Does Insulin Make You Fat?

Luke Tulloch

The article below is adapted from a podcast episode transcript, so please forgive any spelling or continuity errors. You can listen below:

Insulin in a nutshell - it's a hormone. It's secreted by some cells on the pancreas called the beta cells, and they are located on pancreatic islets. The main role of insulin involves directing energy metabolism in the fed state - this means that when we eat our food, we have changes in how our energy is produced and insulin's main role is directing that energy metabolism.

Do we want to metabolize more carbohydrates? Do we wanna metabolize more fats? Insulin helps tell the body what to do.

Now the main focus of insulin is on blood glucose control. So by extension, it also directs fuel usage. So it affects fat burning and it affects what substrates are broken down to feed us. For example, we can use amino acids to generate blood glucose, but maybe if we have a boost of blood glucose, we don't want to do that. Insulin inhibits muscle breakdown so that we don't use the amino acids from our muscles to start making more glucose when we've got plenty floating around in the blood.

The basic way it works is this: When we eat, our blood glucose tends to go up. We don't want our blood glucose to be too high because that's quite dangerous and we don't want it to be too low because that's also quite dangerous. So there's a happy medium. There are two threshold, a lower end and a higher end, that we want to keep blood glucose in between.

After we eat and our blood glucose goes up, insulin helps to chaperone that glucose out of the blood and stick it into some tissues. That could be your muscle tissue. It could be fat tissue, it could be any other organs or tissues that can use that glucose. This is what I mean by directing energy metabolism. If we are directing a cell or a tissue to take up glucose, we're hoping that it's going to actually be using that glucose for its energy production.

This is achieved in a variety of ways. We have some quick actions and some longer lasting actions of insulin. It actually has a multi-step process. In the short term, it can change cell membranes to effect glucose uptake. This could be, for example, promoting the opening of glucose channels on the cells. Some of you might've heard about GLUT4 - it stands for glucose transporter 4. This exists in a few different cells, but in particular in muscle cells. What happens when GLUT 4 opens up is it allows the muscle cell to soak up more glucose from the blood and start using that glucose in a slightly longer timeframe. Insulin can also alter the enzyme activity that is involved with anabolic or catabolic signaling - in other words, it can change the way enzymes work within a cell or a tissue that tell the cell or tissue to build more stuff or break down more stuff in the longer term.

So we're talking a couple of hours now. We have even more interaction with those anabolic or catabolic enzymes and that can affect the outcome of fuel usage in the cell.

Now one of the problems with insulin is that it does affect fat metabolism as well. So while it's telling different tissues to use glucose, what happens to the fatty acids that we want to be burning to lose body fat? Well, it actually suppresses fatty acid oxidation.

However, this is quite a small piece of the puzzle. While insulin does suppress fatty acid oxidation, there are other factors involved with the burning and storage of fat. Some of those include something called hormone sensitive lipase, which actually helps to promote fat burning. And this is inhibited by insulin and another protein called acylation stimulating protein, which helps to store fat independent of insulin. It increases the enzyme action that helps incorporate fatty acids into the fat cells.

It also increases glucose storage in those fat cells and like I just mentioned, it actually inhibits fat burning by inhibiting hormone sensitive lipase. So when people talk about insulin being the primary fat storage hormone, it's not quite true because there are some things that are not related to insulin signaling that are involved in fat storage and fat burning.

Now before we go on, I do want to talk about GI a little bit. GI stands for glycemic index and it basically tells us how much your blood sugar rises when you eat a certain amount of a food. This is obviously important because insulin is trying to control your blood glucose. Glycemic index has a few problems. The first is that everyone's going to have an individual response to whatever food they're eating. The second part is that although the glycemic index is given for a single food, the issue is that we almost never eat a single food in isolation.

It's going to be affected by our previous meal, our level of activity, what we're eating, our current meal with. So for example, you usually don't eat potatoes by themselves. You might have them as part of a bigger meal and so the overall glycemic index of any given meal is difficult to calculate for an individual overall.

