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James Krieger: "Insulin...An Undeserved Bad Reputation"

MR. BMJ

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An interesting 'ongoing' blog series by James Krieger. Brings up some good and interesting points in each entry. Here are 1-4, #5 is not up yet. Anyway, some good reading.


Insulin…an Undeserved Bad Reputation
by James Krieger MS, Nutrition; MS, Exercise Science


I feel sorry for insulin. Insulin has been bullied and beaten up. It has been cast as an evil hormone that should be shunned. However, insulin doesn’t deserve the treatment it has received.
Insulin: A Primer

Insulin is a hormone that regulates the levels of sugar in your blood. When you eat a meal, the carbohydrate in the meal is broken down into glucose (a sugar used as energy by your cells). The glucose enters your blood. Your pancreas senses the rising glucose and releases insulin. Insulin allows the glucose to enter your liver, muscle, and fat cells. Once your blood glucose starts to come back down, insulin levels come back down too. This cycle happens throughout the day. You eat a meal, glucose goes up, insulin goes up, glucose goes down, and insulin goes down. Insulin levels are typically lowest in the early morning since it’s usually been at least 8 hours after your last meal.

Insulin doesn’t just regulate blood sugar. It has other effects as well. For example, it stimulates your muscles to build new protein (a process called protein synthesis). It also inhibits lipolysis (the breakdown of fat) and stimulates lipogenesis (the creation of fat).

It is the latter effect by which insulin has gotten its bad reputation. Because carbohydrate stimulates your body to release insulin, it has caused some people to argue that a diet high in carbohydrate will cause you to gain fat. Their reasoning, in a nutshell, goes like this:

High Carbohydrate Diet -> High Insulin -> Increased Lipogenesis/Decreased Lipolysis -> Increased Body Fat -> Obesity

Using this same logic, they argue that a low carbohydrate diet is best for fat loss, because insulin levels are kept low. Their logic chain goes something like this:

Low Carbohydrate Diet -> Low Insulin -> Decreased Lipogenesis/Increased Lipolysis -> Decreased Body Fat

However, this logic is based on many myths. Let’s look at many of the myths surrounding insulin.




MYTH: A High Carbohydrate Diet Leads to Chronically High Insulin Levels

FACT:Insulin Is Only Elevated During the Time After a Meal In Healthy Individuals



One misconception regarding a high carbohydrate intake is that it will lead to chronically high insulin levels, meaning you will gain fat because lipogenesis will constantly exceed lipolysis (remember that fat gain can only occur if the rate of lipogenesis exceeds the rate of lipolysis). However, in healthy people, insulin only goes up in response to meals. This means that lipogenesis will only exceed lipolysis during the hours after a meal (known as the postprandial period). During times when you are fasting (such as extended times between meals, or when you are asleep), lipolysis will exceed lipogenesis (meaning you are burning fat). Over a 24-hour period, it will all balance out (assuming your are not consuming more calories than you are expending), meaning you do not gain weight. Here’s a graph showing how this works:


After meals, fat is deposited with the help of insulin. However, between meals and during sleep, fat is lost. Fat balance will be zero over a 24-hour period if energy intake matches energy expenditure.



This is just a rough chart that I made, but the green area represents the lipogenesis occuring in response to a meal. The blue area represents lipolysis occuring in response to fasting between meals and during sleep. Over a 24-hour period, these will be balanced assuming you are not consuming more calories than you expend. This is true even if carbohydrate intake is high. In fact, there are populations that consume high carbohydrate diets and do not have high obesity rates, such as the traditional diet of the Okinawans. Also, if energy intake is lower than energy expenditure, a high carbohydrate diet will result in weight loss just as any other diet.




MYTH: Carbohydrate Drives Insulin, Which Drives Fat Storage

FACT: Your Body Can Synthesize and Store Fat Even When Insulin Is Low


One of the biggest misconceptions regarding insulin is that it’s needed for fat storage. It isn’t. Your body has ways to store and retain fat even when insulin is low. For example, there is an enzyme in your fat cells called hormone-sensitive lipase (HSL). HSL helps break down fat. Insulin suppresses the activity of HSL, and thus suppresses the breakdown of fat. This has caused people to point fingers at carbohydrate for causing fat gain.

However, fat will also suppress HSL even when insulin levels are low. This means you will be unable to lose fat even when carbohydrate intake is low, if you are overeating on calories. If you ate no carbohydrate but 5,000 calories of fat, you would still be unable to lose fat even though insulin would not be elevated. This would be because the high fat intake would suppress HSL. This also means that, if you’re on a low carbohydrate diet, you still need to eat less calories than you expend to lose weight.

Now, some people might say, “Just try and consume 5000 calories of olive oil and see how far you get.” Well, 5000 calories of olive oil isn’t very palatable so of course I won’t get very far. I wouldn’t get very far consuming 5,000 calories of pure table sugar either.




MYTH: Insulin Makes You Hungry

FACT: Insulin Suppresses Appetite


It is a well known fact that insulin acutely suppresses appetite. This has been demonstrated in dozens and dozens of experiments. This will be important when we talk about the next misconception…




MYTH: Carbohydrate Is Singularly Responsible for Driving Insulin

FACT: Protein Is a Potent Stimulator of Insulin Too


This is probably the biggest misconception that is out there. Carbohydrates get a bad rap because of their effect on insulin, but protein stimulates insulin secretion as well. In fact, it can be just as potent of a stimulus for insulin as carbohydrate. One recent study compared the effects of two different meals on insulin. One meal contained 21 grams of protein and 125 grams of carbohydrate. The other meal contained 75 grams of protein and 75 grams of carbohydrate. Both meals contained 675 calories. Here is a chart of the insulin response:


Comparison of insulin response between low protein, high carb meal and high protein, low carb meal



Now here’s a chart of the blood sugar response:

Comparison of blood sugar response to low protein, high carb meal and high protein, low carb meal




You can see that, despite the fact that the blood sugar response was much higher in the meal with more carbohydrate, the insulin response wasn’t higher. In fact, the insulin response was somewhat higher after the high protein meal, although this wasn’t statistically significant.

Some people might argue that the “low-carb” condition wasn’t really low carb because it had 75 grams of carbohydrate. But that’s not the point. The point is that the high-carb condition had nearly TWICE as much carbohydrate, along with a HIGHER glucose response, yet insulin secretion was slightly LOWER. The protein was just as powerful at stimulating insulin as the carbohydrate.

I can also hear arguments coming like, “Yeah, but the insulin response is longer and more drawn out with protein.” That wasn’t true in this study either.


Insulin response to high protein and high carb meals




You can see in the chart that there was a trend for insulin to peak faster with the high protein condition, with a mean response of 45 uU/mL at 20 minutes after the meal, versus around 30 uU/mL in the high carb condition.

