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

[Lynne]

I have had KP pretty much my whole life

Me too, but haven't observed any changes with season/sun exposure. I have noticed it better or worse at various times and not known what to attribute the change to, except when I first cut right back on PUFAs I noticed a great improvement. Hoping this low VA eating will help.

Has anyone else doing low VA experienced dry, cracked heels? If so how have they changed on low VA (or anything else)? Mine have got worse, but it's now the end of a long summer of bare feet or flip-flop wearing and beach-going. Though I do think they're worse than this time last year and I'm hoping it's just all the VA being dumped into my system from storage and that they will improve soon...

 

[Atman]

Here are the rules of the Low vitamin A diet, this list is not yet complete so feel free to add anything I forgot:

3. It is helpful to have small amounts of fat added to meals. Olive oil seems to be safest fat, MUFAs are anti-inflammatory. Avoid added saturated fats like butter, beef-fat, cocoa butter and coconut oil. These fats are high in stearic acid and palmitic acid, which are pro-inflammatory by increasing endotoxin production and retinoid acid associated inflammation. Contrary to what most Peatarians believe, saturated fats might turn out to have detrimental effects. The safest fats are MUFAs, and even PUFAs are theorized to have health benefits, as long as enough Vitamin E is present.

The absolute state of this forum...

Well I guess at least the controversy boosts traffic enourmously.
Maybe that's why Charlie is in on it.

Btw sunflower and soy oil is obviously the best oil to cook with.
Very little saturated acids and high in vitamin E.

 

[Amazoniac]

I don't know why. He posts studies that show calcification happened in some sheep (yes, sheep), infants fed 4 million IUs (very high, even for an adult), and people receiving intramuscular injections of 600,000 IU a month. These doses are so high and extreme, they simply wouldn't apply to regular D supplements..... unless you purchased 10 bottles and took every dose the same day.

I could try and dig up the studies from Smith's website, but I'm hoping @Amazoniac can just link to the comment where I already did 83 pages back, and I can get right down to responding with a Michael McDonald video (maybe also staring Nate Dogg and Warren G)

I don't think there is any need to worry if you keep a daily dose in the area of 5,000 to 10,000 IU a day.

The issue with potassium is similar:
- Is Supplemental Vitamin D Safe? "RENAL POTASSIUM-WASTING INDUCED BY VITAMIN D"

But you know my opinion on those doses.

The issue with Accutane was never that the body makes that isomer. That has pretty much always been known. No shock there. The issue with Accutane is that each dose is hundreds to thousands of times what the body would produce naturally, and that dose is taken chronically daily for months.

Yeah, it's not as controlled and converted on demand, the body is forced to process a massive dose of forms that regulate genie expression.

- Handbook of Vitamins (0-8247-0428-2)

@ecstatichamster - Ask your girlfriend to not supplement arotinoid acid (a synthetic poisonoid) in case you plan to manufacture fetuses together. And of course they's way more susceptible than adults.


This is from Garrett's link:

- Modulation of plasma all-trans retinoic acid concentrations by the consumption of carotenoid-rich vegetables

People in the experiment were advised to consume those with their main meals, which probably had a decent amount of fat:

"This nutritional regulation of the active RAR ligand by vegetable consumption could be one of the major mechanisms by which vegetables exert their beneficial potential, especially for RAR-coinfluenced nutritional diseases such as cancer and cardiovascular disease [8]."​

5 liters is the average volume of blood in a guru.

5000 ml ÷ 2 (plasma is about 50%) × 2 ng (all-the-trans-RA concentration after carrot juice) ÷ 1^6 (ng to mg) = 0.005 mg​

Some is taken up by tissues and that's just a snapshot. But consider that on top of what foods provide, the person adds the isotretinoin dose, which can be for example 40 mg a day (depends on duration).

- Determination of isotretinoin in human plasma: Application to pharmacokinetic study

Note the unit.​

It's quite unusual for the body having to handle isotretinoin in such doses.

In a natural diet, if the person is taking excessive amounts of poisonyl esters from foods, the consequences are often nausea followed by vomiting or diarrhea, and both is attempts to avoid the adsorption.

