You may be aware that insulin resistance is the cause of prediabetes and type 2 diabetes, and is a large contributing factor to America’s epidemic of chronic disease.
Despite this, many authors, scientists, and medical professionals argue incessantly about the actual causes insulin resistance, which is admittedly quite frustrating for those looking to reverse insulin resistance quickly, safely, and effectively using their food as medicine.
If you’re like millions of people around the planet searching the internet for ways to reverse insulin resistance using your diet, you’re in the right place.
We like to call this the “insulin resistance diet” – a lifestyle scientifically proven to reverse insulin resistance, based off of more than 85 years of evidence-based research.
Because insulin resistance is the underlying factor present across all forms of diabetes (including type 1 diabetes, type 1.5 diabetes, prediabetes, type 2 diabetes, and gestational diabetes) it is extremely important to fully understand what causes insulin resistance in order to control your blood glucose with precision.
If I asked you to define insulin resistance in 1 or 2 sentences, what would you say? Can you clearly define what single aspect of your diet is the most potent cause of insulin resistance?
Even though you might be tempted to ask your doctor for the ideal insulin resistance diet, it’s imperative to know that the medical community does not understand how to eat to reverse insulin resistance and diabetes.
Why? It’s actually quite simple. Doctors aren’t educated about nutrition in medical school, and as a result of that, many patients are given improper information about how to reverse chronic disease using their food as medicine.
Don’t be mistaken – doctors are wonderful people. They are not to blame for a lack of knowledge about nutrition. They were trained in a system that does not prioritize nutrition education, and therefore are unaware of evidence-based methods to reverse chronic disease, especially prediabetes and type 2 diabetes (1–4).
The answer to the question above is here:
Insulin resistance is caused by the storage of excess fat in tissues that are not designed to store large quantities of fat.
That’s right. Even though you may think that insulin resistance is caused by eating too much sugar, excess dietary fat is significantly more powerful in creating insulin resistance than refined sugar.
Insulin resistance is a very prominent health condition in our world today, and it increases your risk for many chronic diseases. Even though we talk about insulin resistance in the context of diabetes and beta cell death, it actually influences many other health conditions including cancer, coronary artery disease, hypertension, atherosclerosis, obesity, high cholesterol, fatty liver, polycystic ovarian syndrome, Alzheimer's disease, neuropathy, blindness, kidney failure, retinopathy, and erectile dysfunction (5–13).
Take a look at the image below to understand these relationships:
Heart disease is arguably the most important of all of these conditions, because heart disease is the number 1 risk of death of people living with diabetes. Studies have shown that as you become more insulin resistant, your risk for coronary artery disease, atherosclerosis, peripheral arterial disease, hypertension, and high blood pressure increase dramatically (9,10,14–21).
What’s incredible is that not only are those living with some form of diabetes at risk for cardiovascular disease, even non-diabetic individuals are at an advanced risk for heart disease as their level of insulin resistance increases (11).
And the statistics become even grimmer for those living with type 1 diabetes, an autoimmune version of diabetes that generally affects people younger than age 30.
According to recent studies, about 33% of all people living with type 1 diabetes will die before the age of 50 due to heart disease (22).
Most physicians have been trained to believe that insulin resistance is only associated with prediabetes and type 2 diabetes, even though it influences type 1 diabetes, type 1.5 diabetes (an adult onset, slow progressing version of type 1 diabetes), prediabetes, type 2 diabetes, gestational diabetes, and Alzheimer's disease (which is now being classified as type 3 diabetes or insulin resistance of your brain).
The truth is that all versions of diabetes are intricately associated with insulin resistance, and must always be talked about together.
In order to understand the basics of the perfect insulin resistance diet, let's first understand basic pancreas physiology.
Your pancreas has two functions – an exocrine function and an endocrine function. More than 99% of your pancreas has exocrine function, which means that it secretes a collection of digestive enzymes required to digest the food you eat.
Every time you eat, food travels down your esophagus, through your stomach, and into your small intestine where the digestive enzymes from your pancreas begin breaking down carbohydrate, fat, protein, elastin, DNA, and many other cellular components.
The other 1% of your pancreas contains islet cells or islet clusters, which constitute the endocrine function of your pancreas. The term endocrine means “secreted into the blood,” and highly specialized cells inside of islet clusters manufacture and secrete hormones into your blood to regulate your blood glucose at all times.
These islet clusters are collections of thousands of alpha, beta, and delta cells, containing anywhere from 1000 to 4000 cells in total, each with a very specific function:
The most important of these cell types are beta cells, the only cell type in your entire body capable of manufacturing and secreting insulin.
