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Weston A Price's Book: Chapter 18 and Vitamin A Evidence
Chapter 18 of the famous book by Weston A Price, Nutrition and Physical Degeneration, has a lot of animal evidence and some human evidence on the supposed benefits of vitamin A. Has @ggenereux2014 or anyone else here debunked these mostly animal studies about the importance of vitamin A in the diet?
Here is a quote from Price's book about one study about vitamin A in pigs.
One of the most important contributions in this field has been made by Professor Fred Hale, of the Texas Agricultural Experiment Station, at College Station, Texas. He has shown that many physical deformities are readily produced by curtailing the amount of vitamin A in the ration of pigs. He produced fifty-nine pigs (15) that were born blind, every pig in each of six litters-where the mothers were deprived of vitamin A for several months before mating and for thirty days thereafter. In pigs, the eyeballs are formed in the first thirty days. He found, as have several others, that depriving pigs of vitamin A for a sufficient period produced severe nerve involvements including paralysis and spasms, so that the animals could not rise to their feet. He reported that one of these vitamin A deficient pigs that had previously farrowed a litter of ten pigs, all born without eyeballs, was given a single dose of cod liver oil two weeks before mating. She farrowed fourteen pigs which showed various combinations of eye defects, some had no eyes, some had one eye, and some had one large eye and one small eye, but all were blind.
https://gutenberg.net.au/ebooks02/0200251h.html#ch18
@jeremy my first thought is that "Vitamin A deficient diet" is missing other unidentified nutrients and/or includes VA inadvertently. Remember that the so-called VAD chow provided to rats in studies was full of casein --
I have the same question: Does anyone know what happened with these experiments?
Is there any way to find out what was in the "Vitamin-A deficient" ration fed to the pigs who had piglets born blind, with clefts, deformities?
The only study I could find available online (attached) from Hale has the attached pig diet, but it doesn't say what the "Vitamin-A deficient" ration was composed of. Interesting that the deformities were cleared by adding either cod liver oil or green pasture.
This is of personal interest to me. I was born with a cleft lip and palate.
5+ years ago I started reading up on health and nutrition, including Weston A Price's Nutrition and Physical Degeneration.
Me: Nutrition determines everything in health!
My wife: Okay, so what causes cleft lip?
Me (very confidently after seeing it in Chapter 18): Vitamin A deficiency. See these images of pigs here!
<Fast Forward 5.5 years>
Me to wife: I'm learning that Vitamin A might actually be a damaging substance and I will try lowering it in my diet.
My wife: ... Didn't you say Vitamin A deficiency causes clefts?
Me: Yes... yes I did. I need to look into that.
Anyway, I know that Vitamin A excess can cause clefts but I am still curious about what happened in these Professor Hale studies cited by Weston Price. Weston A Price's work is pretty foundational to many of us who care about holistic health, so it would be interesting to be able to speak to what happened in Hale's studies. Anyone have ideas?
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First I thought, as a serious question about any early pig studies:
Who cares about pigs?
-Who takes really good care of any pig?
Even most Germanic languages have mostly negative proverbs and idioms about pigs like:
•As sick as a pig.
•Choosy pigs never get fat. [a proverb not taken from the link below]
•It ain't fitting to roll with a pig.
https://owlcation.com/humanities/pig-idioms
Then in the 1935 Hale study, which you attached in your post, they had only a subjective measurement of what vitamin A deficiency was:
"Symptoms of vitamin-A deficiency in the gilts at the time of breeding were evidenced by their wobbly gait, weaving, and crossing of the hind legs at the walk, drooping of the ears, and loss of weight. After the gilts were bred, they remained on the vitamin-A-free ration for the first 30 days of the gestation period, the time during which it is known that the eye develops in the pig embryo. After the first 30 days of the gestation period had passed, the gilts were given an abundance of vitamin A in the form of cod-liver oil, so as to furnish them every opportunity to complete a full gestation period."
"DR. FREDERICK H. VERHOEFF : I should like to ask if it ever failed when you tried to do that [induce vitamin A deficiency birth defects]?
MR. HALE : Yes, it has, but it is hard to tell when these animals are depleted to the state where vitamin A is practically depleted out of the body. You have to observe that yourself and be enough of an animal husbandman to know the symptoms exhibited by those pigs with vitamin-A deficiency. I doubt if anyone who is not familiar with pigs showing vitamin-A deficiency could ever succeed, except through trial and error for a good many periods.
We succeeded the very first effort we made, after we selected young gilts the same age and weight of the first gilt. When we failed, it was with mature animals. We thought the one-hundred-and-sixty-day period on which we kept the first gilt was of some significance, but found it is not of any significance. The important feature is to deplete the animal to a very low state in vitamin A. We kept mature animals on a deficient ration for one hundred and sixty days and failed, but never have failed when we withheld breeding until the animals showed depletion, by these vitamin-A symptoms, to a very low state."
Why would any real scientist blindly assume that the cause of vitamin A deficiency is the only cause of these seemingly neurolical birth defects?
