Quote from tim on December 19, 2019, 7:33 am

@orion

Ah thanks, so you feel the stress response is from an increase in VA excretion? I thought that we absorb roughly 5 mg of a 100 mg tablet and that the total bodily reserves were about 30 mg, that struck me as something I should be able to replenish quite quickly? It makes sense though over supplying our bodies with the rate limiting nutrients involved in VA excretion.

Yeah I'm intrepidly soaking/fermenting some beans right now to get more molybdenum and B vitamins in my diet. Something I didn't realise until yesterday is that dairy is actually the main molybdenum source for most people.

Quote from Orion on December 19, 2019, 7:37 am

Quote from tim on December 19, 2019, 7:33 am

@orion

Ah thanks, so you feel the stress response is from an increase in VA excretion? I thought that we absorb roughly 5 mg of a 100 mg tablet and that the total bodily reserves were about 30 mg, that struck me as something I should be able to replenish quite quickly? It makes sense though over supplying our bodies with the rate limiting nutrients involved in VA excretion.

Yeah I'm intrepidly soaking/fermenting some beans right now to get more molybdenum and B vitamins in my diet. Something I didn't realise until yesterday is that dairy is actually the main molybdenum source for most people.

I think this link may have some of the explanation of why B2 and B1 are not working properly in people who have VA overload.  I think the minerals are the base of the pyramid and are deficient, DH system is limping along.

 

https://b12oils.com/rnb.htm

 

Quote from tim on December 19, 2019, 7:42 am

@bludicka

Yeah I normally take nutritional yeast when I want more Bs.

Quote from ggenereux on December 20, 2019, 10:56 am

Hi @tim-2,

Re: I really don't understand how you think a VAD diet containing lard and casein can cause toxicity. Both casein and lard have minimal VA and RA, this isn't up for debate.

That’s a critical point for two reasons. Firstly, the tiny amounts of vitamin A that does exist in lard and casein is evidence that their supposed VAD diet was not actually completely devoid of vitamin A. Therefore, the grand VAD theory was not really proven by their experiments. Additionally, even Wolbach & Howe acknowledged in their report that other contemporary 1-yr long studies (using other VAD diet designs) had wholly failed to produce the VAD conditions in their animals. For them to gloss over that fact is not acceptable, and is not valid science. Why should we consider the Wolbach & Howe studies to be any more legitimate or valid? Why aren’t the other ones correct?

But, of course, the small amounts of retinol in the casein on the Wolbach & Howe studies could not, and would not, have diseased and killed these animals in just 8-10 weeks either. And, we now know with certainty that it wasn’t a deficiency. So, what really happened to these animals?

We need to then ask was it a toxicity condition that caused the disease and death in these animals so quickly. If so, there are not a lot of choices as to what that toxin was. One possibility is that it was the vegemite causing the fermentation of the starches in the intestinal tract poisoning them with methanol? But, there a big clue found in Stepp’s 1913 experiments, where he did not use vegemite. The clue is that his animals were killed extremely quickly by the diet when washed and heated in ethanol, and not at all when the same diet was heated and washed in ether.

Additionally, the death rate in Stepp’s experiments was proportional to the heating duration. Therefore, it entirely possible that the heating and processing of the base food was somehow creating an unknown toxic compound. And it was that toxic compound that was then causing rapid disease and death.

Then, we need to consider the very limited number of food-based substances included in these animal diets that can be converted into toxic ones through a process of heating and aeration. Also, consider that ethanol will provide the needed OH group for oxidizing retinol to retinoic acid, and ether does not. Then consider that all the morbidity conditions described in these experiments are a perfect match for RA poisoning.

RE: If I saw rats or mice breeding successfully over multiple generations on a zero VA diet then I would start to question the science.

Please go ahead and conduct that experiment. It would probably only take about 18 months.

But, breeding successfully over multiple generations is not at all the basis of the so-called science that defined the existence of vitamin A in the first place.

Next, let’s consider what we know about vitamin A in humans. Firstly, the “active form” of vitamin A is RA (both the 13-cis and all-trans isomers). But, the FDA has stated that a fetus exposed to “ANY AMOUNT” of RA can result in birth defects. RA is so incredibly toxic to the human fetus, that it’s on par with that of thalidomide.  The NIH has also documented RA to be a “poison”. Yet, we are supposed to believe that same highly toxic substance to be the active form of a vitamin essential for fetal development? How can RA (in any amount) be both a “poison” and a “vitamin” at the same time?

And, how is it that even trace amounts of the “active form of a vitamin” can so easily destroy a human fetus? This toxicity is not theoretical. It has been proven repeatedly in animal studies, and it has been proven thousands of times over with women on Accutane getting pregnant and subsequently having either spontaneous abortions or giving birth to deformed babies.

