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Back in March in my blog post titled: Embryogenesis – the last bastion of hope for “vitamin A” I made the statement:

“And, like with Wolbach and Howe back in 1925 these researchers are so sure of themselves that they completely ignore the contradictory findings from their contemporaries.”

I’ve been asked to provide supporting information to back up that statement. I’ll share that here in just a bit.

First, you might be wondering why we should care at all about some rat study from almost 100 years ago. However, I think it’s tremendously important. The 1925 Wolbach and Howe study was the one that supposedly definitively proved the essential need for vitamin A, and therefore, the one that solidified and confirmed the concept of it being a vitamin. If they got that wrong, and if we can therefore disqualify that study, then it should go a long way in disproving the entire “it’s a vitamin” claim.  

I’m assuming that for most people knowing whether or not vitamin A is truly a vitamin does not matter too much. Vitamin or not, that verdict probably won’t change what they are doing. From a practical perspective, and in the short term, we just need to know that vitamin A is toxic once we’ve accumulated too much of it. We can apply that knowledge and hopefully still recover our health.

However, if we don’t go the extra mile and disprove this “it’s a vitamin” claim then the powers that be will just go on perpetually poisoning much of the human population with it. It will also continue to be very difficult to warn more people about the potential harms of over consuming vitamin A.

Okay, now let’s get back to the 1925 Wolbach and Howe study. One of the most fundamental requirements in scientific experiments is repeatability of results. If results are not repeatable (within some explainable margin of error), then the experiment proves nothing.

Here are some of the statements from the Wolbach and Howe study’s introduction effectively ignoring / dismissing the results of experiments from their contemporaries

  1. Few pathological studies have been made, and the majority of these have resulted in wholly negative results and, therefore, erroneous conclusions as to the sequence of events and importance of infections.
  1. Emmett and Alien in a comparison of changes due to vitamin A and B deficiency respectively in the rat report “no special outstanding pathological findings,” in the absence of fat-soluble A, in contrast to atrophies and hypertrophies found in B deficiency.
  1. Stephenson and Clark failed to find a distinctive pathology in keratomalacia in rats.
  1. Davis and Outhouse 4 studied only the kidneys, spleen, heart, lungs, pancreas, liver, and testes. As they report that the testes were normal in most of their cases, it is certain that either their diet was not deficient in fat-soluble (vitamin) A or that the duration of the experiments was too short.
  1. Cramer, Drew, and Mottram ~ in a study of the effects of vitamin deficiency in rats upon the function of lymphocytes and lymphoid tissue found no pathology in fat-soluble A deficiency.
  1. Wason found no lesions in any organ other than the eyes. She regarded the changes in the cornea as secondary to bacterial invasion.
  1. Meyerstein ~ failed to find any characteristic pathology in either vitamin A or vitamin B deficiency in rats.

There’s yet another study from this era that I want to directly compare with Wolbach and Howe’s (W&H) study. It is:

THE NECESSITY OF CERTAIN LIPINS IN THE DIET DURING GROWTH.BY E. V. McCOLLUM AND MARGUERITE DAVIS.(From the Laboratory of Agricultural Chemistry of the University of Wisconsin.)(Received for publication, June 1, 1913.)

The reason I want to discuss this study is because they detail the diet used, and the outcomes. The diet used in this study was remarkably similar to the W & H study.  However, McCollum’s 1913 study was only investigating the “growth” producing effects of some suspected fat soluble factor. 

Here’s an example diet McCollum that fed his animals.

Here’s a chart for Rat # 104a (female)

Do you notice something? Up until period III, McCollum’s study diet is nearly identical to the one used by W&H. McCollum’s study diet is supposedly devoid of vitamin A too, yet his animals survive quite well to the 20 week mark, and beyond. Whereas, in the W&H study all of the animals were either dead or dying by the 8th-10th week. In the last two weeks of the W&H study the animals needed to be force fed their ration, and that finished them off. Except, here in McCollum’s study, not only have the animals survived at least 2X longer, there is no mention of sickness or disease, at all. In other words, his animals were probably very healthy, and obviously reproductive, at the 20 week mark. McCollum’s study presents similar results for male rats.

Then to investigate growth, in period III he adds in an egg extract, and the animals do gain weight. However, let’s not jump to the conclusion that it’s a good thing. What would you tell someone today who claims that gaining weight is the medical equivalent to growth? I think you’d tell them that they are confused. But, that’s a small technicality we are not too interested in right now (unless we wanted to consider this an inadvertent obesity causation study).

What’s critically important is that apparently the same diet regimen used by McCollum’s and W&H’s studies yielded completely opposite results. How can we explain that? When combined with the other studies mentioned above from this era , it is very clear that the animals in the W&H study did NOT succumb to a vitamin A deficiency. Therefore, with the diametrically opposing results between the McCollum’s and W&H’s studies, we have no experimental repeatability. Thus, we can’t legitimately derive any scientific conclusion from them. Therefore, the claim that vitamin A is a vitamin is completely unsupported, and is quite bogus. 

However, there’s a subtle but very important difference in the diets used by McCollum and W&H. In W&H’s paper they state:

Distilled water, sufficient to make a dough, was added to the ingredients; small cakes were moulded, each containing five gm. of material, and dried in an oven.

For additional information about heat treating milk, and its correlation to early death in experimental animals please read about Wilhelm Stepp’s 1912 work in mice. Stepp kills his mice in just 3 weeks using heat treated milk. And, it looked to me that Stepp’s results (kill rate) correlated with the heating duration times in alcohol.