This tendency for a higher insulin response was associated with a tendency towards more appetite suppression. The subjects had a tendency towards less hunger and more fullness after the high protein meal:

Comparison of low protein, high carb and high protein, low carb meals and their effects on hunger and fullness




Here’s the results of another study that compared the effects of 4 different types of protein on the insulin response to a meal. This study was interesting because they made milkshakes out of the different proteins (tuna shakes???? YUCK!!!!! Of course some people may remember the tuna shake recipes from the misc.fitness.weights days). The shakes contained only 11 grams of carbohydrate, and 51 grams of protein. Here’s the insulin response to the different shakes:

Insulin Response to 4 Different Proteins




You can see that all of these proteins produced an insulin response, despite the fact that the carbohydrate in the shake was low. There was also different insulin responses between the proteins, with whey producing the highest insulin response.

Now, some might argue that the response is due to gluconeogenesis (a process by which your liver converts protein to glucose). The thought is that the protein will be converted to glucose, which will then raise insulin levels. As I mentioned earlier, people will claim that this will result in a much slower, more drawn-out insulin response, since it takes time for your liver to turn protein into glucose. However, that’s not the case, because the insulin response was rapid, peaking within 30 minutes and coming back down quickly at 60 minutes:

Insulin response to different types of protein




This rapid insulin response was not due to changes in blood glucose. In fact, whey protein, which caused the greatest insulin response, caused a drop in blood glucose:

Glucose response to different types of protein




The insulin response resulted in appetite suppression. In fact, the whey protein, which had the highest insulin response, caused the greatest suppression of appetite. Here’s a chart showing the calorie intake of the subjects when they ate lunch 4 hours after drinking the shake:

Calorie intake at a lunch consumed 4 hours after consuming various protein




The subjects ate nearly 150 calories less at lunch when they had whey protein, which also caused the greatest insulin response. In fact, there was an extremely strong inverse correlation between insulin and food intake (a correlation of -0.93).

Here’s data from another study that looked at the insulin response to a meal that contained 485 calories, 102 grams of protein, 18 grams of carbohydrate, and almost no fat:

Insulin response to a high protein, low carb meal in lean and obese people




You can see that the insulin response was exaggerated in the obese subjects, probably due to insulin resistance. Here’s a chart of the blood glucose response. You can see there was no relationship between the glucose response and insulin, which was similar to the study discussed earlier.

Blood glucose response in response to a high protein, low carb meal in lean and obese




The fact is that protein is a potent stimulator of insulin secretion, and this insulin secretion is not related to changes in blood sugar or gluconeogenesis from the protein. In fact, one study found beef to stimulate just as much insulin secretion as brown rice. The blood sugar response of 38 different foods could only explain 23% of the variability in insulin secretion in this study. Thus, there’s a lot more that’s behind insulin secretion than just carbohydrate.

So how can protein cause rapid rises in insulin, as shown in the whey protein study earlier? Amino acids (the building blocks of protein) can directly stimulate your pancreas to produce insulin, without having to be converted to glucose first. For example, the amino acid leucine directly stimulates pancreas cells to produce insulin, and there’s a direct dose-response relationship (i.e., the more leucine, the more insulin is produced).

Some might say, “Well, sure, protein causes insulin secretion, but this won’t suppress fat-burning because it also causes glucagon secretion, which counteracts insulin’s effects.” I mentioned earlier how insulin will suppress lipolysis. Well, some people think that glucagon increases lipolysis to cancel this out.

The thought that glucagon increases lipolysis is based on 3 things: the fact that human fat tissue has glucagon receptors, the fact that glucagon increases lipolysis in animals, and the fact that glucagon has been shown to increase lipolysis in human fat cells in vitro (in a cell culture). However, what happens in vitro isn’t necessarily what happens in vivo (in your body). We have a case here where newer data has overturned old thinking. Research using modern techniques has shown that glucagon does not increase lipolysis in humans. Other research using the same techniques has shown similar results. I will also note that this research failed to find any lipolytic effect in vitro.

It should be remembered why glucagon is released in response to protein in the first place. Since protein stimulates insulin secretion, it would cause a rapid drop in blood glucose if no carbohydrate is consumed with the protein. Glucagon prevents this rapid drop in blood sugar by stimulating the liver to produce glucose.




Insulin: Not Such a Villain After All

The fact is that insulin is not this terrible, fat-producing hormone that must be kept as low as possible. It is an important hormone for appetite and blood sugar regulation. In fact, if you truly wanted to keep insulin as low as possible, then you wouldn’t eat a high protein diet…you would eat a low protein, low carbohydrate, high fat diet. However, I don’t see anybody recommending that.

I’m sure some are having some cognitive dissonance reading this article right now. I know because I experienced the same disbelief years ago when I first discovered this paper and how protein caused large insulin responses. At the time, I had the same belief that others have…that insulin had to be kept under control and as low as possible, and that spikes in insulin were a bad thing. I had difficulty reconciling that study and my beliefs regarding insulin. However, as time went on, and as I read more research, I learned that my beliefs regarding insulin were simply wrong.

Now, you may be wondering why refined carbohydrates can be a problem. Many people think it’s due to the rapid spikes in insulin. However, it’s obviously not the insulin, because protein can cause rapid spikes in insulin as well. One problem with refined carbohydrate is a problem of energy density. With refined carbohydrate, it is easier to pack a lot of calories into a small package. Not only that, but foods with high energy density are often not as satiating as foods with low energy density. In fact, when it comes to high-carbohydrate foods, energy density is a strong predictor of a food’s ability to create satiety (i.e., low-energy density foods create more satiety). There are other issues with refined carbohydrate as well that are beyond the scope of this article.

The bottom line is that insulin doesn’t deserve the bad reputation it’s been given. It’s one of the main reasons why protein helps reduce hunger. You will get insulin spikes even on a low-carb, high-protein diet. Rather than worrying about insulin, you should worry about whatever diet works the best for you in regards to satiety and sustainability. As mentioned in last week’s issue of Weightology Weekly, individual responses to particular diets are highly variable and what works for one person will not necessarily work for another. I will be writing a post in the future on the need for individualized approaches to nutrition.
 

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Insulin: An Undeserved Bad Reputation, Part 2

In a previous issue of Weightology Weekly, I wrote about insulin and how it’s been unfairly demonized by many in the nutrition field. This demonization has been based on a number of misconceptions regarding insulin, its biological effects, and its secretion. I want to continue clarifying these misconceptions.


MYTH: Insulin Spikes are “Bad”

FACT: Insulin Spikes Serve a Normal & Important Physiological Function

In my previous article, I discussed how dietary protein can cause insulin spikes just like dietary carbohydrate, and these spikes are not related to gluconeogenesis from the protein (i.e., the protein being converted to sugar). I also showed how these spikes are partly responsible for the suppression of appetite that is caused by dietary protein (due to insulin’s effects on your brain to inhibit appetite).

