Leah:
Hello and welcome to the Ideal Nutrition Podcast. I am your host Leah Higl and I’m here with my co-host Aiden Muir, and today we’ll be doing a deep dive into insulin, but particularly through the lens of health and body composition. There is quite a lot to unpack here.
So, this is probably going to be a slightly longer episode, but I’m going to start with just defining insulin, just to get us off on the right foot. And then we will kind of go one for one on different points that we want to kind of cover. Hopefully we can wrap this up in 30 minutes, but we shall see.
So insulin itself is a hormone produced by the pancreas that plays the most important role in regulating blood glucose levels or blood sugar levels. It helps glucose move from the bloodstream into the cells within the liver, fat or muscle. In these tissues, the glucose is converted into glycogen or fat.
And then circulating insulin also increases protein synthesis in a wide variety of tissues as well. So it actually has other roles in the body other than just the glucose, blood glucose stuff. It can help amino acids enter muscle cells and it’s actually even more effective at reducing muscle protein breakdown than it is at building new muscle.
Additionally, it helps other hormones like IGF-1, that play a role in muscle growth and repair. So we consider insulin as being an anabolic hormone as it helps with the storage of muscle, fat and glycogen.
Aidan:
Now talking about another piece of background of what we’ll call normal glucose metabolism. When glucose is high in the blood, insulin is released from the pancreas, which will reduce the glucose levels. When glucose in the blood is low, less insulin is released. Vice versa, glucagon does the opposite.
So, when glucose is low, glucagon is increased, and it stimulates the liver to release glucose. I think it’s relevant to know that in almost all cases, or the majority of cases, both insulin and glucagon are in your system. It’s just more about the ratio. Usually, one is more dominant than the other.
And the reason why I’ve kind of added this in here is sometimes when you hear people talking about it, they make it seem like Insulin being in your system ever is a bad thing. It’s like, it was pretty much always in your system. It’s just about the amount and like which one’s dominant at any given time.
Leah:
Talking about some abnormal ways we see glucose metabolism happen in the body. Diabetes is obviously a huge one to bring up. We’re not going to go too in depth on diabetes itself today because we want to keep this a little bit more broad and as an overview of insulin more so than diabetes.
But in this context, we do need to touch on it. So, type 1 diabetes is a condition where the body’s immune system essentially attacks the insulin-producing cells in the pancreas called beta cells. So, the body makes little or no insulin. People with type 1 diabetes need to use insulin injections or an insulin pump for their whole life. So this is something that isn’t quote unquote curable. It’s something that is consistently managed for the entirety of someone’s life.
And then we have type two diabetes. And this is also called lifestyle diabetes because it’s something that is acquired rather than something that you are born with as an autoimmune condition. So, it’s a condition where the body becomes resistant to insulin. So, it’s not that we are not producing any insulin. It’s that our body itself is resistant to it.
So unlike type one, the body still produces that insulin, it just doesn’t respond to it properly. So, you will still find many people with type 2 diabetes like type 1 utilizing things like insulin injections, but that may or may not be needed depending on the situation. That’s a massively oversimplified version of diabetes, just kind of giving you a quick rundown. But since we’re touching on insulin, we had to just give that the time it deserves.
Aidan:
That gives a good background for everything else we’re going to cover throughout this podcast. But as a bit of a segue into this, I wanted to talk about something that I, personally, find very interesting. And that’s a bit of a timeline on synthetic insulin. So, in 1921, insulin in general was first discovered. It was extracted from the pancreas of a dog.
Diabetes had obviously been around for thousands of years. I’m a bit of a history buff. Like, there are so many cases where I’m listings narratives of certain histories and stuff like that and key figures. They’re what historians now go back and look at and like that was very likely diabetes and obviously impacts their lives.
So it’s kind of crazy that 1921 was when insulin was discovered because obviously this diabetes has been relevant for thousands of years. It wasn’t even until the late 1800s that a link between diabetes and the pancreas in general was kind of clarified. So 1921, insulin discovered. 1922 is the first time human treatment occurred using insulin extracted from pigs and cows. After this, for a surprisingly long time, people relied on animal-sourced insulin, which worked, but it did cause immune reactions.
