Article: “Vitamin A Deficiency” Doesn’t Exist?!? The Research Says We’ve Been Blaming the Wrong Thing
“Vitamin A Deficiency” Doesn’t Exist?!? The Research Says We’ve Been Blaming the Wrong Thing
What if the symptoms that have been blamed on “vitamin” A deficiency for the last century aren’t actually caused by a lack of “vitamin” A?
Vitamin A Deficiency Doesn't Exist?!? - RELOADED | LYLL #263
What if the supposedly classic signs—night blindness, xerophthalmia/dry eye, Bitot’s spots, poor growth, skin problems, impaired intestinal function, and more—can be reliably reproduced by deficiencies of things that have absolutely nothing to do with a lack of retinol?
And what if the populations supposedly suffering from “vitamin” A deficiency are exactly the populations you would expect to be deficient in protein, zinc, taurine, calories, and meat?
That is what the research keeps showing.
Over.
And over.
And over again.
The more of this literature I put together, the harder it becomes to defend the conventional story.
Before we even get to the symptoms, however, we have to start with an inconvenient problem:
The Tests Used to Diagnose “vitamin” A Deficiency Aren’t Reliable
One of the biggest problems in the entire “vitamin” A deficiency story is that researchers have been using blood measurements as if they reliably tell us whether somebody is actually deficient.
They don’t.
A 2025 Cochrane review, Selected laboratory-based biomarkers for assessing vitamin A deficiency in at-risk individuals, evaluated the laboratory tests used to diagnose low “vitamin” A.
Their key message?
“The two most common tests, serum or plasma retinol and retinol-binding protein, cannot reliably identify at-risk individuals with or without vitamin A deficiency…”
Read that again.
The two tests that form the foundation of huge amounts of “vitamin” A deficiency research cannot reliably tell you who actually has the deficiency.
It gets worse.
When serum retinol was compared with liver “vitamin” A, the test produced enormous numbers of false positives.
In the example presented in the review, imagine 1,000 people, of whom 100 are considered truly deficient based on the reference standard.
Serum retinol would identify 206 people as deficient.
Of those, 153 would be incorrectly classified as deficient.
Retinol-binding protein performed terribly as well.
Using another reference comparison, 266 out of 1,000 people would be classified as deficient when only 100 supposedly actually were—and 216 of those positive results would be wrong.
This isn’t a minor technical problem.
If your test massively overdiagnoses a condition, and then you go into poor populations and use that test to declare enormous numbers of people “vitamin” A deficient, your entire premise is already standing on extremely shaky ground.
Then comes the next problem.
People Can Have “Deficient” Blood Levels Without the Supposed Deficiency Symptoms
If low serum retinol really represents a clinically meaningful “vitamin” A deficiency, people with severely low serum retinol should predictably develop the symptoms attributed to it.
That is not what the research shows.
In a UK hospital study, Vitamin A deficiency: experience from a tertiary referral UK hospital; not just a low- and middle-income country issue, researchers identified patients with low or “deficient” serum retinol.
What happened?
Eighty percent did not report symptoms.
Their supposed “hypovitaminosis A” was discovered incidentally while their chronic diseases were being managed.
If your blood test says somebody has a deficiency but 80% of them don’t have the symptoms of that deficiency, perhaps the obvious question should be:
Is the blood test actually measuring what we think it is measuring?
Another study looked at patients with primary biliary cirrhosis. In Primary biliary cirrhosis, dark adaptometry, electro-oculography, and vitamin A state, nine patients had low circulating “vitamin A.”
How many had abnormalities of dark adaptation or electro-oculography?
None.
Low blood “vitamin” A.
No night-vision problem.
That should matter.
It happens again in Crohn’s disease.
In Vitamin A deficiency in Crohn’s disease, 21% of patients had low plasma retinol concentrations. Yet the paper itself points toward another massive confounder in these sick, poorly absorbing patients:
Protein depletion.
The authors recommended that protein depletion be corrected.
Keep that in mind, because protein is going to become very important.
Children Can Be “vitamin” A Deficient Without the Eye Problems
Let’s go to the populations where “vitamin” A deficiency supposedly runs rampant.
In a study of marginalized children in Chandigarh, India, 35% of children in one analyzed group had serum retinol below the conventional deficiency cutoff.