I want to expand on the importance of rapid insulin spikes due to feeding, and how they are important in blood sugar regulation. To do this, we need to discuss the phases of insulin secretion. Insulin secretion from your pancreas comes in two phases. The first phase happens very quickly; your pancreas senses rising glucose, and insulin is released within 1-2 minutes of this rise in blood sugar. This rapid-phase response is the result of your pancreas releasing stored insulin. It is typically over within 10 minutes. This rapid-phase response has been found to be impaired in people with impaired glucose tolerance (people who have higher blood sugar responses to meals than normal, and higher fasting levels of blood sugar, but who are not diabetic). This rapid-phase response is completely absent in people with type 2 diabetes.

There is a second phase that continues as long as glucose is elevated. This release of insulin is achieved by the release of stored insulin, as well as the creation of new insulin (insulin is created from a precursor called proinsulin). When you infuse glucose into the blood of healthy people and type 2 diabetics, you get insulin responses that look like this:



Insulin Response to Intravenous Glucose Administration in Healthy People Versus Type 2 Diabetics


You can see that the diabetics completely lack the rapid phase response that is present in the healthy individuals.

There is a drug called exenatide (Byetta), which has been found to restore this rapid phase insulin response in diabetics:



Insulin responses of type2 diabetics and healthy individuals, who have been administered glucose intravenously. Circles represent the insulin response of the type 2 diabetics when given a placebo. Squares represent the insulin response of the diabetics when given exenatide. You can see that exenatide restores the rapid phase insulin response. Black circles represent the insulin response of healthy individuals.


This restoration of the rapid phase insulin response improves blood sugar regulation in diabetics:


Blood sugar response to a meal in type 2 diabetics. Circles represent subjects on a placebo. Dark triangles and circles represent subjects on exenatide. You can see that blood sugar remained steady in the subjects on exenatide, but gradually increased in the subjects on the placebo.


You can see in the above chart that blood sugar remained consistent in response to a meal in the subjects on exenatide, but it increased over time in the subjects on the placebo.

Many people like to blame obesity and weight gain on insulin, but exenatide, which restores insulin spikes in type 2 diabetics, causes weight loss:


Effects of exenatide (Byetta) on body weight


Part of this weight loss is due to an improvement in satiety. Exenatide is a drug that mimics the effects of a hormone called glucagon-like peptide-1 (GLP-1). GLP-1 is an intestinal insulin-stimulating hormone (known as an incretin). GLP-1 potentiates insulin secretion, enhances the synthesis of insulin, upregulates insulin gene expression, and inhibits glucagon (insulin’s opposing hormone) secretion. Yet Exenatide, which mimics GLP-1 and helps stimulate insulin secretion, causes weight loss.

The fact is that rapid insulin spikes in and of themselves are not a bad thing. Protein causes rapid insulin spikes, yet protein reduces appetite and helps with weight loss. GLP-1 and drugs like exenatide contribute to insulin spikes, yet they reduce appetite and cause weight loss. The problem is that people confuse insulin spikes and blood glucose spikes. It is well established that rapid rises and falls in blood glucose can contribute to hunger. Because rapid rises in blood glucose also cause rapid rises in insulin, people end up blaming insulin (and the effects of high glycemic carbohydrates on insulin) for the problem.

MYTH: Since diabetics who inject insulin gain weight, this means that insulin is the reason for weight gain in non-diabetics

FACT: Amylin is co-secreted with insulin in non-diabetics; amylin has appetite suppressant and lipolytic effects

I would like to thank Dr. Stephan Guyenet for this information. I had known about amylin but hadn’t looked into it in any great detail. Amylin is a hormone that is secreted by your pancreas at the same time as insulin. Amylin decreases appetite, and also stimulates lipolysis (the breakdown of fat into fatty acids).

Type 1 diabetics do not produce amylin, and amylin secretion is impaired in type 2 diabetics. Pramlintide, a drug that mimics the effects of amylin, has been found to produce weight loss in diabetics.

This information demonstrates that the effects of insulin injection in a diabetic cannot be compared to the effects of physiological changes in insulin in a non-diabetic, yet many people erroneously make this comparison as if they are similar.

MYTH: Lowering Insulin Will Improve Appetite Regulation

FACT: Insulin Is One of the Many Hormones Critical to Satiety

I already most addressed this myth in my previous article on insulin, showing how protein stimulated insulin secretion and helped reduce appetite, and also showing how insulin injection into the brain reduces appetite. I again want to thank Dr. Guyenet for this information, but when you knock out the insulin receptors of a mouse’s brain, the mouse will overeat and develop obesity.

MYTH: All of this information only applies to healthy people

FACT: The information applies to obesity and diabetes

On other forums, I saw people comment on my previous article and claim that the information I provided only applied to healthy people, and not diabetics or obese individuals. They continued to believe that treating diabetes and obese individuals was all about insulin control. Nothing could be further from the truth. Not only is this evident from information mentioned earlier in this article (such as how exenatide restores insulin spikes and improves blood sugar control and body weight in diabetics), but it is also evident from the fact that high protein diets have been found to help both diabetics and obese individuals, despite the fact that protein is a powerful stimulus of insulin secretion.

As I mentioned earlier, people seem to confuse blood glucose control and insulin control. It is the management of blood glucose itself that is partly responsible for the health benefits of low-glycemic carbohydrates, or reducing carbohydrates, or increasing protein intake, or consuming dietary fiber, or consuming fruits and vegetables, or consuming whole foods over processed foods. It is not the control of insulin; the control of insulin ends up being a byproduct of these other behaviors through improvements in insulin sensitivity (how responsive your cells are to insulin) and reductions in blood sugar swings.

Remember, insulin is not the bad guy. Click here to read part 3 of this series, where I discuss dairy products are extremely insulinemic, yet do not promote weight gain.


SOME Q&A AFTER THE ARTICLE:

This is fascinating.

One of the key hypotheses in Good Calories, Bad Calories (a book I know that you do not endorse in any way) is that insulin is related to many diseases that are part of so-called metabolic syndrome: diabetes, heart disease and cancer to name three big ones. Would you agree that eating refined carbohydrates is likely a (not necessarily “the”) cause of these diseases, but through, in your words, “insulin sensitivity (how responsive your cells are to insulin) and reductions in blood sugar swings.”?

If so, can you elaborate the mechanism of how eating refined carbohydrates and blood glucose control affects insulin sensitivity and how insulin sensitivity then contributes to these diseases?

Part 3 of this series will focus on insulin and blood sugar regulation, but I am trying to push you to link these issues to end points readers care about, like disease.
jAMES: Refined carbohydrate can result in reduced satiety due to the rapid drops in blood glucose that occur after the rapid rises. In turn, the overconsumption of energy intake that is not met by an increase in energy expenditure would result in deposition of fat. This fat, in turn, would result in a rise in NEFA’s in the blood, which would then lead to insulin resistance. Thus, in this model, the problem is still overconsumption of calories. This is supported by research showing that, when you control energy intake so that subjects are in energy balance, consumption of refined carbohydrate does not impair insulin sensitivity. So initial overfeeding that is not met by an increase in energy expenditure is causing the problem.