Because the population of beta cells in your pancreas is quite small, when they fail to secrete adequate insulin, an organism-wide problem is created that can cause death if left untreated.
For those living with type 1 diabetes or type 1.5 diabetes, the problem starts in your pancreas. A collection of environmental triggers tricks your immune system to begin manufacturing antibodies to destroy beta cells, which renders them unable to secrete insulin sufficient insulin to meet your body’s metabolic needs over the course of time (23–30).
Unlike type 1 diabetes, type 2 diabetes begins in your muscle and liver, then progresses to your pancreas over time. The cascade of events follows a predictable pattern, as described below:
We begin when you eat low-carbohydrate diet high in fat and high in protein, with the explicit intent of minimizing carbohydrate-rich foods to control your blood glucose. These foods include dairy products, eggs, red meat, white meat, fish, shellfish, vegetable oil, nuts, seeds, avocados, and coconuts.
When lipids enter your small intestine, they are absorbed directly into your lymph system and then immediately transferred to your blood. A series of complex hormonal signaling patterns between your digestive system and brain reduce your gastric emptying rate, slowing the exit of food from your stomach (31).
As a result of reduced gastric emptying, carbohydrate absorption occurs at a slower rate, slowing the entrance of glucose into your blood.
Fatty acids in circulation enter tissues all over your body, including primarily your adipose tissue, muscle and liver. Your adipose tissue is actually a protective tissue, specifically designed to absorb fatty acids when abundant, and release fatty acids when limited.
Your adipose tissue actually protects your muscle and liver from absorbing excess fatty acids.
This is great news, because even though your adipose tissue can grow over time, it protects peripheral tissues from absorbing excess fatty acids.
As you continue to eat fat-rich foods over time, your adipose tissue can become inflamed. This occurs when adipocytes (adipose cells) become overwhelmed with the amount of fatty acids that they are forced to uptake.
Every time fatty acids appear in your blood in high amounts, adipocytes do their best to absorb as much fatty acids as possible. But as you continue to eat more fat-rich foods, the size of the lipid droplet inside of adipocytes grows beyond that which it was designed to handle.
When this occurs, adipocytes become hyperplastic, and begin increasing in size. Hyperplastic adipocytes then break open and spill their contents into extracellular fluid. Surrounding in-tact cells secrete stress hormones called cytokines, which then attract macrophages to the area to help clean up the cellular debris (32–39).
This process is called adipose tissue macrophage infiltration, which creates a state of low-grade chronic inflammation which then inhibits the ability of insulin to communicate with adipocytes. In other words, adipose tissue macrophage infiltration causes insulin resistance in your adipose tissue.
See the image below for a schematic of how this process unfolds:
Muscle and liver cells have a very difficult time preventing fatty acids from entering. As soon as you eat fat-rich foods, fatty acids enter your muscle and liver within hours. Unfortunately, there is very little that your muscle and liver you can do to stop these fatty acids from entering.
The fatty acids congregate together into a structure known as a lipid droplet, which is fine as long as the total amount of lipids remain small. By design, cells in your muscle and liver are not designed to store large lipid droplets.
Over the course of time, as you continue to eat fat-rich foods, the lipid droplet in each cell grows, which then causes a serious downstream problem – impaired insulin signaling.
When the lipid droplet grows, various lipid molecules communicate directly with insulin receptors, preventing them from functioning properly. Muscle and liver cells choose to cripple the action of the insulin receptor in order to burn the existing lipid droplet first.
Muscle and liver cells effectively say, “I have to burn this lipid droplet first before I can take up any more energy, even if that energy is glucose.”
Next, when you go eat a carbohydrate-rich food like a banana, potato, or piece of bread, the carbohydrate molecules inside break down into glucose. That glucose circulates in your blood, and must be accompanied by insulin in order to get inside of cells.
In the case of type 1 diabetes, you inject insulin in order to get insulin receptors in your muscle and liver to allow glucose to enter. But because they have accumulated large lipid droplets, both tissues reject insulin efficiently. In order to bring your blood glucose down, you inject larger amounts of insulin.
In the case of prediabetes and type 2 diabetes, the beta cells in your pancreas are forced to hypersecrete (secrete large amounts) of insulin to get cells in your muscle and liver to cooperate.
Insulin’s job is to knock on the door of the cell and say, “Hey I have some glucose, do you want to take it up?”
If insulin receptors are inhibited by excess fat accumulation, muscle and liver cells respond by saying, “I can’t take up that glucose right now, I have to burn this lipid droplet first.”
