Thin but Metabolically Unhealthy: Understanding Invisible Visceral Fat

# You Can Be Thin Yet Metabolically Unhealthy: The Problem Isn’t Always Fat Quantity but Where Your Body Stores It

**by Laurent Glatz – for Athletic Carnivore**

You step on the scale: normal weight.

You check your BMI: nothing alarming.

You still fit into the same clothes you wore ten years ago.

Yet inside, your metabolism might be telling a completely different story.

This is one of the major pitfalls of our modern health perspective: we have so strongly linked metabolic disease with visible obesity that we ended up believing a thin person is automatically protected.

They are not.

There is even a phenotype studied under the name **TOFI — “Thin Outside, Fat Inside.”** These are people whose BMI remains normal but who have excessive visceral fat and an unfavorable metabolic profile. A recent review dedicated to this phenomenon describes it as high visceral adiposity despite normal or near-normal weight.

To understand why this matters, we must stop treating all fat as identical.

Your Adipose Tissue Is Not Just an Unsightly Storage Depot

Body fat has an essential physiological function.

When energy needs to be stored, subcutaneous adipose tissue is normally one of the relatively safe places to deposit triglycerides.

Under the skin.

Hips.

Thighs.

Buttocks.

Subcutaneous abdomen.

The problem begins when this storage capacity becomes insufficient or dysfunctional.

In some people, subcutaneous fat can expand considerably without immediately causing major metabolic disruption.

In others, this capacity seems much more limited.

When energy can no longer be properly stored in subcutaneous adipocytes, lipids start to accumulate elsewhere.

Around organs.

In the liver.

In muscle.

Around the heart.

In the pancreas.

This is called **visceral fat** or **ectopic fat**, depending on its location.

Biologically, the difference is immense.

A 2025 review highlights that fat distribution, particularly visceral and ectopic accumulation in organs like the liver, pancreas, heart, or muscle, plays a major role in metabolic disturbances, inflammation, and insulin resistance.

You can weigh 70 kilos yet have a more unfavorable metabolic environment than someone weighing 90.

The scale can’t show you where those kilos are stored.

Visceral Fat Is Not Just “Belly Fat”

There is a fundamental difference between the fat you can pinch under your skin and the fat located deep within the abdominal cavity.

Visceral fat surrounds the organs.

And it is metabolically active.

When it becomes hypertrophied and dysfunctional, it can exhibit more local hypoxia, inflammation, tissue remodeling, and release fatty acids as well as various inflammatory mediators.

Its location makes it particularly significant: some of its secretions enter the portal circulation directly, thus reaching the liver.

A 2024 review on the pathophysiology of visceral adipose tissue precisely describes this communication with the liver as one of the mechanisms contributing to cardiometabolic risk associated with visceral adiposity.

In other words, that belly you sometimes don’t even see in the mirror can start altering your liver’s metabolic function.

And the liver is central to almost everything.

Glucose management.

Glycogen storage and release.

Lipid metabolism.

Triglyceride production.

Gluconeogenesis.

Insulin response.

When fat accumulates in the liver, its insulin response can progressively deteriorate.

Insulin Keeps Talking, but the Liver Listens Less

In a metabolically healthy organism, insulin sends an important message to the liver after a meal:

**there is energy available, reduce glucose production.**

When the liver becomes insulin resistant, this signal loses effectiveness.

It continues producing glucose even though blood glucose is already elevated.

The pancreas must respond.

It secretes more insulin.

For a while, this increased insulin maintains apparently normal blood sugar.

This is fundamental.

You can have relatively normal blood glucose while already compensating with higher insulin levels.

From the outside: nothing.

On the scale: nothing.

Sometimes even on a basic blood test: almost nothing.

Yet the system is working harder to maintain this normality.

This is precisely why visible thinness does not guarantee excellent insulin sensitivity.

Muscle Also Plays a Huge Role

Muscle isn’t just there to look good in photos.

After a carbohydrate-containing meal, it is one of the main tissues responsible for insulin-stimulated glucose uptake.

The more active and metabolically functional muscle you have, the more tissue you possess capable of managing a significant portion of circulating energy substrates.

Conversely, a light person with very little muscle mass may have a completely different situation.

They may be thin simply because they have little subcutaneous fat **and little muscle**.

This is not necessarily an advantage.

Ectopic fat in muscle is also associated with insulin resistance, although the relationship is complex: endurance athletes can have high intramuscular lipids yet remain very insulin sensitive because they have excellent oxidative capacity. This again reminds us that a single number never fully describes metabolism.

What matters is what the muscle does with that energy.

Store it passively?

Or efficiently oxidize it in mitochondria?

This Is Why Exercise Becomes Much More Than a Tool to “Burn Calories”

We come back exactly to the cardio problem.

A thin person might think:

“I don’t need exercise; I don’t need to lose weight.”

This may be one of the costliest mistakes.

Exercise isn’t just about lowering the number on the scale.

Muscle contraction greatly increases energy demand.

Muscle uses glycogen.

It increases glucose uptake.

It improves oxidative capacity with training.

It increases the number and function of mitochondria.

And exercise can reduce visceral fat even when a person is not overtly obese.

A recent meta-analysis specifically on normal-weight or slightly overweight individuals studied the effects of cardio, strength training, and other exercise modalities on visceral fat in these TOFI profiles.

The benefit of exercise is therefore absolutely not limited to:

**“how many kilos have I lost?”**

You can stay exactly the same weight and dramatically improve your body composition.