So, how can anyone legitimately claim that RA is needed for the proper development of a human fetus? Additionally, it’s well documented that retinol is a direct reproductive toxin. This has been known since at least the 1960s. It is also well documented that retinol (and even beta carotenes) are naturally converted into both 13-cis and all-trans RA. So, the notion that this reproductive toxin is also an essential “vitamin” is completely absurd IMO.

But, opinions don’t matter here. So, let’s consider what happens in the real world. There was a study of birth defects in chronic malnourished mothers in Kenya. The researchers were astonished that these mothers were giving birth to anatomically perfect babies. The rate of birth defects was effectively zero among this group of women.  Whereas, here in North America the rate of birth defects is ~ 1/33 babies. How do we square up these glaring contradictions?

Beyond reproductive health, let’s look at what Sommer’s documented for young children (the better-nourished ones) getting a single 100,000 IU dose of vA. The result was that they were 17X more likely to die in the following year, versus those in the placebo control group. How do we square up that information with “it’s a vitamin” claim? I think it’s complete garbage. How can giving a “vitamin” result in children being 17 times more likely to die? Some people will, of course, claim that they were just given too much of it. But, clearly then these “experts” have no clue what they are doing, and clearly their scientific incompetence has directly killed these children. Sorry, I don’t trust them, or their science, one tiny bit.

RE: Here are a couple of more modern studies proving VA is essential for the eye:

I’ve read a lot of similar studies. And almost all of them start off making the same claims:

Vitamin A and its derivatives (retinoids) play diverse and crucial functions from embryogenesis to adulthood and are used as therapeutic agents in human medicine for eye and skin diseases, infections and cancer.

But, that statement is 1) just repeating the prior assumptions from every other similar paper. And, there are other modern studies proving that RA destroys the human eye.

 And, 2) vitamin A used as therapeutic agents in humans has always failed.

VA treatments have failed in dermatology and have only caused more disease. It has failed in treating infections and caused a lot more deaths, and it has colossally failed in treating cancer. The real facts in cancer treatment are that it actually accelerates people into death. And for treating eye diseases, Sommer’s acknowledges in his textbook on VAD that vA supplementation often fails when treating eye diseases in children, and the children just progressively decline a die. His excuse is “we just didn’t get to them soon enough.” Of course, it’s complete BS because if the real cause was VAD, then the treatment with VAS should almost always work.

So, how can these researchers make these claims about the Vitamin A and its derivatives

being therapeutic agents when even just a few hours of research reveals that they almost always fail, and are worse than placebo? Why is there never any mention that the “retinoids” as therapeutic agents have now killed hundreds of teenagers and thousands of babies?

So, obviously, these people have a huge upfront bias, and without knowing all the details of these experiments I don’t put any credibility into their claims. And, how exactly did they abruptly introduce VAD on day 10.5?

As for their claim that : Plasma retinol binding protein (RBP) is the principal and specific vitamin A carrier in the blood and binds vitamin A at 1:1 ratio

I think I’ve proven that to be more junk science based on assumptions. In no way can the RBPs be “carrier” proteins. It is highly, if not completely, implausible.

What I see in so much of the medical research is that any serious critical thinking has been replaced by “studies” and statistical analysis. The epitome of the absurdity in vA research is this one. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832782/

Where the “researchers” have concluded that “tail flick latency” is now a measure of VAD. Yet, what they completely fail to see is that their animals have lasted disease-free at 2.5X longer than those of the disease defining W&H studies.

I think the entire concept of retinol as a “vitamin” is just based on garbage science. With nearly the worldwide supplementation of the human population with so-called vitamin A we are now facing a corresponding global catastrophe in human health. And, it just so happens that most of that chronic disease is a match for vitamin A toxicity. I’m not claiming that all the blame should be placed on VA. Obviously, there are other culprits such as glyphosate etc. 

It is so important for us to get this sorted out and we can only do that by not accepting the prior assumptions.

 

Quote from lil chick on December 20, 2019, 5:42 pm

Quote from ggenereux on December 20, 2019, 10:56 am

...How do we square up these glaring contradictions?

... how can these researchers make these claims about the Vitamin A and its derivatives

being therapeutic agents when even just a few hours of research reveals that they almost always fail, and are worse than placebo?

...So, obviously, these people have a huge upfront bias...

 

I was just shopping for Christmas gifts, and one game was described as "the perfect game for the POST-FACT era!"

Quote from pano200 on December 21, 2019, 12:10 am

Quote from ggenereux on December 20, 2019, 10:56 am

Next, let’s consider what we know about vitamin A in humans. Firstly, the “active form” of vitamin A is RA (both the 13-cis and all-trans isomers). But, the FDA has stated that a fetus exposed to “ANY AMOUNT” of RA can result in birth defects. RA is so incredibly toxic to the human fetus, that it’s on par with that of thalidomide.  The NIH has also documented RA to be a “poison”. Yet, we are supposed to believe that same highly toxic substance to be the active form of a vitamin essential for fetal development? How can RA (in any amount) be both a “poison” and a “vitamin” at the same time?