Some had extraordinarily low serum retinol.
And yet:
None of the children showed ocular manifestations of “vitamin” A deficiency.
None.
Another study looked at preschool children in rural Nigeria: Vitamin A Status and Nutritional Intake of Carotenoids of Preschool Children in Ijaye Orile Community in Nigeria.
About 27% of these children had serum retinol below 10 µg/dL.
Another 48% were between 10 and 19 µg/dL.
By the conventional blood criteria, approximately 75% of these children had low or deficient serum retinol.
How many had night blindness?
1.5%.
How many had xerophthalmia?
None.
Seventy-five percent supposedly deficient.
One-and-a-half percent with night blindness.
Zero xerophthalmia.
At some point, you have to ask whether the thing being measured is actually the thing causing the symptoms?
Because these children had something else in common:
They were malnourished.
And that brings us to the part of the story that the “vitamin” A deficiency narrative desperately needs people to ignore.
Protein-Calorie Malnutrition Produces the Supposed “vitamin” A Deficiency Symptoms
What do many of the populations used to establish “vitamin” A deficiency have in common?
They are poor.
They are undernourished.
They don’t eat enough protein.
They don’t eat enough calories.
And they don’t eat enough meat.
This is not a trivial confounder.
It may be the entire story.
Take xerophthalmia—the dry-eye condition repeatedly held up as one of the classic signs of “vitamin” A deficiency.
A paper appropriately titled Xerophthalmia and protein malnutrition in Bantu children discussed the relationship decades ago.
The literature cited in that paper noted that severe manifestations attributed to “vitamin” A deficiency were accompanied by protein malnutrition.
Another passage describes an ocular condition that always occurred in association with protein malnutrition.
Always.
An additional paper, Influence of diet on tear function, states that adequate dietary protein and zinc may be necessary for normal tear function.
Wait.
Protein?
Zinc?
I thought this was a “vitamin” A problem.
It gets much more obvious.
In Plasma vitamin A, retinol-binding protein and prealbumin concentrations in protein-calorie malnutrition. III. Response to varying dietary treatments, malnourished children were given more protein and calories.
What happened?
Their plasma “vitamin” A increased.
Their retinol-binding protein increased.
Their prealbumin increased.
Did they need to be loaded with “vitamin” A to make the blood “vitamin” A rise?
No.
They needed food.
Even more importantly, the researchers found evidence that hepatic retinol-binding protein synthesis was impaired during protein-calorie malnutrition.
Of course it was.
What do you need to make a protein?
Protein.
Retinol-binding PROTEIN is right there in the name.
If somebody is protein deficient and cannot properly manufacture RBP, why would we expect their blood retinol to behave normally?
And if correcting protein malnutrition makes serum retinol rise without correcting a supposed dietary retinol deficiency, what exactly did the low blood retinol prove in the first place?
Not much.
Another study on Indian children examined the relative significance of protein-calorie malnutrition and vitamin A/carotene levels in xerophthalmia.
The researchers noted that protein-calorie malnutrition was an additional essential factor in the clinical manifestation of xerophthalmia.
Then we have Bangladeshi children.
Protein energy malnutrition, vitamin A deficiency and night blindness in Bangladeshi children found that night blindness was associated with protein-energy malnutrition.
The authors even concluded:
“This may indicate that night blindness is only one aspect of the general protein energy malnutrition problems in this population.”
There it is.
They are starving.
They are not eating enough protein.
They are not eating enough meat.
And somehow the nutritional establishment managed to turn that into:
Give them more “vitamin” A.
Protein Deficiency Also Makes Blood Retinol Look Low
The relationship isn’t merely that protein deficiency can cause similar symptoms.
Protein deficiency directly interferes with the system used to move retinol around the body.
The role of retinol-binding protein in protein-calorie malnutrition addresses this relationship directly.
So does research using RBP to predict “vitamin” A deficiency, where protein malnutrition and the acute-phase response interfere with the interpretation of RBP: Use of serum retinol-binding protein for prediction of vitamin A deficiency.
This means the conventional interpretation can become completely backwards.
A malnourished person has low protein.
Low protein interferes with RBP production.
Serum retinol falls.
