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There is nothing "essential" or "vital" about Poison/"Vitamin A" - Part 3, other things can do the same jobs

See part 1 here.

See part 2 here.

See my article Cod liver oil is a poison and the research has always said so

This paper from 1922 shows that the presence of Poison/”Vitamin A” is NOT uniquely necessary.  As long as there are other agonist ligands for the RXR present in large enough amounts, no Poison/”Vitamin A” is necessary at all.  I will be interspersing other papers in here as well, to show that more recent science agrees with the findings from back then.

Before you read this one, you might want to review Part 2 of this series.  It is important to know before you go further, that science has shown that DHA (docosahexanoic acid), phytanic acid, and ARA (arachidonic acid) have all been shown to exert activity at the RXR receptor...short story is, they induce the exact same necessary biological effects that are attributed to Poison/”Vitamin A”, while not being toxic to the system. Evidence will be provided of all of these things.

A key thing to understand is that I am NOT arguing if Poison/”Vitamin A” has a biological EFFECT or not.  It does. Cocaine has a biological effect too! That’s not the point here. What I’m doing here is showing that real-world experiments from the 1920s showed that there are multiple other compounds in foods--they didn’t know what they were at the time--that activate the same biological effects that Poison/”Vitamin A” does, thus striking this poison off the list of “essential” nutrients for human life/health.  Even the authors are expressing their doubts in Poison/"Vitamin A" by the end of the paper.

Studies on Experimental Rickets - An Experimental Demonstration of the Existence of a Vitamin Which Promotes Calcium Deposition

Note the bolded part below.  They had their doubts about it even back then.

With the discovery in 1913 that certain fats contain a substance or substances which are essential for growth, this class of foodstuffs assumed an importance in nutrition which had not been hitherto accorded it. At first the evidence of the existence of the substance which subsequently became known as fat-soluble A, or vitamin A, rested upon the failure of experimental animals to grow when the fats carrying this substance were lacking in the food, and the resumption of growth when such fats were administered. Later xerophthalmia of a certain type was recognized as a pathological condition which invariably results from specific starvation for fat-soluble A. We have recently, however, convinced ourselves that a similar ophthalmia may be the result of disturbance of the balance of inorganic elements in the diet. Up to the present time no definite evidence has been brought forward to show whether one or more than one substance is contained in those fats which contain fat-soluble A which gives them their unique biological value (1).

What we are about to go into are the real-world, black-box demonstrations of how things other than Poison/”Vitamin A” can prevent the very ailments attributed to this imposter of a nutrient.

Other components are a factor, as meat by itself corrected rickets:

All of Mellanby’s own data cannot be brought into line with this reasoning. For example, Dog 187 was fed bread, yeast, salt, orange juice, separated milk, and 10 cc. of cottonseed oil, but no meat. It developed rickets. Dog 305 had the same diet but with 10 gm. of meat. The bones of this animal are described as “practically normal” (3). Meat is essentially lacking in fat-soluble A. It does, however, contain phosphorus, and but little calcium, and serves to change the ratio between these elements in the diet. This, as has been pointed out, is of great importance in the etiology of rickets (4).

What nutrients does meat contain that also are agonist ligands of the RXR?

  • DHA
  • ARA
  • Phytanic acid
  • Other free fatty acids

Has protein malnutrition itself been associated with so-called “Vitamin A deficiency” in the research?  You bet!

Vitamin A deficiency and protein-energy malnutrition in a sample of pre-school age children in the Kivu Province in Zaire.

This survey suggests that in this population of the South-Kivu Province in Zaire, vitamin A deficiency co-exists with protein-energy malnutrition

Protein energy malnutrition, vitamin A deficiency and night blindness in Bangladeshi children.

Our results showed that night blindness was associated with protein energy malnutrition when using the mid-upper arm circumference (MUAC) as a measure of nutritional status. The odds ratio for a confirmed diagnosis of night blindness among children with a MUAC < 80% of the reference versus normal children was 5.4 (CI 1.9-15.5). Low MUAC was associated with low intake of beta-carotene-rich and vitamin A-containing foods as well as with low serum vitamin A in the total series of cases and controls. This may indicate that night blindness is only one aspect of the general protein energy malnutrition problems in this population.

Back to the initial paper.

In his experiments Mellanby studied cod liver oil, butter fat, lard, suet, bacon fat, peanut oil, olive oil, coconut oil, linseed oil, babassu oil, rape seed oil, palm kernel oil, and hydrogenated fats. He states (3):

“Of the fats tested, cod-liver oil is the best. Suet and butter also have a potent influence on calcification. Lard is poor as compared with suet. Butter, heated and oxidized for four hours, loses some anti-rachitic action. In his experiments Mellanby studied cod liver oil, butter fat, lard, suet, bacon fat, peanut oil, olive oil, coconut oil, linseed oil, babassu oil, rape-seed oil, palm-kernel oil, and hydrogenated fats. Cod liver oil similarly treated still has a strong anti-rachitic effect. The vegetable oils vary in their anti-rachitic action, the order of merit being somewhat as follows: pea-nut and coca-nut oils (best), rape-seed, cottonseed, palm-kernel, olive, linseed, and babassu oils (worst). Hydrogenated fats are poor.”