And, how is it that even trace amounts of the “active form of a vitamin” can so easily destroy a human fetus? This toxicity is not theoretical. It has been proven repeatedly in animal studies, and it has been proven thousands of times over with women on Accutane getting pregnant and subsequently having either spontaneous abortions or giving birth to deformed babies.

I've been thinking about this "active form" form of vitamin A for awhile. Scientists assume that the active form is the ligand that binds the tightest to the receptor and the ligand has to be everywhere the receptor is found. I find this pretty stupid to assume that the natural ligand must be the tightest binding ligand to the receptor. We have RAR and RXR receptors. RAR binds tightly to all-trans-RA and 9-cis RA. Skimming for articles about RXR, it seems like they can't figure out which is the natural ligand for it, a recent article says that many RXR ligands are natural, but only a few are endogenous or nutritionally relevant. https://www.sciencedirect.com/science/article/abs/pii/S0303720719301248

So basically they're trying to find some magic tightly binding ligand where it seems, at least to me, that RAR and RXR are perfectly fine having moderately tight binding ligands, like polyunsaturated fatty acids. https://www.mcponline.org/content/3/7/692 It just seems to me that this whole issue with vitamin A is just overstimulation of the RAR/RXR receptors.

Again, this is all a little out there, but MAYBE that's why if you take a bunch of omega 3 fatty acids it's considered anti-inflam, there are so many omega 3 fatty acids around to moderately activate to the RAR/RXR that they were preventing RAR/RXR from being overstimulated by retinoids. Maybe this is the mechanism of omega 3 fatty acids being anti-inflam? maybe there is some property of omega 3s vs the other polyunsaturated fatty acids that makes it more ideal for this role. i don't know.

Quote from tim on December 21, 2019, 1:29 am

@ggenereux2014

Hi Grant,

Thanks for your response.

Raw lard and raw milk both contain low non toxic levels of retinol and retinoic acid. Thus cooked lard and casein both contain low levels of RA. ATRA is toxic when taken orally but even megadoses do not generally kill people in a matter of weeks. Additionally, cooked liver and cooked butter which are actually high in retinol and thus will have the most RA of any foods can be fed to animals with no or limited ill effect. Thus there is no basis on which to conclude that RA in lard and casein caused detectable harm.

Why can't it be another nutrient deficiency or some other toxin?

But, that statement is 1) just repeating the prior assumptions from every other similar paper. And, there are other modern studies proving that RA destroys the human eye.

The studies are directly showing that retinol not RA is essential for the eye. You can feed a person with xeropthalmia ATRA but it will not cure it because we don't possess the enzymes to convert RA to retinol.

Next, let’s consider what we know about vitamin A in humans. Firstly, the “active form” of vitamin A is RA (both the 13-cis and all-trans isomers). But, the FDA has stated that a fetus exposed to “ANY AMOUNT” of RA can result in birth defects. RA is so incredibly toxic to the human fetus, that it’s on par with that of thalidomide. The NIH has also documented RA to be a “poison”. Yet, we are supposed to believe that same highly toxic substance to be the active form of a vitamin essential for fetal development? How can RA (in any amount) be both a “poison” and a “vitamin” at the same time?

11-cis-retinal and all-trans-retinal are the two active forms involved in vision. all-trans-RA is the active signalling molecule and hormone in the body. 13-cis-RA is naturally present in far smaller amounts than ATRA and isn't considered to have a biological role. Grouping ATRA and 13-cis-RA together when discussing toxicity is very inaccurate IMO as they are two completely different molecules. With regard to ATRA though, of course essential and endogenous molecules can have toxic properties. The essential metals are an example. The body produces substances like methanol and ethanol, carcinogenic formaldehyde is a natural part of our biochemistry.

I think the entire concept of retinol as a “vitamin” is just based on garbage science. With nearly the worldwide supplementation of the human population with so-called vitamin A we are now facing a corresponding global catastrophe in human health. And, it just so happens that most of that chronic disease is a match for vitamin A toxicity. I’m not claiming that all the blame should be placed on VA. Obviously, there are other culprits such as glyphosate etc.

I think it's essential but testing has shown that nobody in the Western countries are deficient and many have clinical hypervitaminosis A. I'm on board with you that excess VA is a major health issue.

Quote from ggenereux on December 21, 2019, 7:21 am

Hi @tim-2,

RE: ATRA is toxic when taken orally but even megadoses do not kill people in a matter of weeks.

