Quote from Dr. Garrett Smith on April 14, 2019, 4:11 pm

This study is a massive proof that either the scientists in the Poison/"Vitamin A" field are massively incompetent at seeing what their own research showed, OR that there is a distinct agenda to convince people that Poison/"Vitamin A" is something they need even when the evidence shows it causes problems.  It also shows how specific deficiencies endemic to the vegan and heavily vegetarian diets allow for Poison/"Vitamin A" toxicity to happen even at low intakes of Poison/"Vitamin A" carotenoids and retinoids.

I'll go over the study and its results first, and then cover how this fiasco caused damage to these children's eyes...and it wasn't from a "lack of Vitamin A".

Failure of massive single oral dose of vitamin A to prevent deficiency.

Forty-seven children between the ages of 2 and 6 years, resident in an orphanage, took part in the study. The children were in apparent good health and none showed clinical signs of vitamin A deficiency; that is, they showed neither dryness and non-wettability of the bulbar conjunctiva by tears (xerosis), nor accumulations of foamy or greasy material on the roughened bulbar conjunctiva exposed in the palpebral fissure adjoining the limbus (Bitot's spots), nor haziness and dryness of the cornea resulting in a ground glass appearance (keratomalacia).

An important note at the start is that what these researchers called "xerosis" is called "xerophthalmia" these days.

We must recognize some very important things here first.

Before the interventions, NONE of these children showed any signs of health problems AT ALL.  I am operating under some ASSumptions here:

1. This study is being done with children in an orphanage (in India, I believe).
2. Orphanages are not known for their stellar nutrition to begin with.
3. Still, these children were "in apparent good health" before the intervention.

This means that ALL problems the kids had at the end of the study were DIRECTLY CAUSED by the researchers and their interventions.  There is no other way around it.

There is an important line in the introductory paragraphs that shows where this is eventually going:

A massive dose of vitamin A (100,000 ug) has been reported as maintaining adequate serum levels for periods of up to 2 years (Susheela, 1969), and able to prevent deficiency when given to preschool children (Swaminathan, Susheela, and Thimmayamma, 1970).
[...]
In a field study, a similar oral dose was accompanied by signs of vitamin A toxicity in 8% of the children to whom it was given (Nutrition Research Laboratories, Hyderabad, Annual Report 1965-66).

A 100,000 ug megadose of Poison/"Vitamin A" has already been demonstrated previously to cause toxicity in 8% of the children it was given to.  They are taking children who have already tested to be "Vitamin A deficient" or just ASSumed to be so...then they gave these supposedly deficient children a megadose of Poison/"Vitamin A" and induced toxicity in 1 out of 12 of them!!!  These researchers were simply hoping that by cutting the megadose in half--to 50,000 ug--that they would avoid this KNOWN problem.  Remember, they KNOW there are problems with megadosing and they are trying to AVOID these problems.  Doesn't that set the stage nicely?

There are important nutritional factors that show up in nearly every study trying to "prove" that Poison/"Vitamin A" deficiency is a real thing and most of them were included in this study.  We will cover those further down.

These orphanage children were likely eating a mixed omnivore diet PRIOR TO the study, probably with dairy in it, possibly with some other animal protein.  That changed once they entered into the study:

For 9 months before the present study, the children were on a diet that provided 2 g vegetable protein and 90 cal/kg per day, and 620-650 ug beta-carotene per day. For the 2 weeks preceding the study the children were on a diet free of vitamin A and carotene. 

Pay attention...620-650 ug of beta-carotene per day for 9 months.  NO ANIMAL PROTEIN.  The researchers later mention that they consider 900 ug of beta-carotene daily to be a "moderate" intake, and 120 ug of beta-carotene daily to be a "low" intake.  So these children were on a moderate-to-low carotenoid intake for 9 months, with a 2-week period of no carotenoids or retinoids before the intervention even started.  The children were"in apparent good health" both before the 9-month + 2-week lead-up diet started, and they were also still "in apparent good health" after that 9-month + 2-week lead-up diet.  Nothing is said anywhere to imply anything different.  Everything was FINE until they were put into the 18-week intervention part!

We also must cover an important point first.  What is the blood Vitamin A level these researchers considered "low"?

By the 18th week, serum values in both groups were below 15 ug/100 ml a level at which serious clinical deficiencies have been encountered (Pereira, Begum and Dumm, 1966).