Then in 1978, scientists put the human insulin gene into E. coli bacteria, which was then able to produce human insulin itself. That was also the first time that bacteria was used to make a human hormone and it allowed insulin to be produced in large amounts, safely and consistently. And then not long after that, so four years later in 1982, Humulin became the first genetically engineered form of insulin approved for human use.
That solved this whole immune reaction problem and it was way more scalable. So it’s crazy to think that not that long ago that all of this happened. I’ve personally found it surprising like the more I think about it, like the more that makes sense, I guess, but crazy how such a life-changing thing, still pretty recently.
Leah:
Yeah, I love that segue because like 1982, like the eighties, like that doesn’t not seem that long ago. So it’s just crazy to think about. But moving away a little bit from diabetes, what we want to cover now is more or less talking about why people have the idea that insulin is bad and it’s a negative thing to have floating around in the human body. Because we can obviously see the ways that it’s very useful in the human body. Like, it is it’s literally essential for life and it has so many important roles but we have this kind of overarching notion particularly in the health and fitness industry that insulin is bad and it’s a negative thing.
Reasons why this could be considered the case are, well, one, it’s involved in fat storage and decreases fat breakdown. So, for anyone looking to lose body fat, that can feel or sound a little scary, like it sounds counterintuitive for it to be circulating in around the body if that’s the case. It also decreases autophagy, which we’ll touch a little bit more on, but even relatively normal insulin levels not long after eating significantly reduce autophagy, which is something that proponents of fasting will often talk about.
We also have the fact that insulin spikes can lead to crashes, which can impact things like energy and mood and consequently things like appetite and lifestyle and nutrition behaviors. And then high insulin levels are often associated with certain health conditions. So such as having type two diabetes, for example. So it’s understandable why there is a lot of myths and misconceptions around insulin and why it’s, it’s often just quite misunderstood.
Aidan:
So we’ll quickly try and go through and unpack each of those things. So, with fat storage, we’re going to talk about that separately, although that does kind of remind me, there are a lot of people I see on Instagram who use pretty much the exact wording, when insulin is in your system, fat burning is completely turned off. And I’m like, well, it’s pretty much always in your system. It’s always there. It’s a problem if it’s not. So, we’re going to unpack that, but we’re going to talk about that later.
I’m going to start with the autophagy side of things. So, autophagy is a process that cleans up and recycles certain components within cells. After eating, especially with adequate protein and carbs, autophagy is suppressed because the cells have plenty of energy and building blocks, so they don’t need to recycle. Insulin does play a role, but what I just said is also relevant with or without insulin, like insulin is just one kind of component there.
And also over a longer timeframe, the best interpretation of the research that I have seen is that autophagy balances out over the longer term if total intake is matched. You see it way more acutely when somebody is doing some form of fasting, whether that is 16, eight, whether that’s like a multi-day fast, you see it way more acutely. But if total intake over a much longer timeframe, say six months was the same, it likely balances out or comes close to balancing out.
And the alternative to that is if total intake was just very low for the long term, autophagy might be higher, but you also run into other issues as well. And since the focus was on insulin, and not total intake. It’s worth mentioning that both carbs and protein raise insulin. Often people are really focused on the carb portion here, but protein also does raise insulin as well. Theoretically, you could get around the total intake problem, but keeping calories appropriate and going low carb and low protein, but that also causes other problems.
So like, I don’t know, I wouldn’t be too focused on the autophagy stuff here, kind of based on that. Like I think a lot of this balances out. And there are a lot of things, a lot of behaviors that we want to be doing for other reasons as well. And I think just focusing on this one thing would be a little bit misleading.
