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 how dairy products are extremely insulinemic, yet do not promote weight gain.

  62 Responses to “Insulin: An Undeserved Bad Reputation, Part 2”

  1. 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.

      

    • Jerrmy,

      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.

        

      • Your points on the large postprandial insulin spike not being deleterious are reasonable. However, I am not so certain your cavalier treatment of fructose is correct.

        You said: “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.”

        Couldn’t it be possible, even likely, that the threshold for fructose induced insulin resistance is considerably lower than 10-20 cans per day? If it is say, 1 can of soda per day, taken daily over multiple years, then it could be the case that the large fructose and glucose spike is injurious to health.

        What comes to mind is non-enzymatic glycosylation and tipping the balance of dynamic equilibrium.

        If you consume refined carbs, i.e. sugar, then there will be a resultant higher than normal concentration of blood sugar. Sugars are reactive. They need to be cleared from the blood as fast as possible for that reason. This augments and strengthens your point about the two phase release of insulin from the pancreas by giving it a rational. The initial phase with it’s consequent massive insulin spike is the body trying to clear the highly reactive glucose from the blood stream.

        If the body can not clear the blood sugar then that give the sugars more time to create aberrant A.G.E.s.

        The body must have some mechanism to deal with the transient AGE products that occur during “regular operations”. What could be happening is that when you consume a huge sugar load and spike your blood sugar you are tipping the equilibrium and giving sugars an opportunity to bind to insulin receptors at a higher rate leading to disease because the body is not able to remove the newly bound sugar from the insulin receptor.

          

        • I don’t think the author endorsed drinking any amount of soda. But is it really likely that one can of soda a day for life would produce insulin resistance? You seem sure it will, but what evidence do you have?

          Insulin resistance is typically found in the overweight and pre-diabetic.
          Drinking 1 can of soda a day regularly may be a factor in some people being overweight, but it doesn’t directly cause insulin resistance.

            

        • There’s nothing worse than some moron who isn’t a scientist, trying to talk like a scientist. Shut the fuck up Derek.

            

          • Unless you personally know Derek, then you don’t know what his background is. He’s asking a perfectly reasonable question – why is that a problem? Or is the blog author only supposed to accept comments that conform to his world view and meet with your approval?

              

    • 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.

        

      • Thanks for the detailed explanation!

        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.

        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC45693/?tool=pmcentrez

        Would you disagree that this type of direct downregulation is a major force in insulin resistance in humans?

          

        • Jeremy,

          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.

            

          • What is causing insulin resistance according to yourself?

            Why is it that long-lived people have this one attribute alike:
            Low levels of insulin.

              

          • There are numerous causes of insulin resistance, including caloric surplus (of any kind), physical inactivity, psychological stress, etc.

            Why is it that long-lived people have this one attribute alike:
            Low levels of insulin.

            First, you need to define exactly what a “low level” of insulin is. Do you have evidence that insulin levels are associated with longevity?

            Second, insulin levels are a result of insulin sensitivity. Chronically high insulin levels are the result of insulin resistance, not the other way around.

              

  2. “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”

    jhale

      

    • Fact: Insulin Resistance goes hand in hand with Leptin resistance. Take a fat guy and give him a Leptin boost and he still eats more and gets hungry. So this does, in fact, only apply to healthy people.

        

  3. “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

      

  4. 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.

      

    • Sam,

      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.

        

  5. Wouldn’t it be funny if insulin is required to get Leptin into the hypothalamus, or other wrench in the “low-carb means low-insulin means no fat accumulation” theory?

    After all, isn’t glucose required for the adipocytes to make leptin in the first place?

    Mr. Hale quoting Freedman and colleagues
    >>…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

      

  6. “low-carb means low-insulin means no fat accumulation” theory”
    Don’t think this claim has reached status as scientific theory, but could be described as an unfounded hypothesis

      

    • >> could be described as an unfounded hypothesis

      Yes, I confuse the layman’s definition of theory with the scientist’s definition.

        

  7. This is an excellent series on insulin James- great work. Enjoying the other articles as well. I had the comment about the misuse of Occam’s Razor on Alan Aragon’s blog that you commented on. I find that the misinformation out there about insulin and carbohydrates that is touted by many low-carb dogmatists ties in nicely with the logical fallacies post as well.

