“Insulin resistance” is a phrase we hear everywhere in conversations about blood sugar, weight, metabolic health and increasingly, perimenopause and menopause.
You may have heard that insulin resistance makes it harder to lose weight. That menopause causes insulin resistance. That carbohydrates cause it. Or that every rise in blood glucose is something we need to prevent.
But what does being insulin resistant actually mean?
Unlike some of the more vague wellness terms I’ve been unpacking in this series, insulin resistance describes a genuine physiological process.
And once you understand what insulin is actually doing, the concept becomes much easier to understand.
In this episode of the Empowered Perimenopause Podcast, I’m going back to basics: what insulin is, why we need it, what changes when our tissues become less responsive to it, how the body initially compensates, and what all of this means for our health in midlife.
First, what is glucose?
Before we can understand insulin resistance, we need to understand glucose.
Glucose is a simple sugar and an important source of energy for the body.
When we eat carbohydrate-containing foods, digestible carbohydrate is broken down into smaller molecules, including glucose. That glucose is absorbed through the small intestine and enters the bloodstream.
As a result, our blood glucose naturally rises after eating carbohydrate.
And that is not inherently a problem.
Our blood glucose is not supposed to remain completely flat throughout the day. The body has sophisticated systems for regulating the amount of glucose circulating in the blood, and one of the most important hormones involved in this process is insulin.
What does insulin actually do?
Insulin is a hormone produced by beta cells in the pancreas.
When blood glucose rises after eating, the pancreas responds by releasing insulin.
Insulin then communicates with tissues throughout the body and helps coordinate how incoming energy is used and stored.
In skeletal muscle, insulin signalling helps increase glucose uptake so that glucose can be used for energy or stored as glycogen for later.
In the liver, insulin helps reduce glucose production and release when there is already sufficient glucose available in the bloodstream.
Insulin also acts on adipose, or fat, tissue, where it helps regulate the storage and release of energy.
So although we often think of insulin simply as a “blood sugar hormone”, it is actually an important metabolic hormone involved in coordinating how our body handles available fuel.
What normally happens after we eat?
Imagine eating a meal containing some carbohydrate.
The carbohydrate is digested and glucose enters your bloodstream.
Your blood glucose begins to rise.
Your pancreas detects this and releases insulin.
Insulin signals to tissues including your skeletal muscle, liver and adipose tissue.
Glucose can be taken up and used or stored, while the liver reduces its own glucose output.
Over the following hours, blood glucose moves back towards its usual range and insulin secretion reduces again.
This is normal physiology.
Your blood glucose rose.
Your insulin rose.
And then both came back down.
A rise in glucose after eating is therefore not automatically a harmful “blood sugar spike” that needs to be prevented.
What matters is how effectively the body regulates glucose.
What is insulin resistance?
Insulin resistance means that insulin-responsive tissues are not responding to insulin as effectively as they should.
The underlying biology is complex, and insulin resistance can affect different tissues and different actions of insulin to varying degrees.
But as a simple way of understanding it, we can think of the insulin signal as becoming less effective.
In skeletal muscle, a given amount of insulin may no longer stimulate glucose uptake as effectively.
The liver can also become resistant to insulin’s effects. Normally, insulin helps suppress the liver’s production and release of glucose when sufficient fuel is already available. With hepatic insulin resistance, this regulation can become impaired.
Insulin resistance in adipose tissue can also alter the normal regulation of stored fat and fatty acid release.
The body therefore needs to find a way to compensate.
And initially, it usually does this by producing more insulin.
The pancreas turns up the volume
This is one of the most important concepts to understand about insulin resistance.
Insulin resistance does not necessarily mean that your blood glucose immediately becomes high.
The pancreas can compensate for reduced insulin sensitivity by increasing insulin secretion.
In other words, if the normal insulin signal is no longer getting the same response, the pancreas effectively turns up the volume.
More insulin creates a stronger signal.
For a period of time, this compensation may allow the body to continue keeping blood glucose within a normal range.
This means someone can have reduced insulin sensitivity while their glucose measurements remain relatively normal because their pancreas is working harder and producing more insulin to achieve that result.
