This is an unreasonable amount of kale :-). I'm going to need to figure out a better meal:kale ratio or use a different vegetable side.
Actually, you're right. They're minutes. I started sampling my blood glucose when I started eating. Let me go ahead and add annotations to some of those data points, especially the data points that correspond to the end of the meal.
Wilted kale and spinach both lose a crazy amount of volume. I wonder how that would affect the experiment. It would be much easier to eat a large volume. Just fry in a pan with a bit of salt and oil.
Also, does caffeine in soda (so often paired with this meal) speed digestion enough to make blood sugar spike? I always assumed that caffeine increases your metabolism, but I didn't consider that speeding digestion is worse for blood sugar.
The experiment with sautéed kale and spinach is worth a try. If it is made too soft though, it may not slow down digestion much.
I hypothesize that a mix of coarse vegetables, for example, one that includes broccoli, kale, red cabbage, and cauliflower, would slow down the digestion rate even more than 10 oz of kale. Replacing the kale with dino kale would make this mix even better.
I didn't drink soda with the meal, simply because I don't normally drink soda with this meal, but an experiment with a caffeinated beverage would be easy enough to do.
One of the things we're working on is quantifying how different things, such as caffeine intake, affect your metabolic rate. This is the subject of an upcoming blog post.
Have you tried using an equivalent amount of water and/or fiber supplements as a control? It seems reasonable to conclude that eating additional food would cause you to feel satiated for longer.
Re: the experiment being bothersome... yes, it was!
I sampled my blood glucose every ten minutes, which might have been unnecessarily frequent. Having to interrupt myself every ten minutes to do a pinprick prevented me from doing anything that required concentration. I basically found myself watching YouTube videos for two hours.
I've heard of people doing continuous blood glucose monitoring, but this may be a bit heavyweight. I really only have to do this a few times for a few different meals to get an idea of what is needed by my body.
This is at best incomplete, armchair science, and at worst dangerous. The founders are all entrepreneurs / engineers, which is to say they don't have a medical degree or any expertise in biochemistry, so their argument is on the whole just skewed to deliver the argument that suits them - which is, "can I stuff enough kale in my mouth to slow down the release of insulin, and therefore reduce blood glucose".
Here's a few other things that reducing insulin does:
1. Decreases amino acid uptake
2. Decreases potassium uptake
3. Reduces brain insulin signaling, reducing control of energy homeostatis.
Insulin, in isolation, isn't bad. It helps increase muscle and improves cognition. What is bad is the way it fluctuates in the body and the ability for the body to regulate glucose and insulin efficiently. It's perfectly normal for a healthy individual to have a blood glucose reading of 140-150 after a carb-heavy meal. The key is how long does it take for their glucose to reduce back down to healthy levels (70-100). If it's 2 hours or less, you're fine. If it's longer than that, now you've got issues. Even then, acute blood glucose levels can vary wildly from individual to individual, particularly if they're on a ketogenic diet low in carbs, and that may report actually higher than normal (because you're constantly looking to the body to make glucose instead of food, so basal levels must remain higher).
Fear not glucose and insulin. Fear insulin resistance and glucose intolerance.
So getting back to the title of the article, the more practical way of making Five Guys less fattening is not to surround a burger in a basket of kale in your stomach, but to either (A) not eat the burger in the first place or (B) improve your insulin resistance/glucose tolerance. All that the article's experiment would do (in reality) is reduce your desire to eat a burger because your stomach is filled with kale - slow or fast, your body still had to break down and consume that burger. But if you exercise, eat right most of the time, and keep your vices in moderation, your improved lipid profile, fasting insulin, fasting glucose (and A1C), and insulin resistance/glucose tolerance will allow you to more efficiently process that burger so it is not as taxing on your body as it would be if you were not as healthy.
Thanks for your comment, Aaron. I will address your points in order.
You start by questioning the background and motives of my colleagues. While I have thoughts on how to respond to this, I choose to stick to discussing the facts.
Then you represent the goal of my experiment in the following way: “can I stuff enough kale in my mouth to slow down the release of insulin, and therefore reduce glucose.” This is not accurate. My goal was to see if I could influence my digestive system to release glucose into the blood more gradually so as to minimize insulin signaling to fat cells. More explicitly, the amount of glucose is about the same in the two meals; it was the amount of insulin signaling by my body that changed.
I will add additional detail that I do not mention in my blog post. Cells that have high need for glucose do not need much insulin signaling. In response to their need, they already have placed more glucose transporters on their cell membrane. Gratuitous insulin signaling causes fat cells to absorb glucose that could have been absorbed by a high-need muscle cell.
