There are lots of theories on what causes insulin resistance. Some would tell you carbs do it while others will tell you it is fat that causes it. Others even say that insulin itself causes insulin resistance. The honest answer is that all of them play a part and it is not any single factor.
My favorite way to understand issues is by looking at various illnesses and the effects they have. There is one in particular that is perfect for this issue. It is called Lipodystrophy. This is a disorder of abnormal fat accumulation in the body.
These people have the appearance of being very lean and even like a ripped up athlete yet they are actually extremely sick. One of the most prominent issues with lipodystrophy is insulin resistance and diabetes. How can someone be so very lean yet be insulin resistant and even diabetic? That is what brings us to the true cause of insulin resistance. We will get back to these poor folks later and how this all ties in but first lets look at the process of how insulin resistance develops.
This is how it starts:
We have storage in our body for carbohydrates. We can store a given amount of glucose in muscles and liver in a form of carbohydrate called glycogen. This will be determined greatly by how much muscle mass a person has. Someone with more lean mass will naturally have more space to store glycogen. When we eat carbohydrate the body will quickly push the glucose into liver and muscle and it gets converted to glycogen where it stays until it is needed. This conversion to glycogen is important. Once it is in the form of glycogen it can’t leave the muscle or liver passively. It has to be converted back to glucose so it doesn’t just flow out all the time. So long as we keep our carbohydrate consumption low enough that we never exceed this storage capacity then we will never become insulin resistant. The problem with todays society is that we do exceed this storage capacity and we rarely empty it out. This is when the issue starts but we are still not insulin resistant yet.
So a bit more about why the conversion of glucose to glycogen is important before we move on. People assume that if we eat carbohydrate we only burn carbohydrate until it is all gone, then we move on to burn fat. This is completely incorrect. We only burn through glycogen in a few scenarios. The rest of the time we use a small amount of glucose but mostly fat. These are the two main scenarios:
- When we first eat carbs and our insulin is elevated.
- Until insulin returns to a low enough level, we will continue to burn carbohydrate because insulin locks up fat cells so fat can’t be used. In a normal person the insulin will be low enough within 2 hours or less. The more insulin sensitive you are the faster it will return to baseline and you will be back to using mostly fat for fuel. That is how the body works and this is partially why most people tend to exceed their glycogen storage. They are eating lots of carbs and filling up glycogen stores then they return to using fat for fuel. They never actually use any of the glycogen because they don’t workout with intensity. Intense exercise is really the only way to pull glycogen out of storage.
- During intense physical activity.
- Intense physical activity, anaerobic/glycolytic, requires glucose for fuel. This is what people are talking about when they say we need carbs to exercise. They are not wrong about that. The part they are wrong about is that we can make all the glucose we need for exercise through gluconeogenesis in the absence of exogenous carbohydrate. Our liver will make glucose when needed through a chain of events that starts with low blood glucose. The body will pull glucose from the blood when needed for intense exercise and this will cause a stress response which pumps out cortisol. Cortisol signals the pancreas to release glucagon which goes looking for glucose. If we have glycogen stores it will start the conversion of the glycogen back to glucose for use but if there are no glycogen stores the glucagon will signal gluconeogenesis to start and make glucose from amino acids. So that is the other instance when we will use primarily carbohydrate.
Besides these two scenarios we primarily use fat for fuel. No matter who you are or what diet you are on. You do not have to use up all the carbohydrate you eat for fuel before you use fat and this is part and partial to the entire issue. Because we move back to fat for fuel when insulin goes back to baseline we end up having all the carbs we ate sit in the glycogen stores. If we don’t engage in high intensity physical activity to empty the stores we will just keep filling them up until they no longer have any more room. Where do the carbs we eat then go?
