We were warned about a coming “vitamin” A toxicity epidemic DECADES ago.

Not hinted at.

Not vaguely concerned about.

WARNED.

By 1953, a paper simply titled Vitamin A Intoxication noted that the diagnosis had already been made with increasing frequency.

Then, in 1981, researchers published a paper with a title that really doesn’t leave much room for interpretation:

Chronic Vitamin A Intoxication: A Multisystem Disease That Could Reach Epidemic Proportions.

Read that title again.

“COULD REACH EPIDEMIC PROPORTIONS.”

That was 1981.

One year later, the warning got even more explicit in Masked Hypervitaminosis a and Liver Injury:

“We may be on the verge of an epidemic of vitamin A toxicity.”

That was 1982.

So here’s the obvious question:

What happened to the epidemic?

Did it magically disappear?

Did the human body suddenly stop storing “vitamin” A?

Did we stop eating it?

Did we stop supplementing it?

Did we stop fortifying foods with it?

Did we stop putting retinoids into medications and skin products?

Nope.

We did the opposite.

We kept adding more “vitamin” A exposures while largely ignoring the place where the body actually STORES the stuff:

THE LIVER.

And THAT is where this story gets really interesting.

WHO Already Told Us When 20% Becomes a Public-Health Problem

Before we get into the liver studies, let’s establish something very important.

What percentage of a population has to be affected before public-health authorities consider something a serious population-level problem?

Conveniently, the World Health Organization already answered that question for “vitamin” A.

Just not in the direction we’re going to be discussing.

In its 1996 report, Indicators for Assessing Vitamin A Deficiency and Their Application in Monitoring and Evaluating Intervention Programmes, WHO laid out thresholds for deciding when supposed “vitamin” A deficiency becomes a public-health problem.

One of the methods WHO discussed was the Relative Dose Response, or RDR, test.

WHO wrote that an RDR response of ≥20% indicated inadequate liver reserves, around <0.07 μmol/g liver.

Then comes the important part:

“A public health problem of moderate or severe importance might be assumed to exist if ≥20%...show abnormal RDR...values.”

Their accompanying table makes this even clearer.

If 20% to less than 30% of preschool children showed abnormal RDR results?

MODERATE public-health problem.

If 30% or more showed abnormal results?

SEVERE public-health problem.

WHO then says “vitamin” A supplementation should be given where a severe problem is detected, and considered where prevalence is moderate-to-severe.

Got that?

This is VERY important to remember.

20% “deficient”?

We have a moderate population-level public-health problem.

30% “deficient”?

SEVERE problem.

Intervention.

Supplementation.

Public-health action.

Fine.

I have no problem with establishing a prevalence threshold and saying:

Once enough people cross it, stop pretending these are isolated individuals. You have a population problem.

What I DO have a problem with is apparently only applying that logic in ONE direction.

Because look at some of the percentages we’re about to see on the OTHER end:

Washington, D.C.: 24%+ had excessive “vitamin” A in their livers.

London: 31%.

Singapore: about 20%.

Modern U.S. cadavers: 33% hypervitaminotic.

South African children: 63.6% hypervitaminotic BEFORE another massive “vitamin” A supplement raised that number to 71.6% (!!!).

Cameroonian children: 42.6%.

South African children in another multi-country analysis: 57.7%.

Burkina Faso: roughly one-third.

Interesting.

When 20% of a population supposedly has too LITTLE “vitamin” A:

PUBLIC-HEALTH PROBLEM!

When 20%, 30%, 40%, 50%, 60%, even 70%+ have excessive or hypervitaminotic stores though…

Where’s the alarm?

Where’s the worldwide surveillance program?

Where’s the massive campaign to STOP adding more?

Where are the public-health authorities screaming:

“WE CROSSED 20%! THIS IS NOW A POPULATION-LEVEL PROBLEM!”

Crickets. Dead silence. Probably calls from Bill Gates to give them all more “vitamin” A supplements! (really)

That’s the double standard I want you to remember throughout this entire article.

Because if 20% is enough to establish a serious population problem when the problem is supposedly too LITTLE “vitamin” A, then why does that same public-health logic suddenly disappear when the problem is TOO MUCH?

But What If “Vitamin A Deficiency” Isn’t Really Vitamin A Deficiency?

There’s another HUGE problem with this whole story.