It will be seen from the foregoing quotations that the question as to whether fat-soluble A exerts an antirachitic effect, or whether such action is to be referred to some other principle which has in many cases at least, a similar distribution is still open.

To insert a quick aside here, it should be noted about the suet and butter performing similarly well, with lard performing poorly compared to suet.

Suet is the hard white fat on the kidneys and loins of cattle, sheep, and other animals.  Butter is the fat obtained from the milk/dairy of animals. We use ruminant animals to source both of these fats.  Ruminant animals, due to their consumption and breakdown of chlorophyll, have phytanic acid in their bodyfat and milk.

Lard is pork fat.  Pigs are not ruminants.  Lard contains no phytanic acid.

It is likely the difference in phytanic acid--which is able to stimulate the RXR--that is why pork didn’t work well, and suet and butter did.

Suet would contain nearly all the same compounds as butter, minus the small bit of Vitamin A, which may explain the small increase in effect of butter over suet.

In July, 1921 (5) we pointed out on the basis of experimental data that: “We have not found it possible to demonstrate experimentally a difference between the effects of cod liver oil and butter fat when the content of the diet in calcium and phosphorus is near the optimum, the other elements in the diet being satisfactory.”

We stated further that “These results suggest the possibility that a dietary essential distinct from the anti-ophthalmic substance (fat-soluble A) may exist. If this is the case this would appear to be present in butter fat in small amounts, but to be very abundant in cod liver oil.”

Again, in January, 1922 (6) we set forth evidence which was all but conclusive that there is a specific calcium-depositing substance. We stated “The results of this series of experiments were so consistent and decisive that we can deduce no other conclusion than that cod liver oil contains in abundance some substance which is present in butter fat in but very slight amounts, and which exerts a directive influence on bone development and enables animals to develop with an inadequate supply of calcium much better than they could otherwise do. This substance is apparently distinct from fat-soluble A, which is essential for growth and which is associated definitely with the prevention of ophthalmia (keratomalacia).”

Our own experience had convinced us that existing methods were incapable of differentiating beyond doubt between fat-soluble A and a special calcium-depositing substance should such exist.

To summarize what they are saying, it’s that some fats that DON’T contain any “fat-soluble A” by their analysis are apparently completely able to do the same biological job as fat-soluble A, and that they are determined to figure out what this compound is. What I can tell you is that it is MULTIPLE compounds, and that all of them have activity as agonist ligands at the RXR.

Now, on to their brilliantly-designed tests, doing REAL science:

Our own experience had convinced us that existing methods were incapable of differentiating beyond doubt between fat-soluble A and a special calcium-depositing substance should such exist. We therefore formulated a plan which involved a comparison of a selected list of fats in respect to three kinds of effects in nutrition. First, we tested cod liver oil, shark liver oil, butter fat, and several vegetable oils for potency in causing the cure of xerophthalmia due to lack of fat-soluble A. Secondly, we made comparative tests of the same fats to determine their value in promoting growth in young rats which were restricted to a diet so low in calcium that satisfactory growth was not possible without the provision of some substance which would make for a greater efficiency in the utilization of calcium than that which could be effected in its absence. Thirdly, we further studied these same fats by means of our “line test” to discover their relative values for inducing the deposition of the line of calcium salts in rachitic bones. With the data which we have secured from these three distinct types of tests, we are now in a position to interpret accurately the results of much of the experimental data in the literature which is otherwise confusing.

The tests have been determined and designed.  What did they find out about these different fats?  First, what did the base diet look like, because that’s of CRUCIAL importance here!

The diet used for testing the value of different fats for the cure of xerophthalmia had the following formula.

Lot 3392.

Rolled oats……….40.0%


NaCl……….1.0% [table salt]

CaCO3……….1.5% [calcium carbonate]

Dextrin……….52.5% [carbohydrate source]

This diet is essentially lacking in fat-soluble A. If 2 per cent of butter fat or cod liver oil is included in place of an equivalent amount of dextrin, xerophthalmia never develops, and the animals are able to grow.

Substituting 2% of the carbohydrate dextrin for EITHER cod liver oil OR butter corrects the xeropthalmia (abnormal dryness and inflammation of the conjunctiva and cornea of the eye) that is supposedly the hallmark symptom of so-called “Vitamin A deficiency”?

First, if you know anything about Vitamin A, you should know that the content of cod liver oil versus butter in terms of Vitamin A is VASTLY different. They do both contain it, but they both were able to fix the same problem at 2% of the diet?

