The Starch We Don’t Digest and What It Could Do to Visceral Fat

An unusual human study

In 2019, researchers studied 19 normal-weight adults in a randomized, double-blind crossover trial.

For four weeks, participants consumed 40 grams per day of resistant starch type 2 derived from high-amylose maize, or an energy-matched control starch. Their diet was controlled during the intervention.

Here is what made the result intriguing:

Body weight did not change significantly, but body-fat distribution did.

MRI scans showed a significant reduction in both visceral and subcutaneous abdominal fat area after RS2. At the same time, metabolic markers, gut hormones and the microbiome changed.

That is a remarkable finding.

Visceral fat is not simply an energy store beneath the skin. It surrounds the internal organs and is metabolically active. Excess visceral fat is closely associated with insulin resistance and cardiometabolic disease.

A dietary intervention capable of influencing this fat depot would therefore be interesting, even if the number on the scale barely moved.

The microbiome as a metabolic organ

A 2024 study published in Nature Metabolism makes the story even more intriguing.

Thirty-seven people with overweight or obesity received 40 grams of resistant starch or a control starch each day for eight weeks in a randomized crossover trial.

During the resistant-starch phase, participants lost about 2.8 kilograms of body weight on average compared with the control intervention. Fat mass and waist circumference also decreased, while insulin resistance improved.

At the same time, the gut microbiome changed.

One bacterium stood out in particular: Bifidobacterium adolescentis. Its presence was associated with the metabolic improvements. In complementary mouse experiments, the researchers found evidence suggesting that this bacterium might contribute to some of the observed effects. They also found changes in bile-acid metabolism, along with signals consistent with improved gut-barrier function, reduced inflammation and reduced fat absorption.

This does not mean that B. adolescentis has been proven to be the decisive mechanism in humans.

But it opens up a fascinating possibility:

Perhaps resistant starch changes our metabolism not simply because we digest less of it, but because our microorganisms turn it into something else.

More than simply “fewer carbs”

That is what makes RS2 more interesting than the simple idea of replacing some digestible starch with fiber.

Fermentation creates new molecules.

Short-chain fatty acids can nourish intestinal cells, interact with receptors and influence metabolic and hormonal signaling. Studies of resistant starch have reported changes in glucose and insulin responses, and some have found improvements in insulin sensitivity.

Gut hormones such as GLP-1 are another possible connection between the intestine and whole-body metabolism. In the small 2019 RS2 trial, acetate and early GLP-1, insulin and C-peptide responses increased.

This creates a network of possible effects:

Starch structure → gut microbiome → fermentation → microbial metabolites and gut hormones → glucose and insulin metabolism → potentially fat metabolism and fat depots.

Which links in this chain actually drive changes in human body fat is not yet fully understood.

But the individual pieces are biologically interesting enough to deserve a closer look.

And then there are bile acids

There is another particularly intriguing mechanism: bile acids are not merely compounds that help us digest fat. They are also signaling molecules.

Gut bacteria chemically modify bile acids, altering the signals they can transmit through bile-acid receptors to metabolic pathways throughout the body.

In the 2024 study, the resistant-starch intervention was accompanied by changes in the bile-acid profile. The researchers also found evidence of reduced fat absorption and improved intestinal-barrier function.

This opens up a much broader perspective:

What we eat as “starch” may influence, through the microbiome, which metabolic messages the gut sends to the rest of the body.

So does RS2 actually reduce visceral fat?

This is where the story becomes more complicated.

Not every human study has found this effect.

In a 12-week trial in people with prediabetes, 45 grams of high-amylose maize RS2 did not change visceral, liver or intramuscular fat. Another study in people with metabolic syndrome found improved insulin sensitivity with 40 grams of resistant starch, but no change in visceral fat.

So the 2019 finding does not mean that taking 40 grams of RS2 will reliably make abdominal fat disappear.

But the null trials should not make the positive finding disappear either.

The studies differ in population, diet, design, duration and metabolic starting point. And for an intervention whose effects may partly depend on the gut microbiome, it is entirely plausible that not everyone responds in the same way.

That leads to a more interesting question:

Not simply, “Does RS2 work?” but “Which form of RS2 works for whom and under what conditions?”

Perhaps the microbiome gets a vote

The 2019 study already found associations between the participants’ baseline microbiome and their metabolic responses to RS2.

The 2024 study strengthens this idea.

If certain microorganisms are particularly good at utilizing resistant starch (or transform it into different metabolites) two people consuming the same amount of RS2 might experience different metabolic effects.

Resistant starch therefore illustrates a much larger idea in nutrition:

We never eat alone.

Part of our food is processed by a microbial ecosystem whose composition differs from one person to another.

The metabolic effect of a food may therefore depend not only on what is in it, but also on who is waiting for it in the gut.

Where do we find RS2?

RS2 occurs naturally in starchy foods in which the starch remains in a relatively intact structure that digestive enzymes find difficult to access.

Sources include:

• raw potato starch
• green or unripe bananas
• high-amylose maize starch
• certain legumes and other starch-rich plants

But there is an important distinction: resistant starch is not one single thing.

Processing, heating, cooling and the surrounding food matrix all alter starch structure. When cooked starch is cooled, for example, some of it can become RS3, another type of resistant starch.

The amounts used in the human trials described here (around 40 grams of RS2 per day) therefore cannot simply be translated into 40 grams of potato starch, banana or another food. These are research doses, not automatically general intake recommendations.

What remains?

RS2 is not an established treatment for visceral fat.

But the story is much more interesting than that sober conclusion suggests.

We have human studies in which resistant starch affects insulin sensitivity. We have a small controlled study in which visceral fat area decreased after four weeks of RS2. And we have a more recent randomized study in which people with overweight or obesity lost body weight, fat mass and waist circumference while taking resistant starch, alongside striking changes in the microbiome.

Other studies have not found these changes in fat depots.

That inconsistency is precisely what makes the question scientifically interesting.

Perhaps RS2 is less like a simple “fat-loss supplement” and more like a way of influencing a complex system: the relationship between starch structure, the gut microbiome, microbial metabolites, gut hormones and our own energy metabolism.

And perhaps what happens to our visceral fat is not determined by the starch alone.

But also by what our gut microbes do with it.