Everything I just showed you about WHO’s deficiency thresholds rests upon an assumption:

That what they are calling “vitamin A deficiency” is actually a deficiency of so-called “vitamin” A.

I don’t believe the evidence supports that assumption.

I went through this topic extensively in my previous Love Your Liver Livestream:

Vitamin A Deficiency Doesn’t Exist?!? — RELOADED | LYLL #263

Here’s the basic problem.

Many of the populations supposedly suffering from “vitamin” A deficiency are also deficient in:

Protein.

Calories.

Zinc.

Taurine.

Often several of them at the same time.

In other words:

THEY’RE MALNOURISHED. THEY DON’T GET ENOUGH MEAT & CALORIES.

Yet somehow the conclusion becomes:

“Vitamin A deficiency.”

That’s a problem.

Zinc deficiency, for example, can interfere with retinol-binding protein and the mobilization of retinol from the liver.

Think about what that means.

You could have “vitamin” A sitting IN THE LIVER.

Zinc deficiency interferes with your ability to mobilize it.

Serum retinol falls.

Somebody measures the serum.

😱😱😱 OMG LOW VITAMIN A! 😱😱😱

Then what happens?

Give them MORE “vitamin” A!

See the problem yet?

The same basic issue applies to protein-calorie malnutrition.

Correcting protein and calorie deficiencies can improve plasma retinol and retinol-binding protein (RBP).

That does NOT automatically mean you corrected a “vitamin” A deficiency.

Maybe you simply restored the machinery needed to move around the “vitamin” A that was ALREADY THERE.

Then there’s taurine.

Taurine has been shown to be critical for retina development and function, fixing dry eye, and skin health…all things typically ASSumed to be heavily connected to “vitamin” A.

Taurine is heavily associated with animal foods, particularly muscle meat, right along with high-quality protein and zinc.

See the pattern?

Meat.

Protein.

Zinc.

Taurine.

Calories.

The very populations that get labeled “vitamin A deficient” are often missing some combination of those things.

So before somebody tells me:

“But vitamin A deficiency is a massive worldwide problem!”

I have some questions.

Was protein adequate?

Were calories adequate?

Was zinc adequate?

Was taurine adequate?

Was retinol-binding protein production adequate?

Were actual LIVER STORES low?

Or did somebody measure low serum retinol in a malnourished population and decide:

“Vitamin A deficiency!”

Those are NOT the same thing.

And this becomes even more absurd when you combine that issue with what we’re about to see.

On one side:

Populations are being declared “vitamin A deficient” and given MORE “vitamin” A.

On the other side:

When researchers actually look at LIVER STORES, substantial percentages of human populations are already HIGH or HYPERVITAMINOTIC.

You might want to know what’s already in the storage tank before you keep pouring more into it.

Just a thought.

The First Problem: We Are Usually Looking in the WRONG Place

If you want to know how much “vitamin” A somebody has stored in their body, where should you look?

Blood?

Sounds reasonable.

There’s just one problem.

THE LIVER IS THE MAJOR STORAGE SITE.

As in, 90%+ of it.

Researchers have known this for decades.

A 1972 human autopsy study, Vitamin A concentration in human tissues collected from five areas in the United States, stated that the best estimates of “vitamin” A nutriture were obtained from liver “vitamin” A concentrations.

Why don’t we routinely measure liver concentrations?

Pretty obvious.

You generally can’t go around cutting chunks out of healthy people’s livers, aka biopsy, just to see how much “vitamin” A is in there.

So we use blood instead.

Unfortunately, blood and liver stores are NOT the same thing.

A 1970 New York City autopsy study, Liver Stores of Vitamin A in a Normal Population Dying Suddenly or Rapidly from Unnatural Causes in New York City, put it plainly:

“Blood levels of vitamin A do not necessarily reflect tissue concentrations.”

The authors also stated that liver reserves are the “best indicator of vitamin A status.”

Then came the 1974 Bangkok study, Plasma and liver concentrations of vitamin A in a normal population of urban Thai.

These were 84 people who died from accidents.

Not people selected because doctors suspected hypervitaminosis A.

Not supplement overdoses.

Accident victims.

The investigators compared plasma retinol with ACTUAL liver “vitamin” A.

Their conclusion?

“Plasma values above 10 μg/100 ml are clearly not predictive of liver storage.”

