I’m hearing a lot about insulin resistance again lately, and it feels a lot like another ‘influencer-wellness’ phrase that’s being misinterpreted. Carbs and sugar intake are being blamed (again). “Spiking insulin” is treated like something dangerous. I even read a recommendation yesterday that we should all go carb-free every few weeks in order to ‘give insulin a break’

But the reality is both simpler—and more nuanced—than that.

Insulin resistance isn’t caused by a single food, nutrient, or meal – not even sugar. It’s something that develops over time, and is shaped by how we eat, move, sleep, and live.

What is insulin resistance?

Insulin is a hormone that helps move glucose (sugar) from your bloodstream into your cells, where it can be used for energy.

When you become insulin resistant, your cells stop responding as efficiently to that signal. This causes your body to compensate by producing more insulin. For a while, this works. But over time, it can lead to higher blood sugar levels and increase the risk of type 2 diabetes and other metabolic conditions.

The biggest driver of insulin resistance is being consistently over-fuelled.

At its core, insulin resistance is strongly linked to a mismatch between: energy coming in (from food) vs. energy being expended (through movement and metabolism).

When we consistently take in more energy than we need, the body has to store the excess somewhere. Initially, it’s stored in fat tissue. But over time, especially when storage capacity is exceeded, fat starts to accumulate in places it shouldn’t - like the liver (non-alcoholic fatty liver disease) and muscles. This is sometimes referred to as lipotoxicity.

This is where the problem begins - these tissues are crucial for managing blood sugar. The excess fat (from consistent excess calorie intake) interferes with how they respond to insulin.

Body fat isn’t just storage – it is metabolically active.

One of the biggest shifts in how we understand metabolism is recognising that body fat isn’t passive – it is metabolically active.

When fat tissue expands (particularly around the abdomen), it can start releasing inflammatory signals into the body. These signals interfere with insulin’s ability to do its job properly. This is often described as chronic low-grade inflammation.

This type of inflammation is not the kind you feel when you’re unwell — it’s silent and ongoing disruption which happens ‘within the body.’

Movement matters!

Your muscles are one of the main places that glucose gets used.

When you move:

• Muscles take up more glucose from the blood.

• Insulin becomes more effective.

• Blood sugar is better regulated.

When you’re inactive, the opposite happens. This is why even short-term increases in activity can improve insulin sensitivity - sometimes even before any noticeable fat loss occurs. This is why exercise is so important regardless of fat loss. *Top tip, go for a 10-minute walk after meals to stimulate glucose uptake into the muscles.

Sleep and stress impact your metabolism.

Two factors that are often overlooked in the context of body fat: sleep and stress.

A few nights of poor sleep can reduce insulin sensitivity. This is partly due to changes in hormones like cortisol, which affect how your body handles glucose.

Chronic stress keeps cortisol elevated, which can increase blood sugar levels and can make cells less responsive to insulin over time.

These aren’t the sole (or main) causes of insulin resistance, but they add to the overall picture.

What about diet?

Diet absolutely matters BUT it’s not about one single nutrient.

There’s no strong evidence that carbohydrates, in isolation, cause insulin resistance.

Instead, dietary patterns that contribute include:

• Regular overeating.

• Diets low in fibre and minimally processed foods.

• Low protein intake (which can affect satiety and body composition).

In other words, it’s the overall dietary pattern that matters, not a single nutrient or ingredient.

Genetics and individual differences.

Some people are more prone to insulin resistance than others. Family history, ethnicity, and where the body tends to store fat (visceral vs subcutaneous) all influence insulin resistance. Two different people can live almost identical lives but have different levels of risk.

In summary…

Insulin resistance is not caused by:

• Eating carbs

• Having sugar

• “Spiking insulin”

It is primarily driven by a long-term mismatch between energy intake and energy use, combined with factors like inflammation, inactivity, poor sleep, and stress.

Insulin resistance isn’t about one meal: it’s the cumulative effect of all the environmental factors that your body lives in. Instead of focusing on avoiding specific foods, it’s more useful to focus on ways to support your body and its environment:

• Eating enough (amount and variety) but not constantly over-consuming.

• Moving regularly (especially resistance training and walking).

• Prioritising sleep.

• Managing stress where possible.

Insulin resistance won’t stop fat loss, but loosing body fat will make you more insulin sensitive.

A final note on PCOS…

The relationship between Polycystic ovary syndrome (PCOS) and insulin resistance is thrown around on social media a lot. Let me explain what we actually know…

PCOS and insulin resistance are deeply intertwined. When cells respond poorly to insulin, the pancreas compensates by producing more — and chronically elevated insulin directly disrupts ovarian function. Unlike most tissues, the ovaries remain highly sensitive to insulin stimulation, responding by overproducing androgens like testosterone, which drives the hallmark features of PCOS: irregular periods, ovulatory dysfunction, acne, and excess hair growth. This is why interventions that improve insulin sensitivity — a high protein, high fibre (lower-glycaemic) diet, regular exercise, or metformin — can improve not just blood sugar, but also menstrual regularity, fertility, and androgen levels simultaneously.