A USDA website search gives us:

If it were Vitamin A that was the key ingredient, then there should NOT be 38x difference in content for the same effect.  Something seems fishy here already! (pun intended) There is probably an additional factor present.

What compounds that have known effects at the RXR does cod liver oil contain?:

  • Retinol (Vitamin A), 38x more than butter
  • DHA, much more than butter
  • ARA
  • Phytanic acid
  • Other free fatty acids

What compounds that have known effects at the RXR does butter contain?

  • Retinol (Vitamin A), 38x less than cod liver oil
  • DHA, much less than cod liver oil
  • ARA
  • Phytanic acid
  • Other free fatty acids

If they contain the same things in terms of the RXR, it must be something other than vastly different levels of Poison/”Vitamin A” doing all that legwork, right?

In making the tests referred to in this paper young rats of 30 to 60 gm. weight were restricted to Diet 3392 until the puffiness of the eyelids was distinctly evident. At this point the eyes were frequently sealed shut while the rats slept, and were opened with difficulty on awakening. The malnutrition induced by this diet progresses rapidly to a fatal termination unless a suitable amount of fat-soluble A is provided at this stage. On the addition of sufficient fat containing fat-soluble A, at the time when the edema of the eyelids is just becoming severe the swelling rapidly disappears, and the eyes return to a normal appearance within a few days. 2 per cent of cod liver oil, 3 per cent of shark liver oil, 3 per cent of burbot liver oil, or 2 per cent of butter fat, were found to effect the prompt cure of incipient xerophthalmia under the conditions of our tests.

The butter fat has WAY less Vitamin A than any of those other fish-derived liver oils.

Although we have data from other experiments which indicate that certain of the vegetable oils when fed liberally (8 to 20 per cent) from the beginning of the experiment tended to defer the onset of xerophthalmia, we have never found that such amounts of vegetable fats would cure the eye condition after it had once developed.

Again, is it simply that the diet they fed these animals was simply lacking in FATS to begin with, and if they had this right from the beginning, there would never have been a problem?

It is, therefore, possible that there are traces of fat-soluble A in some vegetable fats. It should be specially noted here that 15 per cent of coconut oil did not cure or prevent xerophthalmia. We are convinced that a properly conducted curative test such as we have described is much more delicate than a preventive test can ever be made.

Interesting, especially in light of the coconut oil fad.  One thing that coconut oil does NOT contain is phytanic acid (or its precursor phytol, which we can break down to phytanic acid).  It also contains hardly any alpha-linolenic acid that the body could potentially convert to DHA.  The other vegetable oils would contain more alpha-linolenic acid, and could work in this manner. From a veterinary nutrition site, on the difference in alpha-linolenic content between coconut oil and corn oil (a vegetable oil):  “You would need to add 30x as much coconut oil as corn oil to a diet to meet a pet’s requirement for linoleic acid!”  This might explain why coconut oil wouldn’t work at all (nowhere near enough alpha-linolenic acid to convert into DHA to begin with), and the other vegetable oils would only work preventatively and not curatively.

Hopkins (7) was the first to point out that oxidation destroys fat-soluble A.


Well...maybe Hopkins found that heating cod liver oil and butter destroyed/oxidized something in both of them that previously would have stimulated the RXR. There was more of this “something(s)” in the cod liver oil than in the butter, see below:

He showed that if oxygen is allowed to pass through heated butter fat the fat-soluble vitamin is readily destroyed. With this destruction the butter fat loses its power of inducing growth or of curing ophthalmia of dietary origin. Mellanby attempted (3) to make use of this means of destroying fat-soluble A in order to determine whether there is a distinct “antirachitic substance.” He found butter fat of little value for protecting against rickets after it had been oxidized, whereas cod liver oil after the same treatment, i.e. heated to 120°C. for 4 hours while oxygen was passing through it, still protected his animals against rickets. He states:

“If it should happen that four hours’ heating and oxidation at 120°C also leaves a large amount of Fat-soluble A in the cod liver oil, it will go a long way, especially when considered together with the butter results, to clinch completely the identity of fat-soluble A and the anti-rachitic vitamine.”

Mellanby used no method of testing for fat-soluble A as distinct from the calcium-depositing substance since he did not make use of the ophthalmia test for fat-soluble A.

What do we know now?

  • Both Vitamin A and DHA are damaged/oxidized by heat.
  • Cod liver oil contains 38x more Vitamin A than butter.
  • Cod liver oil contains much more DHA than butter.
  • Butter is the equal of cod liver oil, in terms of dosing necessary, to prevent and cure the same issues in these experiments.

The smaller amounts of Vitamin A, and more importantly DHA, in the butter were likely rendered useless through the heating.  Cod liver oil, having started with so much more of both of these things, had enough survive the process to still have an effect.  What happens when they heat the cod liver oil longer?