The correlation?

r = 0.068.

Basically NOTHING.

So when somebody tells me:

“My serum vitamin A was normal.”

My response is:

AND?

What was in your liver?

Because THAT is the storage tank.

What Counts as Excessive Liver Storage?

We need to keep the terminology straight here because different papers use different units, different cutoffs, and different labels.

Modern human studies commonly define liver “vitamin” A (abbreviated vA in the units) of ≥1.0 μmol vA/g liver as hypervitaminosis A.

That works out to approximately:

286 μg vA/g liver

286 mg vA/kg liver

~950 IU vA/g liver

For comparing the older studies, I use approximately 300 μg vA/g or 1,000 IU vA/g as a practical historical comparison point.

Some newer papers reserve the word “toxic” for even higher liver concentrations.

Fine.

I’m not interested in playing semantic games over whether we call something “high,” “hypervitaminotic,” “excessive,” or “toxic.”

Here’s what I want to know:

HOW MANY PEOPLE ARE ALREADY ABOVE THE LIVER LEVEL THE LITERATURE ITSELF CALLS HYPERVITAMINOSIS A?

Because once you start looking there, things get ugly FAST.

New Zealand: Children With ENORMOUS Liver Stores in the 1950s and 1960s

The 1962 study Vitamin A content of human liver from autopsies in New Zealand examined liver samples collected in 1951 and 1960–61.

[reminder, above 1,000 IU vA/g is EXCESSIVE]

The overall mean (average) among 110 subjects:

1,006 IU vA/g liver.

Now look at the CHILDREN.

“Children from 1 to 10 years had higher liver stores.”

How high?

Median:

1,982 IU vA/g liver.

That’s roughly TWICE the modern hypervitaminosis comparison threshold.

Among people dying from accidents, the median was 1,256 IU vA/g liver.

And what did the researchers discuss as possible contributors?

Butter.

Dietary carotenes and preformed “vitamin” A.

Fish-liver-oil preparations (like cod liver oil, aka “fish fatty liver juice”).

In short, food AND “food-based” supplements.

So much for the idea that this story is simply:

“Some idiot swallowed an entire bottle of synthetic vitamin A pills.”

Nope.

Ghana: Nearly HALF the Livers Above 300 μg/g

Now let’s go to Ghana.

The 1963 paper HYPERCAROTENÆMIA IN GHANAIANS examined 49 livers.

[reminder, above 300 ug vA/g is EXCESSIVE]

Here’s what they found:

“Twenty-four of the livers showed vitamin-A levels above 300 ug. per g.”

Twenty-four out of 49.

49%.

Basically HALF.

The average for the entire group was already:

409 μg vA/g liver.

The highest?

3,635 μg vA/g liver.

Remember WHO’s magic public-health number where concern begins?

20%.

Here we have roughly 49% above 300 μg vA/g liver.

More than DOUBLE that prevalence.

Four years later, another Ghanaian study, Distribution of carotene and vitamin A in liver, pancreas and body fat of Ghanaians, examined another group.

The researchers described the hepatic “vitamin” A values as:

“exceptionally high.”

The mean was 490 μg vA/g liver.

The maximum:

1,900 μg vA/g liver.

And what was a major feature of the diet?

Carotene-rich foods.

Palm oil.

FOOD.

We can safely assume that in 1960s Ghana, they were not popping “vitamin” A supplements at all, which is exactly what the research says.

Canada: “Surpluses Are Stored”

A 1969 Canadian survey, Vitamin A Reserves of Canadians, analyzed liver samples from several major Canadian cities.

The authors made a statement that should probably be stapled onto every bottle of “vitamin” A:

“a slight accumulation of vitamin A over the life span, as would be expected of a vitamin whose surpluses are stored.”

Read the last part again.

“SURPLUSES ARE STORED.”

Exactly.

THAT is why chronic exposure matters.

Today’s dose doesn’t exist in isolation from yesterday’s dose.

And yesterday’s dose doesn’t necessarily disappear before tomorrow’s dose arrives.

SURPLUSES ARE STORED.

The Canadian investigators also found that children ages 1–10 had the highest stores and described those unusually large stores as strongly suggesting supplementation.

Maybe repeatedly adding a fat-soluble substance that the body STORES deserves a little more thought than:

“But it’s a harmless vitamin!”