Very cool. I also was doing some searching around, and found this article- How Well Do You Convert Beta-Carotene to Vitamin A?

So, if that's to be believed, then I am also an undercoverter. Go Team Under Convert Carotene!

If true, this means (most of my life) I've been under converting carotene while loading iron (have those genes, too) while living in a country that spiked iron fortification and demonized retinol in favor of Beta Carotene. Oh, and also decided to dump a lot of PUFA into foods, just in case the oxidation issues and metabolism slowing wasn't enough from the first two.

This does connect a lot of dots for me. It does happen to explain the yellow soles of my feet and callouses. Time for this emoji which hasn't been used in this thread it seems (or at least, not often)............

So, for me, this means I'm certainly continuing to keep carotenoids as low as possible. I have had KP pretty much my whole life (just like the writer of the article I linked). Didn't notice high dose retinol having much of an effect...... but sun exposure has seemed to improve it drastically. I might play around with different retinol intakes. Maybe some higher levels with very low carotenoids might be beneficial for me. Looking back, when I tried the low A diet over the winter, I think I was still getting some hidden carotenoids.

Have you read this?

- Vitamin A and β-Carotene Can Improve Nonheme Iron Absorption from Rice, Wheat and Corn by Humans

"The effect of increasing doses of vitamin A on nonheme iron absorption from meals containing rice, corn and wheat is shown in Table 3. Iron absorption from the meal given alone was significantly lower than when vitamin A was included. There were no significant differences in iron absorption from rice meals containing from 0.55 to 2.78 umol (496–2526 IU) vitamin A. The same patterns of iron absorption were observed from the tests containing pre cooked corn flour and white wheat flour."

"In study 4, iron absorption from the rice meal containing vitamin A (meal 2, Table 4), was more than double the absorption from the meal given alone. In the absorption test in which the meal contained 0.58 and 0.95 mmol (342 and 558 IU) b-carotene, iron absorption was more than two and three times greater than the meal given alone. The same pattern of iron absorption was observed for corn and wheat tests. The addition of 8 g of coffee powder as a beverage to meal 3 for rice test (0.58 umol b-carotene) and meal 4 for corn and wheat tests (1.53 and 2.06 umol b-carotene, respectively) (Table 4), produced no difference in iron absorption compared with meals with lower or higher content of b-carotene and without coffee, but the values were still significantly higher than those obtained when the meal alone was consumed."


"b-carotene has the same effect on iron absorption than vitamin A. In the case of rice meal, it was shown that 0.95 umol (558 IU) of b-carotene increases iron absorption more than threefold compared with the meal given alone. Absorption from the other two cereals showed similar behavior. It seems that b-carotene also prevents the inhibitory effect of polyphenols on iron absorption. When coffee was administered with the test meals containing b-carotene, iron absorption did not show a significant decrease as expected. On the contrary, it increased from one- to twofold compared with the meal without b-carotene or coffee."

"The unexpected behavior of vitamin A and b-carotene of improving iron absorption requires further studies to discover the mechanism for this peculiar reaction. A previous publication (Layrisse et al. 1997) showed that spectrophotometric results, elution patterns from high-performance liquid chromatography (HPLC) and solubility of iron with vitamin A at pH 6 suggest that vitamin A binds iron liberated during the digestive process and forms a complex that acts as chelating agent preventing the inhibitory effect of phytates and polyphenols on nonheme iron absorption. This hypothesis agrees with the results of Mejia (1986), who demonstrated interactions between vitamin A and iron metabolisms."​

@haidut When are going to stop forcing people to take poison A against there will?

buying is voluntary. If somebody thinks vitamin A does not sit well with them then they are free to not buy any product containing it.

 

[Amazoniac]

From his other link posted, for comparison:

- 13-cis-Retinoic acid is an endogenous compound in human serum

 

[Amazoniac]

@Blossom - I just realized something. Check out the tomato diet above: gurus had lower levels than people consuming little carotenoids. Isn't it agonizing that it might be antagonizing?

 

[Dolomite]

Has anyone else doing low VA experienced dry, cracked heels? If so how have they changed on low VA (or anything else)? Mine have got worse, but it's now the end of a long summer of bare feet or flip-flop wearing and beach-going. Though I do think they're worse than this time last year and I'm hoping it's just all the VA being dumped into my system from storage and that they will improve soon...

