels were analyzed by ELIZA and HPLC in both groups. Findings: Retinol levels were found to be significantly lower in the patient group (P <0.001). There was no difference in retinol between two different age groups in the patient group (P> 0.05). There was no significant difference in retinol between men and women (P> 0.05). Comorbidity did not affect serum retinol levels (P >0.05). Conclusion: Serum retinol levels were low in patients with severe COVID-19. Drugs preventing retinol excretion were not stopped in the patient group. Some patients took vitamin A externally. Despite this, retinol was low in COVID-19 patients. Retinol depletion impairs Type-I interferon synthesis by impairing retinoid signaling. Retinoid signaling may be the main pathogenetic disorder in COVID-19. This pathogenesis can serve as a guide for adjuvants, drug targets, and candidate drugs. Retinol, retinoic acid derivatives, and some CYP450 inhibitors may work on COVID-19.

Facepalm.

So the conclusion is that retinol and retinoic acid are good for COVID because vitamin A is depleted? No. It's the exact opposite! Most COVID symptoms are caused or exacerbated by elevated levels of retinoic acid!

Mawson on vitamin A and influenza:

According to the model proposed here, influenza-induced increased RAR activation inhibits the production and secretion of retinol binding-protein (RBP) via a process of feedback inhibition [185], thereby lowering serum retinol concentrations and simultaneously increasing the accumulation and expression of retinoids in the liver. These changes induce inflammation and tissue damage, consistent with the known role of excessive vitamin A in inducing liver damage [186] and apoptosis [187].

More Mawson:

A low vitamin D : A ratio has been postulated to increase the severity of influenza infection. The risk of severe illness may be further exacerbated by the effect of illness on the liver and its stored contents of vitamin A. On this model, activation of the retinoid cascade causes liver damage and the spillage of retinoic acid and unbound retinyl esters into the circulation. It is hypothesized that this induces lung damage, multiorgan 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.

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

You have based your refute of the publication on the unfounded claim of retinoid acid toxicity. A model proposed and a postulation.

Have you heard of the concept of homeostasis. It applies here. It can’t be squared with your dogmatic view, granted.

Both A and D are homeostatic modulators of immunity. If (if!) some viral infections lead to a distorted feedback that would lead to universal tissue damage that’s not a proof that high vit a or RA is detrimental in such infections per se.
What if vit A and RA signaling and quantities are crucial in contributing to preventing those infection stages that lead to the hypothesized derangement you present here? (Hint: they do)
It all suddenly comes down to unprecise semantics

 

[tim333]

You have based your refute of the publication on the unfounded claim of retinoid acid toxicity. A model proposed and a postulation.

Have you heard of the concept of homeostasis. It applies here. It can’t be squared with your dogmatic view, granted.

Both A and D are homeostatic modulators of immunity. If (if!) some viral infections lead to a distorted feedback that would lead to universal tissue damage that’s not a proof that high vit a or RA is detrimental in such infections per se.
What if vit A and RA signaling and quantities are crucial in contributing to preventing those infection stages that lead to the hypothesized derangement you present here? (Hint: they do)
It all suddenly comes down to unprecise semantics

No. I simply pointed out that retinoic acid levels are high during infection, not low. Retinoic acid can't be toxic? What?

Nobody has said retinoic acid is not important, you're confusing the issue of elevated levels of retinoic acid with retinoic acid itself.

