Evidence-Based Nutrition For Chronic Disease Prevention

How to Prevent or Reverse Insulin Resistance

Published March 6, 2025

Insulin resistance is a key risk factor for numerous chronic diseases, most notably type 2 diabetes, but also heart disease, chronic kidney disease, or Alzheimer’s disease.

However, most people don’t even know whether they are insulin-resistant, what causes it, or what can be done about it. This is tragic because insulin resistance is almost always preventable and reversible. 

In this blog post, we’ll address the following questions:

First, what is insulin resistance, and why is it important?

Second, how can you assess whether YOU are insulin resistant?

Third, how can you assess WHY you are insulin resistant?

This is particularly important because insulin resistance can have many different causes. Insulin resistance in an 80-year-old frail lady, a 24-year-old male college student, a 44-year-old mom, and a 30-year-old obese truck driver may superficially look the same: they are all insulin resistant. However, the root causes that make each of them insulin-resistant could be fundamentally very different, which means that they need to understand why they are insulin-resistant and take very different actions to reverse it.

We will then discuss …

Fourth, how can you reverse your insulin resistance?

And for those of you who are not yet insulin resistant, or who have managed to reverse their insulin resistance, we will also address …

Fifth, how to maintain normal insulin sensitivity.

My goal with this blog post is to empower you to understand insulin resistance for what it is: one of the most important risk factors for chronic disease, and to fully understand what you need to do to maintain or achieve optimal insulin sensitivity.

What Is Insulin Resistance?

Insulin is a hormone produced by the beta-cells in the pancreas that has numerous functions in the body. Most notably, it binds to the insulin receptor on the surface of cells, which causes these cells to move glucose transporters to the cell surface. Glucose from the blood can then enter the cells through these glucose transporters. What this means is that insulin helps move glucose out of your blood and into your cells, where it can be used for energy. As a result, blood glucose levels fall.

Insulin is a key component of regulating your blood glucose levels after a meal, so if you want to have normal blood sugar levels, it is important that this process works well. Unfortunately, there are quite a few things that can throw a monkey wrench into this process, such that insulin may still bind to the insulin receptor, but for one reason or another, this is less effective at causing glucose transporters to move to the cell surface.

We call such a condition insulin resistance. It means that the amount of glucose that can be taken up into the cells per one insulin molecule is reduced. When this happens, one of two things will follow.

The first is that the body senses that not enough glucose is removed from the blood, and will simply produce more insulin to compensate for the insulin resistance. The blood insulin concentration rises, and this larger amount of insulin now gets the job done; glucose can now readily be taken up into the cells and blood glucose levels will remain in the normal range. So, in this scenario, blood glucose levels remain normal, but blood insulin concentrations would now be chronically elevated. Particularly after eating a meal containing carbohydrates, the insulin concentration in blood can be several-fold higher in insulin-resistant people than in insulin-sensitive people, because more insulin is required to bring all the glucose from the meal out of the blood and into cells. Again, let me emphasize that in this scenario, none of this is apparent if we only measure blood glucose levels. This is not apparent from the fasting glucose concentration, not from the glucose levels in an oral glucose tolerance test, and not from an HbA1c lab test. It’s also not readily apparent from CGM data, but later in the blog post, I’ll share how you can use your CGM data to detect clues that you may be insulin resistant. We’ll also talk about other tests that you could have done to assess whether you are insulin resistant.

Insulin resistance can lead to chronic hyperinsulinemia (scenario 1), or hyperglycemia (elevated blood glucose levels) combined with modestly or substantially elevated insulin levels (scenario 2). The key difference between these two scenarios is that in the first, but not the second, scenario the beta-cells can fully compensate for the degree of insulin resistance.
Insulin resistance can lead to chronic hyperinsulinemia (scenario 1), or hyperglycemia (elevated blood glucose levels) combined with modestly or substantially elevated insulin levels (scenario 2). The key difference between these two scenarios is that in the first, but not the second, scenario the beta-cells can fully compensate for the degree of insulin resistance.

First, however, let’s discuss the second scenario of what can happen if someone becomes insulin-resistant. In that scenario, the pancreatic beta-cells are unable to make more insulin. Or, to be more precise, maybe they can make more insulin, but the key point is that the beta-cells cannot produce enough insulin to fully compensate for the level of insulin resistance. In that case, less glucose can be taken up into the cells. As a result, the blood glucose concentration rises measurably more after a meal, and stays higher for longer. Glucose intolerance develops, which eventually can lead to prediabetes and then type 2 diabetes. In this scenario, insulin levels after a meal and throughout the day are typically slightly or massively elevated. Again, the key point here is that the body is not able to produce enough insulin for the given level of insulin sensitivity.