From looking at a more modern case study from 2018 they mention that there could several other reasons for microphthalmia and I don't think any of these older studies have excluded the possibility of any other possibilities than vitamin A deficiency.
-On top of theat who measures retinoic acid in any of these studies or wonder where the retinol that is usually very high in the liver have gone?
This more recent case study from 2018 is called:
"Congenital Microphthalmic Syndrome in a Swine"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6033249/
"A long-established cause of microphthalmia in swine is hypovitaminosis A [4–6]. Other known or suspected causes include gestational-acquired infections, drugs, and environmental pollutant toxicities [7, 8]. More recently, various genetic aberrations ranging from chromosomal duplications to mutations in a single gene SOX2 [8] were identified to be implicated in microphthalmia development in humans and other animal species.
Teschen/Talfan disease is caused by the ubiquitous Teschovirus A (previously classified as Serogroup 1 porcine enterovirus), a nonenveloped ssRNA(+) virus in the order Picornavirales, family Picornaviridae. There are 13 serotypes (PTV-1 to -13) [9] of different pathogenicity, but all of them exhibit gastrointestinal and neurotropism. Both domestic pigs and wild boars are the only known hosts [10].
"Apart from hypovitaminosis A, several other causes of microphthalmia were reported, including suspected drug toxicities and high levels of selenium in diet [7]. Hereditary microphthalmos has been reported in Yorkshire pigs [1], White Shorthorn cattle, Jersey calves, and Hereford cattle (as a part of encephalopathy-microphthalmos syndrome). The pattern of heritability seems to be autosomal recessive trait in all cases listed above [7]."
What matters is that there is strong evidence for vitamin A being essential during fetal development.
Function of Vitamin A in Vertebrate Embryonic Development
I'm very concerned about people spreading the idea that vitamin A is not a vitamin.
Vitamin A and Pregnancy: A Narrative Review
In a study with animals, severe VAD during pregnancy was associated with fetal renal agenesis [89], whereas mild VAD led to a decrease in kidney weight and the number of nephrons in the newborn [106]. Based on these findings, a study was conducted in 16 mothers with VAD and 64 mothers with vitamin A sufficiency. Newborn babies of the mothers with VAD had significantly lower mean retinol levels and the dimensions of both kidneys were smaller than those of the newborns of mothers with vitamin A sufficiency [63]. A recent systematic review found an association between vitamin A deficiency in pregnancy and a negative effect on kidney function and kidney structure in the child [107].
Even mild VAD may affect the kidney size of offspring.
Quote from David on April 22, 2024, 1:13 amFirst I thought, as a serious question about any early pig studies:
Who cares about pigs?
-Who takes really good care of any pig?Even most Germanic languages have mostly negative proverbs and idioms about pigs like:
•As sick as a pig.
•Choosy pigs never get fat. [a proverb not taken from the link below]
•It ain't fitting to roll with a pig.
https://owlcation.com/humanities/pig-idiomsThen in the 1935 Hale study, which you attached in your post, they had only a subjective measurement of what vitamin A deficiency was:
"Symptoms of vitamin-A deficiency in the gilts at the time of breeding were evidenced by their wobbly gait, weaving, and crossing of the hind legs at the walk, drooping of the ears, and loss of weight. After the gilts were bred, they remained on the vitamin-A-free ration for the first 30 days of the gestation period, the time during which it is known that the eye develops in the pig embryo. After the first 30 days of the gestation period had passed, the gilts were given an abundance of vitamin A in the form of cod-liver oil, so as to furnish them every opportunity to complete a full gestation period."
"DR. FREDERICK H. VERHOEFF : I should like to ask if it ever failed when you tried to do that [induce vitamin A deficiency birth defects]?
MR. HALE : Yes, it has, but it is hard to tell when these animals are depleted to the state where vitamin A is practically depleted out of the body. You have to observe that yourself and be enough of an animal husbandman to know the symptoms exhibited by those pigs with vitamin-A deficiency. I doubt if anyone who is not familiar with pigs showing vitamin-A deficiency could ever succeed, except through trial and error for a good many periods.
We succeeded the very first effort we made, after we selected young gilts the same age and weight of the first gilt. When we failed, it was with mature animals. We thought the one-hundred-and-sixty-day period on which we kept the first gilt was of some significance, but found it is not of any significance. The important feature is to deplete the animal to a very low state in vitamin A. We kept mature animals on a deficient ration for one hundred and sixty days and failed, but never have failed when we withheld breeding until the animals showed depletion, by these vitamin-A symptoms, to a very low state."Why would any real scientist blindly assume that the cause of vitamin A deficiency is the only cause of these seemingly neurolical birth defects?
From looking at a more modern case study from 2018 they mention that there could several other reasons for microphthalmia and I don't think any of these older studies have excluded the possibility of any other possibilities than vitamin A deficiency.
-On top of theat who measures retinoic acid in any of these studies or wonder where the retinol that is usually very high in the liver have gone?This more recent case study from 2018 is called:
"Congenital Microphthalmic Syndrome in a Swine"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6033249/"A long-established cause of microphthalmia in swine is hypovitaminosis A [4–6]. Other known or suspected causes include gestational-acquired infections, drugs, and environmental pollutant toxicities [7, 8]. More recently, various genetic aberrations ranging from chromosomal duplications to mutations in a single gene SOX2 [8] were identified to be implicated in microphthalmia development in humans and other animal species.
