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

[Amazoniac]

Liver retinol accumulates with age, and so does serum retinol. This is plainly demonstrated by the London autopsy data and the NHANES survey.
In the case of the thyroid, I don't think it would be harmful because I have seen no evidence for this. As far as I can tell, this had all started from the misinterpretation of carotenemia's relationship with hypothyroidism.

What about this?

In general, carotene behaves as an inert substance dependent on the lipids for its movements in the body and having no effect upon the body's economy except as a precursor of vitamin A. However, excessive ingestion may in some cases be followed by certain toxic effects, which are similar to those arising from excessive vitamin A ingestion, but are due to carotene and not to vitamin A.

Seems based on observation of patients.

 

[InChristAlone]

• Josephs, Hugh. "Hypervitaminosis A and carotenemia." American Journal of Diseases of Children (1944)

'As has been said above, knowledge of hypervitaminosis A is confined to the effects in animals, particularly in rats and mice, which are especially sensitive to the toxic effects of overt symptoms; the hair, especially about the head, becomes unkempt and falls out and the skin becomes greasy and has a peculiar odor suggestive of hydrous wool fat. Later the eyes become sore, there is a bloody secretion from the nose and diarrhea develops. These symptoms along with the extreme loss of weight and frequent loss of use of the posterior extremities provide a superficial resemblance to vitamin A deficiency. An almost constant feature is the development of multiple spontaneous fractures of the bones of the extremities. Some investigators reported exophthalmos, the cause of which is unknown; others stated specifically that they had never seen this result. [...] Histologically two features stand out, rarefaction of the bones with extreme thinning of the cortex and increased deposition of fat in the reticuloendothelial cells, especially in the Kupffer cells of the liver and in the spleen.' ―Hugh J.

'When vitamin A in large but nontoxic daily doses was given to rats, guinea pigs or rabbits, a rise in cholesterol and in total lipids of the serum occurred. This rise was only temporary, however, and tended to disappear after a time, even while the large doses of vitamin A were being given. The same effect was observed in human beings but not in dogs. In rats previous deficiency intensified and prolonged the response, and a similar reaction was seen after pneumonia in infants receiving vitamin A. Apart from this lipid reaction, the effect of vitamin A on physiologic processes has been little studied. No effect was observed on the formation of blood in animals. The serum calcium and phosphorus were not affected, though there was an increase in excretion of calcium, which was attributed to "décalcification" of the bones. The basal metabolic rate was decreased.' ―Hugh J.

'In contrast to the harmful results of overdosage with vitamin A, toxic effects have not been seen in animals after ingestion of excessive amounts of carotene; the animals have not lost weight or died and have not shown any of the outward manifestations of hypervitaminosis.' ―Hugh J.

'Carotenemia has been considered completely harmless, its only symptom being the development of the characteristic yellow color of the skin which generally disappears as soon as the responsible conditions have been corrected.' ―Hugh J.

Travis, I want to give you the benefit of the doubt that you are not cherry picking but you left out some important information from that paper.

2. Increased Serum Lipids : Anderson and Soley noted an increase in serum lipids and
pronounced fall in basal metabolic rate in several
California farmers who had eaten vegetables in
large amounts. The liver was enlarged in 4 oft the 9 patients. An increase in serum lipid was
noted by two other observers but, in general, little attention has been paid to the blood lipids
in carotenemia.

Case 3.—Carotenemia was diagnosed in a well-to-do,
asthmatic man who enjoyed vegetables in large quantities. No special studies were made, and the case is included only as one in which the patient was not
harmed by the carotenemia.

Case 4.—A 38 year old clergyman had as his only
complaints yellowness of the skin and loss of weight.
He had been supplementing his diet with carrots and
carrot juice for about seven years. When carrots were
removed from his diet, he recovered rapidly.

Case 6.—A well-to-do woman of 45, because of imagined idiosyncrasies to meat, eggs, milk and starchy
foods, had lived largely on vegetables and fruits for a
number of years. In addition to having carotenemia,
she was markedly underweight, with low blood pressure
and asthenia. Hypothyroidism was diagnosed on two
occasions when she was in the hospital. She was greatly
improved by a diet high in calories, given in the hospital.

Case 4 is the link connecting the cases of innocuous carotenemia with those in which
harm has resulted ; in this case there is no doubt
of the primary position of the carotenemia, and
at the same time the patient showed loss of weight, asthenia, high blood lipids and cholesterol and a low basal metabolic rate.

