Carnivore Diet and Minerals: Debunking Myths About Deficiencies

# Carnivore Diet and Deficiencies: Magnesium, Copper, Zinc, Iron, Potassium, Selenium — What Biology Really Says

**by Laurent Glatz – for Athletic Carnivore**

The next big trial against the carnivore diet is already predictable: not enough magnesium, too much copper, excess iron, insufficient potassium, zinc-copper imbalance, lack of this, excess of that.

On paper, it sounds scientific. You take a nutritional recommendation, open a food composition table, compare two numbers, and pronounce the verdict.

But that’s not how the human body works.

**Dietary intake is not absorption. Absorption is not retention. Blood concentration is not necessarily tissue storage. And exceeding or not reaching a reference value does not automatically mean toxicity or clinical deficiency.**

It is precisely this confusion that fuels many myths about “carnivore deficiencies.”

The Human Body Doesn’t Count Milligrams Like a Nutrition App

To understand minerals, you must distinguish at least four levels: what is present in the food, what remains available after digestion, what actually crosses the intestine, and what the body retains or eliminates.

These four values can differ radically.

Bioavailability depends on the nutrient’s chemical form, the food matrix, digestive pH, molecules binding the mineral, the body’s reserve status, and the activity of intestinal and renal transporters.

That’s why two foods containing exactly 10 mg of a mineral do not necessarily provide 10 mg of biologically equivalent mineral.

Phytates, found notably in cereals, legumes, seeds, and nuts, can form complexes with several minerals. A 2024 review of 42 human interventions concluded that most studies on phytate-rich foods find decreased bioavailability of iron and zinc, while phytate degradation often improves it.

This does not mean plants “steal all minerals.” It simply means that **you cannot properly compare two diets based on raw food content without considering absorption.**

For iron and zinc, this difference is particularly well documented.

Magnesium: The Number on the Label Tells Only Part of the Story

Magnesium is probably the most frequently used argument against the carnivore diet.

It’s often pointed out that seeds, nuts, and green vegetables are especially rich in magnesium. That’s true.

Then the conclusion is jumped to: without them, deficiency.

That’s where physiology disappears.

An adult contains about **25 grams of magnesium**. Between 50 and 60% is in the bones, most of the rest in soft tissues, and **less than 1% is in blood serum**. This is precisely why the NIH reminds us that serum magnesium measurement poorly reflects total body stores.

But the most interesting part lies in the intestine and kidney.

Under usual intake, about 30 to 50% of ingested magnesium is absorbed. When intake is low, **fractional absorption can rise to about 80%**. When intake is high, it can drop to around 25% or less depending on experimental conditions.

This is not magic. It’s homeostasis.

Part of magnesium crosses the intestinal epithelium passively; another part benefits from transcellular transport systems whose importance increases when availability decreases. The kidney then does the other half of the work: about **96% of filtered magnesium can be reabsorbed by renal tubules** under physiological conditions.

So when reserves drop, the body can simultaneously **increase intestinal absorption efficiency and reduce urinary losses**.

Conversely, if a lot of magnesium arrives, the absorbed fraction decreases and renal excretion increases.

That’s why “my diet provides 280 mg while the recommendation is 400 mg, so I’m deficient” is not a biological diagnosis.

Another particularly interesting detail for an animal-based diet: a human literature review reports that proteins can improve apparent magnesium absorption, while phytates and some fibers can reduce it.

This doesn’t mean 200 mg suddenly becomes 400 mg.

It means something much more serious: **the amount ingested is not enough to predict the amount retained.**

Can You Still Lack Magnesium on a Carnivore Diet? Obviously. But That’s a Different Statement

Vomiting, chronic diarrhea, alcohol, certain medications, digestive disorders, renal losses, or metabolic disorders can cause magnesium depletion regardless of diet label.

And during the abrupt switch to a very low-carb diet, decreased insulin initially causes more natriuresis. Water, sodium, and sometimes potassium are then lost more during this adaptation phase. This transient phenomenon is documented in ketogenic induction literature.

A cramp during this phase does not prove that “humans need almonds.”

It proves that electrolyte balance is dynamic.

Excess follows the exact opposite reasoning. In someone with normal kidney function, dietary hypermagnesemia is unusual because the kidney eliminates the surplus. Severe intoxications mainly concern pharmacological or high supplemental doses, especially when renal function is impaired.

Again: **it’s not carnivore versus plant. It’s absorption, retention, losses, and regulation.**

Copper: Claiming Carnivores Lack It Is Hard to Defend

Copper makes the “animal deficiency” argument even more fragile.