This second scenario, glucose intolerance, is certainly not ideal because we know that the resulting higher blood glucose levels raise the risk of many chronic diseases. However, the first scenario of insulin resistance is also not great, because even if we can keep blood glucose levels in the normal range, having chronically elevated insulin levels by itself is a risk factor for chronic diseases. And maybe most importantly, most of the factors that can cause insulin resistance are also major chronic disease risk factors in their own right, so you really want to know WHETHER and WHY you are insulin resistant. Knowing that will give you the knowledge to take targeted action to reverse the condition by addressing its root cause or causes. The first step should be …

How to Determine If You Are Insulin Resistant

In clinical research studies, we use some complicated methods to figure out if someone is insulin-resistant. The problem is that these tests are usually not offered in clinical care, so this is not something you could easily have measured. Just in case you are interested and want to google this to learn more, the gold-standard test is called a hyperinsulinemic-euglycemic clamp, or clamp for short. A reasonably solid alternative is the so-called Kraft test.

Fortunately, the gold-standard test correlates pretty highly with two simple tests that are affordable and that you may already get in your routine blood test results, or that you could at least request from your doctor. All that’s required for these two tests is a fasting blood sample.

The first one is HOMA-IR. I have previously covered that one in a separate blog post, so check this out if you’d like more detailed information. In short, HOMA-IR is based on fasting glucose and fasting insulin, using the formulas shown below. Fasting here means the blood should be drawn in the morning, after an overnight fast of at least 12 hours.

Formulas for the calulation of the HOMA-IR insulin resistance index.
Formulas for the calulation of the HOMA-IR insulin resistance index.

The formula was created so that normal insulin sensitivity leads to HOMA-IR values of around 1. I would suggest that everything up to 1.5 can be seen as perfect insulin sensitivity. I would define HOMA-IR values between 1.5 and 2.5 as mild insulin resistance, between 2.5 and 3.5 as moderate insulin resistance, and more severe forms of insulin resistance as values greater than 3.5.

Guide to the interpretation of HOMA-IR values
Guide to the interpretation of HOMA-IR values

There is a second test that may be even easier for you to obtain. For this one, you take your fasting triglyceride concentration in mg/dL and divide it by your fasting HDL-cholesterol concentration, also in mg/dL. If your lab measures these in mmol/L, you must first convert these values to mg/dL. Just pay attention to the fact that the conversion factor is different for triglycerides and HDL-cholesterol. 

Formula for the calculation of the triglyceride-to-HDL-cholesterol-ratio, a surrogate biomarker for the estimation of insulin resistance
Formula for the calculation of the triglyceride-to-HDL-cholesterol-ratio, a surrogate biomarker for the estimation of insulin resistance

In insulin-sensitive people, this ratio tends to be lower than 1.8. Values between 1.8 and 2.5 suggest mild insulin resistance, 2.5 to 3.0 suggest moderate insulin-resistance, and values greater than 3.0 a more severe insulin resistance.

Guide to the interpretation of the triglyceride-to-HDL-cholesterol-ratio
Guide to the interpretation of the triglyceride-to-HDL-cholesterol-ratio

There is a third method that you may already be using to get a sense of whether you may be insulin resistant. If you are using a CGM, observe a typical glucose response to any of your meals that include at least some carbs. What you want this to look like is that the glucose at its peak never reaches 180 mg/dL, and the level is back roughly to your normal baseline two hours after you started eating. So if your baseline in the fasting state and between meals is around 95 mg/dL, you’ll want to be back in that area two hours after starting a meal. If your glucose level still hovers substantially above that after most of your meals, say at 110 or 120 mg/dL, as illustrated in the figure below, that would be suggestive of insulin resistance. If this was me, I would then ask my doctor to measure fasting insulin and glucose so that I could calculate HOMA-IR.

In the postprandial phase, blood glucose levels commonly remain elevated two hours after beginning the meal in individuals who are insulin resistant.
In the postprandial phase, blood glucose levels commonly remain elevated two hours after beginning the meal in individuals who are insulin resistant.

To conclude this portion, please be aware that these tests can only provide estimates of whether or not you may be insulin resistant. One particular problem with these measures is that some forms of insulin resistance may not be apparent in the fasting state. I’ll talk more about that later. So please don’t think this is a conclusive assessment. If you have any questions about this, please speak to your doctor.