Leah:
Unpacking the insulin spike stuff a little bit more. I think the insulin spikes leading to crashes is valid to a degree. But I’d also say it’s not necessarily typical or problematic for most people living their day to day life. In most people, the process is smooth and the appropriate amount of insulin is released to bring blood glucose levels back to within range.
And ideally within the body, this is something that’s quite tightly and well controlled. Obviously that’s not the case for things like diabetes, but also things like reactive hypoglycemia, like that does exist. And case by case basis there, but one example could be someone has a really high intake of carbs, particularly your high glycemic index carbohydrates and on a particularly empty stomach perhaps. And that can lead to insulin being a bit overproduced to the point there is a drop in blood glucose levels below what the healthy range is.
And it can cause symptoms of a hypo, so hypoglycemia. It’s also something that can be quite common in certain conditions, particularly I work a lot in hypermobility and co, so things like MCAS and POTS. And it’s something that I see quite often in these clients and it can lead to or contribute to their chronic fatigue, episodes of shakiness, dizziness and severe brain fog, as well as insomnia. But for the most part, it’s not relevant for most people, but we’re highlighting that, yes, for some people it can be relevant for sure.
Aidan:
High insulin levels are associated with certain conditions, so that is true. But the other angle that I would personally prefer to look at from is that it’s less about the insulin being high and more about the insulin resistance itself being an issue. With insulin resistance, because insulin is less effective, more insulin is required to get the job done. That’s also another thing that we will talk about more when we talk about the body fat thing.
But I’ve thought about that a lot being like, if insulin is having a harder job taking the glucose out of the blood to be stored, is it so much about the insulin being higher or about the insulin resistance? Like I think the insulin resistance matters a fair bit more, but that also can create a bit of a loop where high insulin levels can reduce insulin sensitivity, increasing the requirement for more insulin, particularly the more extreme this gets.
This probably isn’t a thing that really matters at lower levels of insulin resistance. I also think it’s detrimental to focus on that too much, particularly for those with diabetes requiring insulin, since I think the best move is just to inject the amount of insulin you need. Telling a personal kind of anecdote here, in my first year as a dietitian, I remember seeing a client who found out about that kind of loop and then also found out about, he was told by a doctor that if he had higher insulin levels, he would have a tougher time losing weight.
He required relatively high dosages of insulin. was on, he was, he had type two diabetes, but required quite high levels of insulin. So what he did was he just basically stopped injecting and he had very high blood glucose levels. Like they were in the 18 plus type of range and he was just under injecting insulin because of this. it’s like, well, having really high blood glucose levels is very clearly doing harm as well. I think the move is inject the appropriate amount of insulin if you were injecting insulin and then also try to decrease insulin resistance over time and otherwise, for example, getting leaner different dietary choices, different exercise, so on and so forth as well.
Leah:
Yeah, I think that’s a good anecdote highlighting the importance of I guess, practitioners explaining things correctly and not fear-mongering certain things, because that could have been so dangerous. Talking a little bit more about insulin resistance and the things that contribute to insulin resistance, we have things like a calorie surplus over time, but specifically where you are gaining body fat, especially around the abdomen, around your organs, and that leading to more insulin resistance over time. Also, being inactive.
So this is relevant because muscle is the biggest site of insulin-stimulated glucose uptake and also because activity burns through glucose as well. Then we have chronic inflammation. So in general, being chronically inflamed can impair insulin signaling. Sleep deprivation and stress can be another big one. And one example is the increase in cortisol, which specifically reduces insulin sensitivity. And then genetics. So some people are just more prone to insulin resistance than others just based on genetic profile.
Aidan:
Now we’re going to go deep into body composition stuff. I’m going to start from the fat loss slash fat gain side of things. And the impact on fat gain is pretty complex. So if somebody is very insulin resistant, like I spoke about, it can contribute potentially to disproportionately storing calories as body fat. This is partly because insulin resistance is tissue specific and muscles are often resistant before fat becomes resistant, not muscles are often a little bit more resistant.