Now, the problem with the above model is that refined carbohydrate is rarely consumed by itself (this is also a problem with the model that many people believe, which is the rapid insulin spike caused by the refined carbohydrate causes the problem). Mixing in protein and fat moderates the glycemic response quite significantly. In fact, food such as candy bars, which contain a mixture of refined carbohydrate and fat, have low to moderate glycemic responses. Now, one might argue that the fructose component of the candy bars contributes to insulin resistance, but again, controlled studies where subjects are given high sucrose (which is half fructose) intakes in energy balance do not result in an increase in insulin resistance. Second, fructose intake would have to be EXTREMELY high for the fructose to be responsible. And even if the fructose is responsible, it would be an effect of fructose itself on insulin resistance, not high insulin levels. High insulin levels would be secondary to the insulin resistance.

A candy bar, however, is quite energy dense (i.e., it packs a lot of calories into a very small package). In fact, the combination of refined carbohydrate and fat are what allows for the large amount of calories in such a small package. The same holds true for many foods like this (cake, ice cream, etc; I would also note that many of these foods do not necessarily cause large insulin responses). It is well demonstrated that foods with high energy density (often the combination of refined carbohydrate and fat) lead to passive overconsumption. Combine that with the hedonic aspects of these types of foods, which override natural homeostatic mechanisms of regulating energy intake, as well as research showing that these foods don’t result in as great of TEF as whole foods, and you get overconsumption of food that will not be met by an increase in energy expenditure. You again get fat deposition, which leads to elevated NEFA’s and insulin resistance. The insulin resistance then leads to hyperinsulinemia. In fact, elevated NEFA’s are often one of the first signs of insulin resistance.

The fact is, it is very difficult to induce insulin resistance under conditions of energy balance by manipulating macronutrients, unless you have extreme diets and a massive imbalance of one particular nutrient (like fructose). Now, there are a percentage of people who drastically overconsume certain nutrients like fructose or sucrose (some of the clients in our clinic would come in drinking 10-20 cans of soda per day), and in these cases, these habits are likely contributing to insulin resistance directly. But when you look at survey data, many people don’t fall into these extremes.

I should also note that there are many people who do consume a lot of refined carbohydrate yet never have obesity or insulin resistance. They expend the energy through high activity and NEAT (not necessarily formal exercise). Thus, there is an interaction between nutrient intake and energy expenditure that affects the risk of developing insulin resistance, which is why sedentary behavior, the mechanization of our society, etc. cannot be ignored as a component.

The bottom line is that, the “high refined carbohydrate causes high insulin which causes obesity & disease” is overly simplistic and fails to explain numerous experimental and epidemiological observations.

I would also note that there’s a lot of data that large postprandial glucose fluctuations and postprandial hyperglycemia directly contribute to disease processes through increasing oxidation of tissues, inflammation, and endothelial dysfunction. There is quite a bit of evidence for this, which is why poorly controlled diabetics are at a higher risk of disease. Again, in this case, it is not insulin that is causing the disease. Disease is being caused by the fact that insulin isn’t working like it’s supposed to work.


To boil it down, overeating leads to insulin resistance through fat accumulation. Insulin resistance itself and the consumption of certain carbohydrates may contribute to disease through “increasing oxidation of tissues, inflammation, and endothelial dysfunction.” Is that right?

The Wikipedia article on insulin resistance links to this article on glucose receptors, suggesting that insulin directly downregulates these receptors.

Insulin down-regulates expression of the insulin-responsive glucose transporter (GLUT4) gene: effects on transcription and mRNA turnover.

Would you disagree that this type of direct downregulation is a major force in insulin resistance in humans?
JAMES: The problem with the study you reference is that it is an in vitro study, and is not necessarily relevant to what happens to humans in vivo. That said, I do agree that chronic hyperinsulinemia can exacerbate insulin resistance. However, we have to not confuse chronic hyperinsulinemia with high insulin levels caused by diet. They are not the same thing. Chronic hyperinsulinemia means insulin is elevated above normal 24 hours a day; even fasted levels are elevated. This is not the same thing as elevations in insulin caused by meals (even high-carb meals), which are characterized by swings in insulin.

For example, dairy products are extremely insulinemic…as much as white bread. Yet dairy products have been found to actually improve insulin sensitivity in animals, and there is no evidence that dairy increases risk of obesity or diabetes.

Chronic hyperinsulinemia starts with insulin resistance. Over time, this chronic hyperinsulinemia can then exacerbate insulin resistance so that you have a vicious cycle. But there is no evidence that eating insulinemic meals will cause insulin resistance.



“MYTH: Lowering Insulin Will Improve Appetite Regulation

FACT: Insulin Is One of the Many Hormones Critical to Satiety”

Furthermore, Freedman and colleagues (2001, Popular Diets: A Scientific Review) point out:

The role for insulin in the synthesis and storgage of fat has obscured its important effects in
the central nervous system, where it acts to prevent weight gain…

…genetic disruption of insulin signaling in the brain leads to increased food intake and obesity
in animals …demonstrating that intact insulin signaling in the central nervous system is required for normal body weight regulation

Increased insulin secretion has been suggested to protect against weight gain in humans…
Because insulin also stimulates Leptin production, which acts centrally to reduce energy intake
and increase energy expenditure, decreased insulin and Leptin production during the
consumption of high-fat diets could help contribute to the obesity promoting effects of dietary
fat”

Jamie Hale

James:
“The bottom line is that, the “high refined carbohydrate causes high insulin which causes obesity & disease” is overly simplistic and fails to explain numerous experimental and epidemiological observations.”

Definitely over simplified, common case of mistaken correlation with causation. As James points out many individuals who eat tons of so-called junk food maintain lean physiques and don’t suffer from insulin resistance. And on the other end, eating super clean can result in obesity- e.g. Sumo Wrestlers,- and increase the chances of IR


Great stuff Mr. Krieger you’re educating me to no end … a vicarious thanks to Dr. Guyenet as well.

Something i’ve been seeing for a while & can’t find the answer to (yet) : why doesn’t acylation stimulating protein make type 1 diabetics fat without injected insulin?

Hope this is a quick and easy answer for someone whose biochem is more recent than mine.

JAMES: This will be addressed when I write the 3rd part of this series. One of the big misconceptions of insulin is that it stimulates lipogenesis. While this is true, this effect is very weak. Insulin’s main function in the body is not stimulatory…instead it is inhibitory. Insulin acts as a brake on lipolysis, gluconeogenesis, proteolysis, and ketogenesis. Without insulin and this brake, these processes go forth unregulated at very high rates. Lipolysis and ketogenesis then proceed at extremely high rates, and ASP simply can’t make up for the runaway lipolysis and ketogenesis. You also have runaway gluconeogenesis and proteolysis. This is why a type 1 diabetic, without insulin, develops ketoacidosis along with hyperglycemia.