Just a thought.

New York City: Even “Normal” Accident Victims Had Very High Stores

The 1970 study Liver Stores of Vitamin A in a Normal Population Dying Suddenly or Rapidly from Unnatural Causes in New York City deliberately studied people without diseases expected to distort “vitamin” A status.

[reminder, above 300 ug vA/g is EXCESSIVE]

Again:

These were people dying suddenly or rapidly from accidents and other unnatural causes.

The distribution showed:

5% between 301–500 μg vA/g liver.

PLUS

5% above 500 μg vA/g liver.

That means:

10% ABOVE 300 μg vA/g liver.

One additional specimen from a 31-year-old woman measured:

1,000 μg vA/g liver.

And remember what this SAME paper told us:

“Blood levels of vitamin A do not necessarily reflect tissue concentrations.”

There it is again.

Washington, D.C.: 24% Above 300 μg vA/g liver

Now things really start getting interesting.

The 1973 study Vitamin A and carotene levels of a selected population in metropolitan Washington, D.C. examined 329 liver samples.

[reminder, above 300 ug vA/g is EXCESSIVE]

Here’s the published frequency distribution:

300–349: 4.3%

350–399: 6.4%

400–449: 0.9%

450–499: 2.1%

500–599: 2.4%

600–699: 1.2%

700–799: 1.5%

800–899: 1.5%

900–999: 0.6%

≥1,000: 3.3%

Add them up.

24.2%.

Nearly ONE-QUARTER of the entire sample was above 300 μg vA/g liver.

The authors themselves reported:

“11% of the subjects had concentrations of vitamin A above 500 μg vA/g liver.”

Another 3.3% were above 1,000 μg vA/g liver.

One liver reached an absolutely ridiculous:

4,921 μg vA/g liver.

Now remember WHO.

20% supposedly deficient = public-health problem.

Washington, D.C.:

24.2% above our hypervitaminosis comparison level.

This was 1973.

Where was the public-health emergency?

Thailand: Accident Victims, Massive Liver Levels, Worthless Blood Correlation

Back to Bangkok in 1974.

[reminder, above 300 ug vA/g is EXCESSIVE]

Again, these 84 people were accident victims.

Median liver “vitamin” A:

89 μg vA/g liver.

Doesn’t sound scary.

This is why medians can hide things.

The RANGE went all the way to:

3,200 μg vA/g liver.

The authors also reported values of 788 and 1,020 μg vA/g liver.

Their table put 8.3% above 320 μg vA/g liver, with another 6% between 280 and 320 μg vA/g liver.

And what did plasma retinol tell us about who had those stores?

Practically nothing.

Again:

“Plasma values above 10 μg/100 ml are clearly not predictive of liver storage.”

How many times does this need to be demonstrated before we stop pretending that a routine serum retinol test tells us how much “vitamin” A is stored in the liver?

London: About 31% Above 300 mg vA/kg Liver

Now we reach London.

The 1982 study A survey of human liver reserves of retinol in London examined:

364 autopsy specimens.

[reminder, above 300 mg vA/kg liver is EXCESSIVE]

Look at the frequency table.

Add every category beginning at 300 mg vA/kg liver.

You get:

112 out of 364.

That’s:

30.8%.

Call it 31%.

The paper itself emphasized the extreme end:

“11% of the subjects had reserves exceeding 500 mg vA/kg liver.”

Three exceeded 1,000 mg vA/kg liver.

Now go back to WHO again.

20–30% of a population is “vitamin” A deficient?

MODERATE public-health problem.

≥30% deficient?

SEVERE public-health problem.

London:

~31% above 300 mg vA/kg liver.

Same prevalence logic applied.

Completely different reaction.

Funny how that works.

Singapore: About 20% Above 300 mg/kg

Now Singapore.

The 1988 study Vitamin A reserve of liver in health and coronary heart disease among ethnic groups in Singapore examined 363 autopsy samples.

[reminder, above 300 mg vA/kg liver is EXCESSIVE]

The frequency table gives 73 people at 300 mg vA/kg liver or higher.

73 ÷ 363:

20.1%.

There’s that number AGAIN.

20%.

The paper reported:

“9% of the subjects had concentrations above 500 mg vA/kg liver”

and 1% exceeded 1,000 mg vA/kg liver.