Among the foods richest in copper listed by the NIH are beef liver and oysters.

About 85 g of beef liver provide around **12.4 mg of copper**, nearly fourteen times the US daily value. The same amount of wild Eastern oysters provides about **4.85 mg**.

In other words, when someone claims that cutting out plants necessarily condemns you to copper deficiency, they forget that some of the richest copper sources are precisely animal foods.

But the most interesting phenomenon happens after ingestion.

Copper absorption itself is adaptive.

With an intake of about 400 µg per day, the NIH reports bioavailability reaching about **75%**. At 7.5 mg per day, it can drop to around **12%**.

The more abundant the copper, the lower the absorbed fraction.

In the intestine, copper is reduced to Cu⁺ before entering the enterocyte. Transport proteins then ensure its passage, while intracellular chaperones prevent free, highly reactive copper ions from roaming inside the cell.

Copper then reaches the liver. There, it can be incorporated into proteins, notably via ceruloplasmin-associated systems, or directed toward biliary excretion.

We are therefore far from a pipe where all ingested copper automatically ends up in the blood.

Here’s the Zinc-Copper Trap Many Forget

Copper cannot be understood in isolation.

A significant excess of zinc can cause… a **copper deficiency**.

Why?

Because zinc stimulates metallothionein synthesis in enterocytes. This protein binds metals but has a very high affinity for copper.

Copper then remains sequestered in intestinal cells instead of entering circulation. When these enterocytes die and are shed into the digestive lumen, copper leaves with them.

The result can be paradoxical: a lot of zinc absorbed, but progressively less copper available.

This mechanism is real enough that high zinc intake is used in some situations to deliberately reduce copper absorption. Chronically high zinc supplementation is a documented cause of copper deficiency.

That’s why looking only at “zinc: X mg, copper: Y mg” is no longer sufficient.

**Biology also depends on their interaction.**

So Does the Carnivore Diet Provide Too Much Copper?

Not automatically either.

In a healthy person, absorption decreases as intake increases, and the liver helps manage and excrete copper via bile.

But that doesn’t mean quantities are infinite.

The US currently sets the adult tolerable upper intake level for copper at 10 mg per day. A large portion of beef liver alone can exceed this value. Chronic dietary toxicity remains rare in healthy subjects, but accumulation becomes a very different issue in certain copper metabolism disorders, notably Wilson’s disease.

That’s why “eat liver every day because more micronutrients means better” is no more biological than “never eat liver because it has too much copper.”

In both cases, physiology is replaced by a simplistic rule.

Zinc: One of the Few Cases Where Animal Bioavailability Is Hard to Contest

For zinc, animal foods have a well-documented advantage.

Meats and seafood are among the main dietary zinc sources. The NIH explicitly states that zinc from beans, nuts, and whole grains has **lower bioavailability** due to phytate content.

The intestine also has remarkable adaptive capacity.

When zinc intake decreases, expression of the intestinal transporter **ZIP4** increases. Inside the enterocyte, various ZnT transporters and metallothionein then modulate storage and passage into circulation.

Again, the body responds to status.

And again, excess is not automatically harmless: chronically high zinc doses, especially supplements, can eventually cause the copper deficiency described earlier.

**A mineral is never fully understood without considering others.**

Iron: Carnivores Absorb It Better… But the Body Has a Brake

Iron is probably the most striking example of the difference between quantity and bioavailability.

Animal foods contain heme iron, whose bioavailability is higher than non-heme iron. The NIH estimates overall iron bioavailability at about **14–18% in mixed diets containing meat and seafood**, versus about **5–12% in vegetarian diets**. Phytates and some polyphenols particularly reduce non-heme iron absorption.

But that doesn’t mean eating more meat raises iron unchecked.

The main regulator is called **hepcidin**.

This hormone, produced mainly by the liver, responds to iron stores, inflammation, and erythropoiesis needs.

When hepcidin increases, it binds to **ferroportin**, the transporter that allows iron to leave enterocytes and some storage cells. Ferroportin is internalized and degraded: less iron then reaches circulation.

When demand rises, hepcidin decreases and more iron becomes available.

It’s a true thermostat of iron metabolism.

But unlike magnesium, humans lack a powerful physiological mechanism to actively excrete excess iron.

That’s why genetic anomalies of the hepcidin-ferroportin axis, like some hereditary hemochromatoses, completely change the situation.

