(Posted in a different font colour cpl posts below)
Does Insulin Make Us Fat??
This article gives a brief overview of the main effects of insulin, the effects of different macro's on insulin, and ultimately whether it even matters when we are looking at losing bodyfat.
What is insulin?
Insulin is a hormone released from the beta cells of the pancreas in response to a rise in blood glucose or as a direct response from certain amino acids. Insulin is a storage hormone and has a main purpose of regulating the metabolism of glucose and other nutrients. It acts as both a ‘brake’ and an ‘accelerator’ on different physiological mechanisms. For instance as part of the ‘brakes’ it inhibits lipolysis (release of stored fat making it available to be used for energy), inhibits glycogenesis (the breakdown of glycogen into glucose by the liver) and inhibits proteolysis (the breakdown of amino acids). As part of the ‘accelerator’ it increases the rate of uptake of glucose and other nutrients in the blood into liver, muscle and fat cells (adipocytes), as well as increasing the rate of lipogenesis (fat storage). So basically when we release insulin we are in ‘anabolic’ mode (building up of tissues) and when insulin is low we are in a more ‘catabolic’ mode (breaking down of tissues, hopefully from adipose tissue rather than muscle tissue!!).
One misunderstood aspect is the notion that if insulin isn’t present, then our liver, muscle and fat cells are unable to take up glucose which isn’t the case. There are enough glucose transporters on the cells surface to transport glucose from the blood into cells even when insulin isn’t present. An example of this can be seen if a type 1 diabetic doesn’t supplement with insulin and becomes severely deficient in insulin. Glucose still enters cells, the problem that causes high blood glucose levels (hyperglycaemia) is that the ‘brakes’ aren’t on because insulin isn’t present, so the liver is continuously pumping out more glucose even though glucose levels are already high. Therefore the effect of insulin is to increase the rate of uptake rather than it being critical for the process to occur at all.
Insulin, Glycemic Index (GI) and Glycemic Load (GL)
For those unaware, the GI of a food is measured according to how much of an impact 50g of carbohydrate has on blood glucose levels compared to the standard which is most often glucose. Glucose therefore has a GI of 100 and if a food raises blood glucose levels 70% as much as glucose the GI for that food would be 70. There are many flaws to the GI of food, for example it bases all measures on consuming 50g of carbohydrate from that food when in day to day life a portion of that food may contain much less carbs. It also doesn’t take into account cooking methods, if the food is eaten hot or cold or what else the food is eaten with (we rarely consume carbs alone).
The GL gets around one of these problems as it takes into account portion size, for example carrots have a GI of 47 yet when we take into account portion size, an 80g portion has a GL of 3. This is true for most fruits and vegetables however a general rule is that a high GI will also correlate with a high GL.
So if we respond to increased blood glucose levels by releasing insulin then the higher the blood glucose response of a food the higher the insulin spike right? Well not exactly. The insulin index was brought out to try to answer this question although very little research has been done on it compared to the glycemic index. The insulin index measured the effects of 38 different foods (239kcal portion of each) on how much glucose was present in a persons blood as well as how much insulin was in the persons blood after a particular food (as well as the satiety of the foods). As we all have different insulin responses the data cant be considered the exact effect for everyone but it does give us a good idea of what we can expect. To discuss these effects lets look at the impact carbs, protein and fat has on insulin release.
Carbs & Insulin
Let’s use potato as an example. When you eat a potato the carbs are broken down into glucose which is then released into your blood stream, this is sensed by your pancreas which releases insulin in response to the raised blood glucose levels. The insulin helps to clear excess glucose (and other nutrients) in the blood into liver, muscle or fat cells. As blood glucose levels fall we stop releasing insulin and our levels normalise again to pre meal (in healthy people). Nothing new there for most people reading this. So some people take this idea and run (the wrong way) with it and use the logic that spiking insulin stops is burning fat so we should just avoid carbs therefore keep our insulin levels ‘stable’ and keep fat burning roling 24/7. Unfortunately these people don’t take into account the fact that they are still eating lots of protein……..