So, they're saying that <15 ug/100 mL ("less than 15") is the level that "serious clinical deficiencies" start at based on the research.

Serum levels of the children when they were still "in apparent good health" AFTER the 9-month + 2-week lead-up diet BUT before the interventions started (see Table in study):

• Group 1 - Starting average serum retinol level: 12.5 ug/100 mL.
• Group 2 - Starting average serum retinol level: 12.2 ug/100 mL.
• Group 3 - Starting average serum retinol level: 12.7 ug/100 mL.
• Group 4 - Starting average serum retinol level: 13.2 ug/100 mL.

Did you catch that?  ALL of the children were "Vitamin A deficient" by blood test BEFORE the intervention started, yet, ALL of the children were still "in apparent good health" and had NO eye problems! Where are the diseases that should be present with this "serious clinical deficiency"???  They aren't around, because they DON'T EXIST.

What were the four types of interventions in this study?  After the 9 months + 2 weeks of controlled lead-up diet mentioned above, that the kids were "in apparent good health" both before and after, the interventions then went like this:

• Group 1 - Single 50,000 ug dose of retinyl palmitate, then maintained on a diet with 120 ug beta-carotene ("low") per day.
• Group 2 - Single 50,000 ug dose of retinyl palmitate, then maintained on a diet with 900 ug beta-carotene ("moderate") per day.  Note that this is more beta-carotene daily than was in the 9-month lead-up diet.
• Group 3 - No supplement, then maintained on a diet with 120 ug beta-carotene per day.
• Group 4 - No supplement, then maintained on a diet with 900 ug beta-carotene per day.  Note that this is more beta-carotene daily than was in the 9-month lead-up diet.

So, what happened to these kids?  It wasn't good!  Pay close attention to the next quote:

The first signs of vitamin A deficiency appeared 8 weeks after the start of the study. Two children in group III, given the low carotene diet without the load of vitamin A, showed xerosis and Bitot's spots. One child in group IV on the moderate carotene diet also showed a Bitot's spot. In all 3 subjects the deficiency signs persisted until the end of the study. By the 10th week, two children in group I, given the loading dose of vitamin A and a low carotene diet, developed xerosis and Bitot's spots which persisted until the end of the study. At 16 weeks, a third child in group III showed xerosis of the conjunctiva. None of the children in group II, given the dose of vitamin A and maintained on the moderate carotene diet, showed clinical evidence of deficiency. The study was terminated at 18 weeks by which time 6 children of the 46 had xerosis or Bitot's spots; 2 in group I, 3 in group III, and 1 in group IV.
[...]
Despite a loading dose of 50,000 ug vitamin A, 2 of the 12 children maintained on a low carotene diet showed conjunctival xerosis at 10 weeks, and all but 3 had serum levels below 15 Lg/100 ml at 18 weeks.

If you recall from the beginning, giving children a megadose of Vitamin A supplement resulted in 8% of the children getting toxicity.

6 out of 46 children getting eye problems in total = 13% of the children got eye problems from the interventions!

43 of the 46 children by the end of the study STILL had "low Vitamin A" by blood test, which includes the 11 children who got the 50,000 ug Vitamin A supplement AND were on the "moderate carotene" diet!  YET, only 6 had eye problems that are supposedly linked to "Vitamin A deficiency".  Isn't that strange?  Shouldn't those numbers be a lot closer, if the "deficiency" is a real thing?

That includes the children who were in Group III, who should have been a "Vitamin A deficiency" disaster if it was a real thing.  Here was what they went through:

• 9-months of moderate-to-low (620-650 ug/day) beta-carotene diet
• 2 weeks of NO Vitamin A or carotenoid diet
• They got NO 50,000 ug retinyl palmitate supplement (intervention variable #1)
• 18 weeks of low (120 ug/day) beta-carotene (intervention variable #2)
• Starting blood Vitamin A level:  12.7 ug/100 mL ("deficient")
• Ending blood Vitamin A level:  10.7 ug/100 mL ("even more deficient")
• 3 of these children got xerosis or Bitot's spots

Let's compare this to Group I, which was the same intervention as Group III, WITH the addition of the megadose 50,000 mcg retinyl palmitate supplement:

• Starting blood Vitamin A level:  12.5 ug/100 mL ("deficient")
• Ending blood Vitamin A level:  12.1 ug/100 mL ("even more deficient")
• 2 of these children got xerosis or Bitot's spots

Apparently the megadose supplement didn't really "prevent" anything.