Then you say, “Here’s a few other things that reducing insulin does....” From your wording, particularly in your use of “other,” you seem to agree that less insulin signaling means less fat cell growth and that your concern is primarily with its “side effects.” I will address amino acids and potassium in a later post. For now, I will address your point about brain signaling.
Actually, too much insulin signaling interferes with leptin signaling, making you respond less to leptin signaling. Leptin is the satiety hormone that is released by your fat cells. The neurons in your hypothalamus that have receptors for insulin also have receptors for leptin, and unfortunately for us, they have commonalities in their signal transduction pathways. So a lot of insulin signaling interferes with leptin signaling. This makes leptin signaling less effective and makes you want to eat more in spite of having enough body fat. (See the paper, “The First Law of Thermodynamics Revisited” by Robert Lustig of UCSF.)
You state firmly, “Fear not glucose and insulin. Fear insulin resistance and glucose intolerance.” You do not state however how you would advise someone to avoid insulin resistance and glucose intolerance. My view is that slowing down the digestion rate of your meals, such as I have done here, is part of the strategy for doing so.
Unfortunately, I have to run now, but I will address your remaining points later. I am also happy to write another blog post with ample references to primary research literature.
Re: your comment on HbA1c, I will just leave this paper here and comment later.
"A Simple Meal Plan of 'Eating Vegetable Before Carbohydrate' Was More Effective For Achieving Glycemic Control than an Exchange-based Meal Plan in Japanese Patients with Type 2 Diabetes"
Statement: “... slow or fast, your body still had to break down and consume that burger.”
Response: You are saying that the digestion rate of the burger doesn’t matter, because the entire burger is still processed by the body. But the way your body processes the burger is different depending on the digestion rate.
A couple of things can happen after a given amount of glucose enters the digestive system.
Consider when the digestive system releases the glucose into the blood rapidly, much more rapidly than cells are able to absorb it. The pancreas releases a lot of insulin. Muscle and fat cells both significantly increase their blood glucose absorption rate.
Alternatively, consider when the digestive system releases the glucose into the blood gradually. Cells are able to absorb more of the blood glucose as it is coming in, so blood glucose levels do not rise as much. There is some insulin signaling, but there is less of it. High-need muscle cells already have increased their blood glucose absorption rate due to increased energy requirements, while insulin signaling to fat cells is minimized.
In the alternate scenario, high-need cells muscle cells, while fat cell growth is limited.
Statement: "not eat the burger in the first place."
Cutting out something I like is not a sustainable way to eat healthily. Food intake is not just regulated by energy homeostasis; the reward system, e.g. the mesolimbic pathway, is also potent.
Statement: "improve your insulin resistance/glucose tolerance"
Agreed.
There are two ways to avoid excessive insulin signaling. One, you can decrease the rate at which glucose enters the blood. Two, you can increase the rate at which glucose leaves the blood. My article talks about one, and you seem to be an advocate for increasing insulin sensitivity, which is advocating for two. I think most people should do both.
This experiment is quite flawed, at best. At the minimum:
- Oversimplified models of biochemistry (way, way more complex than insulin = fat)
- Sample size of 2 trials (leaving one result)
- No measure of insulin (not a one-to-one relation to blood glucose, also released in complex cycles)
- No control of meal time (blood glucose varies)
- No control of meal contents (assuming both meals are equal in content)
- No control of fasting time (blood glucose varies)
I have had to treat diabetes in cats so I got quite proficient with measuring blood glucose levels. Even when you control every single factor as much as possible (animal eats the same amount, at the same time, every day), blood glucose varies wildly. Non-diabetics have the same massive variance, as I have done blood glucose curves to myself and to others.
This experiment is unfortunately pretty much useless. The body is a very complex organic machine with lots of parts that evolved independently of each other. There aren't neat little one-to-one relationships that can be tested easily. It is full of genes that modify genes that modify genes that secrete hormones that modify pathways and brain patterns and so on.
"Oversimplified models of biochemistry" - when insulin binds to an insulin receptor on a fat cell, the fat cell activates LPL, translocates GLUT4 to the cell membrane, and inhibits HSL. What else am I missing?
"No measure of insulin" -- insulin is not as easy to measure using off-the-shelf devices. If one meal leads to higher blood glucose levels than another, especially if it is vastly higher, it is a reasonable working assumption that it elicits a greater insulin response.
"No control of meal time" -- both meals were dinners.
"No control of fasting time" -- I ate the same amount during the day prior to each meal. Activity levels were also similar.