The high values for blood lipid and cholesterol and the low basal metabolic rate are
definitely part of the picture of carotenemia.

According to this theory the symptoms of hypothyroidism
may exist not only as the result of diminished activity of the thyroid gland, but as the result of "neutralization" of thyroxin by carotene or vitamin A.

The basal metabolic rate was not determined in the patient discussed with hypervitaminosis A, but it was decreased in most of my patients with carotenemia. In fact, the picture of carotenemia
resembles that of hypothyroidism to such an
extent that a distinction may be difficult.
​

I also found this symptom list for hypervitaminosis A very interesting when I see very few of these effects being talked about on this thread......and instead other ones that usually make the list of VA deficiency.

The condition was characterized by hepatomegaly, splenomegaly, hypoplastic anemia, leukopenia, increased serum vitamin A, increased serum lipids, advanced skeletal
development, clubbing of the fingers and sparse,
coarse hair ; it was accompanied with an abnormal
appetite for halibut liver oil, the source of the
vitamin. Most of the symptoms cleared promptly
when the excess vitamin A was removed from
the diet.
​

That was a great paper Travis thanks for sharing.

​

 

[Amazoniac]

Certainly the cases in which there is evidence of harm were those in which the patient had taken the carotene-containing foods for a long time or had lived largely on them.[..]

[..]Case 4 is the link connecting the cases of innocuous carotenemia with those in which harm has resulted; in this case there is no doubt of the primary position of the carotenemia, and at the same time the patient showed loss of weight, asthenia, high blood lipids and cholesterol and a low basal metabolic rate.

 

[Travis]

The high values for blood lipid and cholesterol and the low basal metabolic rate are
definitely part of the picture of carotenemia.​

Of course, this is because they are simply both symptoms of hypervitaminosis A.

 

[InChristAlone]

Of course, this is because they are simply both symptoms of hypervitaminosis A.

But the symptoms of hypervitaminosis A were a bit different. Was there an indication for conversion of the carotene to A in those cases that showed harm? Because carotene is not A as we have been debating about how it isn't harmful like RA is, but you just posted a paper showing excessive carotene cannot be distinguished from hypothyroidism.

 

[Travis]

...but you just posted a paper showing excessive carotene cannot be distinguished from hypothyroidism.

Well it can, because there are other causes of hypothyroidism than hypervitaminosis A and it has strict biochemical definitions—i.e. high TSH, low T₃, low T₄—completely independent of carotene levels. You would expect hypervitaminosis A to cause carotenemia only when sufficient carotenes are also consumed. Carotenemia can of course happen in the absence of hypervitaminosis A, and hypothyroidism, yet the presence high concentrations of retinoic acid actively limit carotene cleavage leading to higher skin levels. Retinol should lower the amount of carotenes needed for skin color changes.

Vegetarian animals consume β-carotene in levels far exceeding what has been shown to induce carotenemia in some people, yet they also consume negligible amounts of retinol. Although fur and feathers can often obscure skin color,* their metabolic rates don't appear any worse for it.

* Ya' gotta 'shave their bellies' first, and then check for orangeness.

 

[InChristAlone]

Well it can, because there are other causes of hypothyroidism than hypervitaminosis A and it has strict biochemical definitions—i.e. high TSH, low T₃, low T₄—completely independent of carotene levels. You would expect hypervitaminosis A to cause carotenemia only when sufficient carotenes are also consumed. Carotenemia can of course happen in the absence of hypervitaminosis A, and hypothyroidism, yet the presence high concentrations of retinoic acid actively limit carotene cleavage leading to higher skin levels. Retinol should lower the amount of carotenes needed for skin color changes.

Vegetarian animals consume β-carotene in levels far exceeding what has been shown to induce carotenemia in some people, yet they also consume negligible amounts of retinol. Although fur and feathers can often obscure skin color,* their metabolic rates don't appear any worse for it.

* Ya' gotta 'shave their bellies' first, and then check for orangeness.

So why did case 4 present with carotenemia without large amounts of retinol? At least I presume, we cannot know from the lack of details given.