WHO sees 20% on the LOW end and starts talking about a public-health problem.

We find 20% on the HIGH end?

Apparently:

Nothing to see here!

And Doctors May Not Even Recognize the Liver Damage

Here’s another MAJOR problem.

Let’s say somebody actually gets a liver biopsy.

Surely the pathologist will immediately recognize “vitamin” A toxicity, right?

Nope.

The 2003 paper Stellate-Cell Lipidosis in Liver Biopsy Specimens: Recognition and Significance reviewed 1,235 non-transplant liver biopsies and found 14 cases of stellate-cell lipidosis.

Stellate cells, aka Ito cells, are a major hepatic storage site for “vitamin” A.

The abstract begins with a major cause of this issue, and its cure:

“Hepatic stellate-cell lipidosis due to hypervitaminosis A can lead to cirrhosis, which can be averted by restricting vitamin A intake.”

The researchers admitted that even their reported prevalence could be an UNDERestimate, because the remaining biopsies had not all been reviewed for missed or uncoded cases.

Five patients were taking oral “vitamin” A.

And clinically?

“None were suspected clinically of having hypervitaminosis A.”

NONE.

The authors ended with this:

“Pathologists should be alert to the diagnosis of stellate-cell lipidosis.”

There’s your detection problem.

The damage can exist.

The biopsy can literally be sitting under a microscope.

The doctor can be LOOKING AT IT.

And if they don’t know what they’re looking for?

MISSED.

Normal Liver Enzymes Don’t Necessarily Save You Either

Now let’s make this even worse.

A 1983 report, Liver damage with reversible portal hypertension from vitamin A intoxication: demonstration of Ito cells, described a woman who developed ascites, hepatosplenomegaly, and “vitamin” A-related liver injury.

There’s those Ito cells again.

Her:

• bilirubin was normal.

• AST was normal.

• ALT was normal.

She had been taking an estimated 90,000 IU of “vitamin” A daily for two years, sometimes increasing it to 300,000 IU daily, while ALSO drinking around half a liter of carrot juice every day.

Yes.

That is an extreme intake.

But before anybody dismisses the carrot-juice part, there’s another historical case you need to know about.

In 1974, the New York Times reported the death of 48-year-old British health-food enthusiast Basil Brown:

Carrot-Juice Addiction Cited in Briton’s Death

Brown reportedly drank as much as:

A GALLON OF CARROT JUICE PER DAY.

He was ALSO taking “vitamin” A tablets, averaging 700,000 IU per day.

At that carrot juice and supplement intake, he lasted only 10 days before he left this world.

The inquest attributed his death to carrot-juice addiction, with severe liver injury described in contemporary reporting.

“Dr. David Haler, the pathologist who performed an autopsy, said that the effect of the enormous intake of Vitamin A from carrots and tablets was indistinguishable from alcoholic poisoning. It produces the same result, he said—cirrhosis of the liver.”

Now, before somebody runs off and says:

“DR. GARRETT SMITH SAYS ONE CARROT WILL KILL YOU!!!”

No.

That is obviously NOT the point.

The point is that here we have another historical case involving:

Enormous carotenoid exposure + preformed “vitamin” A exposure + severe liver damage = DEATH.

And in the 1983 woman?

Remember:

SERIOUS liver effects.

NORMAL AST.

NORMAL ALT.

So let’s see how well our standard detection system is working so far.

Serum retinol does not reflect liver stores.

Routine liver enzymes may be perfectly normal even while the liver is falling apart.

And actually measuring the liver directly requires sticking a needle into it or waiting until somebody dies. If a biopsy is done, the pathologist may not be astute enough to catch the problem.

Wonderful.

Seeing the problems yet?

Then 2018 Happened: 33% of U.S. Cadavers Were Hypervitaminotic

This may be one of the most important modern papers in this entire discussion.

The 2018 study Serum retinyl esters are positively correlated with analyzed total liver vitamin A reserves collected from US adults at time of death obtained matched serum and liver specimens from 27 American cadavers.

This was NOT an estimate.

They had the livers.

They measured them.

What did they find?

“Nine subjects (33%) had hypervitaminosis A.”

33%.

ONE-THIRD.

Now I’m going to beat this WHO comparison into the ground because it deserves to be beaten into the ground.

