Novelty as Scarcity: Does Unfamiliar Food Signal Famine?

This is the second essay in a series. If you haven't read Five Types of Hunger yet, start there, because this piece builds directly on it.

I didn't really learn how to cook until my thirties. Moving abroad and the sudden demands of motherhood pushed me well past simply applying heat to things. I had to learn to experiment with local ingredients since my usual staples weren't available. Looking back, that was a stroke of luck. My weight stabilized, my energy became steady and reliable, and without making a conscious decision, I was eating a lower-carbohydrate, nutrient-dense diet built around whole foods, both new and familiar.

Then I moved back to the US.

Getting meals together became effortless with processed food everywhere, always cheap, always fast. Except I was suddenly incredibly hungry all the time. I started gaining weight despite eating less and moving more. I read labels and found ingredients that hadn't existed in anything I'd been cooking abroad: industrial emulsifiers, refined seed oils, high-fructose corn syrup, artificial sweeteners, preservatives I couldn't pronounce. The combination of rapidly absorbed carbohydrates and these novel compounds spiked my blood sugar, crashed it, and drove the kind of rebound hunger that doesn't respond to will power. Despite living in a world of abundance, my body was reading the signals from my food thinking I lived in a time of scarcity.

I kept asking myself: if I'm eating less and moving more, why is my body holding on to fat?

A paper published in June 2026 finally gave me a name for what I experienced and a plausible biological explanation.

The Novelty-as-Scarcity Hypothesis

Researchers Ben-Dor and Klement, writing in the International Journal for Vitamin and Nutrition Research, propose what they call the Novelty-as-Scarcity (NAS) hypothesis.¹ The core argument is straightforward but striking:

When your body encounters foods that are evolutionarily unfamiliar, whether that means novel ingredients, unusual macronutrient ratios, or new processing methods, it interprets them as "fallback foods": the kind of thing you'd only eat if your real food supply had collapsed. This triggers an ancient fat-storage program designed to protect you from the famine that, in your body's evolutionary logic, must be coming.¹

In other words, your physiology doesn't just count calories. It reads your food environment for signals about stability and safety. Ultra-processed foods, packed with synthetic compounds your ancient metabolic systems have never encountered, send a signal that reads: something is wrong with the food supply. Expect scarcity and famine. Store fat now.

There is a reason to want an explanation of this kind. National data on American energy intake and energy availability rose between 1961 and 2000 and then plateaued or fell, while the trend they were meant to explain kept climbing and physical activity modestly increased.² Something in the standard account is missing a term.

This is an evolutionary mismatch, a survival mechanism that was genuinely useful for hundreds of thousands of years, now firing constantly in response to a supermarket full of novel industrial ingredients.

The novelty-as-scarcity loop

Your body isn't counting calories. It's reading your food environment.

1

Novel food

Ultra-processed ingredients your body has no history with

2

Weak satiety signal

Less GLP-1 and PYY released

3

Brain reads scarcity

Low nutrient yield interpreted as food shortage

4

Fat storage and hunger

An ancient conservation program activates

5

Eat more

The drive toward familiar, energy-dense food intensifies

↻ Step 5 returns to step 1, and the loop runs again

Each step is a proposed link, not a measured one.¹

What's Actually Happening in Your Body

The paper maps out several interlocking biological mechanisms, and each of them has its place in understanding what hunger is and what it means in your body.

Your gut sends weaker "I'm full" signals after novel foods

The lining of your gut is packed with receptors that detect nutrients and release satiety hormones, chiefly GLP-1 and a companion hormone called PYY. These receptors evolved to recognize the chemical signatures of ancestral foods. The paper's proposal is that novel food components may bind them with lower affinity, activate different receptor subtypes, or fail to activate certain pathways altogether.¹ That's a proposal, not a measured effect, and the paper is careful to say so.