Now, if you find that you are insulin-resistant, what should you do about it? And if your test results show that you have very good insulin sensitivity, what should you do to keep it this way in the future? 

That’s what we are discussing next. Let’s look at four key dietary and lifestyle factors that you need to get right to reverse your insulin resistance and that will also help you prevent the development of insulin resistance and glucose intolerance in the future.

It may be one of the best things you can do for your long-term health.

Factor #1: Minimize Visceral and Ectopic Fat

In our body, there is only one space suitable for fat storage: the subcutaneous fat tissue right under our skin. As far as we know, fat stored in this location does not cause metabolic complications. Some people can store a lot of fat there, such that even if they become very obese, they remain metabolically healthy as long as they can store all their excess body fat in their subcutaneous fat tissue. We also say that those people have a high personal fat threshold, meaning they can store a lot of body fat safely in their subcutaneous fat tissue. An example for this would be the person on the left in the image below. Others are less lucky, such as the person on the right: they have a very limited storage capacity in their subcutaneous fat tissue, meaning they have a low personal fat threshold. When they gain weight beyond their personal fat threshold, their body needs to find other places to store fat, and starts to deposit fat in the visceral fat depots surrounding the inner organs, and in tissues that are not made for fat storage, such as the muscle, the liver, and the pancreas. We call this fat storage in organs and the muscle ectopic fat, and it’s very undesirable from a health perspective. We understand well that when this happens, it has several consequences: for one, these tissues that now are forced to store fat become insulin resistant. A liver with too much fat is what we call a fatty liver, which is usually insulin-resistant (by the way, insulin resistance may also contribute to increased fat accumulation in the liver, setting up a vicious cycle). Muscle with fat is usually insulin resistant (an exception being increased fat storage in endurance athletes). And as an aside, a pancreas that is forced to store fat loses some of its ability to secrete insulin, whereas reductions in pancreatic fat tend to improve beta-cell function. Aside from this, we also know that people with more visceral and ectopic fat often suffer from low-grade chronic inflammation, and that inflammation can make insulin resistance worse. 

MRI image across the belly in two men who have the same overall body fat mass, but very different personal fat thresholds, resulting in the accumulation of excess visceral fat (in white) in the man on the right side.
MRI image across the belly in two men who have the same overall body fat mass, but very different personal fat thresholds, resulting in the accumulation of excess visceral fat (in white) in the man on the right side.

I talk about this in much more detail in my blog post about the Personal Fat Threshold hypothesis.

Relevant to this blog post is the question of how you can know whether you have excess visceral and ectopic fat. Of course, you could have a DEXA scan done to measure your total body fat mass and obtain an estimate of your visceral fat mass. Or you could have an abdominal MRI scan done to measure your visceral and liver fat, but that is not a viable option for most people

Unfortunately, we don’t have any one biomarker that we could measure in our blood that would tell us whether we have excess visceral and ectopic fat. However, several measures correlate more or less strongly with visceral and ectopic fat, and by combining these, you can get a good sense of whether you may carry excess visceral and ectopic fat. To help you with this, I have created a poster, which you can download for free. I explain the insulin resistance syndrome and the science behind this in a separate blog post, The Insulin Resistance Syndrome: A Neglected Risk Factor for Chronic Disease. Make sure to use the correct poster for your sex and race, because some cut-offs are different for men vs. women and white vs. non-white people. Then, get measurements of as many of these measures as you can. Waist circumference is a direct measure of how much fat we store in our belly, and because visceral fat directly increases waist circumference, it can be a good surrogate measurement of visceral fat mass. The other measures are all downstream consequences of carrying excess visceral and ectopic fat, so if you find that all or most of these measures are in the green portions of these bars, then you probably don’t have excessive visceral and ectopic fat. If, by contrast, most of these are in the orange and red portions of these bars, you should assume that you have some visceral and ectopic fat. The further on the right these are, on average, the more visceral and ectopic fat you probably have. If yours looks like the one below, I would certainly encourage you to speak to your doctor about this, educate yourself, and take action to address this issue.

Insulin Resistance Syndrome poster, completed by a white man with a very high likelihood of excessive visceral and ectopic fat.
Insulin Resistance Syndrome poster, completed by a white man with a very high likelihood of excessive visceral and ectopic fat.