Re: widely varying blood glucose levels, in my own experience, it is very rare to see a meal cause a blood glucose concentration reach 150 mg/dL. This is very, very high amongst my meals and only happens with meals like this.
The following meal would most certainly be nowhere near 150 mg/dL no matter the time of day: vegetables (kale, broccoli, cauliflower), black beans, sardines, and avocado.
16 comments
[ 1.8 ms ] story [ 42.6 ms ] threadThe graph says "Time (s)", but those can't be seconds. What's up?
So you did a dozen pinpricks to measure glucose? Does that start to get bothersome?
http://www.taylorfarms.com/products/organic-salads/baby-kale...
This is an unreasonable amount of kale :-). I'm going to need to figure out a better meal:kale ratio or use a different vegetable side.
Actually, you're right. They're minutes. I started sampling my blood glucose when I started eating. Let me go ahead and add annotations to some of those data points, especially the data points that correspond to the end of the meal.
Also, does caffeine in soda (so often paired with this meal) speed digestion enough to make blood sugar spike? I always assumed that caffeine increases your metabolism, but I didn't consider that speeding digestion is worse for blood sugar.
I hypothesize that a mix of coarse vegetables, for example, one that includes broccoli, kale, red cabbage, and cauliflower, would slow down the digestion rate even more than 10 oz of kale. Replacing the kale with dino kale would make this mix even better.
I didn't drink soda with the meal, simply because I don't normally drink soda with this meal, but an experiment with a caffeinated beverage would be easy enough to do.
One of the things we're working on is quantifying how different things, such as caffeine intake, affect your metabolic rate. This is the subject of an upcoming blog post.
I sampled my blood glucose every ten minutes, which might have been unnecessarily frequent. Having to interrupt myself every ten minutes to do a pinprick prevented me from doing anything that required concentration. I basically found myself watching YouTube videos for two hours.
I've heard of people doing continuous blood glucose monitoring, but this may be a bit heavyweight. I really only have to do this a few times for a few different meals to get an idea of what is needed by my body.
Here's a few other things that reducing insulin does:
1. Decreases amino acid uptake
2. Decreases potassium uptake
3. Reduces brain insulin signaling, reducing control of energy homeostatis.
Insulin, in isolation, isn't bad. It helps increase muscle and improves cognition. What is bad is the way it fluctuates in the body and the ability for the body to regulate glucose and insulin efficiently. It's perfectly normal for a healthy individual to have a blood glucose reading of 140-150 after a carb-heavy meal. The key is how long does it take for their glucose to reduce back down to healthy levels (70-100). If it's 2 hours or less, you're fine. If it's longer than that, now you've got issues. Even then, acute blood glucose levels can vary wildly from individual to individual, particularly if they're on a ketogenic diet low in carbs, and that may report actually higher than normal (because you're constantly looking to the body to make glucose instead of food, so basal levels must remain higher).
Fear not glucose and insulin. Fear insulin resistance and glucose intolerance.
So getting back to the title of the article, the more practical way of making Five Guys less fattening is not to surround a burger in a basket of kale in your stomach, but to either (A) not eat the burger in the first place or (B) improve your insulin resistance/glucose tolerance. All that the article's experiment would do (in reality) is reduce your desire to eat a burger because your stomach is filled with kale - slow or fast, your body still had to break down and consume that burger. But if you exercise, eat right most of the time, and keep your vices in moderation, your improved lipid profile, fasting insulin, fasting glucose (and A1C), and insulin resistance/glucose tolerance will allow you to more efficiently process that burger so it is not as taxing on your body as it would be if you were not as healthy.
You start by questioning the background and motives of my colleagues. While I have thoughts on how to respond to this, I choose to stick to discussing the facts.
Then you represent the goal of my experiment in the following way: “can I stuff enough kale in my mouth to slow down the release of insulin, and therefore reduce glucose.” This is not accurate. My goal was to see if I could influence my digestive system to release glucose into the blood more gradually so as to minimize insulin signaling to fat cells. More explicitly, the amount of glucose is about the same in the two meals; it was the amount of insulin signaling by my body that changed.
I will add additional detail that I do not mention in my blog post. Cells that have high need for glucose do not need much insulin signaling. In response to their need, they already have placed more glucose transporters on their cell membrane. Gratuitous insulin signaling causes fat cells to absorb glucose that could have been absorbed by a high-need muscle cell.
Then you say, “Here’s a few other things that reducing insulin does....” From your wording, particularly in your use of “other,” you seem to agree that less insulin signaling means less fat cell growth and that your concern is primarily with its “side effects.” I will address amino acids and potassium in a later post. For now, I will address your point about brain signaling.