Insulin is like a stop-light or traffic cop. Without it, you get car wrecks.
 

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Insulin: An Undeserved Bad Reputation, Part 3…MOOOOO!!!!
By James Krieger


This article represents part 3 of a series on how insulin has been unfairly demonized by many in the nutrition field. If you have yet to read the first few parts, you can read Part 1 here, and you can read Part 2 here. In this article, I will discuss how dairy products are among the most insulinemic foods out there, yet do not promote fat or weight gain, which pokes holes in the hypothesis that carbohydrates drive fat accumulation through insulin secretion.


Dairy Products Are Insulinemic Yet Don’t Promote Weight Gain

One of the premises of individuals like Gary Taubes is that carbohydrates stimulate fat accumulation by stimulating insulin secretion. I’ve already shown how this premise is flawed in the last two parts of my series. Namely, I showed how protein also stimulates insulin secretion (sometimes as much as carbohydrate) yet does not promote weight or fat gain. I also showed how the drug exenatide restores rapid-phase insulin secretion in diabetics yet promotes weight loss.

If the carbohydrate/insulin hypothesis were true, then we would predict that foods that are extremely insulinemic would be uniquely fat promoting. What many people do not realize is that dairy foods are among the most insulinemic foods out there. In fact, they create much greater insulinemic responses than you would expect based on their carbohydrate content. Not only that, but lactose, the primary carbohydrate in dairy foods, is actually low glycemic and produces slow rises in blood sugar (lactose has a glycemic index of 46 compared to white bread which is 100). In fact, the glycemic index of many dairy products is quite low, with full-fat milk at 39, skim milk at 37, ice cream at 51, and fruit yogurt at 41.
Glycemic Index and Glycemic Load
Glycemic Index and Glycemic Load

Despite the low blood sugar responses, dairy products create very large insulin responses. For example, in one study, dairy products created similar or greater insulin responses than white bread, despite the fact that the blood sugar response for some of the dairy products was 60% lower than the white bread. In this study, the researchers compared the glycemic and insulinemic responses between white bread, a low gluten/lactose mixture, a high gluten/lactose mixture, cod with added lactose, milk, whey protein with added lactose, and cheese with added lactose. All of the conditions contained 25 grams of carbohydrate and 18.2 grams of protein, except for the white bread and low gluten/lactose mixtures, which contained 25 grams of carbohydrate and 2.8 grams of protein. Thus, lactose was the carbohydrate in all of the conditions except for white bread.
Glycemia and insulinemia in healthy subjects after lactose-equivalent meals of milk and other food proteins: the role of plasma amino acids and incretins -- Nilsson et al. 80 (5): 1246 -- American Journal of Clinical Nutrition

When you look at the insulin area-under-the-curve (AUC) for the various conditions, you can see that the dairy products actually created greater insulin responses than the white bread, despite having similar amounts of carbohydrate:


Insulin response of dairy foods compared to white bread


It is obvious that it is not the lactose that is responsible for the greater insulin response, because the gluten/lactose and cod/lactose mixtures resulted in similar or lower insulin responses to white bread.

The blood sugar response was also not responsible for the greater insulin response. In fact, the blood sugar response was lower in all of the conditions compared to the white bread, with the milk creating the lowest blood sugar response yet 3rd highest insulin response:



Blood glucose response to dairy foods compared to white bread


The insulinogenic index, which relates the amount of insulin secretion to the blood glucose response, was significantly higher in the dairy products, indicating that the dairy products stimulated much greater insulin secretion that you would expect based on the blood glucose response:


Insulinogenic index of dairy products compared to white bread


This is not the only study to show the insulinemic effects of dairy products. I showed in my previous article how whey protein, a dairy protein, created the highest insulin response compared to non-dairy proteins. In a study on type 2 diabetics, the inclusion of whey protein in a meal increased the insulin response by 31-57%, while the blood glucose response was reduced by up to 21%. In another study, the addition of 400 mL of milk to a bread meal increased the insulin response by 65%, despite the fact there was no change in the blood glucose response. In this same study, the addition of 200 or 400 mL of milk to a spaghetti meal increased the insulin response by 300%; again, there was no change in the blood glucose response. In fact, drinking milk with the spaghetti meal created an insulin response that was similar to white bread.
Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects -- Frid et al. 82 (1): 69 -- American Journal of Clinical Nutrition
Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects -- Frid et al. 82 (1): 69 -- American Journal of Clinical Nutrition
Milk as a supplement to mixed meals may elevate postprandial insulinaemia

Here’s the results of another study showing the glycemic and insulinemic indexes of milk compared to white bread:
Inconsistency between glycemic and insulinemic responses to regular and fermented milk products -- stman et al. 74 (1): 96 -- American Journal of Clinical Nutrition





Why Does Dairy Stimulate So Much Damn Insulin?

It is clear that dairy products stimulate large amounts of insulin secretion, as much or more than white bread. One of the reasons dairy products create large insulin responses is due to their amino acid content. In fact, the postprandial insulin response from dairy products correlates with the rise in branched chain amino acids leucine, valine, and isoleucine. I already pointed out in part 1 of this series how leucine will directly stimulate your pancreas to produce insulin.
Glycemia and insulinemia in healthy subjects after lactose-equivalent meals of milk and other food proteins: the role of plasma amino acids and incretins -- Nilsson et al. 80 (5): 1246 -- American Journal of Clinical Nutrition

Another reason that dairy products stimulate so much insulin secretion is their effects on a hormone called glucose-dependent insulinotropic polypeptide (GIP). Like GLP-1 which I wrote about in part 2 of this series, GIP is an incretin. This means that it is a hormone produced by your intestines that stimulates insulin secretion. Dairy products stimulate increased production of GIP. In the study I discussed earlier which compared whey, milk, and cheese to white bread, whey and cheese resulted in 21-67% greater GIP responses than white bread:


Glucose-dependent insulinotropic polypeptide (GIP) response to dairy foods compared to white bread


The above data illustrates one of the problems with the carbohydrate/insulin hypothesis…it assumes that carbohydrate is the primary stimulus of insulin secretion. However, it is clear that amino acids and incretins play significant roles in insulin secretion as well. And as I pointed out in part 1 of this series, the blood sugar response of a food only explains 23% of the variation in the insulin response. Thus, a lot more goes into insulin secretion than the blood sugar response from eating carbohydrate.