Please read the early research on Accutane. They chose to go to market with the 13-cis-retinoic acid isomer of RA because it was LESS toxic than the trans isomers. And, the 13-cis-reinoic acid product has indeed killed many people. Maybe not in a matter of weeks, but many people have been seriously harmed (permanently damaged) by it in just a few weeks. As have many fetuses.

RE: Thus there is no basis on which to conclude that RA in lard and casein caused detectable harm.

See this 1987 HHS Patent HHS Patent 4,696,040. They’ve indeed poisoned to death their mice in just 8-17 days with trans retinoic acid. So, that’s pretty conclusive evidence that RA can indeed kill rodents in just two weeks.

RE: Why can't it be another nutrient deficiency or some other toxin?

I don’t think it can be a deficiency because the base diet did provide for the B vitamins, etc. And deficiencies result in a slow atrophy and wasting; not in a catastrophic disintegration of almost the entire body. The mode of death in these animals in no way approximates a deficiency condition.

What candidate other toxins can you think of? It had to be sourced from their food, and very likely created by heat-treating the food in alcohol. Then it has to be a toxin that is known to attack the basal membrane throughout the body. As you stated, let’s apply Occam's razor here. There are not a lot of possibilities, so I’m going with the most likely one.

RE: The studies are directly showing that retinol not RA is essential for the eye. You can feed a person with xeropthalmia ATRA but it will not cure it because we don't possess the enzymes to convert RA to retinol.

In Sommer’s book on stating the treatment often fails to recover a child from xerophthalmia, they were, of course, using retinol as a treatment and not ATRA.  So, it was retinol that failed to work. 

And it was retinol that poisoned children to death, at a rate of 17X placebo.

Since the body slowly and naturally converts some retinol to RA (into both the cis and trans isomers) we are just splitting hairs debating the relative toxicity of them. Eventually, via the detoxification pathways, they are the same.

RE: I think it's essential

That’s fine. All views are welcome here. 

Agreed, we’ve just gotten way too much of it.

Thanks

Grant

Quote from tim on December 21, 2019, 6:59 pm

@ggenereux2014

Hi Grant,

They’ve indeed poisoned to death their mice in just 8-17 days with trans retinoic acid. So, that’s pretty conclusive evidence that RA can indeed kill rodents in just two weeks.

I don't doubt that but the mice would have been given thousands of times more ATRA than animals would have gotten from lard and casein?

What candidate other toxins can you think of? It had to be sourced from their food, and very likely created by heat-treating the food in alcohol. Then it has to be a toxin that is known to attack the basal membrane throughout the body. As you stated, let’s apply Occam's razor here. There are not a lot of possibilities, so I’m going with the most likely one.

If RA was present in amounts similar to doses that can kill an animal then of course it would have been ATRA but I just don't see that as possible. But you are right, what else could it be? Animals can be sensitive to heat, they can also be sensitive to chemicals, for example parrots are sensitive to non stick fry pan use, dogs to chocolate. If they had straw in their enclosures it would have been pesticide treated. Nothing sticks out as a likely cause to me though.

In Sommer’s book on stating the treatment often fails to recover a child from xerophthalmia, they were, of course, using retinol as a treatment and not ATRA.  So, it was retinol that failed to work. 

Xerophthalmia is a degenerative process. If caught really early when it is simply dry eyes then it can be totally reversed but a lot of the time it can't. If a man got extreme gum disease from scurvy we wouldn't expect Vitamin C sufficiency to return his gums to a pristine state. Our eyeballs must be in a pristine state in order to be considered functional. As we know, nutrients do not operate in isolation either and third world children with VAD are malnourished in both calories and a range of nutrients.

And it was retinol that poisoned children to death, at a rate of 17X placebo.

Yes that makes sense to me, do you have a link to that, 17x is so high? Many of these children would have marginal zinc status as well as being close to or deficient in a range of nutrients including protein. A megadose of 100,000 IU retinol will further deplete other nutrients and is a stress for a small person's body to deal with all at once. However, a one off dose of 100,000 IU retinol is far less toxic than a course of Accutane, this is also a relatively small amount compared to the amount of retinol I have ingested when I was consuming both liver and cod liver oil regularly. Many here have consumed more retinol than that over a period of just a few weeks at some point during a chronic dietary program of self poisoning. We are examples of very high retinol consumption and we are still alive. We could conclude that that is due to us being well nourished and so being able to deal with more VA but I think these children probably died of infectious disease right? Infectious disease such as influenza often creates a state of hypervitaminosis A and when one is in a very weakened state, VA toxicity could be the final death blow. So I don't think a dose of 100,000 IU kills without the infectious disease element. It seems that low VA liver stores possibly protect against mortality from infectious disease. This doesn't prove though that low VA liver stores are beneficial the rest of the time.

That’s fine. All views are welcome here.

Thank you, hopefully discussion like this leads to greater understanding for all.