Does Menopause Cause Insulin Resistance?

An article about insulin resistance in menopause

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In this blog, I am going to talk about the common diets used to ‘treat’ insulin resistance and also explore whether it is possible to improve the management of insulin resistance and blood glucose levels in the absence of weight loss. Let’s start with what insulin resistance is.

What is Insulin Resistance?

Quick bit of biology then – insulin is released from the pancreas in response to rising sugar (glucose) levels in the blood. Its role is to act as a key, opening up the ‘doors’ on the cell walls of muscle and liver cells to allow glucose to pass in, where it is converted into energy or stored for later as glycogen. Muscle cells account for up to 90% of our glucose uptake after a meal – this is really key and we’ll come back to this later.

Our fat cells are also able to take glucose in, in the presence of insulin, and store it as body fat. 

Insulin resistance isn’t to do with not having enough insulin (although insulin deficiency can develop as part of type 2 diabetes). The word ‘resistance’ refers to the fact that the cells that are supposed to respond to it by opening up their doors, stop listening. The body responds by releasing more insulin in the hope this will help, but we’re dealing with a rusty lock on those doors and it’s not easy.

Insulin is a storage hormone so lots of circulating insulin will tell the body to store – whether this be glycogen or triggering fat cells to accept glucose and store it as fat, which creates a vicious cycle as it can cause weight gain– and this isn’t your fault!

When cells become resistant to insulin, they fail to benefit from all of its effects. Normally insulin will switch off the liver from producing glucose, but if the cells don’t respond to insulin as well, then the liver continues to produce glucose, which compounds the problem.

If it goes on for a long time, the cells in the pancreas that produce insulin get overworked and insulin levels may start to decline. This is the insulin deficiency we just spoke about.

How Do You Detect Insulin Resistance?

NICE guidance says that if fasting blood glucose is between 5.5-6.9mmol/l then this is suggestive of insulin resistance, the theory being that if fasted, blood glucose levels should be lower so if they’re staying above 5.5mmol/l, it shows our system is struggling to cope.

The other measure you may be familiar with is HbA1c.

With more glucose hanging around in the blood, it joins to haemoglobin – this HbA1c has a life of about 3 months so when tested, gives an idea of how much glucose has been in the blood in the previous 3 months. In type 2 diabetes the aim is to keep this under 48 mmol/mol.

What Causes Insulin Resistance?

The causes are complex and not fully understood. There are lifestyle components, such as diet and exercise as well as genetic ones, and it’s a bit of a chicken and egg as to which kicks the whole thing off. It’s connected to increased inflammation, changes in how we metabolise fat and shifts in our gut bacteria. These are some of the reasons insulin resistance is more prevalent after menopause.

What Are the Physical Symptoms of Insulin Resistance?

So aside from someone with insulin resistance probably feeling like it’s all their fault, we also have to consider how they’re feeling day to day. Despite there being glucose (fuel) in the blood, it’s not getting where it’s needed so tiredness is common. As far as the body is concerned it still needs fuel, so appetite will also go up and there are strong links between the pathway that controls insulin and the pathway that controls leptin which is the hormone that tells us we’re full. So, we might feel lethargic, hungry and confused – before we even add in any menopausal symptoms on top!

How Does Insulin Resistance Relate to Menopause?

Research highlights menopause as a potential risk factor for developing insulin resistance independent of age, all linked to a reduction in circulating oestrogens. Prior to menopause our oestrogen seems to stand us in good stead and is the main reason why our cardiovascular risk pre-menopause is much lower than men. 

Oestrogen does a lot to protect the body against insulin resistance. It has lots of roles, acting on major organs such as the pancreas, liver and muscle to ensure fuels are taken up and broken down as they should be, and metabolism functions well.

Replacing the lost oestrogen has benefits. A meta-analysis pulling together all the available data has shown that HRT confers a significant improvement in insulin sensitivity and a reduction of new onset of diabetes. It also protects our hearts and lowers our cardiovascular risk again.

The bottom line is oestrogen goes hand in hand with our metabolic health, specifically with respect to how we distribute our body fat mass and respond to glucose. With less of it our energy metabolism is affected.

Does Gaining Weight with Menopause Mean We Will All Become Insulin Resistant?

Higher body weights are associated with insulin resistance but the key word there is associated. We can’t say for sure that higher body weights cause insulin resistance, without also considering how much of a role insulin resistance plays in contributing to weight gain in the first place as we’ve just discussed under ‘causes’.

Visceral fat (fat around our organs and therefore associated with weight gain around the middle) is more metabolically active and is definitely connected to disease risk, such as diabetes and cardiovascular disease (as opposed to subcutaneous fat under our skin). We know where we store fat changes after menopause and why this occurs (you can read more about this in Myths and Facts about Menopausal Weight Gain, but it isn’t a given that this weight gain will always be associated with insulin resistance. There is a large variation in levels of ‘resistance’ due to all the confounding factors including:

  • Genetics
  • Family History
  • Ethnicity
  • Stress
  • Sleep
  • The balance of foods we eat or have access to eating in relation to all of those factors above.