(Note here that several of these biomarkers can individually be elevated for reasons other than carrying excess visceral and ectopic fat. For example, someone with untreated type 1 diabetes may have elevated blood glucose, and someone with genetically elevated cholesterol levels could have elevated LDL-cholesterol. Therefore, this poster is best used by (a) considering all factors together, because an increase in visceral and ectopic fat is most commonly associated with a right-ward shift in several of these markers, and (b) consider each biomarker in your individual historical context. What is meant with the last point is that if you always had LDL-cholesterol of under 100 mg/dL, and suddenly it’s 110 mg/dL, and then the next year it’s 120 mg/dL, that’s when you want to start thinking about whether an increase in visceral and ectopic fat may be underlying this shift.)

OK, what can you do to prevent or reverse excess visceral and ectopic fat? Well, if you currently don’t see evidence of excessive visceral and ectopic fat, try not to gain weight. If you already have excess visceral and ectopic fat, losing at least some excess body weight would be helpful. The good news here is that even losing just 5 or 7% of your body weight can reduce both visceral and ectopic fat by 20, 30, 40, 50, or more percent.

What do I see as the best way to prevent weight gain, or to lose weight and have a chance to keep it off? My approach of choice would not be to count and actively restrict calories, but to focus on maximizing the quality of your diet, in very specific ways, to make sure you consume fewer calories spontaneously because the foods you eat are more filling, or more satiating, per calorie.  

So what should you do if you want to be comfortably satiated with fewer calories and lose weight? I have just published a blog post on this topic entitled How to Lose Weight Without Counting Calories, and I certainly recommend you check it out after this one here if you see evidence of excessive visceral and ectopic fat. I don’t want to repeat that entire blog post here, so let me just summarize the seven key strategies.

Key recommendations to make meals more satiating per calorie while minimizing the risks of overconsumption.
Key recommendations to make meals more satiating per calorie while minimizing the risks of overconsumption.

Now, if you currently do not have excess visceral and ectopic fat, adopting these strategies, or most of them, will most likely be sufficient to prevent weight gain in the future. However, if you find that you need to lose excess visceral and ectopic fat, you will probably need to apply these strategies more rigorously. If you cannot lose enough weight using this approach, experiment with different implementations of these general strategies. For example, for some people, using these strategies to design a highly satiating low-carb diet can be a great approach. For others, using the principles outlined here to design a plant-based low-fat diet can be something they enjoy long-term and can lose weight with. I am pretty confident, however, that whichever specific diet you decide on, prioritizing these six strategies here will be an important foundation to help you control your calorie intake naturally in the long run. 

If you find that you cannot lose weight using this approach, or not enough, I would also recommend that you talk to your doctor about other weight loss approaches. I believe in a food and lifestyle first approach, but I also see some of the new GLP-1 medications as a blessing for people who cannot get to a healthy body weight otherwise. And, taking medication and improving the quality of your diet don’t have to be mutually exclusive.

Factor #2: Increase Your Muscle Mass

Just like having too much visceral and ectopic fat causes insulin resistance, we can have the opposite problem when it comes to our muscle mass. Too little muscle mass is strongly associated with insulin resistance, which is often a core problem in lean and elderly people who become insulin resistant. 

How do you know if you may have too little muscle mass? Well, you could certainly have a DEXA-scan done to measure your lean body mass, some of which is muscle mass. However, that would not be my primary suggestion. Instead, I would say that if you do not currently do any form of exercise and particularly resistance training, you will undoubtedly benefit from these activities.

So, I strongly suggest engaging in some form of resistance training at least twice weekly. If you are currently insulin-resistant and not engaged in resistance training, you may see very profound improvements in your insulin sensitivity. And really, don’t think you need to register at a gym and lift enormous weights immediately. That can be an intimidating thought for many people. Start where you are right now: even a short routine consisting of bodyweight exercises such as push-ups, squats, lunges, and crunches can be a great way to start. And if you cannot do a push up, do it against the wall or a countertop. There are also great workout programs available on YouTube or on apps that can work great to get you going with no or little equipment requirements. And once you are more comfortable with the idea of training to build muscle mass, you can always take it a step further and consider a gym. Whatever you do, however, make sure to do each exercise with good form and give it an honest effort such that you go close to what your muscles can currently do to give them a reason to grow. Muscles grow when we work and challenge them. And, of course, if you are not sure you can safely engage in an exercise routine, make sure to talk to your doctor first.

Before we move on, one more suggestion. Engaging in resistance training is particularly important if you are trying to lose weight. Because ideally, you would lose your excess visceral and ectopic fat, but hold on to your muscle tissue. Also, remember that earlier in the blog post, I briefly mentioned the value of increasing protein intake, because a high-protein diet is more satiating per calorie than one low in protein. A higher protein intake has another benefit: it provides building blocks, amino acids, for your body to make muscle tissue. And this is particularly important when you are trying to build muscle, and also when you are losing weight to minimize muscle loss.