This compensatory increase in circulating insulin is often referred to as hyperinsulinaemia.
Over time, however, some people’s pancreatic beta cells are no longer able to produce sufficient insulin to compensate for the degree of insulin resistance.
Blood glucose can then begin to remain elevated.
Insulin isn’t the enemy
Insulin has acquired quite a bad reputation in the wellness and weight-loss world.
It is often described simply as our “fat-storage hormone”, with the implication that every rise in insulin is something we should try to avoid.
But insulin is essential.
We need insulin to regulate glucose and coordinate energy metabolism.
Insulin rising after a meal is not evidence that something has gone wrong, it is exactly what we expect to happen.
The problem in insulin resistance isn’t that insulin exists or that it rises.
The issue is that tissues aren’t responding appropriately to its signal, meaning the body may need to produce greater amounts of insulin to achieve the necessary metabolic effect.
What contributes to insulin resistance?
There is no single cause of insulin resistance.
Risk is influenced by a combination of factors, including:
- Genetics and family history
- Age
- Body composition and body fat distribution
- Physical activity
- Muscle mass and muscle function
- Sleep
- Certain medications
- Some endocrine and metabolic conditions
- Polycystic ovary syndrome (PCOS)
- A history of gestational diabetes
Excess energy storage and accumulation of fat in tissues such as the liver and around the abdominal organs can also be strongly associated with impaired insulin sensitivity.
However, it is important not to reduce insulin resistance to simply being a consequence of body weight.
Not everyone living in a larger body has insulin resistance, and people in smaller bodies can also develop insulin resistance and type 2 diabetes.
Individual metabolic risk is much more complex than body size alone.
Why muscle matters for insulin sensitivity
Skeletal muscle has an important role in glucose metabolism and is a major destination for glucose after eating. You can learn more about this in episode 98, here.
Physical activity can improve glucose uptake and insulin sensitivity.
Muscle contraction can also increase glucose uptake through pathways that are not entirely dependent on insulin, which is one reason why physical activity, including something as simple as walking after a meal, can help with post-meal glucose regulation.
Over the longer term, regular physical activity and resistance training can help improve metabolic health while maintaining and building skeletal muscle.
This becomes particularly important in midlife, when preserving muscle mass has benefits far beyond strength and appearance.
Muscle is metabolically important tissue.
Do carbohydrates cause insulin resistance?
Because eating carbohydrate causes glucose and insulin to rise, it can be tempting to conclude that carbohydrates therefore cause insulin resistance.
But these are not the same thing.
Insulin is supposed to rise after eating carbohydrate.
And carbohydrate-containing foods are not all metabolically identical.
Lentils are not the same as sweets.
Oats are not the same as a sugary drink.
Fruit is not metabolically identical to cake.
The amount and type of carbohydrate matters, but so do fibre, the overall food matrix, portion size, what else is eaten with the meal, physical activity, overall energy intake and an individual’s existing metabolic health.
For someone with impaired glucose tolerance or diabetes, carbohydrate quantity and quality may be particularly important and individualised dietary support can be helpful.
But this is very different from saying that everyone needs to avoid carbohydrates to prevent insulin resistance.
Insulin resistance, prediabetes and type 2 diabetes are not the same thing
These terms are sometimes used interchangeably, but they describe different things.
Someone can have insulin resistance without having diabetes.
In the earlier stages, increased insulin production may allow the pancreas to compensate sufficiently to maintain glucose within the normal range.
Prediabetes describes blood glucose levels that are above the normal range but below the diagnostic threshold for diabetes.
Type 2 diabetes develops when glucose regulation becomes sufficiently impaired to meet established diagnostic criteria. Insulin resistance is commonly involved, alongside insufficient pancreatic beta-cell compensation.
Importantly, having insulin resistance does not mean that someone will inevitably develop type 2 diabetes.
Insulin sensitivity and metabolic risk can be influenced by many modifiable factors.
Can you tell if you’re insulin resistant from symptoms?
Social media is full of lists of supposed “signs of insulin resistance”.