 

[Travis]

• Maharshak, Nitsan. "Carotenoderma–a review of the current literature." International journal of dermatology (2003)

'Carotenoderma is a phenomenon characterized by orange pigmentation of the skin, resulting from carotene deposition mainly in the stratum corneum. It is associated with a high blood β-carotene value, and is regarded as a significant physical finding, but a harmless condition.' ―Maharshak

'The most common is excessive dietary consumption of β-carotene. Carotenemia may be observed 4–7 weeks after initiation of a diet rich in carotenoids. Foods with high β-carotene contents are listed in Table 2. In these cases of carotenemia, serum levels of vitamin A may be normal or elevated, although never high enough to cause hypervitaminosis A.' ―Maharshak

'Lycopen [sic] is a physiologically inert isomer of carotenoid that is not converted into vitamin A. It is found in tomatoes, rose hips and bittersweet berries. Its metabolism is similar to that of β-carotene. Skin pigmentation in lycopenemia has a deeper tinge than that in carotenemia and occurs on the palms and soles but also on the palate. The sclerae are also unaffected in this condition. It can be differentiated from carotenemia on the basis of spectrophotometeria.' ―Maharshak

'Riboflavinemia has also been reported to cause yellow skin.' ―Maharshak

'In diabetes mellitus, in addition to hyperlipidemia, the conversion of β-carotene into vitamin A in the liver may be impaired and thus an elevation of serum β-carotene levels may occur.' ―Maharshak

'Liver disease may cause carotenemia due to impaired conversion of β-carotene into vitamin A. In these cases carotenenoderma may be masked by jaundice [a.k.a. hyperbilirubinemia]. Kidney diseases, particularly nephrotic syndrome and chronic glomerulonephritis, may be associated with elevated serum levels of β-carotene. In nephrotic syndrome it is attributed to hyperlipidemia. An interesting finding is the absence of carotenoderma in patients who suffer from renal disease in spite of elevated serum β-carotene.' ―Maharshak

'Carotenoderma is a well-known physical finding which is considered to be harmless. The importance of recognizing this condition is chiefly in calming the patient and in avoidance of unnecessary examinations, which can be unpleasant to the patient and may have economic implications.' ―Maharshak

'Apart from anecdotal complications of carotenemia, we did not find any evidence of long-term complications or benefits resulting from carotenemia.' ―Maharshak

 

[InChristAlone]

So you are still saying that excessive carotene is harmless despite what that paper said about low metabolic rate. You blame it on retinol or maybe other underlying diseases? They said there was no doubt case 4 had carotenemia but you are saying maybe the hyperlipidemia is a separate underlying condition?

 

[Hans]

I have yet to see a dog excited to eat offer of raw liver

Lol then you clearly never had dogs or they were very spoiled and picky. Our dogs would prefer to eat liver any day over any other food. They like it "raw and wriggly" (quote from smeagol).
When they just get a whiff of raw liver they get pretty excited all right.
And it's definitely not just the two dogs we have now. My family and I only had two dogs when I was very young and I can't remember that we ever tried giving them liver; but my wife and her family had dogs all the time while moving around (even to two other countries), and all of her dogs loved liver just the same.

 

[Elchupanibrain]

Due to severe acne, i had 3 treatments with accutane. I guess i should be poisoned like sh**

 

[Amazoniac]

The vitamin A spectrum: from deficiency to toxicity (!)

"nd-carotene toxicity was described by Leo et al (30) in the livers of alcohol-fed animals, which showed swollen mitochondria after b-carotene feeding. Of interest is the possibility that retinoid metabolites of b-carotene could also have biological and possibly toxic potential. Wang et al (31) [previous page] showed that b-carotene molecules in an in vitro system, in addition to splitting into retinal, could also be split at several double bonds, yielding apo carotenals and apo carotenoic acids. They showed that at low doses, these carotenoic acids could be converted directly to retinoic acid (32–34). That is, for retinoic acid to be formed, b-carotene need not be converted to retinal first because in the presence of citral, which blocks the oxidation of retinal to retinoic acid, retinoic acid was still detected (35). Yeum et al (36) showed that this eccentric [asymmaetric] cleavage of b-carotene could occur by a cooxidation mechanism in the cytosol. These investigations showed that when lipoxygenase was incubated with b-carotene alone, very small amounts of eccentric cleavage products of b-carotene appeared; however, when the substrate linoleic acid was added to the system, the cleavage metabolites of b-carotene increased dramatically. Thus, it appears that eccentric cleavage can be initiated in tissues by a cooxidation mechanism and then possibly completed by either conversion to retinaldehyde to form retinoic acid or by a mitochondrial mechanism, as Wang et al (37) described, to form retinoic acid. However, the question arises as to what happens when these eccentric cleavage products accumulate in large amounts? Do they have biological activity of their own? Could these metabolites interfere with the action of retinoic acid? This may, in fact, partially explain the results from 2 carotene intervention trials in which the effects of high doses of b-carotene supplements were studied in smokers and in asbestos-exposed workers (38, 39). These studies showed a higher incidence of lung cancer in smokers who consumed high doses of b-carotene than in smokers who did not take b-carotene supplements."