Researchers measure the low serum retinol.
They call it “vitamin” A deficiency.
Then they attribute the malnutrition symptoms to “vitamin” A deficiency.
See the problem yet?
Zinc Blows an Even Bigger Hole in the Story
If protein is bad for the conventional “vitamin” A deficiency narrative, zinc is devastating.
Nearly every classic symptom attributed to “vitamin” A deficiency can also be found in zinc deficiency.
Night blindness?
Zinc.
Bitot’s spots?
Zinc.
Growth retardation?
Zinc.
Anemia?
Zinc can be involved.
Skin problems?
Zinc.
Abnormal intestinal villi and brush-border enzymes?
Zinc.
Problems with water and electrolyte transport?
Zinc.
And zinc also directly affects retinol-binding protein.
Let’s start with the eyes.
Zinc Deficiency Causes Night Blindness
The relationship between zinc deficiency and night blindness has been known for decades. See Zinc and its deficiency diseases.
Yet night blindness continues to be treated as if it uniquely demonstrates “vitamin” A deficiency.
It doesn’t.
Then we get to Bitot’s spots.
These are repeatedly described as a classic, even “pathognomonic,” sign of “vitamin” A deficiency.
Except apparently nobody told zinc.
A 2025 case report titled Zinc deficiency: a spot diagnosis described a patient with a recurring Bitot’s spot.
His serum “vitamin” A was normal.
His zinc was low.
After zinc supplementation, the lesion and ocular symptoms disappeared.
No “vitamin” A was required to fix the supposed “vitamin” A deficiency sign.
The paper states:
“In this case, however, it was related to an isolated zinc deficiency.”
That’s about as straightforward as research gets.
The authors also acknowledge that zinc is required for hepatic synthesis of retinol-binding protein.
Which brings us right back to the blood testing problem.
If zinc deficiency lowers RBP, and low RBP lowers circulating retinol, then a zinc-deficient person can appear “vitamin” A deficient on the very blood measurements used to diagnose the condition.
Zinc Can Raise Blood “vitamin” A Without Giving More “vitamin” A
This is one of the most important pieces of this entire puzzle.
Researchers took zinc-deficient rats and gave them zinc.
They did not need to give them more “vitamin” A.
What happened?
Their plasma “vitamin” A rose back toward normal.
The study is Vitamin A metabolism during the repletion of zinc deficient rats.
After zinc repletion, plasma “vitamin” A returned toward the normal range.
When zinc was injected, there was a short lag followed by a significant rise in plasma “vitamin” A.
By the fifth day, plasma “vitamin” A was back within the normal range.
Again:
They didn’t fix a dietary “vitamin” A deficiency. They gave zinc.
The authors concluded that adequate food intake as well as zinc appeared necessary to completely reverse low plasma “vitamin” A concentrations associated with zinc deficiency.
So when a malnourished person has low serum retinol, what should be your first thought?
“Quick! Give them retinol!”
Or:
Are they zinc deficient and underfed?
The research gives us a pretty strong clue.
Zinc Deficiency Interferes With Retinol-Binding Protein
Research on the effect of zinc deficiency on retinol-binding protein metabolism found very low plasma “vitamin” A in zinc-deficient rats despite adequate liver stores.
Read that carefully.
Low “vitamin” A in the blood.
Adequate “vitamin” A in the liver.
Is that a deficiency?
Or is it a transport/mobilization problem?
The researchers concluded that zinc deficiency interfered with synthesis of retinol-binding protein and impaired the ability to mobilize “vitamin” A from the liver.
Another paper, Zinc deficiency reduces hepatic cellular retinol-binding protein in rats, found liver cellular RBP reduced by more than 50% in zinc-deficient animals.
This matters because retinol-binding protein isn’t a magical chauffeur whose job is to deliver your precious “vitamin” A where it “needs” to go.
RBP literally protects tissues from unbound (“free”) retinol.
A review of Vitamin A Metabolism in the Fetus and Neonate describes hypervitaminosis A occurring when plasma retinol exceeds the availability of RBP to bind it, producing elevated free retinol.
In other words:
RBP protects you from retinol toxicity.
Now the pieces start fitting together very differently.
Protein deficiency → less ability to make RBP.