The result: you eat a calorie-equivalent meal of ultra-processed food, but your gut releases significantly less GLP-1 than it would after a whole food meal. A randomized feeding study cited in the paper found that a Paleolithic style meal produced significantly higher GLP-1 and PYY levels than a calorie and macronutrient matched meal that included more evolutionarily novel foods like rice.³ Your brain receives a weaker satiety signal, interprets it as poor nutrient yield, or in other terms, scarcity, and pushes you to keep eating.

Your microbiome doesn't know what to do with these ingredients

Your gut microbiome co-evolved with the foods your ancestors ate, and a novel food may introduce substrates that community is poorly equipped to handle. That can mean inefficient fermentation, an unusual profile of short-chain fatty acids, or outright disruption of the microbial community. Those shifts alter gut peptide secretion, which feeds back into the same circuits regulating appetite and storage.¹⁶

The paper treats this as one of its more speculative routes and rests it largely on reviews.

There is one rung above a review, though. A human gut microbiota, kept alive in a bioreactor and exposed to twenty commonly used dietary emulsifiers, showed altered density, composition and gene expression under some of them, though not all.⁵ A bioreactor isn't a person, which is exactly the limitation.

But there is a human trial worth knowing about, and it isn't in the paper either.

In a double-blind controlled-feeding study, healthy adults ate either a completely emulsifier-free diet or the identical diet with fifteen grams a day of carboxymethylcellulose, a synthetic emulsifier that turns up in an enormous quantity of packaged food. Eleven days. The emulsifier group showed disrupted gut microbiota composition and reduced microbial diversity, and their stool metabolomes were depleted in short-chain fatty acids and free amino acids. Those changes were detectable within three days and held for the rest of the study.⁴

Two of the seven people eating the emulsifier showed something more serious: bacteria pushing into the inner mucus layer of the gut wall, which is normally kept sterile and whose breach is a defining feature of intestinal inflammation.⁴

Sixteen people in total, so treat it accordingly. But it is human, randomized, double-blind, and the diets were fully controlled, which almost never happens in nutrition research. It's the closest thing I've found to a direct test of whether your gut notices an industrial additive.

The individual variation is worth thinking about too. Most participants were relatively unaffected. Two were not. Which is either noise in a very small study, or a hint that the answer to "does this hurt you" depends on whose gut you're asking.

Novel components and low-grade inflammation

Then there's the immune route, which the paper gives more space than any other.

In fat tissue, the liver, and the hypothalamus itself, certain dietary components can activate immune cells and produce chronic low-grade inflammation.⁷ The paper's proposal is that historically unrecognized ingredients: synthetic emulsifiers, artificial sweeteners, novel lipid structures, preservatives contribute to this both through the microbiome and directly, through oxidative stress.¹⁶ The inflammatory signals that follow, TNF-alpha and interleukin-6 among them, promote insulin resistance, which raises blood glucose and pushes fat into places it doesn't belong, including the liver and skeletal muscle.⁸

The part I find genuinely interesting is what the paper does with this. In an ancestral environment, internal inflammation would have correlated with injury, infection, or an insecure environment. Conditions that tend to arrive alongside a food shortage.

So under this framework the inflammation isn't only damage. It's a signal, and the signal says the same thing everything else in this article says: conditions are deteriorating, hold onto reserves.¹

That's an elegant argument. It's also, so far, an argument rather than a finding.

The set point

There's a second reading of all this, and it's the one I find most unsettling.

Everything so far describes a signaling problem: a weaker satiety message arrives, the brain reads it as poor nutrient yield, and you eat more. That's the version most people mean when they talk about ultra-processed food and appetite, and I think it's real.

But the paper proposes something else alongside it. Signals of dietary novelty, arriving via the gut or the senses, could be read by the hypothalamus as evidence that the environment itself has become unreliable. And the hypothalamus doesn't just regulate appetite. It defends a level of body fat. The proposal is that a persistent novelty signal shifts the level being defended upward.¹

If that's right, the problem isn't only that you eat more. It's that your body has revised its opinion about how much reserve it ought to be carrying, and will now work to keep it there.