Additionally, there is an even more fundamental problem with the McCollum and W&H studies. That problem is now revealed by the modern-day work of Collin Campbell et al with their work on the direct toxicity of casein on its own. 

Therefore, with that huge red flag and confounding factor no rat study in history that’s used casein can be considered legitimate and valid. Clearly then, Wolbach and Howe’s 1925 study is complete junk science.  Moreover, we have the previously ignored studies from Wolbach and Howe’s contemporaries actually proving that there is no dependency on vitamin A.

But, there’s a much bigger problem with the 1925 Wolbach and Howe study. The foundational claim of their study is that they’ve used a vA free diet. This fundamental claim is based on their assumption that since vA is a fat soluble substance, and they’ve removed all dairy fats from the ration, by boiling in alcohol leaving only the casein portion remaining, that they’ve removed any possible vA.  Turns out, they were completely wrong in that assumption. 

Here’s a paper, documenting that casein has a high affinity to both vA and to retinoic acid, and almost on a 1:1 ratio.

Binding of vitamin A with milk α-and β-caseins

P Bourassa, CN N’Soukpoe-Kossi, HA Tajmir-Riahi – Food chemistry, 2013 – Elsevier

The binding sites of retinol and retinoic acid with milk α-and β-caseins were determined, using constant protein concentration and various retinoid contents. FTIR, UV–visible and fluorescence spectroscopic methods as well as molecular modelling were used to analyse retinol and retinoic acid binding sites, the binding constant and the effect of retinoid complexation on the stability and conformation of caseins. Structural analysis showed that retinoids bind caseins via both hydrophilic and hydrophobic contacts with overall binding …

The number of bound retinol molecules per protein (n) was 1.5 (±0.1) for α-casein and 1.0 (±0.1) for β-casein, while 1 molecule of retinoic acid was bound in the α- and β-casein complexes. Molecular modelling showed different binding sites for retinol and retinoic acid on α– and β-caseins with more stable complexes formed with α-casein. Retinoid–casein complexation induced minor alterations of protein conformation. Caseins might act as carriers for transportation of retinoids to target molecules.

And ..

Caseins play an important role in stabilising retinol, which does not degrade over time or during heat treatments. 

With that, I think we have more than enough circumstantial evidence here to conclude that the 1925 Wolbach and Howe study was not a vA free diet, but rather it was a high retinoic acid diet .

The W&H study is the foundational cornerstone of the grand vitamin A theory. Their conclusions were wrong, and they made the assumption that they had narrowed it down to this one molecule. Quite remarkably they made this assumption in 1925 even though the structure of the molecule had not been determined until 1931. Sadly, every vitamin A study since W&H’s has been layered upon that flawed foundational assumption. Very few follow-on researchers have had the courage to stick their heads above the parapet and call this out for what it is. But, there have been a few. Here’s a prophetic quote from Pitt:

… people seem curiously reluctant to recognize just how toxic is vitamin A. I have long asserted that considered as a chronic poison vitamin A is probably more harmful than cyanide, but I have usually been disbelieved …

I think that if modern day researchers stopped fabricating ridiculous follow-on theories and sub-theories to rationalize what they are seeing, and reevaluated their finding through the lens of vitamin A being a toxin, and nothing but a toxin, then all of it will make so much more sense. 

The W&H study is garbage science, and needs to be tossed into the trash can. With that, so does the entire bogus claim of this toxic molecule being an “essential” vitamin.

Of course, vitamin or not, there’s no debate about the potential toxicity of so-called vitamin A. But, if we can finally correct the science on it then we might have a chance in stopping the global supplementation nonsense going on. Let’s consider this report:

WHO Library Cataloguing-in-Publication Data
Report: WHO technical consultation on vitamin A in newborn health: mechanistic studies, Geneva, Switzerland, 1–3 December 2009.
1.Vitamin A – administration and dosage. 2.Vitamin A deficiency – prevention and control. 3.Infant, Newborn. 4.Infant nutrition.
I.World Health Organization.
ISBN 978 92 4 150316 7

High doses of retinyl ester are commonly provided to at-risk populations in areas where vitamin A deficiency is a problem. For women, 400 000 IU given as two doses of 200 000 IU at least 1 day apart and within 6 weeks postpartum are being recommended. Vitamin A supplementation programmes have been highly successful in addressing vitamin A deficiency but are not without risk. The doses administered are at toxic levels (200 000 IU retinyl ester is 85 times the recommended daily allowance (RDA) and 400 000 IU retinyl ester is 172 times the RDA). Acute toxicity may occur at dosages >100 times the adult RDA.

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Do they warn these women and get their signed informed consent for the likely harm from that toxic dose? I highly, highly doubt it.  Of course, they’ll claim that this deliberate poisoning of young women with known acute toxic doses is somehow necessary, ostensibly claiming that it’s to prevent vA deficiency. 

But, what’s really going on here? Clearly, it might not be just bad science and there’s another possibility to consider. In the 1970’s the WHO and the global elites were absolutely obsessed with the runaway growth in the human population. It was viewed as the biggest threat to the planet.  Then factor in that it’s been known since the 1960s that vitamin A is a reproductive toxin. 

Check out the last entry in this table of lethal doses of some common substances:

Then in the 1970s the WHO’s vitamin A supplementation programmes were started up in about 100 countries, and vitamin A was added to the low fat dairy, etc., in North America and to sugar in South America, etc. Then, surprise, surprise, there’s been a massive drop in human fertility around the planet. And, by the early 2000s the WHO had gone mostly quiet about the risk about the global population. The WHO’s primary focus has now shifted to vaccines.  Do you trust these guys? I sure hope not.