We have found that cod liver oil treated with a stream of air bubbles at the temperature of boiling water for 12 to 20 hours no longer contains sufficient fat-soluble A to relieve rats from xerophthalmia when administered to the extent of 2 per cent of the diet. Cod liver oil which had been oxidized 4 hours, when fed as 2 per cent of the diet, cures xerophthalmia. Untreated cod liver oil under these conditions invariably causes complete recovery within 5 days. Likewise, 2 per cent of fresh butter fat, under exactly comparable experimental conditions, effects the disappearance of ophthalmia within 5 to 10 days. These results are sufficient to serve as a basis of comparison for our present purpose of the relative values of cod liver oil and butter fat for the cure of ophthalmia.

Let’s get into their discussion, where they wrap all this up:

We have shown experimentally that cod liver oil oxidized for 12 to 20 hours does not cure xerophthalmia in rats. It does, however, cause the deposition of calcium in the bones of young rats which are suffering from rickets. This shows that oxidation destroys fat soluble A without destroying another substance which plays an important role in bone growth.

My guess is that the substance is the Vitamin D3 in the cod liver oil that survived the heating.

Coconut oil is shown to be lacking in fat-soluble A, since it will neither prevent nor cure xerophthalmia. This oil, on the other hand, contains a substance which stimulates the deposition of calcium salts in rickets in a manner similar to cod liver oil.  It is, like butter fat, far less effective from a quantitative standpoint.

Coconut doesn’t contain any DHA, ARA, phytol, phytanic acid, Vitamin A, or Vitamin D.

However, coconut oil does contain lauric acid, myristic acid, palmitic acid, decanoic acid, caprylic acid, oleic acid, and a small amount of other fatty acids (including a tiny amount of linolenic acid).  From the study referenced in Part 2, we know that myristic, oleic, stearic, and linolenic acids all have some effect at the RXR.

Cod liver oil, shark liver oil, and burbot liver oil, are highly effective for curing xerophthalmia, for protecting the body against the effects of a deficiency of calcium, and for the deposition of lime salts in rachitic bones.

Certain vegetable fats, among which are cottonseed oil, maize oil, sesame oil, and olive oil, do not possess the property of curing xerophthalmia, nor do they raise the efficiency of the tissues in utilizing calcium when there is an inadequate provision, nor of initiating healing in rickets.

Butter fat contains the calcium-depositing factor but in much smaller amounts than the fish oils we have examined. It is a much better source of fat-soluble A than of the substance which regulates calcium metabolism.

Butter has less DHA and Vitamin A than cod liver oil, these things are true.  I saw it has 9 IU of Vitamin D per Tablespoon, which is a miniscule amount.

DHA has appeared to help with osteoporosis in multiple studies, so I’m going with that one as the “calcium-depositing factor”.

Our results are in harmony with those of Mellanby in that they show that coconut oil has an antirachitic effect. They prove conclusively, however, that this effect is not due to the presence of fat-soluble A in this fat. Mellanby did not appreciate the importance of calcium and phosphorus in his experimental diets as a factor in the causation of rickets. Many of his apparently discordant results can, we believe, be accounted for on this basis rather than on the content of his diets in the calcium-depositing vitamin (3).

The question might be raised as to whether the effect of the substance which is designated fat-soluble A in protecting the functional activity of the eyes, is not one, and the calcium-depositing effect of certain oils which contain it, another physiological effect of one and the same substance. A controversy involving this principle has been carried on for many years over the identity or non-identity of pepsin and rennin. It may be postulated that the two properties which cod liver oil and certain other fats can be shown to possess, are referable to two side chains on the same molecule, and that in oxidation we have destroyed one and left the other intact. It is, of course, not possible at present to prove or disprove either of these views. The only evidence which bears on the question is the observation that coconut oil which had received no chemical treatment whatever, has been shown to possess demonstrable calcium-depositing properties, whereas it does not show a comparable antixerophthalmic effect. This points to the two properties under discussion being due to distinct substances.

The evidence set forth in this paper demonstrates that the power of certain fats to initiate the healing of rickets depends on the presence in them of a substance which is distinct from fat-soluble A. These experiments clearly demonstrate the existence of a fourth vitamin whose specific property, as far as we can tell at present, is to regulate the metabolism of the bones.

Even back then, scientists were questioning if the effects they saw were from “fat-soluble A” or not.  What they were seeing and didn’t know how to interpret was that multiple things in fats can affect the RXR and do the exact same things biologically that they attributed to Poison/”Vitamin A”.

That’s the end of this little series for now.  I hope you can now see that Poison/”Vitamin A” is not a vitamin, it’s not “essential”, and that proper RXR activity (not too much, not too little, the Goldilocks effect) without the use of Poison/"Vitamin A" is what we are after.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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