Protein & Insulin
The fact that adding protein to a meal containing carbs lowers the GI is well known by now. The problem is that in some cases people assume this also lowers the insulin response when in fact protein has a synergistic effect and actually raises the insulin response (meaning we release more insulin than eating the carbs without the protein). Another reason to avoid carbs you say. Well if we look at protein consumed alone without carbs you will find that, although blood glucose is not raised that much, the subsequent insulin release is actually greater than that of some popular carb choices. If we look back to the insulin index beef caused a greater amount of insulin to be released than white pasta and fish more so than popcorn. Whey is the most insulinemic protein type, with a general rule that the higher the quality of the protein, the greater the effect on insulin (predominantly due to the fact leucine seems to exert the greatest effect).
The release of insulin occurs due to the direct action of predominantly leucine, arginine and phenylalanine on the pancreas, and there appears to be a synergistic effect of some of the other aminos. It is a good thing as it helps our cells take up the amino acids. Glucagon is also released to prevent blood glucose levels dropping too low in the presence of insulin and the absence of glucose. Glucagon is released from the alpha cells of the pancreas to stimulate the liver to release glucose to into the blood when levels become low. If liver glycogen stores are not depleted the majority of glucose comes from the breakdown of glycogen. Stimulation of gluconeogenesis (synthesis of glucose from molecules that arent carbohydrates, eg amino acids and glycerol) in the liver can also produce glucose that can be released into the blood stream to increase blood glucose levels if glycogen stores are depleted. The glycogen stored in the muscle cells cannot be released back into the bloodstream to help normalise blood glucose levels.
Some people believe the release of glucagon counteracts the effects of insulin on lipolysis however this is not the case as glucagon has been shown to have no effect on lipolysis in living humans.
Fats and Insulin
Fats eaten alone have a negligible effect on insulin release. Consuming fats with carbs again will lower the GI but again isn’t the full story. Saturated fats tend to increase the insulin response and unsaturated fats tend to either lower the insulin response or have no effect. However don’t assume that insulin must be present for dietary fats to be stored in fat cells. Acylation stimulation protein levels can go up just fine without insulin present and has been described as the most potent stimulator of fat storage in the fat cell. Inhibition of hormone sensitive lipase when we eat fats can also occur without insulin present which again has similar effects as insulin on lypolysis.
So, does insulin ‘make us fat’?
No is the short answer. Although insulin levels are spiked after eating a meal and have this ‘bad’ quality of making us store more fat and stopping us using it for energy, whether we lose bodyfat comes down to our caloric intake (of course amounts of each macro matter but if we eat too much of them we are more likely to spend a greater amount of time in ‘anabolic mode’ vs ‘catabolic mode’ which invariably leads to gains in bodyfat).
So after we eat, insulin is released and it only takes small amounts of insulin to put a complete halt to fat burning, even in a fasting state insulin is still present and inhibits lipolysis by around 50%. However if we are hypocaloric due to eating less or being more active we will spend a greater amount of time burning stored nutrients (catabolic mode) than we will storing ingested nutrients (anabolic mode) such as between meals (after insulin returns to lower levels) and during sleep. So in a nutshell fat burning is only relevant when we look over a 24hr period or weekly period rather than just looking at the effects directly after a meal.
The above also applies to macros consumed at each meal. High levels of fats whilst insulin is spiked probably isn’t a great idea however high protein, high carb and high fat meals are rarely a staple of a trainers diet especially in a hypocaloric diet, but again what counts is what happens over the whole day rather than just at each meal. Neurotically separating all carbs and fats whilst consuming high protein in fear of increasing insulin levels is, as we’ve discussed, fighting a losing battle due to the insulin response of protein. This is not an article that advises everyone should eat protein, carbs and fat at each meal but rather the basis for splitting them shouldn’t be due to a fear of insulin. Diets containing a mix of macros in each meal during a hypocaloric diet versus minimising levels of carbs or fats has shown no significant effects on body fat losses. But these kind of studies are mainly conducted on untrained or obese people you cry, well this actually works in our favour in that we can expect to have far better glucose and insulin metabolisms than the untrained obese people.
This is by no means a conclusive article about insulin, rather it focuses on how insulin is not the enemy it’s often made out to be when we talk about fat loss.