 

[Amazoniac]

A publication posted here a while ago touched on this issue:

- The Effect of Isotretinoin on Biotinidase Activity

Spoiler

"According to the literature, neurological and ocular manifestations were mainly reported in patients with profound (total) biotinidase deficiency. The absence of such symptoms in our patients could be due to their acquired ‘partial’ biotinidase deficiency which was presented only with dermatological symptoms [13]. Additionally, the highest specific activity of biotinidase was found in liver and serum [10, 11], kidney and adrenal glands, but relatively low in the brain [15, 16]. Pispa [17] noted a 50% decrease in the biotinidase activity in liver, and a 30% decrease in serum activity of partially hepatectomized rats. It was concluded that the liver was the likely source of serum biotinidase. Furthermore, the serum biotinidase activities in patients with chronic hepatic diseases were detected below the lower limit of activity found in healthy adults [16–18]. Thus, it could be suggested that isotretinoin impairs the liver function [8], resulting in low biotinidase activity as it was previously reported [19]. On the other hand, the unaltered biotin serum levels that were evaluated for the first time in patients with cystic acne before and after 1-month treatment as well as the results of the in vitro experiments, which showed no direct isotretinoin effect on biotinidase activity, could lead to the following preliminary suggestions. The absence of an in vitro effect of the drug on biotinidase could possibly be due to physicochemical factors such as polarity since isotretinoin was pretty insoluble in water. At this point it should be noted that there was also no indication that any spectral isotretinoin properties have interfered in the in vitro assay. As regards the in vivo effect of isotretinoin therapy, it seemed that isotretinoin isomers-metabolites, such as tretinoin, oxotretinoin or 4-oxo-isotretinoin, might play a pivotal role towards biotinidase activity [16]. The latter hypothesis deserves to be investigated through future experiments. However it could be concluded that the dermatological lesions (xerosis and thinning of the skin, cheilitis, erythema etc.), which were found in almost all the patients on treatment, could be related to initial symptoms of their low biotinidase activities. These findings are clinically important since patients on isotretinoin treatment may develop symptoms similar to those observed in patients with partial enzyme deficiency. Biotinidase deficiency is a potentially treatable disorder, and empirical evidence suggests that a supplement of biotin (10 mg/day) in patients prevents its clinical manifestations [10]. Therefore, adequate biotin should be prescribed as a supplement during isotretinoin treatment in order to restore biotinidase function and offer more free metabolically available biotin."

 

[ursidae]

What is the reason behind the headaches it causes?

 

[ursidae]

Asking this question as I kept my retinol intake around 290 iu a day for a couple of months while supplementing vitamin d and eating fish/some avocado daily. by the end of this period my sebum production was completely recovered back to how it was as a teenager. I developed extreme dry skin last January after overdosing on liver. Skin seems less prone to infection with all the oil however it’s a bit too much so I took a multi with 600 iu retinol acetate three days in a row. Oil on my cheeks has been reduced already and I feel significantly warmer even though temps are not much higher. Problem is I got a headache very soon after the first dose, vision became less focused, very strong fatigue happening, an almost constant low grade headache and a very tense jawline.

could all this be happening from this small dose (1800 iu) and is it caused by something that has been depleted?

 

[GorillaHead]

I now believe vitamin A causes Ulcerative colitis.

Check these charts out. One is prevalence of UC and the other is prevalence of considered vitamin a deficiency.

studies shows UC is related to tretinoin use and in fact there are hundred of people claiming that after they got on accutane they developed some gut issue or disease

There reason i brough this up is because i was diagnosed with UC.

i have been symptom free for 3 years with no drugs until yesterday when I consumed 10k iu of retinol acetate. 4-5 hours later gas.

next day symptoms in my stool.

When i developed UC i was pounding 1-2 mass gainers a day. Today i checked the nutrient profile apparently each serving has 4000iu of vitamin A.

the reason the body doesnt convert much carotenoids to retinol is probably because in high levels it is toxic and perhaps the levels that are considred RDA are way too much.

Just look at japan. 2nd highest average life span. Low vitamin A consumption.

literally the countries that consume the most vitamin A. Have the highest prevalence of autoimmune diseases.

megadosing vitamin C. Vitamin D and Naicin right now. I theorize this should put me back in remission within a day

i do want to point out that today i feel warmer than usual which is nice. So unless its an off chance incident retinol may provide energy and perhaps we should be getting it through carotenoids