To review:

All the children were tested "Vitamin A deficient" to begin.
0% had eye problems to begin.

50% (2 of the 4 groups) of the children were given a 50,000 ug Vitamin A supplement.
13% of ALL the children had eye problems at the end.
2 of the 6 children who ended up with eye problems had been given the megadose Vitamin A supplement (33%)!

This study in total was 9-months + 2-weeks + 18-weeks long.  That's close to 14 months!  At the end of the 9-month + 2-week lead-up diet, there were NO EYE PROBLEMS in spite of diagnosed-by-blood-test "Vitamin A deficiency".  However, within the 18-week intervention, 6 children showed eye problems.  The interventions CAUSED the eye problems!  At the very least, the researchers should be saying, "whatever we did to these kids, it should be avoided in the future!".

Some of you may not be able to wrap your head around all that above.  I understand, I didn't get it right at the start too.

Let's head into the dietary mechanisms here.

No good information was given about what the kids were eating or weren't eating, so further analysis is impossible beyond what was provided. Other than hitting the vegetable protein and Calorie marks, we must assume that the children received significantly different foods to get their beta-carotene intakes nearly 8x different 120 ug versus 900 ug, so that is a real factor here.  Different foods affect other nutrient profiles as well, which is extremely important for what I'm about to go into.

Here's a video showing a charity organization's assistance in getting Indian orphans decent meals (remember, at the start of this study, whatever they had been eating had been keeping them in decent health!):

https://youtu.be/VPTqZhPjouE

This study was done in 1971, that video was from 2017.

There are specific nutrients that the body needs to protect itself against Poison/"Vitamin A" damage.  These nutrients include:

• Adequate protein
• Adequate zinc
• Adequate taurine (an amino acid that is almost exclusively from animal products)
• Adequate Vitamin E

We'll address each of these topics, as they are quite important.

Protein:

Before this study started, these children who were in "in apparent good health" were likely eating some dairy, and possibly some other animal protein on occasion.  However, during this study, they specifically mention "2 g of vegetable protein" per day.  This likely means that they didn't give these children any dairy or other animal proteins, and basically made them vegan for the duration.  This would help control the Vitamin A intake even further (since milk contains it).  However, it probably also induced protein malnutrition.  It would also eliminate nearly ALL taurine (addressed further below).

Retinol-Binding Protein (RBP), the very protein your body needs to protect your EYES and skin from the diseases caused by Poison/"Vitamin A", requires that a person eats enough PROTEIN to be able to make it.  It also requires enough zinc (addressed further below).  I have covered RBP many other places in this blog-forum, search for it if you need more info.

What types of problems does protein malnutrition cause, you wonder?  Kwashiorkor is "a form of malnutrition caused by protein deficiency in the diet, typically affecting young children in the tropics."  The southern parts of India are in the tropics, just as an aside.

Kwashiorkor - Approach | BMJ Best Practice

A child may complain of eye symptoms such as photophobia or eye soreness, which can be a sign of xerophthalmia.

So, protein malnutrition can cause xerophthalmia (dry eye) and photophobia (extreme sensitivity to light).  Hey, did you know that photophobia is a classic symptom of Poison/"Vitamin A" toxicity?  Pay attention to the dry eye part, it will show up again.

If you don't understand how vegan diets are drastically different in protein content and protein bioavailability than omnivorous diets, I simply do not have the time or desire to back up that far for you.

Zinc:

Is it common for vegan/vegetarian diets to be deficient in zinc, especially since the highest dietary zinc sources are all in animal products?  Yes.

Effect of vegetarian diets on zinc status: a systematic review and meta-analysis of studies in humans.

 Populations that habitually consume vegetarian diets have low zinc intakes and status.

Is adequate zinc important in preventing eye (ocular) disorders?  Yes.

Zinc in the eye.