Kind of complex to understand or for me to understand how much of a difference that matters. But it does seem to make a difference. I don’t think it necessarily should change behavior for a few reasons because it’s like, if you are very insulin resistant, you want to be resolving that anyway. But one of the things that makes it complex is it very clearly doesn’t cause fat gain. You still need a surplus. It just increases the odds that a slightly higher percentage of calories can be stored as body fat if you’re in a surplus.
If you’re in a deficit, regardless of how insulin resistant you are, you’re likely to be losing a decent amount of body fat in the process. We also know that this does not matter outside of extremes, which is kind of why I’m being pretty cautious with how I’m talking about this, because some people could interpret this as being like, if insulin resistant, that’s going to disproportionately make you store body fat. The reason why I want to pump the brakes a little bit on that is we previously recorded a podcast looking at this quite closely from another angle where we were looking at the topic of should you cut before you bulk?
Where we were really exploring the concept of whether being leaner at the start of a muscle gain journey would improve the ratio of muscle versus fat gain. And a large reason the theory exists that being leaner at the start should help is based on a logic that you become more insulin resistant as you gain body fat. And as you become more insulin resistant, the ratio of muscle versus fat that you gain would get worse and worse. But when looking at evidence on this topic, that didn’t really seem to be the case. There didn’t seem to be evidence that that mattered in a trained population.
And in that kind of trained population, the only time it really seemed to fall apart and potentially make a difference were at extremes where the body fat levels were so high that it was less likely to about the insulin, more likely to be about other variables. For example, maybe it wasn’t as practical to train at the exact same levels and stuff like that, at quite high levels of body fat.
So while insulin is involved in fat storage, I wouldn’t focus on insulin resistance really being a relevant factor in this case outside of extremes. And in those extremes, it also doesn’t prevent fat loss. It just means that when you’re in a surplus, potentially a slightly higher percentage of calories will be going towards body fat. If you’re in a deficit, fat loss would still occur.
Leah:
The other angle that we could look at this from is that insulin is involved in muscle growth. And what is quite interesting here is it’s not uncommon for bodybuilders to use insulin injections like a performance enhancing drug to actually improve body composition outcomes. When combined with a high carb intake and a high protein intake, it does help to push glucose and amino acids into the muscle cells, assisting with muscle growth. And the goal is to improve nutrient partitioning. And if used well, it can actually be quite effective in producing more muscle mass over time.
Again, why a lot of bodybuilders would like to add it onto their stack. And ideally steps are also taken to limit fat growth. So, heaps that we could unpack there, but not really the point of this podcast. It really comes down to risk management for these people. So, it does put you at a greater risk of hypoglycemia when you’re using insulin that is technically not required. It’s intentionally above what is like a biologically normal dose. Otherwise it wouldn’t be worth doing. And it could potentially increase insulin resistance if done long term.
So, that’s something that may have to be managed as well. And if generally, if it’s not managed well, it can also, like I said, increase fat gain. So, the reason we’re mentioning this is because there are people who demonise insulin for body composition. But then on the flip side, we have professional bodybuilders that are using it to improve body composition. So, I just think it highlights the fact that if anyone is kind of saying insulin is bad for body composition, that that is an oversimplification and it’s not necessarily true.
Aidan:
When I was preparing for this podcast, I was starting to write some stuff about strategies that they could use to minimise fat gain, like from a nutrition perspective, other certain compounds that stack.
Leah:
Yeah. I was thinking in my brain, I was like, let’s not even go there.
Aidan:
We’re just saying that like, we’re just talking about the fact that we shouldn’t demonise it for body composition.
Leah:
I love how we both almost took the same tangent and was like, hold on, not this episode.
Aidan:
So, getting back onto what we should be talking about is we’re to be talking about the other health angles with insulin resistance as well, or just insulin as well, sorry. So, being insulin resistant is linked with a lot of risks. It’s linked with blood pressure, high cholesterol, atherosclerosis, cognitive decline, certain cancers, PCOS, and a bunch more. We also have this whole metabolic syndrome kind of concept as well.