My heels aren’t more cracked but I wear shoes most of the time. I did notice that right after lifting my foot to look at my heels the yellow orange tint is much more noticeable. I guess I need to look more closely at the fruit I am eating.

 

[Blossom]

@SB4
Here’s what the person on Grant’s site shared with me.
rs12934922-rs12934922(A;T)

Reduced conversion of beta-carotene to retinol Associated with Rs7501331 and reduced BCMO1, lower ability to convert beta-carotene to retinyl esters and higher serum beta-carotene levels. See also Rs7501331
rs12934922 (R267S) and rs7501331 (A379V) double mutant have a reduced catalytic activity of beta-carotene by 57%. Female volunteers carrying the T variant of rs7501331 (379V) had a 32% lower ability to convert Beta-carotene, and those carrying at least one T in both SNPs show a 69% lower ability to convert Beta-carotene into retinyl esters. rs7501331: the frequency of the wild-type C allele and variant T allele was 76 and 24%, respectively; 56% of the population was CC wild-type genotype, and 39% was heterozygote CT with the TT variant present in 5% of the population. rs12934922: the frequency of the wild-type A allele and variant T allele was 58 and 42%, respectively; 38% of the population was AA wild-type genotype, 40% was heterozygote AT, and 22% was TT homozygote
more info
rs6564851(T;T)
normal
rs6564851(G) associated with higher beta-carotene (p = 1.6 x 10(-24)) and alpha-carotene (p = 0.0001) levels and lower lycopene (0.003), zeaxanthin (p = 1.3 x 10(-5)), and lutein (p = 7.3 x 10(-15)) levels, with effect sizes ranging from 0.10-0.28 SDs per allele. Note that low plasma levels of carotenoids and tocopherols are associated with increased risk of chronic disease and disability, yet dietary intake of these lipid-soluble antioxidant vitamins is only poorly correlated with plasma levels, leading to the hypothesis that it isn't what you eat, it's your SNPs that regulate your carotenoid levels. This is one of the SNPs reported by NutraHacker SNPs.
more info
rs6420424(A;G)

This is one of the SNPs reported by NutraHacker SNPs. Common variation in the beta-carotene 15,15'-monooxygenase 1 gene affects circulating levels of carotenoids: a genome-wide association study.
rs12934922(A;T)
Reduced conversion of beta-carotene to retinol Associated with Rs7501331 and reduced BCMO1, lower ability to convert beta-carotene to retinyl esters and higher serum beta-carotene levels. See also Rs7501331
rs12934922 (R267S) and rs7501331 (A379V) double mutant have a reduced catalytic activity of beta-carotene by 57%. Female volunteers carrying the T variant of rs7501331 (379V) had a 32% lower ability to convert Beta-carotene, and those carrying at least one T in both SNPs show a 69% lower ability to convert Beta-carotene into retinyl esters. rs7501331: the frequency of the wild-type C allele and variant T allele was 76 and 24%, respectively; 56% of the population was CC wild-type genotype, and 39% was heterozygote CT with the TT variant present in 5% of the population. rs12934922: the frequency of the wild-type A allele and variant T allele was 58 and 42%, respectively; 38% of the population was AA wild-type genotype, 40% was heterozygote AT, and 22% was TT homozygote.
I just compared my raw data to the
above. I hope that helps you some.

*I don’t think this is necessary for everyone to be concerned over. I was just curious because my mom’s side of the family has lots of serious, hard to explain health problems and early deaths. Since I’ve seen myself following a similar trajectory and I have had great results from low A I wanted to try to understand it all better as applied to my own inherited traits.*

 

[schultz]

I wanted to try to understand it all better as applied to my own inherited traits.

Do you think these traits could be "switched" on or off, or altered, during the lifetime of a person?