More muscle.

Less visceral fat.

Better insulin sensitivity.

Improved mitochondrial capacity.

The mirror and scale may show almost nothing while biologically your terrain changes profoundly.

This Is Also Where Low Carb Becomes Particularly Interesting

If the central problem is chronic poor management of energy substrates, it makes sense to consider the quantity and frequency at which these substrates arrive.

A carbohydrate-rich diet means that after meals, more glucose must be handled.

In a very active, muscular, and insulin-sensitive person, this load can be remarkably well managed.

In another person, with little muscle, sedentary, and already insulin resistant at the liver or muscle level, the same intake can produce a very different metabolic response.

That’s why simply asking:

**“Are carbohydrates good or bad?”**

is probably not the right question.

The question becomes:

**what is your body capable of doing with them today?**

By drastically reducing carbohydrates, a low-carb diet mechanically decreases the amount of dietary glucose to be managed after each meal.

Postprandial insulin can decrease.

Fat mobilization becomes easier when insulin remains low.

The body gradually increases its use of lipids.

And under certain conditions, the liver increases ketone body production.

In other words, you progressively change fuel circulation.

Carnivore Takes This Logic Even Further

A properly constructed carnivore diet practically eliminates major sources of dietary carbohydrates while placing animal proteins and fats at the center.

This can produce several interesting effects in this context.

First, a dramatic reduction in exposure to ultra-processed foods combining flour, sugar, oils, starch, and hyperpalatability.

Next, a high protein density, with a significant effect on satiety and muscle mass maintenance.

Finally, a very large reduction in dietary carbohydrate load.

The liver obviously continues producing necessary glucose via gluconeogenesis.

The body does not become “glucose-free.”

But it no longer has to manage multiple massive glucose arrivals each day.

For someone already glucose intolerant, this difference can become metabolically very interesting.

But beware of the reverse shortcut.

Carnivore Does Not Mean Immune to Visceral Fat

This is probably one of the most important nuances to understand.

Eating zero carbs does not biologically make energy storage impossible.

You can still consume more energy than your body uses.

You can still be extremely sedentary.

You can still sleep five hours.

You can still lose muscle mass.

You can still have a terrain where certain fats accumulate more easily in the liver or around organs.

Science on ectopic fat shows precisely that this problem corresponds to a mismatch between energy arrival, storage, and use—not simply the presence of an isolated macronutrient.

That’s why carnivore can be an extremely coherent strategy without becoming a license to ignore everything else.

And Here’s the Most Interesting Paradox: You Can Also Be Obese and Relatively Insulin Sensitive

It sounds contradictory.

Yet classic studies have identified obese individuals with much more favorable insulin sensitivity than others of similar weight.

In a particularly interesting study, two groups of obese people had comparable total and visceral adiposity, but the insulin-sensitive group had much less liver and intramuscular fat and far superior insulin sensitivity.

This is essential information.

It means that **weight itself is not the metabolic problem.**

The real problem is much closer to:

where is energy stored?

how is it used?

what is the adipose tissue’s capacity to accommodate it?

how much muscle is available?

how do mitochondria function?

how does the liver respond to insulin?

That’s why two people with exactly the same BMI can have radically different metabolic risks.

The Body Can Hide the Problem for Years

This is probably what makes the TOFI phenotype so deceptive.

If you gain a lot of weight, something pushes you to react quickly.

Your clothes change.

The mirror changes.

The scale changes.

But if your weight remains stable?

You can keep eating exactly the same way.

Never do strength training.

Walk very little.

Gradually lose muscle with age.

Slowly accumulate visceral fat.

And consider yourself protected because your BMI still reads 22 or 23.

Yet recent literature confirms that excess visceral fat is a metabolic risk factor independent of obesity defined simply by weight or BMI.

This is where our collective obsession with the scale reaches its limits.

So the Real Goal May Not Be to Weigh Less

It could be to have a body capable of better energy management.

A muscle able to consume huge amounts of fuel when you ask it to work.

Mitochondria capable of oxidizing it.

A liver not overloaded with triglycerides.

Adipose tissue able to properly fulfill its role.

Good insulin sensitivity.

A diet that doesn’t continuously stimulate energy arrivals your body has no reason to use.

That’s why **strength training, cardio, daily activity, and low carb or carnivore diets can become extremely complementary.**

Cardio increases expenditure and oxidative capacity.

Strength training gives the body a reason to preserve or build muscle tissue.

Low carb drastically reduces carbohydrate load.

Carnivore can simultaneously boost protein density, simplify diet, and promote a very low-carb environment.

But none of these strategies should be viewed in isolation.

Because the real issue is never simply what you eat.

It’s what your body does with what you give it.

You can be thin and metabolically healthy.

You can be overweight and still have good insulin sensitivity.

But you can also be perfectly thin in front of your mirror while starting to accumulate exactly the fat you don’t want to accumulate: the fat you don’t see.

And at that point, asking only:

**“What is my weight?”**

becomes almost the least interesting question.

The much more relevant question is:

**“Where does my body store its energy, and why might it be starting to store it there?”**

This is exactly why a personalized analysis should not start by arbitrarily deciding how many kilos you need to lose. It should start by understanding your body composition, muscle activity, diet, carbohydrate tolerance, metabolic history, and how these elements interact.

**What if your silhouette reassured you simply because it shows you the fat you can see, but not the fat that may matter more for your metabolism?**

**Understanding My Metabolic Terrain**

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