WHO:

≥30% deficient = SEVERE public-health problem.

U.S. cadavers:

33% hypervitaminotic.

Same type of prevalence.

Where’s the severe public-health response?

The study gets even better.

Liver “vitamin” A versus serum retinol:

r = 0.00.

P = 0.95.

ZERO relationship.

Not “weak.”

Not “less than ideal.”

ZERO.

And the researchers concluded that:

“population biomarkers diagnosing hypervitaminosis before toxicity are urgently needed.”

Exactly.

Because the routine blood marker isn’t telling you anything about what’s in the storage tank.

Direct Liver Measurement Was STILL Finding Excess in 2024

Maybe all of this is just old data.

Maybe this somehow stopped happening.

Nope.

The 2024 study Hepatic Vitamin A Concentrations and Association with Infectious Causes of Child Death directly analyzed postmortem liver specimens from children and stillbirths in Kenya and South Africa.

Among 366 viable liver samples, researchers found:

6.0% high

8.7% hypervitaminotic

So ~15% of these children had EXCESSIVE stores, while absolutely STARVING as a whole:

“Eight in 10 cases had evidence of malnutrition based on anthropometry at death, and the prevalence of underweight (79.4%) and stunting (69.9%) was significantly higher among neonates.”

They need MEAT and CALORIES.

Yet 1 in 6 of them still have excessive “vitamin” A in their livers.

Still, the simple-minded public-health approach has only focused on one direction:

MORE “VITAMIN” A.

What About Retinol Isotope Dilution?

Obviously, we cannot routinely biopsy the livers of healthy living people.

So researchers developed another method:

Retinol Isotope Dilution, or RID.

RID gives somebody a small dose of stable isotope-labeled retinol, lets that tracer mix with existing body stores, then estimates total-body and liver reserves based upon the resulting dilution.

Important distinction:

RID estimates liver stores.

Direct chemical liver analysis MEASURES liver stores.

I do NOT consider those equivalent.

But here’s what makes this interesting:

Even the indirect RID method keeps finding the SAME basic problem.

Nicaragua: Fortified Sugar More Than Doubled Estimated Stores

The 2004 study Use of the deuterated-retinol-dilution technique to monitor the vitamin A status of Nicaraguan schoolchildren followed children during the first year of Nicaragua’s national “vitamin” A sugar-fortification program.

[reminder, above 1.0 μmol vA/g liver is EXCESSIVE]

Median estimated total-body “vitamin” A stores increased from:

0.33 → 0.72 mmol.

Mean estimated liver “vitamin” A increased from:

0.57 → 1.20 μmol vA/g liver.

One child went from an already-high:

1.35 → 3.24 μmol vA/g liver.

And what did his plasma retinol look like?

“the corresponding plasma retinol values were unremarkable”

There it is AGAIN.

Liver stores go sky-high.

Blood looks boring.

After only one year:

9 of 21 children had estimated liver stores above 1.05 μmol vA/g liver.

That’s:

43%.

The fortification program was designed to put more “vitamin” A into their bodies.

Well...

MISSION ACCOMPLISHED.

South Africa: 63.6% Hypervitaminotic BEFORE Another High-Dose Supplement

This one is absolutely ridiculous.

The 2019 paper’s title says almost everything:

South African preschool children habitually consuming sheep liver and exposed to vitamin A supplementation and fortification have hypervitaminotic A liver stores.

They assessed 94 preschool children using RID.

BEFORE the supplement:

63.6% were already hypervitaminotic.

Read that again.

SIXTY-THREE POINT SIX PERCENT.

Then, “in line with current practice,” the children were given:

200,000 IU OF “VITAMIN” A.

Afterward?

71.6% hypervitaminotic.

You cannot make this stuff up.

Nearly TWO-THIRDS of the children were already classified as hypervitaminotic.

So what did the system do?

GIVE THEM MORE.

Remember WHO again?

≥30% deficient?

SEVERE public-health problem.

Here we have:

63.6% HYPERVITAMINOTIC.

More than DOUBLE the prevalence WHO calls severe when the arrow points the other way.

Where’s the emergency?

Where’s the policy reversal?

Where’s the giant red:

Five African Countries: Hypervitaminosis Was NOT Some Isolated Fluke

Maybe Ghana and South Africa were just some weird outliers.

Nope.