Actually, too much insulin signaling interferes with leptin signaling, making you respond less to leptin signaling. Leptin is the satiety hormone that is released by your fat cells. The neurons in your hypothalamus that have receptors for insulin also have receptors for leptin, and unfortunately for us, they have commonalities in their signal transduction pathways. So a lot of insulin signaling interferes with leptin signaling. This makes leptin signaling less effective and makes you want to eat more in spite of having enough body fat. (See the paper, “The First Law of Thermodynamics Revisited” by Robert Lustig of UCSF.)
You state firmly, “Fear not glucose and insulin. Fear insulin resistance and glucose intolerance.” You do not state however how you would advise someone to avoid insulin resistance and glucose intolerance. My view is that slowing down the digestion rate of your meals, such as I have done here, is part of the strategy for doing so.
Unfortunately, I have to run now, but I will address your remaining points later. I am also happy to write another blog post with ample references to primary research literature.
"A Simple Meal Plan of 'Eating Vegetable Before Carbohydrate' Was More Effective For Achieving Glycemic Control than an Exchange-based Meal Plan in Japanese Patients with Type 2 Diabetes"
http://search.informit.com.au/documentSummary;dn=12049472055...
Response: You are saying that the digestion rate of the burger doesn’t matter, because the entire burger is still processed by the body. But the way your body processes the burger is different depending on the digestion rate.
A couple of things can happen after a given amount of glucose enters the digestive system.
Consider when the digestive system releases the glucose into the blood rapidly, much more rapidly than cells are able to absorb it. The pancreas releases a lot of insulin. Muscle and fat cells both significantly increase their blood glucose absorption rate.
Alternatively, consider when the digestive system releases the glucose into the blood gradually. Cells are able to absorb more of the blood glucose as it is coming in, so blood glucose levels do not rise as much. There is some insulin signaling, but there is less of it. High-need muscle cells already have increased their blood glucose absorption rate due to increased energy requirements, while insulin signaling to fat cells is minimized.
In the alternate scenario, high-need cells muscle cells, while fat cell growth is limited.
Statement: "not eat the burger in the first place."
Cutting out something I like is not a sustainable way to eat healthily. Food intake is not just regulated by energy homeostasis; the reward system, e.g. the mesolimbic pathway, is also potent.
Statement: "improve your insulin resistance/glucose tolerance"
Agreed.
There are two ways to avoid excessive insulin signaling. One, you can decrease the rate at which glucose enters the blood. Two, you can increase the rate at which glucose leaves the blood. My article talks about one, and you seem to be an advocate for increasing insulin sensitivity, which is advocating for two. I think most people should do both.
- Oversimplified models of biochemistry (way, way more complex than insulin = fat) - Sample size of 2 trials (leaving one result) - No measure of insulin (not a one-to-one relation to blood glucose, also released in complex cycles) - No control of meal time (blood glucose varies) - No control of meal contents (assuming both meals are equal in content) - No control of fasting time (blood glucose varies)
I have had to treat diabetes in cats so I got quite proficient with measuring blood glucose levels. Even when you control every single factor as much as possible (animal eats the same amount, at the same time, every day), blood glucose varies wildly. Non-diabetics have the same massive variance, as I have done blood glucose curves to myself and to others.
This experiment is unfortunately pretty much useless. The body is a very complex organic machine with lots of parts that evolved independently of each other. There aren't neat little one-to-one relationships that can be tested easily. It is full of genes that modify genes that modify genes that secrete hormones that modify pathways and brain patterns and so on.
"Oversimplified models of biochemistry" - when insulin binds to an insulin receptor on a fat cell, the fat cell activates LPL, translocates GLUT4 to the cell membrane, and inhibits HSL. What else am I missing?
"No measure of insulin" -- insulin is not as easy to measure using off-the-shelf devices. If one meal leads to higher blood glucose levels than another, especially if it is vastly higher, it is a reasonable working assumption that it elicits a greater insulin response.
"No control of meal time" -- both meals were dinners.
"No control of fasting time" -- I ate the same amount during the day prior to each meal. Activity levels were also similar.
Re: widely varying blood glucose levels, in my own experience, it is very rare to see a meal cause a blood glucose concentration reach 150 mg/dL. This is very, very high amongst my meals and only happens with meals like this.
The following meal would most certainly be nowhere near 150 mg/dL no matter the time of day: vegetables (kale, broccoli, cauliflower), black beans, sardines, and avocado.