Factor #3: Minimize Sedentary Time

In addition to engaging in intentional exercise, as I just described, I also recommend reducing your sedentary time, or time spent sitting and not moving during waking hours. So, if you spend multiple hours sitting while working, commuting, eating, reading, watching television, crafting, or for whatever reason, consider getting up and moving around for a few minutes at least once per hour. Formal exercise is very important, but even if you formally exercise a few times per week, you may still suffer the negative consequences of too little physical activity if you sit for much during the day. So, I suggest that you start thinking about yourself in the same way as you would think about, say, a dog or a horse that needs to be moved to be healthy. It’s not that different with your body. Humans evolved moving for a good part of most days, and if we want to remain healthy and insulin-sensitive, we need to move our bodies regularly.

Factor #4: Meet All Of Your Micronutrient and Fiber Needs Regularly

We have good evidence that several micronutrient deficiencies can or may cause insulin resistance, and that meeting the daily requirements can improve insulin sensitivity in people with deficiencies in these micronutrients. Similarly, we have good evidence that increasing fiber intake can improve insulin sensitivity in people with low fiber intake.

I am not going to discuss all of the different micronutrients that affect insulin sensitivity separately here – I don’t want to make this about just a few minerals or vitamins, because then everyone will simply take these as supplements. There is potentially room for supplementation, but the much more significant point here is to remind you that one key objective of a healthy diet is to regularly provide our bodies with all the essential vitamins, minerals, and trace elements.

So here is what I suggest: make sure to eat a diet rich in a variety of nutrient-dense foods, mostly in their unprocessed or minimally processed form. Ideally, these include plant foods such as vegetables of all kinds, fruit and berries, legumes such as beans and lentils, mushrooms, whole grains, nuts and seeds. And also animal foods such as unprocessed meats, fish and shellfish, eggs, and dairy products.

Examples of the most nutrient dense foods
Examples of the most nutrient dense foods

It is similarly vital to know which foods to avoid or minimize as much as possible. The figure below shows what we call empty-calorie foods. These do not provide fiber and they also all have a very low concentration of micronutrients. To maximize the nutrient density of your diet, minimize refined grains, added sugars and syrups, added fats and oils, and all foods made from these, such as white bread, pancakes, cakes, pretzels, cookies, donuts, or candy bars. This category also includes many ultra-processed foods such as soda, chips, crackers, sweetened breakfast cereals, and the like. All of these have a lot of calories, but provide almost nothing else of any nutritional value to you.

Examples of foods with the lowest micronutrient density.
Examples of foods with the lowest micronutrient density.

You can use this general information to create your own way of eating that you enjoy: if you want to make this more plant-heavy and lower in fat, just prioritize veggies, fruit and berries, legumes, mushrooms, and whole grains, with just an occasional piece of meat if you want to eat meat, fish or seafood, yogurt or cheese, or an egg every once in a while. 

Or, vice versa, if you prefer low-carb, focus more heavily on meat, fish and shellfish, eggs, dairy foods, nuts and seeds, olives, and avocados, and add as many non-starchy vegetables and leafy greens as you like. My suggestion is always to include plenty of plant foods, even if your diet is low-carb and largely animal-based, and always to include some animal foods even if your diet is heavily plant-based or low-fat. That is because some of the essential micronutrients lacking in plant foods can be found in a high concentration in animal foods, and vice versa. 

For those of you who are not sure that you meet all micronutrient requirements regularly and would like to take it a step further, here is another suggestion. For at least three days, better more, keep track of everything you eat and enter it into a nutrition analysis software. I find Cronometer to be a very good choice for this because it provides detailed micronutrient information (note that we have no affiliation or other relationship with Cronometer).

Keep track of everything you eat and drink, with as much detail as possible. Try to be precise with the amounts of everything you eat. While you do this, try to eat the same way you always eat; this is an assessment, so try not to make any changes yet. Include weekdays and at least one weekend day if your diet differs on weekends. Then examine whether you regularly meet the recommended intakes for fiber and all micronutrients. The point here is not that you need to meet requirements for each mineral, trace element, and vitamin every day, but across several days, you should be at 100% or at least close, for all. For fiber, I would try to comfortably hit 100% of the recommended amount daily.

