Recognizing and Reversing Insulin Resistance: The Silent Engine Behind Belly Fat

You are standing in front of the mirror. Your arms are as slim as ever, your face has barely changed. Only your belly has quietly pushed its way forward over the last few years.

You are not eating more than you used to. Maybe even less. And yet your waistband feels tight. In the afternoon your energy slumps, and you reach for the chocolate as if on autopilot.

Then come the results from your check-up: fasting blood sugar unremarkable. Everything in the green zone. And you wonder why it doesn't feel that way.

May I ask you an uncomfortable question? What if your blood sugar is only normal because your body is working overtime in the background?

In the article Insulin resistance and weight loss, I described why the kilos often stay put with insulin resistance. This text starts one step earlier. It is about how you can recognize insulin resistance before your blood sugar rises. Which values reveal more than fasting blood sugar. And what large studies say about whether it can be reversed.

One thing up front: this text does not replace a medical examination. It is meant to help you ask the right questions.

Slim arms, big belly: how do you recognize the pattern?

Some people carry their weight evenly. Others look slim from a distance. Only in profile do you notice that everything collects in the middle. I come across this second picture strikingly often in my practice when insulin has fallen out of rhythm.

Around one in five normal-weight adults is metabolically unhealthy and carries a more than threefold higher risk of death or cardiovascular events (Stefan 2017).

This story does not stand alone. The scale measures your weight. It does not measure where the fat sits and what it does there. And that is exactly what can be decisive for your insulin.

Why does location matter so much? Imagine the fat under your skin as a large wardrobe. It is built to store supplies neatly. If the wardrobe is full or badly organized, things end up in the hallway. In the body, this hallway is the abdominal cavity, the liver and the muscles. Experts speak of ectopic fat, meaning fat in the wrong place.

You don't need an MRI for a first look. An international expert panel led by Ross calls for waist circumference to be measured in every practice as a standard vital sign, because BMI alone does not adequately reflect risk. The panel's good news: even moderate exercise and dietary changes can noticeably reduce waist circumference (Ross 2020).

The ratio of waist to height may be even more telling. A systematic review of 78 studies found the same guide value for men and women: 0.5. Its message is refreshingly simple: keep your waist circumference below half your height (Browning 2010). A meta-analysis with data from more than 300,000 adults showed that this ratio indicated diabetes and high blood pressure better than BMI and waist circumference alone (Ashwell 2012).

And now you know why a tape measure sometimes reveals more than a scale.

Why does fasting blood sugar raise the alarm so late in insulin resistance?

Imagine carrying a backpack every day that gets heavier week by week. At first you notice nothing. You walk a little more upright, tense more muscles, compensate. From the outside, nobody sees you wobble. Until one day you stumble.

Something similar can happen to your glucose metabolism. And that is why an unremarkable fasting blood sugar can be deceptive.

In the Whitehall II study, fasting blood sugar only began to rise steeply about three years before the diabetes diagnosis, while insulin sensitivity had already fallen markedly before that (Tabák 2009).

Insulin is the key that unlocks the door of your cells for sugar. With insulin resistance, the locks in muscle, liver and fat tissue stick. Your pancreas reacts the way a hard-working caretaker would: it sends more keys. Sugar keeps getting into the cells. Just with more and more effort.

This is exactly where the blind spot lies. Fasting blood sugar measures the result, not the effort. As long as the caretaker can manage the overtime, the result stays unremarkable.

One detail from the same study is fascinating. Between the fourth and the third year before the diagnosis, insulin production actually rose further, from 85.0 to 92.6 percent. Only after that did it fall, reaching 62.4 percent by the time of diagnosis (Tabák 2009). That is the caretaker giving it everything one last time.

Researchers at the US National Institutes of Health (NIH) in Phoenix led by Weyer tracked what this compensation looks like over several years. They followed members of the Pima people in Arizona with elaborate metabolic measurements. In those who stayed healthy, the insulin response rose as insulin sensitivity fell. In those who developed diabetes, insulin sensitivity and insulin secretion declined together (Weyer 1999).

And now you know why fasting blood sugar tends to tell the end of a story rather than its beginning.

Fasting insulin, HOMA and the insulin curve: which values show it earlier?

Maybe you are picturing your last lab report right now. Glucose, HbA1c, cholesterol. And you look in vain for insulin. That is not an oversight. It is routine.

Standard testing with fasting blood sugar, HbA1c and the glucose tolerance test is well researched and makes sense. It is designed to reliably identify prediabetes and diabetes. For the phase before that, functional medicine also looks at insulin itself.

In a large database of glucose tolerance tests, around half of the people with normal glucose tolerance still showed an excessive insulin pattern (Crofts 2016).

The HOMA index: a simple calculation that says a lot

The HOMA index was described in 1985 by Matthews and colleagues. It uses fasting blood sugar and fasting insulin to estimate how strongly your cells respond to insulin. Compared with the elaborate gold standard, the clamp test, it agreed closely, with a correlation of 0.88. In individual cases, however, its precision was limited, with a variation of about 31 percent (Matthews 1985).

Where is the cut-off?

Let's be honest here: there is no single worldwide cut-off. Insulin is measured with different test methods depending on the laboratory. As early as 2003, a team at Stanford University noted that a standardized insulin test is lacking (McLaughlin 2003).

A Spanish population study of 2,459 adults shows how much the cut-off depends on the method. If you simply counted the top ten percent as abnormal, it was 3.46. When actual metabolic risk was taken into account, it dropped to 2.05, and to 1.85 in men without diabetes (Gayoso-Diz 2013).