By Neil Deighton
Does Insulin Make Us Fat??
This article gives a brief overview of the main effects of insulin, the effects of different macro's on insulin, and ultimately whether it even matters when we are looking at losing bodyfat.
What is insulin?
Insulin is a hormone released from the beta cells of the pancreas in response to a rise in blood glucose or as a direct response from certain amino acids. Insulin is a storage hormone and has a main purpose of regulating the metabolism of glucose and other nutrients. It acts as both a ‘brake’ and an ‘accelerator’ on different physiological mechanisms. For instance as part of the ‘brakes’ it inhibits lipolysis (release of stored fat making it available to be used for energy), inhibits glycogenesis (the breakdown of glycogen into glucose by the liver) and inhibits proteolysis (the breakdown of amino acids). As part of the ‘accelerator’ it increases the rate of uptake of glucose and other nutrients in the blood into liver, muscle and fat cells (adipocytes), as well as increasing the rate of lipogenesis (fat storage). So basically when we release insulin we are in ‘anabolic’ mode (building up of tissues) and when insulin is low we are in a more ‘catabolic’ mode (breaking down of tissues, hopefully from adipose tissue rather than muscle tissue!!).
One misunderstood aspect is the notion that if insulin isn’t present, then our liver, muscle and fat cells are unable to take up glucose which isn’t the case. There are enough glucose transporters on the cells surface to transport glucose from the blood into cells even when insulin isn’t present. An example of this can be seen if a type 1 diabetic doesn’t supplement with insulin and becomes severely deficient in insulin. Glucose still enters cells, the problem that causes high blood glucose levels (hyperglycaemia) is that the ‘brakes’ aren’t on because insulin isn’t present, so the liver is continuously pumping out more glucose even though glucose levels are already high. Therefore the effect of insulin is to increase the rate of uptake rather than it being critical for the process to occur at all.
Insulin, Glycemic Index (GI) and Glycemic Load (GL)
For those unaware, the GI of a food is measured according to how much of an impact 50g of carbohydrate has on blood glucose levels compared to the standard which is most often glucose. Glucose therefore has a GI of 100 and if a food raises blood glucose levels 70% as much as glucose the GI for that food would be 70. There are many flaws to the GI of food, for example it bases all measures on consuming 50g of carbohydrate from that food when in day to day life a portion of that food may contain much less carbs. It also doesn’t take into account cooking methods, if the food is eaten hot or cold or what else the food is eaten with (we rarely consume carbs alone).
The GL gets around one of these problems as it takes into account portion size, for example carrots have a GI of 47 yet when we take into account portion size, an 80g portion has a GL of 3. This is true for most fruits and vegetables however a general rule is that a high GI will also correlate with a high GL.
So if we respond to increased blood glucose levels by releasing insulin then the higher the blood glucose response of a food the higher the insulin spike right? Well not exactly. The insulin index was brought out to try to answer this question although very little research has been done on it compared to the glycemic index. The insulin index measured the effects of 38 different foods (239kcal portion of each) on how much glucose was present in a persons blood as well as how much insulin was in the persons blood after a particular food (as well as the satiety of the foods). As we all have different insulin responses the data cant be considered the exact effect for everyone but it does give us a good idea of what we can expect. To discuss these effects lets look at the impact carbs, protein and fat has on insulin release.
Carbs & Insulin
Let’s use potato as an example. When you eat a potato the carbs are broken down into glucose which is then released into your blood stream, this is sensed by your pancreas which releases insulin in response to the raised blood glucose levels. The insulin helps to clear excess glucose (and other nutrients) in the blood into liver, muscle or fat cells. As blood glucose levels fall we stop releasing insulin and our levels normalise again to pre meal (in healthy people). Nothing new there for most people reading this. So some people take this idea and run (the wrong way) with it and use the logic that spiking insulin stops is burning fat so we should just avoid carbs therefore keep our insulin levels ‘stable’ and keep fat burning roling 24/7. Unfortunately these people don’t take into account the fact that they are still eating lots of protein……..