 

[stargazer1111]

I’m just going with how I feel these days because science is really disappointing me time and again. I’m not sure which scientific research is accurate and which is phony. We’ve talked about this issue on the forum before but here’s a recent news story about more lies, greed and corruption in science.
Duke University to pay $112 million to US government after accusations of faking research for grants
@stargazer1111, if you learn anything on the A/casein issue would you mind posting it or sending me a PM? Thanks

No doubt. I took a "critical analysis" course last year for my graduate studies and an investigation into the most prominent scientific journals (Science, Nature, Cell) revealed that roughly 50% of the studies were either totally fabricated, partially fabricated, or the conclusions were just plain wrong based on the raw data.

Be very careful with interpreting research. The funding source is the very first thing I look at. Then, I see if I can guess what the results will be based on the funding source and am more often than not correct.

For instance, most of the pro-dairy literature I have read was funded by either Danon or Yoplait.

 

[Blossom]

Do you think these traits could be "switched" on or off, or altered, during the lifetime of a person?

I think it’s possible. I’m sure environment plays a larger part in all of this too. Peat’s ideas have helped me more than anything I’ve tried before going low A and I’m sure a big part of that was using thyroid. If a person knew they had a lower ability to convert carotenoids to A they could avoid getting caught up in certain eating styles that would end up causing them health problems. I’m not sure how much can be changed by middle age so I’m just going to work with what I know to be my own individual predispositions at this point.

 

[Inaut]

Not sure if this had been posted on any of the 222 pages of this threat so forgive me if so.....

Quick summary?

How A "Healthy" Diet Can Make You SIck...

My question is.....if liver function is restored and working as it should, is vitamin A really s big deal? Would autoimmune still be an issue

 

[Blossom]

No doubt. I took a "critical analysis" course last year for my graduate studies and an investigation into the most prominent scientific journals (Science, Nature, Cell) revealed that roughly 50% of the studies were either totally fabricated, partially fabricated, or the conclusions were just plain wrong based on the raw data.

Be very careful with interpreting research. The funding source is the very first thing I look at. Then, I see if I can guess what the results will be based on the funding source and am more often than not correct.

For instance, most of the pro-dairy literature I have read was funded by either Danon or Yoplait.

Thanks @stargazer1111! It’s nice to hear a perspective from someone in the field without ulterior motives.

 

[stargazer1111]

I asked Grant about this on his forum, and there are no studies that have directly test this, we need an actual lab to take heated milk casein and test for retinoic acid. We know that in the past before retinoic acid was discovered(1920s to 1950s), they heated the casein and retinol disappeared, so we assume it turned to RA via oxidation.

Retinol in Casein bypassing liver

Any reason you are not using rice for carbs?

We are on similar paths, I took high dose retinyl palmitate as well after reading that same study. 300K/day for few months, also two rounds of accutane in the past, different body chemistries, different reactions. Main symptoms for me were; sleep issues, cognitive decline-depression, skin worsening(acne, dandruff, oiliness, flakiness), eye site decline in left eye, continued hair shedding.

Now into my 6 months of low VA, symptoms very slowly fad, come and go, but continue in a positive direction.

I am intolerant to rice, unfortunately. I develop bad acid reflux and stomach pain when I eat it.

 

[stargazer1111]

Not sure if this had been posted on any of the 222 pages of this threat so forgive me if so.....

Quick summary?

How A "Healthy" Diet Can Make You SIck...

My question is.....if liver function is restored and working as it should, is vitamin A really s big deal? Would autoimmune still be an issue

Even with a perfectly healthy liver, it most likely depends on genetics. It would depend a lot on how much retinol-binding protein you produce and everyone is probably different in that regard.

 

[stargazer1111]

Thanks @stargazer1111! It’s nice to hear a perspective from someone in the field without ulterior motives.

Well, I am still an amateur at this point working on my PhD. But, I am learning quite a lot as I progress.

I used to just sort of believe what studies told me back in the day until I learned how to read them critically. Oh, how naive I was....

 

[Blossom]

I used to just sort of believe what studies told me back in the day until I learned how to read them critically. Oh, how naive I was...

Yes, me too (with medicine). It’s important to for us to be open minded yet skeptical and keep trying to grow in our understanding. I’m sure you are well on your way to being a great scientist.

 

[charlie]

Kidney stones, bladder stones, nephrolithiasis, urolithiasis...all caused by Poison/"Vitamin A"

 

[Mito]

Do you think these traits could be "switched" on or off, or altered, during the lifetime of a person?