"An animal model was used to try to mimic the results of these studies in humans (40). Ferrets were divided into 2 groups: b-carotene supplemented and non-b-carotene supplemented (control group). The dose of b-carotene used was equivalent to 30 mg/d in the human intervention trials. The b-carotene–supplemented and non-b-carotene–supplemented groups were further divided into smoke-exposed and non-smoke-exposed groups. The smoke-exposed group was exposed to cigarette smoke within a chamber twice in the morning and twice in the afternoon for 30 min each time, providing an exposure equivalent to that from 1.5 packs of cigarettes/d in humans. The animals tolerated this exposure well; they experienced no decrease in appetite or weight and behaved no differently from nonsmoke-exposed animals. Animals were treated for 6 mo and then killed. b-Carotene concentrations in the plasma and lungs were greater in the b-carotene–supplemented ferrets than in the nonsupplemented ferrets; however, b-carotene concentrations in the lungs were significantly lower in the smoke-exposed ferrets than in the non-smoke-exposed ferrets in both the b-carotene–supplemented and nonsupplemented control animals. Retinoic acid concentrations in the lung tissue were also significantly lower in all 3 treatment groups than in the control group (Table 3). The dramatic decreases in lung and blood b-carotene concentrations as a result of smoke exposure correlated with the enhanced breakdown of b-carotene into eccentric cleavage oxidation products."

"When the lung sections of the 4 groups of ferrets were examined, it was found that smoke exposure alone caused mild aggregation and proliferation of macrophages. However, localized proliferation of alveolar cells and alveolar macrophages and keratinized squamous epithelial cells were observed in the ferrets in the 2 b-carotene–supplemented groups. The most severe proliferation of alveolar cells and squamous metaplasia was observed in the b-carotene–supplemented, smoke-exposed ferrets. Keratinized squamous metaplasia was confirmed by immunohistochemical staining with anti-keratin antibody in the lung sections of all ferrets in the b-carotene–supplemented, smoke-exposed and non-smoke-exposed groups. Retinoic acid concentrations were lower in the smoke-exposed ferrets than in the nonsmoke-exposed ferrets, presumably because of increased oxidative breakdown. In turn, the expression of RARb (a subtype of RAR) activity was down-regulated in the lungs of the 3 treatment groups compared with that in the control group. RARb is known to play an important role in normal lung development, and primary lung tumors and lung cancer cell lines lack RAR b expression (41–46). Thus, a role for RARb as a tumor suppressor gene in the lung has been proposed (47). Because lung carcinogenesis is also associated with an alteration in retinoid signaling involving the AP-1 complex, AP-1 transcriptional activity was studied in these ferrets (48). c-Fos and c-Jun expression were up-regulated in the b-carotene–supplemented, smoke-exposed group. Additionally, AP-1 expression in this study was positively correlated with squamous metaplasia and inversely with RARb expression in these animals.

Thus, it appears that high doses of b-carotene under highly oxidative conditions result in many eccentric cleavage oxidative breakdown products, which could have biological activity of their own. One possibility is that these products interfere with retinoic acid binding to retinoid receptors, but another likely possibility is that these metabolites induce local enzymes in the lung, such as P450 enzymes, which increase the catabolism of retinoic acid and thus diminish retinoic acid signaling. A local deficiency of retinoic acid can then result in squamous metaplasia. Salgo et al (49) reported that b-carotene oxidation products promote the binding of benzo[a]pyrene (a smoke-borne carcinogen) to calf thymus DNA. Incubation of DNA with intact b-carotene decreased such binding, whereas incubation with b-carotene oxidation products (eg, 5,6-epioxide) for 1, 2, 3, and 4 h significantly increased the binding. These are all possible explanations for why toxicity occurs after high doses of b-carotene and may explain the increased incidence of lung cancers observed in the 2 large intervention trials mentioned previously (38, 39)."​