Dairy and Weight Gain/Loss

It is clear that dairy products are extremely insulinemic, moreso than many high carbohydrate foods. Thus, if the carbohydrate/insulin hypothesis were true, then we would predict that a diet high in dairy products should promote weight and fat gain. However, studies fail to show any relationship between dairy product intake and weight gain. For example, there is no relationship between intake of dairy products and BMI in Japanese women. In U.S. men, there is no relationship between an increase in dairy consumption and long-term weight gain. In perimenopausal women, high intakes of dairy products are actually inversely associated with weight gain (i.e, higher dairy product intakes are associated with less weight gain).
Elsevier
Calcium and dairy intakes in relation to long-term weight gain in US men -- Rajpathak et al. 83 (3): 559 -- American Journal of Clinical Nutrition
Association between dairy food consumption and weight change over 9 y in 19 352 perimenopausal women -- Rosell et al. 84 (6): 1481 -- American Journal of Clinical Nutrition

While these are observational studies, the results from controlled studies on animals and humans are similar. In fact, animal studies show less weight gain when they are fed dairy products. In mice, yogurt supplementation results in less weight and fat gain than controls on isocaloric diets. In another study, transgenic mice lost weight on energy restricted diets. The mice were then allowed to eat ad libitum (i.e., as much as they felt like). The mice fed dairy products regained less fat and weight during refeeding. In a third study, the intake of dairy products, but not a calcium supplement, decreased weight gain and body fat in mice fed a high-fat diet. In a fourth study, dairy protein attenuated fat gain in rodents fed a high-fat, high-sugar diet. In a fifth study, a dairy diet attenuated weekly weight gain in Sprague-Dawley rats.
Elsevier
Calcium and Dairy Products Inhibit Weight and Fat Regain during Ad Libitum Consumption Following Energy Restriction in Ap2-Agouti Transgenic Mice -- Sun and Zemel 134 (11): 3054 -- Journal of Nutrition
Dietary Calcium Source Influences Body Composition, Glucose Metabolism and Hormone Levels in a Mouse Model of Postmenopausal Obesity ? In Vivo
Obesity - Abstract of article: Dairy Protein Attenuates Weight Gain in Obese Rats Better Than Whey or Casein Alone
Mary Ann Liebert, Inc. - Journal of Medicinal Food - 0(0):

Of course, these are animal studies. What about humans? In one study, low-fat dairy products did not promote weight gain, while high-fat dairy products did. Hmmm, could it be that the weight gain in this study was simply caused by excess calories and not insulin? In another study, increased intake of dairy products did not affect body composition. In a third study, increased intake of dairy products did not impair weight loss. In a one-year study, increased intake of dairy products did not affect changes in fat mass. In a 6-month follow-up to this study, high dairy product intake predicted lower levels of fat mass. In a 9-month study, increased intake of dairy products did not affect weight maintenance, but the high dairy group exhibited evidence of greater fat oxidation.
The effect of low-fat versus whole-fat dairy product intake on blood pressure and weight in young normotensive adults - Alonso - 2009 - Journal of Human Nutrition and Dietetics - Wiley Online Library
Dairy products and metabolic effects in overweight... [Am J Clin Nutr. 2009] - PubMed result
Effect of energy-reduced diets high in dairy produ... [Obes Res. 2005] - PubMed result
Dairy products do not lead to alterations in body ... [Am J Clin Nutr. 2005] - PubMed result
Effect of 1-year dairy product intervention on fat... [Obesity (Silver Spring). 2006] - PubMed result
Effects of dairy intake on weight maintenance. [Nutr Metab (Lond). 2008] - PubMed result

Why Am I Not Fat?

My own personal experience with dairy fits right in with the science. I consume a lot of dairy and have for many years. I go through 2-3 gallons of milk per week. I also go through a lot of Greek yogurt, cottage cheese, regular cheese, and whey protein. I have some type of dairy with just about every meal. Thus, I have large amounts of insulin flowing through my body pretty much all day. If insulin was truly the fat-promoting, weight-gaining hormone that some have made it out to be, then I should be obese by now. Yet, I am not…not even close.

Not only that, but the people who think insulin makes you hungry, that would imply that I should be starving all of the time with all of the insulin that is flowing through my body all day. Yet, I’m not.


Got Milk? Got Insulin!

The evidence is overwhelming that dairy products do not promote weight gain, and they actually inhibit weight gain in animal studies. This is despite the fact that dairy products produce very large insulin responses, as much or greater than many high carbohydrate foods. Thus, it is clear from this article, as well as my previous articles, that the carbohydrate/insulin hypothesis is incorrect. Insulin is not the criminal in the obesity epidemic; instead, it is an innocent bystander that has been wrongly accused through guilt by association.

Read part 4 of my series, where I address the misconception of how insulin regulates blood sugar.


Q&A After the Article:

First let me thank you for sharing such excellent content. It is a genuine honor to stop by and read your work.

While I would still not make any sort of wild claims about promoting weight gain, per se, the fact that this series is on insulin did make me want to ask your general take on a somewhat related topic. With wide variation in individual sensitivities to various foods, and coupled with the often high stress nature of modern life (both beyond our control and oftentimes even more from self-imposed stress) is it possible that dysfunctional insulin signaling/responses are often the product of unwittingly eating foods that we (the collective “we,” that is) may be sensitive to and/or from having blood glucose elevated rather chronically due to inappropriate chronic elevation of cortisol (again, as opposed to it serving its proper physiological role on an acute basis)?

These sort of extenuating circumstances may potentially make what would otherwise be a relatively innocuous dietary choice into something that might be more problematic in that context, no? Or perhaps I am wildly off base here. Either way I will be more than happy to allow you to school me with your expertise, as I consider it a true honor to learn from people who blend the mental acuity and graciousness in sharing their knowledge as you do.
JAMES: Thank you for your comment and I’m glad you like my work!

There is some evidence that stress-induced cortisol secretion can induce insulin resistance, which, in turn, would then lead to appetite dysregulation. There is also evidence that some people are stress “hyperresponders” in terms of cortisol while others are not, and also that some people overeat in response to stress while others do not. I would highly agree with you that the high stress nature of modern life certainly is a contributor to the obesity epidemic, and there is sufficient scientific data to support that. There is also evidence that high fat/high sugar foods can truly operate as “comfort” foods which actually alleviate distress and pain. I hope to write about these things here in the future.



Krieger, you’ve done it again. You’ve completely thrown my head into a spin. Very nice and now I really understand more clearly the effect of carbs and diet. From what I gather, it’s not ingesting of carbs, but rather making sure I get the right amount of calories that are sustainable. Better carbs equals more satiety? More fats and better proteins to help the process? Very Nice! Thank you so much, because I am following a low carb diet but high amounts of protein and fats. My losses are due to calorie reduction and satiety, because I do feel full longer after a post workout shake of 45 g of Whey Protein. Thanks again old friend!
Jason

I really hope you’re angling all this work to be re-useable, angling toward ending up with something publish-able to compete against the pseudo science in the diet industry.