Zinc deficiency → impaired RBP production.
Less RBP → low circulating bound retinol and impaired handling of stored retinol.
Researchers see low serum retinol and call it “vitamin” A deficiency.
But the “vitamin” A may still be sitting right there in the liver.
The Supposed “vitamin” A Deficiency Symptoms Keep Turning Into Zinc Deficiency
Let’s keep going.
Anemia is sometimes attributed to “vitamin” A deficiency.
But Association of Zinc with Anemia describes zinc deficiency contributing to anemia and notes its frequent coexistence with iron deficiency, growth retardation, edema, hypoproteinemia, water transport, and intestinal issues.
What’s an excellent dietary source of both zinc and iron?
Meat.
Growth retardation?
See Zinc nutrition and growth retardation.
Edema and hypoproteinemia?
Edema, hypoproteinemia, and zinc deficiency in low-birth-weight infants reported rapid resolution of edema after zinc supplementation, with serum proteins increasing as well.
Problems with water transport?
Transport of electrolytes, water, and glucose in zinc deficiency found significantly impaired water and sodium transport in zinc-deficient rats.
What about the intestine?
A paper titled Vitamin A-Deficient Rats have Only Mild Changes in Jejunal Structure and Function found only mild intestinal changes even with severe experimental depletion.
The changes that eventually appeared included reduced villus height and altered brush-border enzymes.
Guess what controls those?
Zinc.
A review, Zinc in Gut-Brain Interaction in Autism and Neurological Disorders, notes that zinc status affects villus height and that zinc deficiency causes shortening and narrowing of the intestinal villi. It also alters brush-border enzyme activity.
So once again:
A symptom gets attributed to “vitamin” A deficiency.
Then you look up zinc deficiency.
There it is.
Then There Is Taurine
The conventional “vitamin” A deficiency narrative becomes even harder to defend when taurine enters the picture.
Taurine is particularly abundant in the retina.
And unlike the vague associations made with low serum retinol, actual taurine deprivation can produce retinal degeneration.
Taurine: evidence of physiological function in the retina states that visual dysfunction in human and animal subjects results from taurine deficiency and can be reversed by taurine supplementation.
Taurine depletion produces significant retinal lesions.
Where do you get meaningful dietary taurine?
Meat.
Now go back and look at the populations in the “vitamin” A deficiency literature again.
Poor children.
Protein-energy malnutrition.
Low meat intake.
Low zinc.
Low taurine.
Low calories.
And we’re supposed to assume the eye problems are because they didn’t get enough retinol?
Why?
Taurine Deficiency Causes Retinal Degeneration in Multiple Species
This isn’t based on one study.
Cats develop retinal degeneration when deprived of taurine:
Retinal degeneration associated with taurine deficiency in the cat
Retinal degeneration induced by taurine deficiency in light-deprived cats
Then we have rhesus monkeys.
Retinal degeneration in 3-month-old rhesus monkey infants fed a taurine-free human infant formula
Long-term effects on retina of rhesus monkeys fed taurine-free human infant formula
Visual acuity loss in rhesus monkey infants fed a taurine-free human infant formula
And the title of another paper says it about as plainly as possible:
Dietary taurine is necessary for normal retinal development in monkeys.
Necessary.
For normal retinal development.
But tell me again how retinal problems prove “vitamin” A deficiency.
Taurine Also Protects the Ocular Surface
Dry eye/xerophthalmia is supposed to be another classic “vitamin” A deficiency symptom.
Yet taurine shows protective effects in experimental dry-eye models.
Antioxidant and Osmoprotecting Activity of Taurine in Dry Eye Models found that a taurine-containing formulation significantly reversed altered dry-eye parameters and was more effective than hyaluronic acid alone.
Again:
Eye problem supposedly caused by “vitamin” A deficiency.
Taurine improves it.
And now we get to the really interesting part.
Zinc and Taurine Protect Against “vitamin” A Toxicity
Not only can zinc and taurine produce or correct symptoms that have been blamed on “vitamin” A deficiency, they also protect against retinoid toxicity.
In Effect of taurine on toxicity of vitamin A in rats, increasing “vitamin” A produced toxic effects involving body weight, liver, kidneys, oxidative stress markers, and other measures.