- The toxicity of antioxidants and their metabolites

"Despite this suggested beneficial role of b-carotene, several large, randomised supplementation trial could not support this suggestion. Two major trials even found increased cancer incidence after b-carotene suppletion in both smokers and asbestos workers (Pryor et al., 2000). It has been thought that this could result from b-carotene only being effective as an antioxidant at low O2 tension, whereas at high O2 tensions it may even stimulate lipid peroxidation (Bast et al., 1998). The free radical addition as depicted in Fig. 4, leads to the free radical form of the carotenoid molecule. Lipid peroxyl radicals (LOO'[savage solution]) that arise during lipid peroxidation may undergo such a radical addition reaction. Subsequent oxygenation of the radical-carotenoid adduct is possible:

LOO-carotenoid' + O2 -> LOO-carotenoid-OO'​

<stop eating spaces>
This LOO-carotenoid-OO' might have a pro-oxidant activity. Its formation has been used to explain the stimulation of lipid peroxidation by b-carotene at relatively high oxygen tensions.

The instability of b-carotene or its metabolites (including oxidised products) in the lungs of cigarette smokers or asbestos workers have been suggested to be responsible for the carcinogenic response (Wang and Russell, 1999). The oxidised products of b-carotene facilitate carcinogenesis by promoting DNA damage or by inducing cytochrome P450 enzymes that promote carcinogen activation (Wang and Russell, 1999; Paolini et al., 1999). Carcinogens are abundantly found in cigarette smoke. The cytochrome P450 induction might also enhance the catabolism of retinoic acid decreasing its levels. Retinoic acid regulates epithelial cell growth through its nuclear receptors (RARs). RAR, which is induced by retinoic acid, can inhibit activator protein 1 (AP-1) activity via a protein-protein interaction. In addition, oxidative stress induced by smoking enhances AP-1 expression. AP-1 binds to the AP-1 responsive element in DNA, and affects the actions of signal transduction pathways, usually resulting in cell proliferation. It is plausible that the b-carotene-induced decrease in retinoic acid level in the lung, or the down-regulation of RARb might reduce the inhibitory effect of retinoids on AP-1, so enhancing lung cell proliferation and potentially tumor formation (Wang and Russell, 1999)."​

 

[Richiebogie]

Seeing the countless studies that restricting VA for long periods in cattle disturbs reproductive health is not good enough evidence that VA is essential?

If retinol and beta carotene are bad for mammals, then we might expect that ruminants rely on their large bacterial colonies to process the beta carotene from the grass they eat into safe chemicals for their intestines to absorb.

This is probably how beef fat ends up pretty low in beta carotene and vitamin A.

On the other hand, Vitamin A is quite high in cows' milk. This might be to feed the calves' rumen bacteria. This way the appropriate bacteria are ready to multiply when the calf is weaned from milk to grass.

Since humans do not need to rely on grass or other high beta-carotene, high cellulose foods, our intestinal flora is much smaller.

We may be better off avoiding high fat dairy, vitamin A-fortified foods and supplements, liver and high sources of beta carotene.

 

[Richiebogie]

I can't believe you are still taking that book seriously.

The author's engineering mind uncovered a logical error in the deficiency experiments.

To prove dietary component Z contains something essential that is missing from diet X, you need to show

X causes disease
X + Z does not

Instead what was shown was:

X + Y causes disease
X + Z does not

Notice the difference?

Not only did they add Z, they also removed Y.

From this we can conclude either:
1) Z is essential or
2) Z contains something essential or
3) Z is less toxic than Y.

In the experiments of the 1920's, we can conclude either
1) butter is essential or
2) something in butter is essential, or
3) butter is less toxic than air cooked casein and rendered lard!

In other words, the experiments did not prove 1) or 2).

They may have demonstrated 3).

If so, X might be superior to X + Z.

This might be more likely since part of Y was an oxidized form of Z.

 

[Richiebogie]

I also found this symptom list for hypervitaminosis A very interesting when I see very few of these effects being talked about on this thread......and instead other ones that usually make the list of VA deficiency.