For a long time I’ve been favoring the more expensive and horrid-tasting casein products over whey products, reasoning that casein’s slower-release protein would be better for hunger control, and partly this had to do with insulin control, (whey releasing more insulin, so preference goest to casein).

This series on insulin is making me rethink my approach – the only argument left standing is the slower gastric emptying time for casein, and therefore the better hunger control of casein over whey.

Also, I never have protein powder alone. I use a blender to liquify spinach and toss the powder in that and also have some solid food – eggs or chicken or my new favourite, squid.

Where do you come down on this issue – is the increased gastric emptying time for casein significant, and is it significant FOR hunger control, or is there some kind of diminishing return – another hour in the stomach does not buy you much in terms of hunger control hormones after say the 2nd or 3rd hour?
JAMES: The research definitely supports slower gastric emptying times to help with appetite. In fact, there was a recent study published that compared casein to whey and satiety was superior in the casein condition.
 

MR. BMJ

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Insulin: An Undeserved Bad Reputation, Part 4: The Biggest Insulin Myth of Them All
By James Krieger


In part 1, part 2, and part 3 of this series, you learned how there are a lot of misconceptions on how insulin works in the body, and how it has been unfairly blamed for weight and fat gain in our society. In this article, I am going to dismantle one of the biggest insulin myths of them all…a myth that has been perpetuated in textbooks and is still taught in college classrooms, despite the fact it was shown to be wrong over 25 years ago.

Insulin Is Not Required for Cells To Take Up Glucose

Are you surprised by the heading above? Many people think that your cells need insulin to take sugar out of the blood. One of the pieces of evidence that is offered for this is the type I diabetic. When a type I diabetic has no insulin, blood sugar skyrockets. This is supposedly because sugar can’t get into cells.

However, the above scenario is not what happens in a type I diabetic that has been taken off of insulin. Sugar can get into the cells just fine. There’s actually something else going on. A review paper published in the Journal of Anasthesia thoroughly describes how insulin has been misunderstood in its role in blood sugar regulation, and I will summarize this paper here, along with some of my own comments.
Insulin: understanding its action in health and disease ? Br J Anaesth


A Man Ahead of His Time

In 1916, Sir Edward Schafer, a professor of physiology, published a book called The Endocrine Organs. In this book, he hypothesized the existence of what we now call insulin:

The results of pancreas extirpation and pancreas grafting are best explained by supposing that the islet tissue produce an Autacoid which passes into the blood stream and effects carbohydrate metabolism and carbohydrate storage in such a manner that there is no undue accumulation of glucose in the blood. Provisionally it will be convenient to refer to this hypothetical substance as insuline.
Insulin would go onto be discovered 8 years later. Schafer also hypothesized that insulin was created from an inactive precursor:

It must however be stated that it has yet to be determined whether the active substance is produced as such in the pancreas or whether it exists there as pro-insuline which becomes elsewhere converted into an active autacoid.

Pro-insulin was discovered nearly 50 years later. Schafer was truly a man ahead of his time.

Schafer avoided using the term “hormone” to describe insulin. Instead, he used the terms “autacoid” and “chalone.” An autacoid was a substance with excitatory action, meaning it stimulated things to happen in your body. An autacoid can be thought of as similar to the gas pedal in your car; you step on the pedal and it stimulates your car to go faster. A chalone was a substance with inhibitory action; it slows things down in your body. A chalone can be thought of as similar to the brake in your car. Schafer correctly hypothesized that insulin acted as both an autacoid and chalone in your body. He also considered that insulin acted as much more of a chalone than an autacoid in your body. In other words, he felt that insulin’s inhibitory functions were much more important than its excitatory or stimulatory functions. He would be proven correct many years later.


The Black Age of Endocrinology

However, before Schafer was proven correct, the “Black Age of Endocrinology” ensued. This was the time period between 1950 and 1980, where scientists extrapolated beyond their discoveries. They took in vitro animal data (research performed in a test tube or culture), and then assumed that the same thing happens in humans in vivo (inside the body). In fact, one of the reasons I am so highly critical of Gary Taubes and his Good Calories, Bad Calories book is that he relies heavily on research from this period, despite the fact that much of what was thought then has either been overturned by better research, or at least significantly altered. Taubes even stated around the 31 minute mark in this interview that he doesn’t pay attention to modern research because “all of this should have been obvious decades ago.” This is a surprising stance for a science writer; I would think that he would understand that conclusions in science are always tentative. This is particularly true in the nutritional and physiological sciences, where advances in measurement techniques have allowed us to measure and discover things that we could not measure before; this has overturned or modified many hypotheses and thoughts over the years. But I digress.
Good Calories, Bad Calories: The Mythology of Obesity, or The Mythology of Gary Taubes? » Weightology
http://www.thelivinlowcarbshow.com/...ncore-week-gary-taubes-interview-episode-213/
Knowledge Summit: Science Might be Wrong

The Black Age of Endocrinology is what led to the now mistaken belief that insulin is needed for your cells to take up glucose. Experiments in the 1950s showed that insulin could stimulate bits of rat muscle and fat to take up glucose. This data was extrapolated to humans, and it was then incorrectly hypothesized that a lack of insulin results in glucose not being able to get inside your cells, and thus blood glucose climbs to dangerous levels. This erroneous thinking has now been taught in textbooks and college classes all over the world for many years, resulting in dogma. Unfortunately, it is very difficult to overcome dogma, and even though this concept of insulin was shown to be wrong in the 1970′s, it still continues to be taught to this day.


Glucose Transport is Not Insulin Dependent

The erroneous hypothesis that insulin withdrawal results in high blood glucose because “glucose can’t get into cells” was based on the assumption that insulin is required for cells to take up glucose, rather than insulin merely enhancing glucose uptake. What the scientists in the 1950s failed to note was how tissues can take up considerable amounts of glucose even when insulin is absent.

Glucose enters your cells via a family of transporters. A primary transporter in muscle and fat cells is known as GLUT-4. Insulin stimulates GLUT-4 to move from the interior of a cell to the cell surface, where the glucose can then bind to the GLUT-4 transporter and enter the cell. However, there are plenty of glucose transporters on the cell surface, even when there is no insulin. In fact, there are enough transporters on the cell surface to allow the cell to get enough glucose to sustain its energy needs. Thus, glucose transport into cells is never truly dependent upon insulin. Insulin enhances the uptake of glucose into cells, but it is not required for it. In fact, when you knock out the insulin receptor in mice so that insulin cannot stimulate glucose uptake into muscle or fat cells (yet you keep the insulin receptor intact on other cells like brain and liver), the animals do not become diabetic and they have normal blood sugars.
Transgenic rescue of insulin receptor-deficient mi... [J Clin Invest. 2004] - PubMed result