Fatigue.
Sugar cravings.
Brain fog.
Difficulty losing weight.
Feeling hungry.
Carrying more weight around the middle.
The problem is that these experiences are extremely non-specific.
Feeling tired does not diagnose insulin resistance.
Having sugar cravings does not diagnose insulin resistance.
Finding it difficult to lose weight does not diagnose insulin resistance.
And many people with insulin resistance or prediabetes may have no obvious symptoms at all.
Risk factors and certain clinical signs can provide useful information, but insulin resistance should not be self-diagnosed from a list of symptoms on social media.
If you’re concerned about your metabolic health or have risk factors for type 2 diabetes, speak to your GP or healthcare practitioner about appropriate assessment and testing.
What happens to insulin sensitivity during menopause?
Midlife can bring several changes that influence metabolic health.
Ageing itself affects body composition.
Without appropriate activity and resistance training, we tend to lose skeletal muscle as we age.
Sleep can become more disrupted.
Physical activity may change.
And body fat distribution often shifts across the menopausal transition, with a tendency towards greater central or abdominal fat accumulation.
Changes in ovarian hormones may also contribute to changes in body composition and insulin sensitivity.
But menopause does not automatically make you insulin resistant.
Nor does reaching a particular age mean that your metabolism has suddenly “broken”.
Instead, midlife is a useful opportunity to pay attention to metabolic health and to the lifestyle factors that help maintain insulin sensitivity as we age.
How can we support insulin sensitivity?
The encouraging thing about insulin sensitivity is that there are many ways we can support it.
Regular physical activity is one of the most powerful.
Both aerobic exercise and resistance training can improve metabolic health, while resistance training also helps us preserve and build metabolically active muscle.
Movement after eating can also help with post-meal glucose regulation.
Diet matters too, of course, but that does not mean eliminating carbohydrates.
A dietary pattern centred around minimally processed, nutrient-dense foods and containing adequate fibre, protein, vegetables, fruit, whole grains, pulses, nuts and seeds can support metabolic health.
Sleep matters.
Not smoking matters.
And if someone is carrying excess body fat and weight loss is appropriate for them, even relatively modest weight loss can improve metabolic health and reduce the risk of developing type 2 diabetes.
However, weight loss should not be the only conversation.
Physical activity, maintaining muscle, dietary quality, sleep and other health behaviours can be valuable regardless of what happens on the scales.
Do we all need to monitor our blood glucose?
Blood glucose has become another area of wellness optimisation.
Continuous glucose monitors can be extremely valuable medical tools for people who need them.
But increasingly, people without diabetes are using them to monitor every rise and fall in glucose, sometimes becoming anxious when a perfectly nutritious food such as fruit produces a post-meal rise.
Our blood glucose is supposed to change after eating.
And insulin is supposed to respond.
The goal is not to create a completely flat glucose line throughout the day.
The goal is effective metabolic regulation.
More health data is not always more useful health information, particularly if we don’t understand how to interpret it.
So, what does insulin resistance actually mean?
At its simplest, insulin resistance means that insulin-responsive tissues are no longer responding to insulin as effectively as they should.
The pancreas may initially compensate by producing more insulin, effectively turning up the volume on the insulin signal.
For a time, this can keep blood glucose relatively well regulated.
But if the pancreas can no longer compensate sufficiently, blood glucose can begin to rise, potentially progressing to prediabetes and, in some people, type 2 diabetes.
Insulin itself isn’t the enemy.
Carbohydrates aren’t automatically the enemy.
And menopause does not mean you are destined to become insulin resistant.
But metabolic health does matter, and midlife is an excellent time to start thinking proactively about maintaining muscle, moving regularly, eating well, sleeping as well as possible and understanding your individual risk.
And next in this series, we’re staying very close to this subject and unpacking another phrase we hear everywhere:
Blood Sugar Balance: What Does It Actually Mean?
Do we really need to keep our blood sugar “balanced”?
What is a blood sugar spike?
And should we be trying to flatten our glucose response after every meal?
That’s what we’re exploring in Episode 105.
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