Leptin is the hormone at the center of this. Released by fat tissue in proportion to how much of it you have, its job is to tell the hypothalamus that reserves are adequate.¹³ Under this reading, the brain isn't failing to hear leptin. It's hearing leptin, weighing it against a signal that says conditions are deteriorating, and deciding the anticipated shortage matters more than the current surplus.

The paper calls this a shift from reactive homeostasis, which corrects a deficit you already have, to predictive allostasis, which alters your internal state to meet a shortage it expects.¹⁴ That distinction is the most speculative thing in the paper.

Novel foods activate your stress axis

Consuming novel foods, particularly when your body registers them as poor-quality fallback options, has the potential to activate the hypothalamic-pituitary-adrenal (HPA) axis and release cortisol.¹ The paper presents this as a route worth investigating rather than a demonstrated one, and the section heading in the original says "potential activation," which I'd rather preserve than sand off.

Elevated cortisol is well established as a driver of fat accumulation around the organs and of appetite for energy-dense foods.¹⁵

The irony is that the foods marketed as convenient and satisfying may be chemically triggering the same stress response as an actual food shortage.

Some novel compounds directly block satiety hormones

One of the paper's most striking citations: digested wheat gluten, a food component humans encountered relatively recently in evolutionary terms, has been shown to inhibit the binding between leptin and its receptor.⁹

This is a binding study, done in vitro. It shows the interaction is chemically possible. It does not show that eating bread meaningfully changes leptin signaling in a living person, and as far as I can find, nobody has tested that in people at all. I went looking for the human study and there isn't one. Which makes this the weakest link in the paper's mechanistic chain, and also the most obvious thing for somebody to go and test.

Artificial sweeteners aren't neutral

The paper reviews evidence that non-caloric sweeteners drive fat storage despite contributing no calories, and one proposed route is genuinely surprising: the liver carries the same sweet-taste receptor as your tongue. It's called T1R3.¹

In high-fat-fed mice, and in human liver cells in a dish, sucralose activates that receptor and drives fat accumulation in the liver independently of calories.¹⁰ Mice and human cell culture, so the mechanism is suggestive not settled. But note that second part, because it matters: those weren't only mouse cells. The human liver cell result means the receptor route isn't a rodent quirk.

Then there's the human evidence, which is stronger than I expected and isn't in the paper at all.

A randomized controlled trial took a hundred and twenty healthy adults who had never used non-nutritive sweeteners and gave them two weeks of saccharin, sucralose, aspartame or stevia, at doses below the accepted daily intake. Below the limit regulators consider safe. All four altered the gut microbiome and the plasma metabolome. Two of them, saccharin and sucralose, measurably impaired glucose handling.¹¹

Here's the part I keep coming back to. The researchers took the gut microbiomes of the people who responded most strongly and transplanted them into germ-free mice. The mice went on to reproduce their human donors' glucose patterns.¹¹

That's not an association any more. Something in those people's altered gut communities was carrying the effect, and it was transferable.

Let's be precise about what this does and doesn't establish. It establishes that saccharin and sucralose are not metabolically inert in people, which is the opposite of what we were told for thirty years. It does not establish that sucralose makes your liver store fat, and it didn't measure appetite at all. There is also a six-week pilot in which only the sucralose group gained weight despite eating less, but a pilot is a reason to run a bigger study, not a conclusion.¹²

What all of it fits, under this hypothesis, is a single pattern: a sweet signal arrives without the nutrition it has always predicted, and the mismatch itself reads as a degraded food supply.

Seven signals, one message

The routes the paper proposes, and what each one rests on

Weaker fullness signals

Novel foods may bind gut receptors poorly, so less GLP-1 and PYY is released after the same number of calories.

A confused microbiome

Emulsifiers, industrial seed oils and artificial sweeteners can disrupt the microbial community your gut evolved with.

Low-grade inflammation

Unrecognized ingredients may activate immune cells in fat tissue, the liver and the hypothalamus. Inflammation itself reads as an unsafe environment.

A raised set point

A persistent novelty signal may shift the level of body fat the hypothalamus defends, not only the amount you eat.

An activated stress axis

Foods the body registers as poor-quality fallback options can trigger the HPA axis and release cortisol.