If you find that you are commonly low in fiber or any of the essential micronutrients, consider including specific foods in your diet to address that deficiency. This is a case where googling can be very helpful: just type in foods rich in magnesium, foods rich in fiber, or foods rich in vitamin B1, and let yourself be inspired. Alternatively, there is also nothing wrong with considering a supplement, as long as you also make an effort to prioritize a nutrient-dense diet rich in unprocessed or minimally processed foods.

Why do I suggest that we benefit from prioritizing getting our nutrients from foods and not supplements? Well, look at all of these nutrient-dense foods in the figure above: these are not just nutrient-dense, but they are also the very foods we should be eating to make our diet more satiating per calorie. And vice versa, those foods that are mostly empty calories also happen to be those that tend to make us overeat calories and gain weight. So you can kill two birds with one stone if you eat a variety of mostly unprocessed or minimizally processed plant and animal foods: you increase your micronutrient and fiber intake, AND you make your diet much more satiating per calorie, which will automatically lower your spontaneous calorie intake and help you achieve or maintain a healthy body weight.

If you want to reverse insulin resistance, it is impossible to overstate the importance of eating a variety of these nutrient-dense foods, ideally mostly in their unprocessed or minimally processed form, while minimizing liquid calories such as sugar-sweetened and alcoholic beverages, ultra-processed foods, and all of these empty calorie-foods here.

If you find yourself overwhelmed with this exercise, consider consulting with a registered dietitian who can help you do this assessment to determine whether your diet is chronically deficient in fiber or any essential micronutrient. This is a good idea, particularly if you don’t eat any animal foods, or maybe even no plant foods, or any other extreme diet that relies mostly on a few food groups while excluding others.

If you have a medical condition that is associated with malabsorption, such as celiac disease, inflammatory bowel disease, or if you’ve had bariatric surgery, speak to your doctor about potential micronutrient deficiencies. Similarly, if you have a medical condition in which a high fiber diet could cause problems, such as irritable bowel disease, also speak to your doctor. 

There is one micronutrient worth mentioning separately: vitamin D. Vitamin D is actually a hormone that our body can produce from cholesterol in the skin whenever you are exposed to UV-light. Depending on where you live, your skin color, how much time you spend in the sun, how many clothes you wear when you are in the sun, and other factors, you may not be able to produce enough vitamin D yourself, though. I suggest you ask your doctor to measure your plasma level of 25-hydroxy-vitamin D, and make sure it’s above 20 ng/mL (50 nmol/L) at all times. In my opinion, ideally, you’d aim for the higher end of the normal range, somewhere between 30-50 ng/mL. That would be between 75-125 nmol/L.

Other Potential Causes of Insulin Resistance

In my interpretation of the literature, if everyone got these four key points right, this would reduce the burden of insulin resistance and type 2 diabetes very substantially: eating in a way that minimizes weight gain and specifically visceral and ectopic fat, engaging in resistance training, generally reducing sedentary times, and eating a high-fiber micronutrient-dense diet. These address the most common and also most actionable root causes of insulin resistance and type 2 diabetes.

However, even if you get all of these right, there are a few issues that could still make you insulin-resistant. These are less common, and less actionable, meaning in some cases they are more challenging to address by our diet or lifestyle, and I will only mention them here briefly.

These factors are circadian disruption, sleep issues, chronic stress, certain medications, and certain medical conditions. I have previously discussed these in a separate blog post entitled Insulin Resistance: Top Causes & Contributing Factors, and will discuss these only briefly here.

Let’s start with certain medications and medical conditions. This is a big topic because there are a lot of medications and diseases that can cause insulin resistance, some of them in a very significant way. Among medications, chronic corticosteroid use and also statins are such examples, and among medical conditions, sleep apnea and thyroid dysfunction come to mind. My recommendation here is that if you are insulin resistant or have prediabetes or type 2 diabetes, and you regularly take a medication, or if you have a chronic medical condition, talk to your doctor about the connection to insulin resistance. There are cases where you can switch to a different medication, or lower the dose of a medication, and that could certainly help you improve your insulin sensitivity. Similarly, work with your doctor to treat any medical condition that may make you insulin-resistant. Two prominent examples here are sleep apnea and thyroid disease. In both cases, getting these diagnosed and treated can have a very profound impact on insulin sensitivity. 