Taurine significantly reduced those toxic effects.
But here’s the part you need to pay attention to:
The serum “vitamin” A level was higher in the rats receiving taurine plus “vitamin” A than in rats receiving “vitamin” A alone.
Think about what that means.
Taurine reduced toxicity while raising blood “vitamin” A.
Does that sound familiar?
Protein raises blood “vitamin” A.
Zinc raises blood “vitamin” A.
Taurine raises blood “vitamin” A.
And all three can improve problems that researchers want to call “vitamin” A deficiency.
Maybe rising blood retinol isn’t proof that you “corrected a vitamin A deficiency.”
Maybe you’re finally able to mobilize and detoxify what was already stored in the body.
Another study makes the protective relationship even clearer.
Protective effect of taurine, zinc and tocopherol on retinol-induced damage in human lymphoblastoid cells exposed human cells to retinol and retinoic acid (called “active vitamin A”).
Cell viability fell in a time- and dose-dependent manner.
More exposure?
More damage.
Higher dose?
More damage.
When taurine and zinc were present, they protected the cells against retinol-induced injury.
Taurine and zinc together dramatically increased cell viability.
What’s an excellent source of both?
Meat.
Do you see the pattern yet?
What Happens When Humans Are Actually Deprived of “vitamin” A?
This should be the simplest experiment in the world.
If “vitamin” A is an essential nutrient and its absence predictably produces a recognizable deficiency disease, then deliberately removing it from the human diet should eventually reproduce that disease.
So what happened when researchers actually tried?
The results are nothing like the clean story people are taught.
A 1945 report, Vitamin A Deficiency and the Requirements of Human Adults, described volunteers placed on a diet designed to be deficient in “vitamin” A and its precursors while otherwise nutritionally complete.
After a year:
“…none of the sixteen deprived subjects became depleted within a year.”
Some continued considerably longer.
Most showed no changes attributable to “vitamin” A deficiency other than gradually falling plasma “vitamin” A.
One subject did not even show that deterioration after 22 months.
Where was the rapidly developing blindness?
Where was the skin falling apart?
Where was the supposedly obvious deficiency syndrome?
It wasn’t there.
Different Human Depletion Experiments Produced Wildly Different Results
This is another giant red flag.
In some experiments, subjects supposedly developed problems relatively quickly.
In others, people went a year or two with little or nothing happening.
Why would an essential nutrient deficiency behave so inconsistently?
One obvious answer is:
The diets were different.
A diet designed to contain almost no “vitamin” A can accidentally become deficient in all sorts of other things.
Protein.
Zinc.
Taurine.
Calories.
Minerals.
Remember: making a diet artificially devoid of a widely distributed group of food compounds is not the same thing as constructing a nutritionally adequate low-“vitamin” A diet.
That distinction is everything.
One human experiment described in The Experimental Induction of Vitamin A Deficiency in Humans highlights just how inconsistent these experiments became.
Some subjects showed deterioration after relatively short periods.
Others took a year or two.
In one experiment, severe weight loss occurred in all subjects before the visual problems appeared.
Hmm.
If everyone starts severely losing weight before they develop “vitamin” A deficiency symptoms, is it possible they are simply being inadequately fed?
Apparently that question wasn’t interesting enough.
Another Human Experiment Couldn’t Produce the Supposed Symptoms
In Effects of Vitamin A Depletion in Young Adults, young adults were placed on a low-“vitamin” A diet for months.
Researchers measured dark adaptation, blood “vitamin” A, carotene, white blood cells, skin, conjunctiva, and other parameters.
Their conclusion?
“None of these measurements showed any definite changes from those found prior to the deficiency for the length of time studied.”
And then comes the line that should have changed the entire direction of this field:
“…these signs that are said to be vitamin A deficiency are not merely the result of uncomplicated vitamin A deficiency.”
There it is.
The researchers themselves couldn’t reproduce the supposed deficiency syndrome with uncomplicated “vitamin” A depletion.
Maybe the problem requires something else.
Protein deficiency?
Zinc deficiency?
Taurine deficiency?
Mineral imbalance?
General starvation?
Exactly.
Researchers Knew a Century Ago That the Eye Disease Could Be Produced Without “vitamin” A Deficiency
This is one of my favorite papers in the entire pile because it comes from 1923.