A later multi-country analysis, Association between Biomarkers of Inflammation and Total Liver Vitamin A Reserves Estimated by 13C-Retinol Isotope Dilution among Preschool Children in 5 African Countries, looked at children in Burkina Faso, Cameroon, Ethiopia, South Africa, and Tanzania.

Using ≥1 μmol vA/g liver as hypervitaminosis A:

Burkina Faso:

24.2%.

Cameroon:

42.6%.

South Africa:

57.7%.

Across the analyzed groups:

20.9% hypervitaminotic.

THERE’S THAT NUMBER AGAIN.

20%.

When it means deficiency:

PUBLIC-HEALTH PROBLEM!

When it means hypervitaminosis:

[…silence…]

Hello?

Anybody home?

Burkina Faso, 2025: One-Third Hypervitaminotic, ZERO “Vitamin A Deficiency” by RID

Now we get to one of my favorites.

The 2025 study Association between vitamin A status, inflammations, and infections in children 36–59 months of age in rural Burkina Faso used 13C-retinol isotope dilution.

Rural Burkina Faso.

Surely these children are all terribly “vitamin” A deficient, right?

That’s what we’ve been told to expect.

What did RID find?

“One-third of study participants were found to have hypervitaminosis A.”

32% hypervitaminotic.

How many were “vitamin A deficient” by RID?

ZERO.

***ZERO***.

Let’s compare that to WHO one more time.

≥30% deficient = severe public-health problem.

Burkina Faso:

~32% hypervitaminotic.

Same prevalence.

Where’s the severe public-health declaration NOW?

And remember what we already discussed earlier.

If “vitamin A deficiency” itself is being confused with deficiencies of protein, calories, zinc, taurine, and the resulting problems with retinol transport...

Then what exactly have these supplementation programs been “correcting”?

Especially when direct or isotope-based assessments keep finding huge stores?

And Then There Is the Filipino Study

This one is particularly revealing because it shows exactly where DATA and INTERPRETATION can part company.

The 2022 study Filipino Children with High Usual Vitamin A Intakes and Exposure to Multiple Sources of Vitamin A Have Elevated Total Body Stores of Vitamin A But Do Not Show Clear Evidence of Vitamin A Toxicity studied 123 children only 12–18 months old.

Most had retinol intake ABOVE the Tolerable Upper Intake Level (abbreviated UL).

If you weren’t aware, intakes above the UL threshold moves the individual into a range where “toxicity or other negative physiological consequences become more likely.”

Their estimated liver “vitamin” A concentrations were generally above the proposed hypervitaminosis cutoff.

Yet the specific biomarkers the researchers chose for overt toxicity did not show the type of toxicity they were looking for.

So what interpretation did they entertain?

Maybe the cutoff should be higher.

Ah.

There it is.

This distinction matters:

FINDING:

Very young children exposed to multiple “vitamin” A sources had very high intake and very high estimated body stores.

INTERPRETATION:

Maybe the level we call hypervitaminosis should be moved upward because the toxicity markers we chose weren’t abnormal yet.

Those are NOT the same thing.

My question is MUCH simpler:

WHY ARE BABIES ACCUMULATING THAT MUCH “VITAMIN” A IN THE FIRST PLACE?

And what happens after another year?

Five years?

Ten years?

Thirty years?

Remember Canada in 1969?

“SURPLUSES ARE STORED.”

This Is NOT One Study. THAT Is the Point.

Anybody can nitpick one study.

Small sample.

Old study.

Different laboratory technique.

Different population.

Different diet.

Accident victims.

Sick people.

Autopsy data.

RID estimate.

Different country.

Fine.

Now ZOOM OUT.

New Zealand.

Ghana.

Canada.

New York City.

Washington, D.C.

Thailand.

London.

Singapore.

The United States.

Nicaragua.

South Africa.

Cameroon.

Burkina Faso.

Kenya.

The Philippines.

Different continents.

Different decades.

Different diets.

Different methodologies.

Adults.

Children.

Babies.

Accident victims.

Community populations.

Cadavers.

Direct liver analysis.

Retinol isotope dilution.

And the SAME basic problem keeps showing up:

HUGE AMOUNTS OF “VITAMIN” A STORED IN HUMAN BODIES.

At some point you have to stop staring at each individual tree and realize:

YOU’RE STANDING IN A FOREST.