We can sum this up to say how the genetic hand we’ve been dealt collides with the environment we find ourselves in has the potential to be the perfect storm, but it’s also a storm we can weather really well if we have the right tools, understanding, support and attitude.

What Is the Best Diet for Someone with Insulin Resistance?

We often hear that weight loss will improve insulin resistance – whilst this isn’t incorrect, simply knowing this, doesn’t automatically mean we can achieve and maintain it. I’m sure Michael Moseley would have us all bashing through our midlife admin on less calories than it takes to nourish a toddler, but in reality, research shows this isn’t very sustainable.

We can’t ignore that there are consequences to our continued pursuit of weight loss and yet often we keep going because we’re made to feel guilty and to blame for having these health issues in the first place.

It’s a little more complicated than that and there’s lots to consider.

But Can You Reverse Insulin Resistance with Diet?

If you google that, you’ll probably get bombarded with keto or fasting information. These methods do work, but clearly not for everyone. Let’s look at the Direct trial which sought to find out if type 2 diabetes could be put into remission using a very low-calorie diet of 850 calories. Participants had 850 calories per day for 3 months, followed by food reintroduction for 2 months and then a weight maintenance phase. 

Let’s whizz to the conclusion at 2 years because this is what we really want to know – so 45 out of 272 people that they had data on achieved a maintenance of at least 10 kg and of these, 29 achieved remission. So, what about the other 243 people?

We have to consider the fallout from following such strict regimes and also whether they are sustainable long term, as weight cycling i.e. repeatedly losing and gaining weight can increase insulin resistance, is a predictor of type 2 diabetes development, increases stress levels, increases inflammation and adds to emotional distress.

Couple of other studies to throw in here. The Dietfit trials which sought to answer which was best for weight loss, low fat or low carb, found there weren’t any significant differences in weight loss between the two at 12 months and interestingly in the low carb dieting group, their carb intakes were getting progressively higher as the months rolled on. In other words, it’s bloody hard to stick to!

Then we have the Look Ahead Study – a massive trial looking to prove that weight loss would improve cardiovascular health risks and mortality in those diagnosed with diabetes. They followed 2 groups of people for 9 years – one randomised to receive intensive weight loss support and the other more basic education and support. Weight losses weren’t that impressive in the intensive group (again proving there’s probably other stuff going on here and it’s not simply calories in, calories out) but more importantly the health risks didn’t improve with weight loss. They couldn’t prove what they wanted to and the trial was stopped early due to futility. This gives more weight to the argument that it’s more about what you eat and how you behave, than it is about the number on the scale.

Very low calorie diets which severely restrict carbs do suit some people, but the evidence is lacking that weight regain won’t occur for many, which as we’ve established can in itself worsen insulin resistance. I know it’s tough and there’s no easy answers. Here’s what you can trust in though: 

  1. Amounts of carbohydrate do make a difference to blood glucose levels independent of weight loss – eating slow release, high fibre carbs in conjunction with protein and healthy fats helps to ease the pressure put on the cells. This doesn’t mean going very low carb or keto.

Keeping carbs in the diet allows you to meet your fibre requirements – high fibre diets are associated with a reduced risk of developing diabetes and plant-based protein like pulses, beans and lentils also seems to offer benefits to reducing insulin resistance. As does type of fat with monounsaturated and polyunsaturated fats seeming to improve insulin resistance.

  1. Consider your relationship with exercise. If you’re insulin resistant and trying to maintain a strict calorie deficit, you’re going to find exercise more effortful. Exercise is a treatment for insulin resistance irrespective of what you’re eating. It takes glucose into your cells without the need for insulin. Resistance training is particularly beneficial as it increases your muscle’s capacity to store glycogen. Remember what I said about how much glucose is taken up by and stored in muscle cells. In menopause our lean muscle mass will decline so we have to look after it and use resistance training to our advantage. Strict calorie deficits will also strip muscle out of the body as we break it down for fuel, another reason why it’s best to avoid these.
  1. If you feel the focus has become all about the diet – if you’re second guessing your every food decision and it’s stressing you out, just stop. Just pull back and look at what else might be contributing to your health and wellbeing. Sometimes the pursuit of weight loss can distract us from the stuff that really counts – health behaviours and the right mindset that can actually improve our physical and mental wellbeing. Those things can reduce stress levels, regulate your blood glucose levels, reduce inflammation and give you more energy to move more and have a better quality of life. This is particularly important in perimenopause and beyond as our body’s resilience to cope with stress reduces. That’s not a sign of weakness, that’s a biological fact we need to get on board with to empower us to view health in a different way.

I hope this has been a helpful read. If you’re interested in exploring support to improve your insulin resistance which doesn’t involve strict dieting and takes a more holistic look at things, whilst still being grounded in science, then the Pause to Nourish Programme is a great first step. For more information, you may like to read the article Menopausal Weight Gain – is this where we’re going wrong?

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