The highest concentration of this trace element in the human body is measured in the eye, particularly in the pigment-containing components. The deficiency of zinc has a dramatic effect on ocular development especially when it occurs during early prenatal period. Zinc is required for the structure and activity of many ocular metalloenzymes. Although the exact mechanism of its molecular and cellular functions are largely unknown the essentiality of this element in the component of the eye, including the retina, choroid, cornea and lens, is well established; it is also well known that zinc deficiency causes functional impairments in various parts of the eye.

So they are saying above that:

• The eye contains more zinc than ANY OTHER PART of the human body
• The essentiality of zinc to the eye is "well established".
• A zinc deficiency can cause "functional impairments in various parts of the eye".

If these children were fed a zinc-deficient vegetarian diet, do you think it could cause eye problems then?

Taurine:

Taurine is an amino acid, which means it comes as part of protein.  It only comes from animal protein sources, it DOES NOT come from any vegan sources.

Taurine concentrations in the diet, plasma, urine and breast milk of vegans compared with omnivores.

Taurine was absent from the vegan diet...

Is taurine critically important to proper eye function?  Yes.

Review: Taurine: A “very essential” amino acid

All ocular tissues contain taurine, and quantitative analysis of ocular tissue extracts of the rat eye revealed that taurine was the most abundant amino acid in the retina, vitreous, lens, cornea, iris, and ciliary body. In the retina, taurine is critical for photoreceptor development and acts as a cytoprotectant against stress-related neuronal damage and other pathological conditions.

So taurine is a "cytoprotectant", a "cell protector"?  Gosh, do you think it might be "protecting the eye cells" from Poison/"Vitamin A" damage then?  Not having any around would allow for more damage to occur, yes?

Vitamin E:

Vegetarian children are particularly low in Vitamin E as well.  As you'll see below, almost no one (vegan, vegetarian, or otherwise) is even getting the RDA on a daily basis!

The effect of vegetarian diet on selected essential nutrients in children.

Significantly lower concentration of serum vitamin E in vegetarian children in comparison to nonvegetarians may be reflected with statistically significant lowering of total antioxidant status.

Is Vitamin E considered to be protective to the eye against oxidative damage? Yes.

Nutrients for the aging eye

α-Tocopherol attacks free radicals to prevent a chain reaction of lipid oxidation. This is important, given that the retina is highly concentrated in fatty acids.2
[...]
Other functions of α-tocopherol that would be of benefit to ocular health include effects on the expression and activities of molecules and enzymes in immune and inflammatory cells.
[...]
Only men and women in the 95th percentile of vitamin E intake or greater have intakes of vitamin E from diet that meet the RDA.

So Vitamin E is a potential factor here as well.

I'm going to try to sum all this up now.  Is there a single study that showed taurine + zinc + tocopherol (Vitamin E) completely protected cells from Poison/"Vitamin A" induced damage?  YES.  Yes there is!

Protective effect of taurine, zinc and tocopherol on retinol-induced damage in human lymphoblastoid cells.

Cultured human lymphoblastoid cells exposed for short times to retinol and retinoic acid, undergo a time- and dose-dependent decrease in viability, accompanied by cell swelling. The presence of taurine (5-20 mM) and zinc (50-100 microM) protected cells from retinol-induced injury. Taurine 20 mM and zinc 100 microM added simultaneously abolished cell swelling and increased cell viability from 7 to 55%. Tocopherol (200 microM) was also effective in protecting these cells from retinol. The three compounds together afforded complete protection. The effects of retinol and of taurine, zinc or tocopherol seem to be unrelated to lipid peroxidation. A membrane stabilizer action is proposed as the mechanism underlying the protective effect of taurine and zinc or of tocopherol.

A diet severely deficient in those three nutrients would quite likely make cells more susceptible to Poison/"Vitamin A" damage, would it not?  That's what they were doing to these children!

A lack of protective nutrition against Poison/"Vitamin A" allows almost any amount of Poison/"Vitamin A" in the system to cause a TON more damage.  That's how it works.

Summary:

• These children were COMPLETELY FINE before the interventions.  All the children were "low Vitamin A" before the intervention started.
• 6 of the children developed eye problems AFTER the interventions. 93% of the children were still "low Vitamin A" AFTER the intervention.
• The intervention made the children WORSE.
• The children were given a multiple-nutrient-deficient diet.  This is what caused the problems, and in my opinion, allowed the Poison/'Vitamin A" to cause damage that it wasn't able to before, when the children likely had more animal protein sources in their diet.