The Blood-Test Problem May Be the Biggest Problem of ALL

If excessive “vitamin” A storage showed up clearly on a routine blood test, this whole situation would be MUCH easier.

It doesn’t.

Researchers have known this for decades.

1970:

“Blood levels of vitamin A do not necessarily reflect tissue concentrations.”

1974:

“Plasma values above 10 μg/100 ml are clearly not predictive of liver storage.”

2018:

Liver “vitamin” A versus serum retinol:

r = 0.00.

The WHO itself acknowledged that serum retinol is under homeostatic control and is reliable for estimating stores mainly at the extremes.

Think about what this means.

You go to the doctor.

They order serum retinol.

It comes back “normal.”

Everybody relaxes.

Meanwhile, that test may tell you VERY LITTLE about how much “vitamin” A is sitting in the liver.

The test answers:

“What is the serum retinol concentration?”

It does NOT necessarily answer:

“How much ‘vitamin’ A is stored in this person’s liver?”

Those are TWO DIFFERENT QUESTIONS.

Yet we act like they’re interchangeable.

They’re not.

So Where Did the “Epidemic” Go?

It didn’t disappear.

WE STOPPED LOOKING FOR IT PROPERLY.

Direct liver studies are difficult.

Liver biopsies are invasive and carry risk.

You cannot ethically biopsy huge populations of healthy people just to measure their “vitamin” A.

So easier biomarkers took over.

Unfortunately:

The easier biomarkers do NOT answer the same question.

Meanwhile, the human liver data NEVER told us:

“Relax, everybody is deficient.”

Quite the opposite.

When researchers actually measured or estimated liver stores, substantial percentages of human populations repeatedly landed in ranges the literature itself labels:

HIGH.

HYPERVITAMINOTIC.

And at still higher concentrations:

TOXIC.

No single paper proves a worldwide epidemic.

That’s not the argument.

THE ACCUMULATION OF THE PAPERS IS THE ARGUMENT.

Different countries.

Different decades.

Different populations.

Different methods.

Same pattern.

And remember where we started.

The researchers warned us long ago.

We Were Warned

1953:

Vitamin A intoxication was already being diagnosed with increasing frequency.

1981:

Chronic Vitamin A Intoxication: A Multisystem Disease That Could Reach Epidemic Proportions.

1982:

“We may be on the verge of an epidemic of vitamin A toxicity.”

They didn’t say:

“Maybe someday, under some bizarre circumstances, a handful of supplement abusers could become toxic.”

They warned about an:

EPIDEMIC.

Then the liver studies kept accumulating.

And now, more than four decades later, modern studies are STILL finding children and adults with hypervitaminotic stores while simultaneously showing that ordinary serum retinol does a TERRIBLE job of revealing what is stored in the liver.

So here’s the bottom line.

“Vitamin” A Toxicity Is NOT Some Freak Event Limited to Somebody Swallowing a Bottle of Supplements.

Excessive liver storage has been documented in human populations for more than 70 years.

Normal serum retinol does NOT rule it out.

Food contributes.

Supplements contribute.

Fortification contributes.

Medications contribute.

Topical retinoids contribute.

These multiple sources STACK.

However, it only truly takes ONE source used long enough to cause the same problem.

Most importantly:

The body STORES surpluses.

Remember WHO’s own public-health logic.

If 20–30% of a population is supposedly deficient?

Public-health problem.

If ≥30% is supposedly deficient?

Severe public-health problem.

Fine.

APPLY THE SAME LOGIC BOTH WAYS.

When 20%, 30%, 40%, 50%, 60%, and 70%+ of studied populations show excessive or hypervitaminotic stores, stop pretending these are isolated curiosities.

And before reflexively treating supposedly low serum retinol with MORE “vitamin” A, maybe ask whether the actual problem is:

Protein deficiency.

Calorie deficiency.

Zinc deficiency.

Taurine deficiency.

Impaired retinol transport.

Or some combination of them.

Because the question public health has spent decades asking is:

“HOW DO WE GET MORE VITAMIN A INTO PEOPLE?”

The liver studies suggest we should have been asking the EXACT OPPOSITE question first:

HOW MUCH IS ALREADY IN THERE?

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Vitamin A Toxicity is a Modern Epidemic — RELOADED | LYLL #265