Blocked satiety hormones

In laboratory studies, digested wheat gluten inhibited the binding between leptin and its receptor.

Sweetness without payload

Non-caloric sweeteners deliver a sweet taste with no matching calories, a mismatch the body may read as scarcity.

One message

Each proposed route points the same direction: your body reads unfamiliar food as a sign that the food supply is unstable.

Proposed mechanisms. Evidence type varies by route and is labeled in the text above.¹

The Evidence from Migrating Populations

What happens when a population's food changes

The NAS hypothesis is still a hypothesis, and the authors are explicit about how hard "novelty" is to isolate in a study.¹ But it rests on a pattern that keeps turning up, and the pattern is more interesting than the hypothesis.

A systematic review examined four populations that went through a documented dietary transition, chosen because the before-and-after data were good enough to say something.¹⁶ Three of the four moved in the same direction and got the same result. The fourth moved the opposite way and didn't. That fourth case is the one that convinced me there's something here.

The Yemenite Jews

We start with the case that rearranged my thinking, because the direction of the change is the opposite of what you'd expect. After migrating to Israel, Yemenite Jews cut their saturated fat intake by more than forty percent. Less saturated fat. Their sugar intake rose roughly six hundred percent. Men's BMI climbed nineteen percent. And diabetes rates rose roughly fortyfold.¹⁶

Read that again, because it's the whole argument in one population. They did precisely what every dietary guideline of the era told them to do. They cut the saturated fat. What they also did, without anybody framing it as a change worth noticing, was replace foods their families had eaten for generations with refined ones nobody in that lineage had ever encountered.

The Tokelauans, in the same review, did the same thing. Fat down, saturated fat down sharply, sugar up around six hundred percent. Same outcome.¹⁶

The Maasai

The Maasai went the same direction and got the same result.

Traditionally a very high fat, very high saturated fat diet built on milk, blood and meat. Post-transition: less fat, less saturated fat, and a great deal more carbohydrate. Total carbohydrate intake rose thirty-nine percent in men and three hundred and sixty-two percent in women. BMI rose with it.¹⁶

Three hundred and sixty-two percent. That isn't a dietary adjustment, it's a different food supply, and it arrived inside a generation.

Tanushimaru, Japan

Here's the case that makes the pattern mean something.

The Tanushimaru Japanese are the fourth population in that review, and they transitioned in the opposite direction. More fat. Less carbohydrate. Exactly the shift the other three moved away from.

Their outcomes broadly improved. Stroke rates fell. Breast cancer rates fell. Heart disease held steady. What rose was the use of blood pressure medication, which is interesting and worth mentioning.¹⁶

So three populations that moved toward refined carbohydrate saw BMI and diabetes increase. One that moved toward fat did not. If saturated fat were the driver, Tanushimaru should be the disaster case. It's the control.

China

Which brings me to the one I'd hand to anyone who thinks this is an anti-carbohydrate argument in a costume.

Across the China Health and Nutrition Survey, between 1991 and 2015, the share of energy from carbohydrate fell from sixty-three percent to fifty-one, while energy from fat rose from twenty-four percent to nearly thirty-six.¹⁷ Over the same period the proportion of Chinese adults carrying excess body fat went from twelve percent to thirty-seven.¹⁸

Read too quickly, that looks like an argument for fat being the problem, and the authors of the second study make exactly that case. But look at where the fat came from.

Energy from plant oil nearly doubled, from eight and a half percent to almost sixteen. Energy from animal fats, lard and tallow and duck and mutton fat, fell by nearly two thirds.¹⁷ Industrial seed oil didn't add itself to the traditional fats. It replaced them, and then some.

The same thing happened inside the carbohydrate decline. Refined grain fell sharply, from fifty-two percent of energy to thirty-six. But added sugars more than tripled, and coarse grains halved.¹⁷

So the honest summary of China's transition isn't less carbohydrate and more fat. It's familiar foods out and novel foods in, in both directions at once.