Right around the era when this whole “vitamin” A story was being constructed.
The paper is titled:
Yes.
You read that correctly.
The animals had fat-soluble A (aka “vitamin” A as it was called way back when) in their diets.
But when the mineral mixture was wrong, they developed the same eye pathology.
The researchers concluded:
“The two conditions are clinically and pathologically identical…”
Identical.
The eye disease produced by a diet supposedly deficient in fat-soluble A was clinically and pathologically identical to the disease produced while fat-soluble A was present but the mineral composition was unfavorable.
It gets better.
One severely affected rat was switched to a diet containing a better mineral mixture.
What happened?
“Photophobia disappeared, the discharge diminished, and the conjunctiva became moistened.”
Without needing to prove that “vitamin” A deficiency was the cause.
In 1923.
Maybe someone should have followed up on that.
Instead, we built an entire global deficiency narrative around “vitamin” A.
A global deficiency narrative that the WHO and Bill Gates are fully behind, by the way.
Extremely Low Blood Retinol Does Not Necessarily Mean Low Liver Stores
Now we get to what may be the most important practical misunderstanding of all.
People assume:
Low blood retinol = low body stores.
That assumption can be spectacularly wrong.
The paper Role of Fat-Soluble Vitamins A and D in the Pathogenesis of Influenza: A New Perspective notes that serum retinol concentrations do not reflect liver “vitamin” A concentrations over a wide range of liver values because circulating retinol is under homeostatic control.
It also notes that cases of hypervitaminosis A can show serum retinol within normal limits.
So serum retinol doesn’t reliably tell you what’s sitting in the liver.
Then comes a case report that demonstrates exactly how backwards the interpretation can become.
Reversible hepatotoxicity associated with hepatic vitamin A accumulation in a protein-deficient patient described a man with protein malnutrition and abnormal liver function.
He had consumed 40,000–50,000 IU of “vitamin” A supplements per day for seven years, plus his dietary intake.
His liver contained massive amounts of “vitamin A.”
Yet:
“both the serum concentration of vitamin A and RBP were below normal.”
Let that sink in.
Massive liver accumulation.
Low blood “vitamin” A.
If somebody had simply looked at his serum retinol and followed the conventional logic, what would they have concluded?
“Vitamin A deficiency.”
While his liver was loaded with the stuff.
That is exactly the problem.
When His Nutrition Improved, Blood “vitamin” A Went UP While Liver “vitamin” A Went DOWN
This case becomes even more important during recovery.
His nutrition improved.
His liver “vitamin” A fell dramatically.
At the same time:
His serum “vitamin” A rose.
This is the opposite of what the simplistic deficiency model would lead you to expect.
His blood “vitamin” A increased as the amount stored in his liver decreased.
Why?
Because he was finally mobilizing it.
Protein improved.
RBP improved.
The stored retinol could move.
This is exactly why I keep telling people that you cannot look at one serum retinol test and pretend you know what is happening inside the body.
The direction of movement matters.
The nutritional context matters.
Protein matters.
Zinc matters.
Taurine matters.
And liver storage matters.
Even Apparently Healthy Infants Have Been Reported With Zero Liver “vitamin” A
The National Academies’ Dietary Reference Intakes chapter on Vitamin A contains another fascinating observation.
Reported liver “vitamin” A stores in apparently healthy infants ranged from:
***0*** to 320 µg/g liver.
Zero is not “a little low.”
Zero is ZERO.
Apparently healthy infants have been reported at the bottom of that range.
Yet we are told “vitamin” A is absolutely required for normal development and that deficiency should produce devastating consequences.
Apparently these healthy infants didn’t get the memo.
Carotenoids Aren’t Even Essential
And before we finish, let’s go all the way back to the beginning of the biochemical pathway.
Retinoids come from carotenoids.
Yet the review Carotenoids states:
“None of the carotenoids are considered essential nutrients.”
It also notes that no carotenoid is directly involved in a vital metabolic pathway and that the absence of a carotenoid has not been exclusively linked to a specific deficiency disease.
So the compounds upstream aren’t essential.
But we’re supposed to believe that compounds produced downstream from them suddenly become indispensable dietary nutrients?