If we continue to consume carbohydrate after the glycogen stores are full it has to go someplace. It cannot sit in the blood as glucose is toxic to the blood. The next step is to convert the excess carbohydrate to fat. Now this is not necessarily a problem and this is why people are so stuck on the calories in vs calories out (CICO) story. In this sense it is absolutely correct. If you exceed your daily capacity to store carbs in glycogen and start storing fat, this is still not an issue so long as you use more calories than you store. See how that works? When you have exceeded your glycogen stores by eating carbs and never use the stored glycogen then CICO 100% applies but if you never eat carbohydrate and never exceed that storage, the story changes dramatically. We won’t get too far into that now. Lets get back to insulin resistance.
So lets now look at what happens when we consume a normal diet that is high in both fat and carbs and how this is what causes insulin resistance. You have exceeded your glycogen stores and never empty it out. You continue to eat carbs so the carbs have no place to go so they get converted to fat and get stored in fat cells. What exacerbates the issue is that you are also eating fat. That fat also has to be stored in fat cells as well. So we now have a double whammy. We are turning carbs to fat and because insulin is high we are also storing fat as fat. We are now starting to develop an issue. We all have a genetic ability to grow and create new fat cells. This is why some people can seem to eat whatever they want and never get fat, we hate these people, while others can get to 600lbs and still not be diabetic. We call this the personal fat threshold.
Once a person hits this threshold, this is when the problem really begins to snowball out of control. This is the beginning of insulin resistance. Once we reach maximum fat capacity the cells become insulin resistant. The insulin can no longer push fat into the cell because they are full. This is when we stat building up fat in the organs. I am sure you’ve heard of non alcoholic fatty liver disease. This is the point where one is officially insulin resistant. This is when blood sugar starts to rise and stay elevated. The body will not allow glucose to stay elevated without trying to fix it. Its response is to increase its insulin production. The increased insulin production will actually force the body to create new fat cells. This is why people will suddenly start to gain more weight when they have been at a set weight for a long time regardless of wether they are eating more. In order to actually grow fat cells in a lab insulin must be used. Insulin can create new fat cells and this can be seen in people who inject insulin. If they do not rotate spots of injection they will start growing lipomas (fat growths) in the injection spots.
The next step in the process is the burnout of the cells in the pancreas that produce insulin. After the body trying to fix the problem of high blood glucose by forcing the pancreas to over produce insulin, the cells will actually start burn out. At this point the diabetic person will need to start injecting insulin to maintain the process because the pancreas is now unable to produce the increasing amount that is required. Most people with T2D will notice they get a spurt of weight gain when they start injecting and this is because the increased insulin load results in further creation of fat cells. It is a viscous cycle.
Sorry this has been so long but it is a complex story that few people actually understand. Now that I have layed that out, I will get back to why people with lipodystrophy perfect display the idea of personal fat threshold and how that leads to insulin resistance.
Because they cannot create adequate fat storage they do not have the inherent protection that fat cells create. They cannot take any of the glucose they eat and convert it to fat so they immediately start developing fatty liver and other visceral fat stores. They immediately become insulin resistant because they have no place to put the excess glucose or fat. You can see how this perfectly demonstrates the idea of the personal fat threshold. If they never exceed their glycogen storage they would also be completely fine. This leads me to believe it was a genetic adaptation. Likely these people evolved in a place where there was inadequate carbohydrate available. They never developed the need to create fat cells. I am sure there is some inherent advantage in this type of environment as there tends to be with this type of issue. What that advantage is, I have yet to figure that out.
So it is not carbs alone or fat alone or insulin alone or even lack of exercise alone that causes diabetes and insulin resistance. It is especially not obesity that causes either of them. You can be as lean and ripped out as an elite athlete yet still be insulin resistant if you have a low personal fat threshold. You can also be 600lbs and super morbidly obese and not be insulin resistant or diabetic.
I hope this was clear and helped further your understanding of these complex issues. I tend to brain dump all of the data in my head sometimes. It all makes sense up in the attic of my mind but sometimes I wonder if it translates to paper. Let me know what you think. 🙂
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