As a result, insulin can’t communicate with tissues, and remains trapped in your blood, causing hyperinsulinemia (excess insulin in circulation). In addition, glucose can’t enter tissues and also remains trapped in your blood, causing hyperglycemia (high blood glucose).
When you go check your blood glucose a few hours after eating a carbohydrate-rich food, you are likely to see a high blood glucose and get frustrated.
Over time, beta cells that are forced to secrete excess amounts of insulin experience apoptosis (programmed cell death).
The reason for this is simple – just like cells in your muscle and liver, beta cells also absorb fatty acids over time. Unfortunately, beta cells are a fragile cell type that are not designed to withstand large amounts of fatty acids, and as you continue to eat more fat these cells not only increase the amount of insulin they secrete, but they generate free radicals which result in cell suicide.
Beta cells can only withstand fatty acid accumulation for a finite period of time, and when the amount of fat in your diet exceeds the ability of beta cells to absorb fat, you increase your risk for lipid-induced beta cell death.
In order to reverse the series of steps outlined above, what could you do?
In truth, all three of the steps outlined above will help you reverse insulin resistance. Evidence-based science shows that the most effective way to reverse insulin resistance and gain insulin sensitivity is by dropping your fat intake to between 10-15% of your total calorie intake.
Remember, the problem is that excess lipid accumulation inside muscle and liver cells has crippled the action of insulin receptors. If you want to gain insulin sensitivity and allow glucose to enter your muscle and liver, it’s time to wake up those insulin receptors!
By reducing your fat intake to 10-15% of your total calorie intake, you will enable cells in your muscle and liver to oxidize (burn) the existing lipid droplet. As that lipid droplet becomes smaller, the insulin receptors gain function once again, making insulin dramatically more powerful.
Now every time that glucose molecules come to the door of cells, smaller amounts of insulin help glucose get inside of cells, preventing your blood glucose from getting too high.
Glucose is allowed to enter muscle and liver cells in large quantities, and these cells either use it for energy or store it for later as glycogen. Over time as you continue this process, cells in your muscle and liver shift away from being reliant on fatty acids and become more reliant on glucose.
This is the beauty and simplicity of the insulin resistance diet.
Exercise is also an incredibly powerful insulin sensitizer, because it accelerates the rate at which your muscle and liver cells burn stored lipid droplets. That’s why most people and medical professionals turn to exercise as their first line of defense when improving blood glucose values, however it’s incredibly important to understand that exercise is less powerful when your diet contains medium or high-fat foods.
The goal is to burn stored fatty acids inside muscle and liver cells but not refill these fatty acid stores at the same rate. If you exercise and burn fatty acids frequently but then refill these fatty acid stores at a fast rate without adopting the insulin resistance diet, you may never fully reverse insulin resistance.
And that’s part of the problem with mainstream diabetes information – whether you have type 1 diabetes, prediabetes, type 2 diabetes, or gestational diabetes, most people will tell you to eat a diet high in fat and high in protein, and even though you can “control” your blood glucose well, you become more insulin resistant over time, increasing your risk for long-term chronic disease.
Many health professionals will tell you that the most effective way to reverse diabetes is to eat a low-carbohydrate, high-fat, high-protein diet and perform frequent intermittent fasts (also known as time restricted feeding), citing research papers documenting evidence that a high-fat diet combined with time restricted feeding increases insulin sensitivity.
There are thousands of research papers that describe the cellular mechanisms at play during calorie restriction, intermittent fasting, and time restricted feeding. It is important to understand that there are thousands of chemical reactions that occur during intermittent fasting which constitute a "program" that optimizes you for excellent metabolic health.
In the research world, calorie restriction is so effective that it is considered one of the most powerful methods of improving all aspects of glucose metabolism, including:
There is no doubt that time restricted feeding is a powerful technique to oxidize the stored lipid droplets in your muscle and liver tissues, however without adopting an insulin resistance diet containing a maximum of 15% calories from fat, any improvement in insulin sensitivity that you gain from a single intermittent fast is inhibited the moment you at fat-rich foods.
Since the name of the game is long-term health, it’s imperative to design a system that works today and over time, otherwise any attempt at decreasing insulin resistance is only temporary. That’s exactly why the insulin resistance diet is your best chance at reversing insulin resistance in the long-term.
The truth is that without first adopting the insulin resistance diet, any attempt to exercise or perform time restricted feeding will only slightly improve your diabetes health. We strongly suggest adopting the insulin resistance diet first, then adding frequent movement and intermittent fasting as secondary habits.