The assertion that insulin can inhibit fatty acid oxidation and fat burning is definitely true. With that said, there came the insulin hypothesis of fat gain. There are a few aspects to this hypothesis. The first part of this hypothesis of fat gain caused by insulin says that insulin inhibits lipolysis (fat burning). Since insulin inhibits fat burning, that means that those fatty acids that aren't being burned have to be stored in fat cells.

The second part of the insulin hypothesis of fat gain is that we can develop something called insulin resistance. What this means is that the muscle or other tissues, but usually the muscle can't efficiently take up glucose from the blood. That glucose that is sitting in the blood has to go somewhere and because it's dangerous to have too much glucose, remember? And so this glucose is converted into fatty acids. The fatty acids are then stored in fat cells. Development of insulin resistance happens when we have a signal of insulin that is not being heard by the muscles and we then get greater fatty acid storage in fat cells.

The third part, lower glycemic index foods will lower the insulin response. They will cause greater satisfaction or satiety from your food and then you won't eat as many calories.

And lastly, the fourth part going low carb means that you will have a lower glycemic index and then you will have a lower insulin response and therefore you will not gain as much fat.

So four separate points. Most of these revolve around the idea that when our insulin is high, we store more fat. When our insulin is high, we don't feel as satisfied from our food and therefore we eat more calories. When our insulin is high, we can develop resistance to insulin signaling, which just compounds the problem even further because we have this resistance to insulin. It means our body has to keep pumping out more and more and more insulin to try and make up for the deaf signal that the cells aren't hearing. Let's examine this part of the argument for insulin causing fat gain.

Firstly, it's true that insulin inhibits fat burning. It's a small piece of the puzzle though. Like I said before, there are other mechanisms involved like acylation stimulating protein and a couple of other things as well that I won't really get into cause they get a little bit too complicated overall. Although insulin inhibits fat burning, it doesn't override overall caloric intake.

Circulating insulin levels are tied to some extent to body weight regardless of diet composition. If you weigh less, you're going to have lower values of circulating insulin at no matter what diet you eat. And therefore the correlation between your base insulin levels and your body fatness may actually be the other way around. Meaning that the higher your body weight, the higher your plasma insulin and not the higher your insulin secretion, meaning that you have higher body weight. So this throws a bit of a spanner in the works for insulin inhibiting fat burning.

We have seen cases where we put people on very high glycemic index diets and they tend to lose weight even compared to low glycemic index diets. There seems to be no difference from the current research. This means that insulin can't possibly inhibit fat burning to the extent that it stops you from losing body fat, provided that you're in a caloric deficit. At some point, the body does have to use a certain amount of energy, whether that energy is coming from carbohydrate or coming from fat is not really that important because overall it means that if you are eating a lot of carbohydrate and your insulin is very high but you're still in a deficit, your body has to come up with the difference in your energy expenditure somewhere. And that will come from body fat regardless of the level of insulin to address.

The second point of the efficacy of eating a lower glycemic index diet, meaning lower insulin and creating a higher satiety, meaning that you eat less calories. Well, this is just completely false. We have a study from Bowen et Al that tested how much people ate at a buffet after ingesting either glucose, fructose, whey protein, or a combination of whey protein and fructose. There were no differences between any of those groups despite drastically different glycemic index indices and therefore drastically different insulin levels.

To give you an example, glucose produces much more insulin than fructose. Fructose doesn't actually raise your insulin. So despite the fact that one group had a raised insulin level and the other group did not, there were no differences in how much they ate at a buffet. After ingesting the liquid, there was another study which looked at different ratios of glucose to fructose in a drink. And again, the more glucose you have, the more insulin you're going to produce. The highest insulin response actually caused the highest satiety levels out of anything.

