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Health Newsletter · September 2026 · Week 2 of 4

Insulin, Sugar, and Refined Carbs

The Obesity Code · Dr. Jason Fung

Last week we established that insulin, not calories, is the hormone that decides whether energy is stored or burned. This week, we go straight to the source: what sugar and refined carbohydrates actually do to insulin — and why not all of them do it the same way.

A medical insulin vial and syringe resting on a clinical white surface
01

Insulin 101: The Hormone That Controls Fat Storage

Insulin is best known as the hormone diabetics manage, but Fung reminds us it has a second, universal job: it is the body's primary fat-storage signal. Every time blood glucose rises, the pancreas releases insulin, which tells cells — including fat cells — to pull that glucose in and, when there's a surplus, lock it away as fat.

This isn't a flaw in the system; it's exactly what insulin evolved to do. The problem is frequency and magnitude. A hormone designed to manage occasional feasts is now triggered dozens of times a day by a food supply built around sugar and refined starch.

Understanding insulin as a storage switch — not just a blood sugar regulator — is the single most important shift in how to think about weight. If the switch is on most of the day, the body simply cannot access its own fat for fuel.

Key TakeawayInsulin's core job is signaling fat storage, not just managing blood sugar — and modern eating patterns keep that switch on nearly all day.

A tall glass of soda with condensation and ice on a table
02

Sugar's Double Hit: Glucose and Fructose

Table sugar and high-fructose corn syrup are roughly half glucose, half fructose — and Fung walks through why that combination is uniquely disruptive. Glucose spikes insulin directly. Fructose, on the other hand, is processed almost entirely by the liver, where it is readily converted into fat.

So a sweetened drink delivers a double hit: an immediate insulin spike from the glucose half, and a slower, liver-based fat-production process from the fructose half — happening in the same glass, from the same pour.

This is also why sugar behaves differently than starch alone, and why Fung singles it out as one of the most insulin- and fat-liver-provoking ingredients in the modern diet, regardless of its calorie count.

Key TakeawaySugar is metabolically a two-part problem: glucose spikes insulin while fructose is converted to fat by the liver — both from a single serving.

A basket of white bread rolls and sugary pastries on a bakery counter
03

Refined Carbs and the Insulin Spike Cycle

White bread, pastries, and other refined carbohydrates behave almost like sugar once they hit the bloodstream. Stripped of fiber and bran, they digest quickly into glucose, producing a sharp insulin spike — followed, a couple of hours later, by a sharp drop in blood sugar.

That crash is what drives the familiar mid-morning or mid-afternoon hunger pang, often satisfied with another refined-carb snack. Fung describes this as a self-perpetuating cycle: spike, crash, crave, repeat — each cycle another wave of elevated insulin.

Whole, fiber-intact versions of the same foods produce a far gentler glucose and insulin curve, which is why food quality — not just carbohydrate quantity — is central to breaking the cycle.

Key TakeawayRefined carbs spike insulin fast and crash blood sugar just as fast, creating a hunger-and-craving cycle that keeps insulin elevated throughout the day.

A tired office worker resting their head on their hand at a desk in the afternoon
04

Insulin Resistance: When Cells Stop Listening

With years of chronically elevated insulin, cells begin to respond less to its signal — a state called insulin resistance. The pancreas compensates by producing even more insulin to achieve the same effect, and blood sugar management still holds together for a while, masking the problem underneath.

But insulin resistance doesn't just affect blood sugar — it deepens the fat-storage signal at the same time it blunts fat-burning. This is why insulin resistance so often shows up alongside stubborn weight gain, particularly around the abdomen, well before a diabetes diagnosis appears.

Fung frames insulin resistance as the hidden mechanism connecting fatigue, cravings, and weight gain — and, encouragingly, as something that responds directly to lowering insulin exposure, not just to eating less.

Key TakeawayInsulin resistance forces the body to produce even more insulin to compensate — deepening fat storage long before blood sugar problems become visible.

An anatomical model of a human liver on a doctor’s desk
05

The Liver's Secret Role: Fructose and Fatty Liver

The liver is where fructose metabolism happens almost exclusively, and Fung points to this as an underappreciated driver of modern metabolic disease. Excess fructose is converted into fat inside liver cells — and over time, this can accumulate into non-alcoholic fatty liver disease, now startlingly common.

A fatty liver becomes less sensitive to insulin, so the pancreas has to produce still more insulin to compensate — deepening insulin resistance from a second direction, separate from the muscle and fat-cell resistance discussed earlier.

This is one reason sugary drinks are singled out so consistently in the research: they deliver fructose in a concentrated, rapidly absorbed form that solid, fiber-rich foods rarely do.

Key TakeawayExcess fructose is converted to fat in the liver, and a fatty liver becomes insulin resistant itself — compounding the body's overall insulin burden.

An empty plate and a clock on a table, suggesting a fasting window
06

Why Fasting Windows Lower Insulin

If frequent eating keeps insulin elevated, the most direct lever isn't necessarily what you eat in a given moment — it's how often you ask the pancreas to release insulin at all. Fung highlights that insulin naturally falls during extended periods without food, giving the body a real chance to access stored fat.

This doesn't require an extreme approach. Even modestly extending the overnight fast — skipping the habitual snack right before bed, or delaying the first meal by an hour or two — reduces the number of daily insulin spikes without requiring any calorie math.

We'll dedicate all of next week to eating windows and timing specifically, but the underlying principle is the thread that connects everything covered this week: fewer insulin spikes, not just fewer calories, is the lever that matters.

Key TakeawayExtending time between meals lowers insulin naturally, giving the body real opportunity to burn stored fat instead of storing more.

A glass of soda being poured down a kitchen sink drain
07

Your Week 2 Commitment

This week, pick one concentrated source of sugar or refined carbohydrate you consume regularly — a sweetened coffee, a soda, a pastry — and replace it with a whole-food alternative for the week. You are not trying to overhaul your entire diet at once.

Pay attention to how you feel a couple of hours after meals with and without that swap: energy level, hunger, and whether a craving shows up on schedule. That pattern is your own insulin response showing itself in real time.

Hold onto the food journal you started last week — next week we build directly on both of these habits as we look at eating windows and timing.

Key TakeawaySwap one regular sugar or refined-carb source for a whole-food alternative this week, and notice how it changes your energy and cravings.

Coming Next Week

Week 3: Timing, Eating Patterns, and Metabolic Health

Next week we shift from what we eat to when we eat — how meal timing and eating windows affect insulin and metabolic health independent of food choice, and what the research says about fasting.

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