Let’s talk briefly about circadian disruption. Circadian disruption means that your inner circadian clock is out of sync with the natural light-dark rhythm. We experience this for a few days when we are jet-lagged and more chronically in people who do shift work, but this can occur to some degree in everyone. A common manifestation of circadian disruption is that it causes insomnia or other sleep issues. The best thing you can do to maintain a normal circadian rhythm is to, first, expose yourself to bright, natural light during the day, particularly early in the day; second, to limit bright and particularly blue light in the later part of the evening and at night; and third, to consume food mostly during the daylight and early evening hours. The latter is called early time-restricted eating, where most typically, food intake is restricted to an eating window of 6-10 hours, with no food intake after about 6 or 7 PM.

Aside from circadian disruption, sleep deprivation could be caused by many other factors, not all of which are under our control. If you have trouble getting at least seven hours of good quality sleep every night, I suggest you discuss this with your doctor. 

And lastly, chronic stress can be a major contributor to insulin resistance. Now, this is a tricky one, because, just like sleep deprivation, no one chooses to be chronically stressed, and in many cases, we cannot immediately change whatever causes us to be stressed. If you are stressed at work, it is not a simple act to switch jobs or reduce hours at work. And if you have stress with a family member, that may also not be just under your control to resolve that immediately. So, I am aware that this can be a big challenge. I am listing this here because if you are chronically stressed, it is important to understand that this alone could contribute to insulin resistance and glucose intolerance. Try to address whatever causes you to be stressed, and consider adopting stress-management techniques such as meditation, yoga, walks in nature or a park, and regular exercise.

Summary & Conclusions

Insulin resistance is a significant risk factor for several chronic diseases, and – in my opinion – everyone should regularly have a test to assess whether they are insulin resistant. Fasting insulin and HOMA-IR should really be part of the routine lab test panel, because insulin resistance clearly is as much a risk factor for chronic disease as all of the other biomarkers we measure routinely such as fasting lipids, fasting glucose, or blood pressure. As this is not the case yet, you may need to pay for the test yourself, but whatever you need to do, get it done every few years.

Then, make sure to get the four big diet and lifestyle factors right, and to do this, I recommend all of the following:

First, stop drinking sugar-sweetened and alcoholic beverages.

Second, replace ultra-processed foods with unprocessed or minimally processed foods.

Third, minimize your consumption of hyperpalatable foods consisting of fat and sugar, fat and salt, or refined grains and salt. 

Fourth, consume mostly meals with a low energy density by using added fats and oils, added sugars and syrups, and refined grains and starches sparingly. 

Fifth, center each meal around a solid portion of a protein-rich food and high-fiber plant foods.

Sixth, follow time-restricted eating and eat only in a 6-10 hour window each day.

And seventh, identify what may be contributing to any non-hunger eating, and find other ways to respond to these triggers. 

Following these seven rules will make your meals much more satiating per calorie and minimize your exposure to the highly tempting foods we tend to overeat. Together, this will lower the number of calories you spontaneously need to consume to feel full, reducing your risk of weight gain and possibly even leading to weight loss. I have discussed these strategies in much more detail in my YouTube playlist Keys to a Healthy Body Weight.

By following these strategies, your diet will also have a very high content of fiber and essential micronutrients. And again, these rules can be implemented very flexibly, as a low-fat mostly plant-based diet, as a low-carb, mostly animal-food-based diet, or anything in between.

Then eighth, engage in muscle-building exercises, ideally resistance training. At least two to three times per week.

Ninth, minimize long, uninterrupted periods of sitting. Make it a habit to move more, go on short – or long – walks throughout the day, or just stretch a bit while you are watching TV, or do 5 minutes of bodyweight exercises – a few squats and a few pushups – as a break from working at a desk.

If you get these dietary and lifestyle factors right, in a way that you can maintain happily forever, you will dramatically reduce your risk of becoming insulin resistant and glucose intolerant. In my experience running clinical trials in people with metabolic disease, I’d say that if everyone ate food that is supportive of our biology rather than nutrient-poor and energy-dense junk that makes us overeat chronically, and if everyone made it a habit to move a lot and engaged in at least some resistance training, most of the epidemic of insulin resistance and type 2 diabetes would just disappear. Considering that currently more than 1 BILLION people worldwide have diabetes or prediabetes, and many more suffer from insulin resistance, isn’t that mind-blowing?

Now, that’s not to say that these are the only causes of insulin resistance and type 2 diabetes. As we discussed, if you suffer from any of the other potential causes of insulin resistance, such as sleep deprivation, chronic stress, or a medical condition, speak to your doctor and try your best to address the issue. 