Make that make sense.
“vitamin” A Deficiency Is Rare in the United States—Where People Eat Plenty of Meat
Finally, even the NIH’s Vitamin A and Carotenoids Health Professional Fact Sheet acknowledges that “vitamin A deficiency” is rare in the United States.
What do Americans generally consume far more of than the impoverished populations where “vitamin A deficiency” is diagnosed?
Protein.
Zinc.
Taurine.
Meat.
Interesting coincidence.
Because the research we just went through shows that:
Protein status affects serum retinol and RBP.
Zinc status affects serum retinol and RBP.
Zinc deficiency can produce night blindness and Bitot’s spots.
Protein-calorie malnutrition accompanies xerophthalmia.
Taurine deficiency damages the retina.
Taurine affects dry eye.
Zinc and taurine protect against retinol-induced injury.
Correcting zinc deficiency can raise serum “vitamin” A without giving more “vitamin” A.
Correcting protein malnutrition can raise serum “vitamin” A without giving more “vitamin” A.
Taurine can raise serum “vitamin” A while reducing “vitamin” A toxicity.
And a person can have massive liver “vitamin” A accumulation while his serum retinol says he is deficient.
At what point do we stop calling this a “vitamin” A deficiency?
We’re Blaming the Wrong Deficiency
Here’s the pattern I see in this literature.
Researchers go into populations that are poorly nourished and frequently consume very little meat.
Those populations are likely to be deficient in protein, zinc, taurine, calories, iron, and other nutrients.
Their ability to manufacture retinol-binding protein is impaired.
Their circulating retinol falls.
Researchers measure the low serum retinol.
They label them “vitamin A deficient.”
Then the symptoms of malnutrition, zinc deficiency, protein deficiency, taurine deficiency, and mineral imbalance get attributed to the low serum retinol.
Give them food, protein, zinc, or taurine and the serum retinol can rise.
Then everybody says:
“See? Their vitamin A status improved!”
No.
Maybe their ability to handle and mobilize and DETOXIFY the retinol already inside them improved.
That is a very different interpretation.
And unlike the conventional story, it actually connects the observations.
This is why the research on “vitamin” A deficiency has looked so inconsistent for so long.
Some people with supposedly deficient serum levels have symptoms.
Most don’t.
Some experimentally depleted humans develop problems.
Others go a year or two without them.
Some people with extremely low blood retinol have plenty of retinol in the liver.
Some people with massive hepatic “vitamin” A toxicity have blood tests that say they’re deficient.
Meanwhile protein, zinc, taurine, and general food intake keep appearing in the background.
Maybe they aren’t in the background.
Maybe they’re the actual story.
The Bottom Line
I don’t believe the evidence supports the conventional concept of “vitamin” A deficiency as it is currently presented.
What gets labeled “vitamin” A deficiency is, in the research itself, repeatedly tangled up with:
Protein-calorie malnutrition, zinc deficiency, taurine deficiency, inadequate food intake, mineral imbalance, and impaired retinol-binding protein production.
The supposed deficiency symptoms can occur without low “vitamin” A.
Low serum retinol can occur without the symptoms.
Low serum retinol can occur while liver stores remain adequate.
And, most damning of all, low serum retinol can occur while the liver contains massive, toxic amounts of “vitamin” A.
That isn’t a small problem with the theory.
That’s the theory falling apart.
When you correct protein, zinc, taurine, and food intake, blood “vitamin” A can rise without adding more “vitamin” A.
When that happens, conventional researchers see “correction of vitamin A deficiency.”
I see something completely different.
I see the body finally becoming capable of handling the poison that was already there.
So when somebody tells you that night blindness, dry eye, Bitot’s spots, skin problems, poor growth, intestinal dysfunction, or a low serum retinol test proves that you need more “vitamin” A, ask the questions they should have asked from the beginning:
How much protein are they eating?
What is their zinc status?
Are they getting enough taurine?
Are they eating enough calories?
Are they eating enough meat?
Can they make enough retinol-binding protein?
And most importantly:
How do you know the “vitamin” A isn’t already sitting in their liver?
Because a blood test sure as hell doesn’t prove that it isn’t.
Written by Garrett Smith