What I observe clinically: a HOMA value above about 2 with unremarkable blood sugar is a reason for me to take a closer look. That is a guide from clinical practice, not a diagnostic criterion. A single value can fluctuate. That is why it always belongs in context with waist size, blood lipids and symptoms.

The insulin curve: what its course can reveal

The timing of the insulin peak may also matter. A team from Seattle led by Hayashi followed 400 Japanese American women and men without diabetes for 10 to 11 years. If insulin only reached its peak after two hours in the glucose tolerance test, 37.5 to 47.8 percent developed diabetes, depending on the shape of the curve. If the peak came early, at 30 minutes, the figure was 3.2 to 9.8 percent (Hayashi 2013).

Two clues that are already on your lab report

A team at Stanford University led by McLaughlin and Reaven examined 258 overweight adults without diabetes using an elaborate insulin suppression test. Apart from insulin itself, two simple values identified the insulin-resistant participants best: triglycerides of 130 mg/dL or higher and a triglyceride-to-HDL ratio of 3.0 or higher. Both were right in about two out of three cases (McLaughlin 2003).

The TyG index combines triglycerides and fasting blood sugar into one number. In a meta-analysis of 14 cohort studies with 270,229 people, a high TyG index was associated with an approximately 3.5-fold higher risk of diabetes. From a value of about 8.6, the risk curve became markedly steeper (Pranata 2021).

A glucose sensor can also show how your blood sugar responds to meals in everyday life. It does not replace a diagnosis, but it can make patterns visible. With your first sensor, it is worth having it applied and evaluated with guidance. More on this in Blood sugar and weight loss: what a CGM sensor shows.

And now you know why I still ask about insulin when blood sugar is unremarkable.

Is insulin the silent engine behind belly fat?

Maybe you have already tried a lot. Eating less, running more, counting calories. The scale barely moves, your belly even less. At some point, you start to doubt yourself.

I would like to offer you a different explanation. Not as an excuse, but as a map.

In an analysis with data from more than 300,000 people, those with a genetically higher insulin release after sugar had a higher BMI on average (Astley 2018).

Insulin is not only the key for sugar. It is also a signal: time to store. As long as insulin is high, it slows the breakdown of fat from the fat cells. Imagine high insulin as a bouncer who happily lets fat in but hardly lets anyone out.

This can create a cycle. Belly and liver fat release fatty acids and messenger substances that can increase insulin resistance. The pancreas responds with even more insulin. And more insulin can in turn mean more storage. How insulin interacts with the satiety hormone leptin is described in the article Leptin and insulin.

How closely insulin is linked to your hormones is explored in more depth in the articles Insulin resistance and female hormones, Excess weight, insulin resistance and testosterone and Blood sugar and cortisol. You can read about the role of silent inflammation in Silent inflammation and weight.

A second perspective comes from anthroposophic medicine. It also understands health as rhythm: waking and sleeping, eating and pausing, tension and relaxation. A metabolism that has to release insulin from morning until late at night hardly gets a break anymore. That is a way of thinking, not a study result. But early studies on meal timing and sleep fit well with it (Sutton 2018, Broussard 2012).

And now you know why fewer calories alone sometimes don't get through to your belly.

Can insulin resistance be reversed?

Maybe you are thinking right now: fine, now I know what is going on inside me. But can I still change anything about it?

Here, the evidence is decidedly encouraging. And it does not come from small niches, but from some of the largest prevention trials in medicine.

In two large randomized trials, a lifestyle program lowered the risk of diabetes in people with prediabetes by 58 percent each (Knowler 2002, Tuomilehto 2001).

At almost the same time, the Finnish Diabetes Prevention Study with 522 overweight people reached the same result: minus 58 percent. In the first year, participants had lost only a little over 4 kilos on average (Tuomilehto 2001). A meta-analysis of seven randomized trials with 4,090 people confirms the effect and shows that it can last for many years after the programs end (Uusitupa 2019).

And if diabetes is already there?

A team at Newcastle University led by Lim and Taylor used MRI to make visible what happens in the body. Eleven people with type 2 diabetes ate a very low-calorie diet for eight weeks. After just one week, their fasting blood sugar fell from 9.2 to 5.9 mmol/L. Liver fat fell from 12.8 to 2.9 percent by week eight, and the early insulin response of the pancreas moved closer to that of healthy people (Lim 2011). The liver seems to be a key place where insulin resistance can ease first. You can read how sugar and fructose can strain the liver in Sugar, fructose and the liver.

Important: in the studies, very low-calorie programs like these were carried out under professional supervision, and medications were adjusted in a controlled way. Please never try this on your own, especially not if you take diabetes medication.

Belly fat can shrink before the scale shows it

A randomized study from the University of Sydney shows how quickly things can change. Four weeks of endurance training on a bike lowered belly fat by 12 percent and liver fat by 21 percent in 19 people with obesity. Their weight did not change (Johnson 2009). The HOMA index, however, stayed the same during these four weeks, a sign that insulin values may need more time.

Strength training can make its own contribution. In a randomized study at Newcastle University, eight weeks of strength training lowered liver fat by a relative 13 percent. The HOMA index improved from 5.9 to 4.6, also without weight loss (Hallsworth 2011). You can find more on this in Strength training for diabetes and insulin resistance.

Timing can matter too

You can read how fasting can influence blood sugar and who it suits in Fasting, blood sugar and insulin resistance.

And now you know why it is worth taking prediabetes seriously: this is where your lever is longest.

Three levers you can start with this week

Maybe this is a lot at once. Numbers, curves, studies. Take a breath. You don't have to change everything at the same time.

And now you know why: your blood sugar tells you where you stand. Your insulin can tell you where you are heading. If you know both, you can change direction in time.

Frequently asked questions about insulin resistance

Connections to other topics