Teschen/Talfan disease is caused by the ubiquitous Teschovirus A (previously classified as Serogroup 1 porcine enterovirus), a nonenveloped ssRNA(+) virus in the order Picornavirales, family Picornaviridae. There are 13 serotypes (PTV-1 to -13) [9] of different pathogenicity, but all of them exhibit gastrointestinal and neurotropism. Both domestic pigs and wild boars are the only known hosts [10].
"Apart from hypovitaminosis A, several other causes of microphthalmia were reported, including suspected drug toxicities and high levels of selenium in diet [7]. Hereditary microphthalmos has been reported in Yorkshire pigs [1], White Shorthorn cattle, Jersey calves, and Hereford cattle (as a part of encephalopathy-microphthalmos syndrome). The pattern of heritability seems to be autosomal recessive trait in all cases listed above [7]."
Thank you for this analysis, David.
I'm going to try to restate what you're saying to see if I'm comprehending it the way you are laying it out.
- Pigs and humans are very different, so the relevance is questionable.
- The "Vitamin A deficiency" was purely subjective, not any kind of outright measurement of Vitamin A levels. Therefore the "deficiency" could have been any number of nutritional issues. And on top of that... since the "deficiency" was marked as a deficiency only once the pigs started having myriad health issues, it makes sense that the pigs born to sick mothers would have defects. Circular reasoning: "Despite depleting them of Vitamin A for 160 days, they aren't deficient because we don't see them sick yet. Once they're sick and feeble, then we will know they are Vitamin A deficient and breed them."
- There are no measurements to show serum retinol levels or anything similar.
- 80 years later, there are other known causes of the same defects showing up in pigs and these were not known to be investigated or controlled for at the time of the original studies.
Does that do a decent job at capturing what you are laying out?
Quote from tim on April 22, 2024, 2:33 amWhat matters is that there is strong evidence for vitamin A being essential during fetal development.
Function of Vitamin A in Vertebrate Embryonic Development
I'm very concerned about people spreading the idea that vitamin A is not a vitamin.
Vitamin A and Pregnancy: A Narrative Review
In a study with animals, severe VAD during pregnancy was associated with fetal renal agenesis [89], whereas mild VAD led to a decrease in kidney weight and the number of nephrons in the newborn [106]. Based on these findings, a study was conducted in 16 mothers with VAD and 64 mothers with vitamin A sufficiency. Newborn babies of the mothers with VAD had significantly lower mean retinol levels and the dimensions of both kidneys were smaller than those of the newborns of mothers with vitamin A sufficiency [63]. A recent systematic review found an association between vitamin A deficiency in pregnancy and a negative effect on kidney function and kidney structure in the child [107].
Even mild VAD may affect the kidney size of offspring.
So, Tim, you do not share Grant G's view that Vitamin A is a toxin, full-stop. Correct?
It sounds to me that you favor limiting A (avoiding hypervitaminosis) but also including enough to avoid hypo.
Thanks for sharing the studies; I have skimmed the rat study. From my brief skim it does seem very interesting in how meticulously they tested out adding Vit A back in and the differences noted. Adding Vit A seems (again, at a skim) to resolve defects. Of course, it also seems to demonstrate how difficult it would be to truly become deficient in a real world environment (especially in relation to our societal trend of likely being more towards hyper than hypo).
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Vitamin A is so ubiquitous that I find it hard to imagine any healthy diet/lifestyle for pigs that doesn't have some. And anything I can think of seems horribly non-pig.
And the fact that cod liver oil seems to help? A bit of cod liver oil in an unhealthy diet (especially given to those who are NOT VA Toxic) might do some good, or else why would it enjoy its current reputation? It's got some nutrition.
One of the biggest problems is the experiments is on pigs, not humans. Pigs need different things than chickens, different than cows, different than humans.
I find Price's results looking into human mouths much more interesting than any pig study. IMO Price does show that you can be healthy despite having VA in your diet. You don't have to be zero-VA to be healthy.
I suppose one of his "wrong notions" was thinking that every aspect of the food in the bags he sent home from the successful tribes was beneficial. He was looking for commonality between successful food ways, and of course VA is going to be one!
Here on Earth food is based on plants (even our meat animals eat plants) and plants rely on VA as their protection from the sun. All natural diets are going to have VA, but it doesn't mean HUMANS need it.
One of the interesting things is that he was studying people in situ, so that they had been eating that way for generations and probably micro-evolved to the unique challenges of each environment. A good example of this is that probably many Swiss were lactose tolerant.
I suppose you can choose the tribe who most closely resemble your genetics and try that diet, for myself that would be the Swiss.
And the closer you can approximate the entire lifestyle the better. You can't go picking and choosing. "I'm going to eat oats like a Scot, but I don't like fish and want to eat tomatoes..." or whatever.