The condition was characterized by hepatomegaly, splenomegaly, hypoplastic anemia, leukopenia, increased serum vitamin A, increased serum lipids, advanced skeletal development, clubbing of the fingers and sparse, coarse hair; it was accompanied with an abnormal appetite for halibut liver oil, the source of the vitamin. Most of the symptoms cleared promptly when the excess vitamin A was removed from the diet

Earlier in the article:

Whether or not it is justifiable to label as "abnormal" a liking for an article of food which most people would not eat by choice, there is no doubt that the child's liking for halibut liver oil was a factor in the case which is reported. It is interesting that this desire for the oil was replaced by a desire for butter and carrots after the administration of the oil was discontinued, and that as the patient improved clinically he lost all such desires.

Henschen's patient with carotenemia had developed such an appetite for carrots that she was impelled to search garbage cans to satisfy her craving.

Well I am sure we all can all relate to that!

Britney warns about dangerous cravings, particularly on long haul flights:



"I'm addicted to you
Don't you know that you're toxic?"

That champagne bubble dress is quite flash!

 

[InChristAlone]

Earlier in the article:

Well I am sure we all can all relate to that!

Britney warns about dangerous cravings, particularly on long haul flights:



"I'm addicted to you
Don't you know that you're toxic?"

That champagne bubble dress is quite flash!

But there's gotta be a reason for the desire, we just don't know why. I know I've had some weird cravings in my past. Raw cookie dough was one. I wouldn't even bake the sugar cookies, just eat the dough over the course of a few days. Its disgusting looking back on it. But why?? I was nursing and required more calories? But why not just eat cookies? Why eat it raw?

 

[franko]

Due to severe acne, i had 3 treatments with accutane. I guess i should be poisoned like sh**

Presumably, you are one of the lucky ones who was able to handle it.

Just do a google search for "Accutane ruined my life" if you want to hear the stories of the "unlucky" ones.

Or watch this rundown of Accutane side effects:

 

[InChristAlone]

I was brave yesterday and ate 2 oz of beef liver!!! hadn't eaten it in a couple months. My lips are smooth! No skin peeling. Folks I think liver is a great thing once in a while. It comes with both vitamin A and E, and as @Amazoniac has been talking about they should go together. And of course don't overdose on polar bear liver

 

[franko]

I tracked down a similar image to the one in the video I posted previously because I think it's a good visualization of what Grant has said about Retinoic Acid causing "head to toe destruction of the human body." That's no exaggeration.

Source: Accutane (isotretinoin) - How it Works, Side Effects, and Reviews

Some may still ask: What does this have to do with Vitamin A?

Well, Accutane is isotretinoin. And isotretinoin is an isomer of retinoic acid (it is an "isomer" because it has the same molecular formula [C20 H28 O2] but in slightly different "arrangement" — the important point for the layman to understand is that they are virtually equivalent in function in the human body).

So basically: isotretinoin (Accutane) ≈ retinoic acid.

And Vitamin A can and does convert to retinoic acid in the human body (especially under certain conditions).

As Grant says in his book:

"Where and when does this conversion take place in the body? It’s well documented in Retinoic Acid: Structure, Mechanisms and Roles in Disease (Microbiology Research Advances: Cell Biology Research Progress), both at the cellular and molecular levels. It's also documented in this 2006 report The acute and chronic toxic effects vitamin A.

From these two sources, it’s clear to see that the body will convert excess vitamin A (retinol) to retinoic acid. It’s going to happen and it happens normally. It will happen in the intestine and at the cellular level in any other tissues. Here is the key fact to remember:

Retinol is metabolized to retinoic acid in normal cells."

- p. 125, ETFOH​

This is why a key feature of Grant's theory is to explain a general association between excess Vitamin A consumption and taking Accutane — the key difference being a matter of degree.

Just for general illustration purposes, you could think of taking Accutane as being similar to consuming a huge amount of VA. Or, by consuming an excessive amount of VA chronically, it may have a similar effect to taking a small amount of Accutane.

But the key point for the theory is to understand the mechanism. Because this gives a mechanistic explanation as to why there could be such a thing as "subclinical" hypervitaminosis A from seemingly normal diet/lifestyles.

 

[Travis]

The author's engineering mind uncovered a logical error in the deficiency experiments.

All that's fine, yet oxidized retinol is not exclusively retinoic acid. The lipid chain of course can become peroxided thus abrogating all hormonal properties. This is an important fact to consider when reinterpreting that historical feeding trial.