Protein & Insulin
The fact that adding protein to a meal containing carbs lowers the GI is well known by now. The problem is that in some cases people assume this also lowers the insulin response when in fact protein has a synergistic effect and actually raises the insulin response (meaning we release more insulin than eating the carbs without the protein). Another reason to avoid carbs you say. Well if we look at protein consumed alone without carbs you will find that, although blood glucose is not raised that much, the subsequent insulin release is actually greater than that of some popular carb choices. If we look back to the insulin index beef caused a greater amount of insulin to be released than white pasta and fish more so than popcorn. Whey is the most insulinemic protein type, with a general rule that the higher the quality of the protein, the greater the effect on insulin (predominantly due to the fact leucine seems to exert the greatest effect).
The release of insulin occurs due to the direct action of predominantly leucine, arginine and phenylalanine on the pancreas, and there appears to be a synergistic effect of some of the other aminos. It is a good thing as it helps our cells take up the amino acids. Glucagon is also released to prevent blood glucose levels dropping too low in the presence of insulin and the absence of glucose. Glucagon is released from the alpha cells of the pancreas to stimulate the liver to release glucose to into the blood when levels become low. If liver glycogen stores are not depleted the majority of glucose comes from the breakdown of glycogen. Stimulation of gluconeogenesis (synthesis of glucose from molecules that arent carbohydrates, eg amino acids and glycerol) in the liver can also produce glucose that can be released into the blood stream to increase blood glucose levels if glycogen stores are depleted. The glycogen stored in the muscle cells cannot be released back into the bloodstream to help normalise blood glucose levels.
Some people believe the release of glucagon counteracts the effects of insulin on lipolysis however this is not the case as glucagon has been shown to have no effect on lipolysis in living humans.
Fats and Insulin
Fats eaten alone have a negligible effect on insulin release. Consuming fats with carbs again will lower the GI but again isn’t the full story. Saturated fats tend to increase the insulin response and unsaturated fats tend to either lower the insulin response or have no effect. However don’t assume that insulin must be present for dietary fats to be stored in fat cells. Acylation stimulation protein levels can go up just fine without insulin present and has been described as the most potent stimulator of fat storage in the fat cell. Inhibition of hormone sensitive lipase when we eat fats can also occur without insulin present which again has similar effects as insulin on lypolysis.
So, does insulin ‘make us fat’?
No is the short answer. Although insulin levels are spiked after eating a meal and have this ‘bad’ quality of making us store more fat and stopping us using it for energy, whether we lose bodyfat comes down to our caloric intake (of course amounts of each macro matter but if we eat too much of them we are more likely to spend a greater amount of time in ‘anabolic mode’ vs ‘catabolic mode’ which invariably leads to gains in bodyfat).
So after we eat, insulin is released and it only takes small amounts of insulin to put a complete halt to fat burning, even in a fasting state insulin is still present and inhibits lipolysis by around 50%. However if we are hypocaloric due to eating less or being more active we will spend a greater amount of time burning stored nutrients (catabolic mode) than we will storing ingested nutrients (anabolic mode) such as between meals (after insulin returns to lower levels) and during sleep. So in a nutshell fat burning is only relevant when we look over a 24hr period or weekly period rather than just looking at the effects directly after a meal.
The above also applies to macros consumed at each meal. High levels of fats whilst insulin is spiked probably isn’t a great idea however high protein, high carb and high fat meals are rarely a staple of a trainers diet especially in a hypocaloric diet, but again what counts is what happens over the whole day rather than just at each meal. Neurotically separating all carbs and fats whilst consuming high protein in fear of increasing insulin levels is, as we’ve discussed, fighting a losing battle due to the insulin response of protein. This is not an article that advises everyone should eat protein, carbs and fat at each meal but rather the basis for splitting them shouldn’t be due to a fear of insulin. Diets containing a mix of macros in each meal during a hypocaloric diet versus minimising levels of carbs or fats has shown no significant effects on body fat losses. But these kind of studies are mainly conducted on untrained or obese people you cry, well this actually works in our favour in that we can expect to have far better glucose and insulin metabolisms than the untrained obese people.
This is by no means a conclusive article about insulin, rather it focuses on how insulin is not the enemy it’s often made out to be when we talk about fat loss.
By Neil Deighton