I think it’s possible.

One example might be the infamous MTHFR polymorphism which slows down the MTHFR enzyme’s ability to methylate folate. It turns out that this genetic variant might be “fixed” simply by improving riboflavin status.

“One of the fascinating things we stumbled on is the possibility that the famous MTHFR polymorphisms — variations in the gene that uses riboflavin to make the methyl group of methylfolate — only decrease MTHFR activity because most people in whom the activity has been measured have mediocre riboflavin status.

Alex found some key studies supporting this and blogged about them here.

Here are the key findings:

• Using experiments in bacteria, where the part of the MTHFR enzyme that binds riboflavin is similar to humans and other animals, the reason that the polymorphisms decrease enzyme activity is because they make the enzyme bind to riboflavin more weakly. At low riboflavin concentrations, the enzyme has poorer activity. However, at high enough riboflavin concentrations, enzymatic activity is restored to normal.
• In humans who have the MTHFR C667T polymorphism, all of the elevated homocysteine is concentrated among people who have poor riboflavin status.
• 1.6 milligrams of riboflavin per day decreases homocysteine, and this decrease is highly concentrated among people with the C677T MTHFR polymorphisms who also have poor riboflavin status. In them, 1.6 milligrams of riboflavin decreases homocysteine a whopping 40%!”

https://chrismasterjohnphd.com/2019/02/26/mthfr-just-riboflavin-deficiency/

So it’s possible there is a similar nutritional factor that could “fix” the BCMO1 genetic variants.

 

[Pulstar]

@Kram @Orion

Anyone have an idea if the hormonal damage from accutane (3 course user...even though I had mild acne...sigh) is permanent? I am four weeks into a poison A elimination diet and I had noticeable improvements after the first two weeks but the benefits have subsided. I plan to keep at it for awhile though.

Seems the main factor could be time under low VA, and I truly hope the damage is not permanent.

@Travis doesn't think that Accutane damage is permanent. Here's his reply to the similar post and I think it is in the context of Accutane. Well, I really hope Travis is right.

And you could perhaps stop eating vitamin A. You're liver could be saturated with retinol that had been absorbed, stored, yet not used since you had so much circulating pseudo‐retinoic acid (Accutane™).

There is no way this could cause permanent damage, but you'd think it could cause a partitioning of retinol in the body. This retinol–retinoid acid system is under tight control with many enzymes and feedback loops. Taking pseudo‐retinoic acid (Accutane™) might logically affect retinol stores, and elevated liver retinol has been linked to aggression. I would guess that most Americans have enough retinol to last four months on a totally retinol–β-carotene-deficient diet

 

[Blossom]

One example might be the infamous MTHFR polymorphism which slows down the MTHFR enzyme’s ability to methylate folate. It turns out that this genetic variant might be “fixed” simply by improving riboflavin status.

“One of the fascinating things we stumbled on is the possibility that the famous MTHFR polymorphisms — variations in the gene that uses riboflavin to make the methyl group of methylfolate — only decrease MTHFR activity because most people in whom the activity has been measured have mediocre riboflavin status.

Alex found some key studies supporting this and blogged about them here.

Here are the key findings:

• Using experiments in bacteria, where the part of the MTHFR enzyme that binds riboflavin is similar to humans and other animals, the reason that the polymorphisms decrease enzyme activity is because they make the enzyme bind to riboflavin more weakly. At low riboflavin concentrations, the enzyme has poorer activity. However, at high enough riboflavin concentrations, enzymatic activity is restored to normal.
• In humans who have the MTHFR C667T polymorphism, all of the elevated homocysteine is concentrated among people who have poor riboflavin status.
• 1.6 milligrams of riboflavin per day decreases homocysteine, and this decrease is highly concentrated among people with the C677T MTHFR polymorphisms who also have poor riboflavin status. In them, 1.6 milligrams of riboflavin decreases homocysteine a whopping 40%!”

https://chrismasterjohnphd.com/2019/02/26/mthfr-just-riboflavin-deficiency/

So it’s possible there is a similar nutritional factor that could “fix” the BCMO1 genetic variants.

That’s a great example, thanks @Mito! I really appreciate your contributions.