Low-carbohydrate diets have been recycled over the course of time. In the 1970’s, the Atkins diet was the first mainstream low-carbohydrate diet, which then was popularized in the 1990’s once again, and became one of the most famous fad diets of all time.
Next came the South Beach diet and the Zone diet in the late 1990’s and early 2000’s, followed by the Paleo diet and now the ketogenic diet. In addition, for people with type 1 diabetes, Dr. Bernstein has created the ultra-low carbohydrate solution, which is effectively the same as a ketogenic diet.
All low-carbohydrate diets will help you control your blood glucose well, but they all have the same effect –they increase your level of insulin resistance and therefore increase your chronic disease risk.
The truth is that low-carbohydrate diets work…in the short term. Low-carbohydrate diets are not an effective long-term dietary strategy because they are hard to maintain and because they increase your risk for diabetes complications, chronic disease, and premature death from any cause.
The problem is that it’s very hard to visualize what will happen in the future, and it’s easier to focus on the changes you see in the present moment. Because low-carbohydrate diets can promote rapid weight loss, significantly drop your A1c value, reduce your blood glucose variability, reduce your total insulin use, and reduce your LDL cholesterol, it’s easy to be “tricked” into believing that they are a great long-term solution.
The scientific literature clearly describes that people who eat low-carbohydrate diets in the long-term increase their risk for all-cause mortality, or premature death from any cause.
Low carbohydrate-diets are associated with an increased risk for many cardiovascular conditions including heart disease, hypertension, high LDL cholesterol, high triglycerides, and atherosclerosis (40–47).
In addition to an increased risk for cardiovascular disease, low-carbohydrate diets increase your level of insulin resistance by increasing fatty acid accumulation in your muscle and liver, which in turn increases your risk for cancer (48).
Low-carbohydrate diets also significantly increase your risk for kidney failure due to high protein loads and chronic kidney inflammation (22,49–53), and cause low energy, impaired digestion, and intense food cravings over the course of time.
An overwhelming amount of scientific research shows that the most effective insulin resistance diet is the exact opposite of a low-carbohydrate diet – a low-fat, plant-based, whole-food diet (22,49,54–57,57–72).
Extensive research shows that increasing your intake of fruits, starchy vegetables, non-starchy vegetables, legumes, and intact whole grains has a tremendous insulin sensitizing effect, which is more powerful than any other intervention studied to date.
For people living with all forms of diabetes, we recommend eating 70-80% calories from carbohydrates, a maximum of 10-15% of calories from fat, and a maximum of 10-15% of calories from protein. In addition, we recommend maximizing your intake of plants and minimizing or completely eliminating your intake of animal products altogether.
You might be wondering what you can actually eat. The simplest way to think about what to eat is to divide foods into green light, yellow light, and red light categories.
The green light category are foods that you can eat in abundance, and should form the base of your calorie intake. This category contains the following foods:
The green light category are foods that you can eat in abundance, and should form the base of your calorie intake. This category contains the following foods:
The yellow light category are foods that you can eat in small quantities, and should contribute no more than 10% of total calories. This category contains the following foods:
It is true that nuts and seeds have documented anticancer effects, anti-diabetic activity, and can significantly improve your cardiovascular health, but we place them in the yellow light category because it is very easy to overeat them. We also put pastas and breads in this category because they tend to be highly refined foods that can contribute to increased blood glucose values.
The red light category are foods to minimize or avoid entirely, because they increase your risk for chronic disease as described earlier. This category contains the following foods:
Take a look at the following recipes below to get an idea of what types of meals you can construct using the lists above:
[cooked-browse columns=”2″ search=”false” pagination=”false” show=”4″ category=”dinner”]
Not only are the foods listed above incredibly tasty and filling, science has proven that this specific insulin resistance diet will help you reverse insulin resistance, reduce your fasting blood glucose, reduce your hemoglobin A1c, and reduce your chronic disease risk from the inside out.
If you want to read more about people who have transformed their lives using low-fat, plant-based, whole-food nutrition, click here to read and listen to amazing case studies.
And if you’re interested in transforming your diabetes health from the inside out, then join the Mastering Diabetes Program and maximize your insulin sensitivity in a supportive community of thousands of other people just like you.
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Cyrus Khambatta earned a PhD in Nutritional Biochemistry from UC Berkeley after being diagnosed with type 1 diabetes in his senior year of college at Stanford University in 2002. He is an internationally recognized nutrition and fitness coach for people living with type 1, type 1.5, prediabetes and type 2 diabetes, and has helped hundreds of people around the world achieve exceptional insulin sensitivity by adopting low-fat, plant-based whole foods nutrition.
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