So the stuff with the most glucose in it caused the highest insulin response and caused the highest level of satiety. Anderson et Al preloaded subjects before they ate a meal and found that the higher the glycemic of the preload, the less energy was consumed in the meal after. In other words, the more insulin produced, the less energy was consumed in a following meal. And finally, Flint et Al found that the greater the insulin response, regardless of the GI, was equal to greater subjective feeling of fullness. So the higher your GI the greatest objective feelings of fullness.

So this concept that the lower the GI, the higher your satiety levels is actually completely false. It, if anything, it appears that the opposite is true. At worst, there's no difference.

Let's examine the part of this theory that says lower carb equals lower insulin and therefore leads to greater fat loss.

Again, like I mentioned before, if the energy intake and the protein intake is the same, there is no difference in fat loss. There was a study by McLaughlin in 1999. They compared insulin sensitive subjects. So these people produced the least amount of insulin with insulin resistant subjects and they produced a lot of insulin on a hypo caloric diet, so they were in an energy deficit. They had no differences in weight loss. Again, if you're insulin sensitive, it means you don't have to produce very much insulin to get the signal through the muscles. If you're insulin resistant, it means that your muscles are deaf to the signal of insulin to some extent, and so your body pumps out more and more and more insulin to try and get the message through. Even though those people produced more insulin, they did not lose any different amount of weight. Louis did the same thing with the same results in a 2006 study.

There've been a lot of other studies that were led by various authors that compared varying GI diets with no differences in weight loss. Even one giving people insulin suppressing drugs. They had no differences in weight loss or appetite compared to placebo when on a hypo-caloric diet. So no matter how we manipulate the insulin levels of people, we don't see any differences in weight loss in practical studies.

Next, what I am going to do is summarize a Kevin Hall study, which was examining this insulin hypothesis very closely at the behest of Gary Taubes, who some of you might know I'm not a huge fan of.

I don't call people out, but I'm happy to call Taubes out cause I think he is morally bankrupt. But I'll get into that in the next section. If you don't know Gary Taubes published a book called Good Calories, Bad Calories, and another book called Why We Get Fat and What To Do About It. And in this he blames carbohydrates for all the reasons we mentioned previously for the obesity epidemic in the Western world. He later founded a foundation to publish research or conduct research on the topic that he feels a was missing from the overall picture. So he feels that the research currently refuting his claims was not done to his standard. And so he founded this foundation called NuSci to try and provide funding for some really well-constructed studies.

And they definitely did that. They definitely came up with some very well constructed studies. Now Kevin Hall was the principal investigator in the first major publication coming out of funding from NuSci. He collaborated a little bit with Gary Taubes in the design of this and some other members of the foundation. They addressed all of those aspects of the insulin hypothesis of fat gain that I mentioned before. Now if you want to learn a little bit more about exactly how this was done, I recommend looking at the Sigma nutrition podcast where Danny Lennon actually interviewed Kevin Hall. It's episode number 165 on this particular study. So I'm not going to go into much depth of the actual study in this particular podcast because I do want to keep it simple, but suffice to say that this was a very well conducted study.

I will do a future episode on the limitations, drawbacks and the methodology of researching human in the human model. But this was a very well conducted study and basically it found that insulin at this point has a very minor effect on body composition, if any. And so our current evidence does state that the amount of insulin you produce on average probably does not matter whatsoever for fat loss, and it really is down to the degree to which you are in a calorie deficit. Now, I will acknowledge that in some individuals this may not be true for overall health. Some people who do have issues with insulin resistance, for example, may do better on a lower GI diet. A lot of the research that we have has not seen that to necessarily be the case. But I do think we can't close the door to that completely.

Okay. At this point. I'm going to end the podcast there. If you enjoyed it, please leave me a rating. Give me some feedback. I'd absolutely love your feedback because I plan to take, listen to feedback into huge accounts so I can produce the best possible podcasts for your listening.

Thanks for reading,

Luke.