Lastly, I’d like to thank the Patrons of this website and the associated YouTube channel who generously support the generation of this free content through a regular contribution. I make these blog posts without accepting any sponsorship deals, I don’t do any affiliate marketing, and I do not in any way affiliate myself with the food, supplement, or pharmaceutical industry. If you value unbiased, evidence-based content, and would like to also support this website and YouTube channel, you can become a Patron here.

Thank you, and take care.

References

  1. Kim. Hyperinsulinemic-euglycemic clamp to assess insulin sensitivity in vivo. Methods in Molecular Biology 2009; 560: 221-38.
  2. Crofts et al.; Identifying hyperinsulinemia in the absence of impaired glucose tolerance: an examination of the Kraft database. Diabetes Research and Clinical Practice 2016; 118: 50-7.
  3. Barber et al.; Metabolic-associated fatty liver disease and insulin resistance: a review of complex interlinks. Metabolites 2023; 13: 757.
  4. Machann et al.; Intramyocellular lipids and insulin resistance. Diabetes, Obesity and Metabolism 2004; 6: 239-48.
  5. Wu. Diabetes remission and nonalcoholic fatty pancreas disease. World Journal of Diabetes 2024; 15: 1390-3.
  6. Kim and Park. Association of muscle mass and fat mass with insulin resistance and the prevalence of the metabolic syndrome in Korean adults: a cross-sectional study. Scientific Reports 2018; 8: 2703.
  7. Haines et al.; Association between muscle mass and insulin sensitivity independent of detrimental adipose depots in young adults with overweight/obesity. International Journal of Obesity 2020; 44: 1851-8.
  8. Srikanthan and Karlmangla. Relative muscle mass is inversely associated with insulin resistance and prediabetes. Findings from the third National Health and Nutrition Examination Survey. Journal of Clinical Endocrinology and Metabolism 2011; 96: 2898-903.
  9. Jiahao et al.; Effects of resistance training on insulin sensitivity in the elderly: a meta-analysis of randomized controlled trials. Journal of Exercise Science and Fitness 2021; 19: 241-51.
  10. Garcia-Hermoso et al.; Exercise and insulin resistance markers in children and adolescents with excess weight: a systematic review and network meta-analysis. JAMA Pediatrics 2023; 177: 1276-84.
  11. Al-Awadi et al.; Are strategies to increase muscle mass and strength as effective in people with type 2 diabetes? Reviews in Endocrinology and Metabolic Disorders 2025; online published ahead of print on February 25, 2025.
  12. Carbone and Pasiakos. Dietary protein and muscle mass: translating science to application and health benefit. Nutrients 2019; 11: 1136.
  13. Kokura et al.; Enhanced protein intake on maintaining muscle mass, strength, and physical function in adults with overweight/obesity: a systematic review and meta-analysis. Clinical Nutrition ESPEN 2024; 63: 417-26.
  14. Hamburg et al.; Physical inactivity rapidly induces insulin resistance and microvascular dysfunction in healthy volunteers. Arteriosclerosis Thrombosis and Vascular Biology 2007; 27: 2650-6.
  15. Smorawinski et al.; Effects of three-day bed rest on metabolic, hormonal and circulatory responses to an oral glucose load in endurance or strength trained athletes and untrained subjects. Journal of Physiology and Pharmacology 2000; 51: 279-89.
  16. Bowden Davies et al.; Short-term decreased physical activity with increased sedentary behavior causes metabolic derangements and altered body composition: effects in individuals with and without a first-degree relative with type 2 diabetes. Diabetologia 2018; 61: 1282-94.
  17. Carneiro et al.; Vitamin and mineral deficiency and glucose metabolism – a review. e-SPEN Journal 2013; 8: e73-9.
  18. Weickert and Pfeiffer. Metabolic effects of dietary fiber consumption and prevention of diabetes. The Journal of Nutrition 2008; 138: 439-42.

 

5 Responses

  1. Amazing explanation and recommendations. Thank you! I wish more people would follow your blog posts.

  2. I have type1 diabetes. Can I still get valid results on the fasting insulin test if I am taking basal insulin that, per the manufacturer, stays I my bloodstream for 24 hours?

  3. Many Asian friends who are very fit, follow a good exercise and diet regime and otherwise healthy become pre-diabetic in their 50’s. Can you elaborate on the genetic disposition to insulin resistance? In addition to following all the recommendations you outlined, if they still have insulin resistance, should they follow a long-term low-carb diet to manage blood sugar?

Leave a Comment

Discover more from Nourished by Science

Subscribe now to keep reading and get access to the full archive.

Continue reading