Saying “meat causes iron overload” without considering this regulation is too simplistic.

Saying “you can never have too much iron on carnivore” would be equally simplistic.

Potassium: No, It’s Not Only Found in Bananas

Potassium is another interesting example.

Meat, fish, and dairy naturally contain potassium. For illustration, the NIH reports about 315 mg per 85 g of beef sirloin, 326 mg for salmon, and 332 mg for chicken breast.

For someone consuming many animal foods, this obviously adds up to significant amounts.

About **85 to 90% of dietary potassium is absorbed**.

More importantly, its concentration is tightly regulated because the potassium-sodium gradient is essential for nerve conduction, muscle contraction, and cellular electrical potential.

The kidneys quickly adjust excretion to intake.

In a healthy person with normal kidney function, the NIH indicates hypokalemia from simply low dietary intake is rare. Major clinical causes are more often digestive losses, certain medications, potassium shifts between compartments, or kidney disorders.

The same logic applies the other way: in someone with normal kidneys, high dietary potassium usually does not cause hyperkalemia. However, kidney failure and some medications can completely alter this balance.

Selenium: Again, Animal Foods Are Far from Poor Sources

Fish, seafood, meat, poultry, offal, and eggs are among the main dietary selenium sources.

A serving of beef can provide roughly two-thirds of the daily value; sardines and shrimp even more.

The idea that a diverse animal-based diet is naturally low in selenium is therefore hard to support.

Yet excess exists here too.

Selenium has a narrower safety window than some other minerals. Chronic excessive exposure can cause selenosis with nail and hair abnormalities, digestive or neurological symptoms. The NIH currently sets an upper limit at 400 µg/day for adults, while EFSA in 2023 adopted a lower limit of 255 µg/day.

Again, the real question is the actual amount consumed, not the “carnivore” label.

Calcium: The Point Where We Must Avoid Spreading Myths

Calcium shows why this discussion demands precision.

A carnivore including cheese, tolerated dairy, sardines, or salmon with bones can obtain a lot of highly available calcium. Calcium absorption from dairy is around 30%, while calcium from some oxalate-rich plants can be extremely low: NIH gives about 5% for spinach versus 27% for milk.

But someone eating only muscle meat without bones or dairy will obviously have much less dietary calcium.

Hiding this difference does not defend the carnivore diet.

It simply shows that **“carnivore” is not a single nutritional composition.**

Here Is the Real Myth to Destroy

The mistake is not to say that mineral deficiency or overload can exist.

Of course they do.

The mistake is to look at a nutrition table and believe it directly predicts an individual’s biological status.

For magnesium, the intestine adapts absorption and the kidney strongly modulates losses.

For copper, absorption varies with intake, zinc can modify it, and the liver organizes distribution and elimination.

For zinc, phytates presence or absence changes bioavailability and intestinal transporters adapt to status.

For iron, heme form is better absorbed and the hepcidin-ferroportin axis regulates iron entry into circulation.

For potassium, absorption is very high but renal excretion adapts quickly.

For selenium, meat and seafood already provide extremely important sources.

We are no longer dealing with a simple story of “milligrams per day.”

We face **a dynamic system of absorption, transport, competition, storage, recycling, and excretion.**

And that’s precisely why the statement:

**“The carnivore diet inevitably causes mineral deficiencies”**

is not a scientific conclusion.

It’s an extrapolation.

But the opposite claim — “a carnivore can never be deficient” — is no more scientific.

The biologically defensible position is much more precise:

**A properly constructed carnivore diet provides many minerals in highly bioavailable forms, removes several absorption inhibitors present in some plant matrices, and benefits from the body’s normal homeostatic mechanisms. Nothing justifies turning the absence of plants into an automatic diagnosis of magnesium, copper, zinc, iron, potassium, or selenium deficiency.**

And above all, a theoretical nutritional value never tells you what’s happening inside you.

Your digestive absorption, losses, kidney function, physical activity, supplements, medications, exact diet composition, and metabolism can completely change the equation.

That’s why blindly adding magnesium, zinc, or copper “just in case” isn’t necessarily smarter than fearing them.

**Blind supplementation can even create the imbalance it was supposed to prevent.**

At this point, the right question is no longer:

**“Does the carnivore diet lack magnesium or contain too much copper?”**

The biologically interesting question becomes:

**“What do I actually absorb, retain, eliminate, and what is my real biological status?”**

That’s precisely where individual analysis begins.

**Understanding My Metabolic Terrain**

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