Whether the novelty or the fat is doing the work there is genuinely unresolved, but interesting. Also, it is worth noting that the study making the fat argument states it had no data on fatty acid types, and that so many of the edible oils it collected were mislabeled as to their actual contents that the individual oil data was unusable.¹⁸

What the four cases share

Not a macronutrient. Not a direction. The Maasai moved toward carbohydrate and gained. China moved away from carbohydrate and gained. Tanushimaru moved away from carbohydrate and didn't.

What the transitions that went badly have in common is that the new foods were new. Industrial seed oil was as unfamiliar in a Chinese kitchen in 1991 as refined maize flour was to a Maasai one. Tanushimaru's shift toward fat came from foods already inside that food culture.

That's the claim, and it's the only reading I can find that accounts for all four.

The evidence from migrating populations

What happens when a population's food changes

Yemenite Jews

Migration to Israel

Before

Established Yemenite diet; high saturated fat

Transition

Saturated fat down more than 40%
Sugar up roughly 600%

Outcome

Men's BMI up 19%
Diabetes up roughly 40-fold

Tokelauans

Dietary transition

Before

Traditional island food pattern

Transition

Fat and saturated fat down sharply
Sugar up roughly 600%

Outcome

BMI and diabetes rose

Maasai

Dietary transition

Before

Milk, blood and meat; high fat and saturated fat

Transition

Fat and saturated fat down
Carbohydrate up 39% in men, 362% in women

Outcome

BMI rose

Tanushimaru, Japan

Transition in the opposite direction

Before

Food culture already included the foods driving the shift

Transition

Fat up
Carbohydrate down

Outcome

Stroke and breast cancer down
Heart disease steady
Blood-pressure medication use up

China

1991 to 2015

Before

Traditional animal fats and coarse grains declined

Transition

Carbohydrate 63% to 51%
Fat 24% to nearly 36%
Seed oils and added sugar up

Outcome

Excess body fat 12% to 37%
Causation remains unresolved

Population-level observational data. Four-population review¹⁶; China survey data¹⁷¹⁸. Dietary novelty is difficult to isolate, and none of these cases establishes cause.

Reporting that four-population review, Ben-Dor and Klement conclude that dietary novelty tracked the rise more closely than calories or physical activity did.¹¹⁶

What This Means for Your Kitchen

Here's the practical takeaway. The hunger you feel: the relentless, doesn't respond to will power hunger may not be a character flaw. It may be a biologically accurate response to a food environment your body correctly identifies as unstable and unfamiliar.

The five types of hunger we covered in the first essay (sensory, social, rebound, processed-food, and stress hunger) don't operate in isolation. They're amplified when the underlying NAS signal is already firing. Your brain is already in scarcity insurance mode, and every processed snack, synthetic sweetener, or seed-oil-laden convenience food turns up the volume.

The intervention isn't another restrictive diet. It's changing the signal.

Each time you eat a meal built around foods your own grandmother would recognize, you send your body a "safe, familiar environment" message. Note the "your own." The paper is explicit that no universally correct diet falls out of this. What counts as familiar depends on where your people ate and what they ate, which is why it cuts against tidy ancestral prescriptions as firmly as it cuts against the supermarket.¹

Eating how your grandmother ate doesn't just taste good. You're speaking a language your metabolic systems actually understand.

The Bottom Line

If you have been eating less, moving more, doing everything right, and still feeling like your body is bracing for famine, you are not weak. There is a compelling explanation on the table: an ancient fat-storage program, activated by foods your body has no evolutionary framework for recognizing as safe.

The path forward isn't more restriction. It's returning to foods your biology already understands.

One familiar meal at a time. The signal, not just the calories, is what changes.

Stay Resilient,
Heidi

If you have any questions you would like me to answer, please reach out at info@originalketone.com.

References

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This article is for informational and educational purposes and describes a published scientific hypothesis that has not been experimentally confirmed. It is not medical advice. Consult your healthcare provider before making significant changes to your nutrition, particularly if you are pregnant or nursing, manage a metabolic condition, or take medication that must be taken with food.