To an extent, there is potential that reducing carbs a bit and or the glycemic index a bit could help with these. For example, there’s even a chance that the slight reduction in circulating insulin reduces the resistance. Or alternatively, it could reduce the spikes in people with diabetes or pre-diabetes and reduce the risk of complications associated with them. But it’s also worth addressing anything else leading to insulin resistance if relevant, such as sleep, stress, overall body composition, micronutrients, activity levels, and anything else.
As much as I have mentioned that maybe reducing carbs a little bit could be relevant, going the alternative angle, many of the world’s longest lived populations have relatively high carbohydrate intakes proportionally as a percentage of their total calorie intake. But they also tend to have better insulin sensitivity due to these other reasons. So I want to kind of make it clear to them like, yes, the carbs are relevant. The glycemic index might also be relevant in certain cases as well. But, so are all of these other variables too.
Leah:
The final major topic that we do want to touch upon is appetite. So, if you go deep down the carbohydrate insulin model of obesity, there’s a pretty interesting history there. Initially, it was sort of simplified as insulin causes fat storage and limits fat breakdown. Therefore, we should reduce insulin. But with all of the research looking at matched calorie and protein intake, when there was even different insulin levels, we can pretty easily conclude that fat loss comes out the same regardless, where it kind of just destroys this entire concept.
And then following that, the goalposts kind of shifted a little bit. So it moved towards, well, if that’s not the case, then insulin makes you want to eat more calories and that’s the problem. And if that were the case, the calorie matched data and research that we were looking at becomes less relevant. So, this often does fall apart as well for a few different reasons. And one is that there have now been many studies where people have been able to eat ad-libitum in situations with noticeably different insulin levels, particularly looking at your low carb versus low fat studies. And the average fat loss does not come out significantly differently. So, that kind of makes that a little bit redundant as well.
And then another angle to consider is that if this concept was true, if this was the case, we should be able to see it in the reverse, but not really something that we see. And actually remember you Aidan saying once that you read, if you want to stimulate your appetite, you should have 15 to 30 grams of simple carbs like 30 to 60 minutes before a meal and that the logic behind this was that it’ll spike your insulin and then leave you like really, really hungry and ready to get into a meal and eat a lot of food.
And I did find that like an interesting concept because like mechanistically we’re like, yeah, I guess that could make a little bit of sense if that’s how it works. But it’s not something we’ve actually seen evidence for and even anecdotally. I mean, I don’t see it being effective and I think you probably would would agree with that.
Aidan:
Yeah, I tried it personally as well.
Leah:
Oh, did you really?
Aidan:
Yeah, it was during my mass-gaining phases. Yeah, and then I’ve never seen it anecdotally from anyone else either, really.
Leah:
Yeah, yeah, interesting. So overall, while insulin might play a role in appetite, it clearly isn’t hugely practical to use either way.
Aidan:
So this was a bit of a longer one and there is so much more we can cover. It’s very big topic, but this is all we will cover. A few things we’re going to we want to summarise on is that insulin is a very important hormone. A lot of people simplify it down to just insulin and they’re often ignoring, or at the very minimum, just not talking about other things. If you focus on one hormone, it does simplify things, but it also misses all of the complex interactions in the human body.
Even simply highlighting that insulin is just one of many relevant hormones is important because you can focus on insulin’s mechanisms and come to strong conclusions while also missing that the other hormones might be having a larger influence at the same time. For example, that glucagon example. And doubling down on that, like there could be times that insulin could be in somebody’s system and technically reducing fat breakdown and increasing storage.
Well, at the same time, glucagon could be playing the dominant role and causing more fat breakdown. So many more examples like that, even if you go outside of this glucose metabolism kind of concept. It’s impossible to cover everything, but hopefully at least some of this was relevant or interesting.
Leah:
This has been episode 211 of the Ideal Nutrition Podcast. If you haven’t yet left a rating or review, it’s always greatly appreciated that you do so, but otherwise, thanks for tuning in.