What Really Happens in a Type I Diabetic

Metabolic tracer studies have allowed us to learn how insulin operates in humans in vivo. When you take a type I diabetic off insulin, blood glucose climbs sharply. However, it’s not because glucose can’t get into cells. In fact, glucose uptake into cells actually increases. This is because the concentration of glucose in the blood is so much higher than the cellular concentration that glucose must move into the cells (remember, there’s already enough glucose transporters on the cell surface even if there’s no insulin). So why does blood glucose climb so high? Remember that the amount of glucose in your blood is both a function of how much glucose is entering the blood (the rate of appearance), as well as how much glucose is leaving the blood (the rate of disappearance). In a fasted diabetic without insulin, all of the glucose is coming from the liver. Remember that your liver helps maintain blood sugar levels when you are fasted by releasing glucose; this glucose comes from both gluconeogenesis (the formation of glucose from non-carbohydrate sources, like protein) and glycogenolysis (the breakdown of glycogen stored in your liver). Insulin acts as a brake (a chalone as Dr. Schafer described it) on these processes. Thus, when you do not have insulin, you have runaway gluconeogenesis and glycogenolysis. The high blood sugar in an uncontrolled diabetic is thus caused by overproduction of glucose from the liver, not because glucose can’t get into cells.
Mechanism of action of insulin in diabetic patient... [Br Med J. 1978] - PubMed result

In fact, since insulin is not present, many processes go forth at high rates, completely unregulated. Insulin normally inhibits the production of ketones by your liver; without insulin to slow down ketone production, ketones are produced at high rates, resulting in diabetic ketoacidosis. This is why hyperglycemia and ketoacidosis occur simultaneously. Without insulin, you also have accelerated proteolysis (the breakdown of protein) and lipolysis (the breakdown of fat). The elevated amino acids in the blood provide further substrate for the liver to continue to produce large amounts of glucose. The elevated fatty acids provide substrate for the liver to continue to produce large amounts of ketones.

Thus, insulin is like a traffic cop or a stop light at an intersection. It helps slow down and control traffic. Without a stop light or traffic cop, cars go through the intersection uncontrolled and you get traffic accidents. Likewise, without insulin in the body, gluconeogenesis, glycolysis, proteolysis, ketogenesis, and lipolysis all proceed at high rates without anything to stop them. The end result is hyperglycemia, ketoacidosis, and eventually death.

When you inject insulin into an uncontrolled diabetic, you are now providing a brake on all of the processes mentioned earlier. You inhibit production of glucose by the liver, so blood sugar falls. Because there is no longer hyperglycemia, glucose uptake into cells actually decreases. Lipolysis is inhibited, so free fatty acid concentration falls to near zero. Because there are no longer free fatty acids to make ketones, ketone production slows down. Proteolysis is also inhibited.


Insulin…More of a Traffic Cop Than a Storage Hormone

Metabolic tracer studies have proven what Schafer had hypothesized nearly a century ago…that insulin’s main role in the body is inhibitory rather than excitatory. While insulin certainly does have excitatory functions, it is not primarily a “storage hormone” that many individuals claim that it is. Insulin is not needed for your cells to take up and store glucose. Certainly, it enhances uptake, but there is a big difference between enhancing uptake and being needed for uptake.

Of course, this research only tells us what happens when insulin is present versus when it is not present. What about the normal situation of a healthy person, who ingests a meal and sees a rise in blood glucose? What is happening to bring glucose back to normal? And what happens in a type II diabetic in this situation? I will cover these in part 5 of this ongoing series. Stay tuned…


REFERENCE: Sonksen, P., and Sonksen, J. Insulin: understanding its action in health and disease. British Journal of Anaesthesia. 85(1):69-79, 2000.


QUESTIONS AND ANSWERS AFTER THE ARTICLE:

Jamie Hale says:

“Taubes even stated around the 31 minute mark in this interview that he doesn’t pay attention to modern research because “all of this should have been obvious decades ago.” This is a surprising stance for a science writer;”

Sounds like a science writer who doesn’t understand science. Which is not an uncommon characteristic in popular science writers.

When you start to dig into the works of many science writers it becomes evident that they don’t realize that science data is tentative. You also find they may not understand the distinction of various types of scientific research- descriptive, correlational, and experimental. Then, taking it a step further they may not understand the concepts of internal validity and external validity.

Many science writers could do them says a big favor and invest some time in becoming educated in research methodology, philosophy of science and logic. However, these endeavors may result in writers’ lessening their sensational writing style.

Poster KD states:

Me thinks you are giving a very incomplete picture focusing solely on weight loss. Carbohydrate restriction significantly improves glycemic control in people with IGT/IFG/T2 even with out caloric restriction or weight loss. I am, however,waiting to pass judgment until In see part 5.
Poster Sam responds:

KD, in this context, you’ve posted a non-sequitur.

James is dispelling popular myths. What POPULAR myths are there about this?

Poster KD responds:

Actually, what he’s doing is presenting a very lawyer like argument against a very narrow set of “myths” of his own choosing. He is then furthermore setting the conditions of those myths to suit his own counter arguments. In effect, doing exactly what the insulin antagonists do, but in reverse.

JAMES: KD, I’ve done nothing of the sort. This series of posts is about insulin myths in relation to weight management, not whether carbohydrate restriction improves glycemic control. Your statement regarding carbohydrate restriction and glycemic control is a red herring.

To illustrate why your statement is a red herring, exercise improves glycemic control even without caloric restriction or weight loss, just like carbohydrate restriction. Since you failed to mention exercise, that would mean, using your same reasoning, that you are also presenting a very “lawyer-like argument against a narrow set of myths”.


Poster KD responds,

You were the one who broached the subject of glycemic control. The first sub heading of this article is ” Insulin Is Not Required for Cells To Take Up Glucose”. While technically correct, saying it merely “enhances” uptake is a gross understatement. It up-regulates glut4 fusion x 60. I originally stated that you were giving an incomplete picture. I stand by that statement.

JAMES:
KD,

Your statement is still a red herring. The stimulation of GLUT4 translocation is irrelevant to your statement regarding carbohydrate restriction and glycemic control (which was your original statement; you said nothing about GLUT4 translocation). Also, you are committing the very error that I discussed in this article…relying on in vitro data. The insulin-stimulated metabolic clearance rate in vivo is what we’re interested in, which I will discuss in the next part of this series.


Poster KD responds,

It sounds to me like you are asserting that glut4 fusion/translocation is irrelevant in vivo. If you have studies in human beings I would be most interested, and eagerly await your next article.
JAMES: No, that’s not what I’m saying; that would be a strawman. Glut-4 translocation is not irrelevant in vivo; it’s simply not required for glucose entry into cells, and it is not the reason a type I diabetic is hyperglycemic when insulin is not present.
 

MR. BMJ

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If a Mod or staff has time, if there is a way to update the "photobucket" pics without having to click on them as links, it helps with the flow of the articles.

If there is a way I can do this myself, please let me know how to do it, and i'll do so:)

I cannot figure out how to make the pictures show without having them as links:confused:

Thanks!


BMJ
 

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