    In my second comment here (scoll down about 1/3 of page):
    http://robbwolf.com/2010/03/02/the-paleolithic-solution-episode-17/
    I address the confirmation bias at work when a popular paleo blogger looked at the Okinawan diet and credited the positive results from a high-carb diet (which would usually run counter to paleo tenets) on the fact that yams were the primary carb source and not wheat/grains. I pointed out that if you look at the paper I linked to (the same one you linked to in part I of this series), you will find that the Okinawans seemingly violate many other tenets of the paleo approach:

    *They get most of their protein from soy and very little from animal meat, seafood, or eggs.
    *They prepare meats like pork by boiling them which removes most of the fat

    So I stated you could just as easily credit eating a soy-based, low-fat diet as being the key to health. I do not agree with that conclusion either, but it makes the point that looking to support your beliefs by cherry picking some of the data and ignoring the rest does not make a solid case at all.

    Looking forward to the rest of the series; keep up the good work!

      

    • Preston,

      Thanks for your comment. That was a great comment you made on the misuse of Occam’s Razor, and thanks for linking to your comments on Robb’s site.

      By the way, I love your statement here from Robb’s site: “I prefer the ‘construct a model and then look for data to DESTROY it’ method. “ This is so true. I try to do the same thing myself. I’m always asking the question, “Is this really true?”, and then look how the information can be potentially falsified. The process of falsification is a very important part of the scientific process and one people often don’t consider.

        

    • Some people have argued that Okinawans eat lots of pork, like this non-scientific site

      http://www.wonder-okinawa.jp/026/e/pork.html

      I am wary of anyone trying to definitively state the Okinawan diet without lots of evidence.

        

  8. “cherry picking some of the data and ignoring the rest does not make a solid case at all.”
    This is the norm in the exercise and nutrition industry

    It is difficult to breakdown a strong Ideological immune system:

    “Ideological immune system
    ‘In day-to-day life, as in science, we all resist fundamental paradigm change’ Jay Snelson (social scientist) calls this resistance an ideological immune system. According to Snelson, the more knowledge individuals have accumulated, and the more well-founded their theories have become the greater the confidence in their ideologies.

    Consequence we build up and “immunity” against new ideas that do not corroborate previous ones.

    Sometimes if we have so much vested interest (whether that be time or financial interests) it is hard to change our stance on a subject”
    http://jamiehalesblog.blogspot.com/2009/06/introduction-to-skeptical-thinking.html

    jhale

      

  9. Thanks James- Couldn’t agree more. Falsification is a key process practiced by far too few, especially in the nutrition/fitness world. I thought it was actually a poignant comment when Robb talked about building a model and then looking for data to support it because without knowing it he exposed one of the main problems with any approach not looking to falsify. They miss the holes in their schema because they are not looking for weaknesses, only strengths and support. Not to uniquely pick on him, he is actually far less guilty of it than many others, just a good single example.

    Jamie- I like the idea of the ideological immune system. I think the old saying- ‘You should keep an open mind, but not so open your brains fall out’ is a good way to remain receptive to new information but not jump on any trend or new claim that pops up.

      

  10. Mr. Krieger. Thank you for this. Could I ask you of your opinion on this article I saw some time back in Men’s Health? My BF is probably around 12% and I eat well, but I take in a pile of carbs (mix of high and low GI) after heavy weight training every 2nd day and I’m just afraid I’m going to burn out my pancreas eventually. There is a lot of Type 2 Diabetes in my family history as well.
    http://www.menshealth.com/men/health/other-diseases-ailments/the-deadly-truth-about-diabetes/article/d4bdb78301459110vgnvcm10000013281eac

    Thank you in advance.

      

    • Post-workout carbohydrates shouldn’t cause you any trouble in the long-run as you are extremely insulin sensitive after training. As long as you maintain a good diet, good activity, keep your body fat low, and your fasting blood sugar remains normal, then you should be fine.

        

  11. Great post. Seems like you have a little spelling mistake, or missing a word, in the last sentence though..

    “…where I discuss dairy products are extremely insulinemic, yet do not promote weight gain.”

      

  12. Fantastic, reminds me of the Malcolm Gladwell article from Martin Berkhan’s site

    http://www.leangains.com/2010/06/malcolm-gladwell-on-low-carb-diets.html

      

  13. Thank you for the articles; very interesting. Please help me understand one thing about the first two graphs in this section. They seem to indicate lower insulin levels in type 2 diabetics than in the control group of normal individuals. I was under the impression that type 2 diabetics actually tend to have higher insulin levels than normal individuals; their bodies simply don’t respond to it (insulin resistance). Am I misreading the graphs, or am I just wrong about type 2 diabetes? (Quite possible, and I won’t be offended if that’s the case!)

      

    • Greg,

      The graphs show the rate per unit time of insulin secretion by the pancreas. This is not the same thing as overall insulin levels in the blood (which are function of both secretion and removal).

        

      • So you are maintaining that any calories controlled diet will work equally well? So 2000 kcal is 2000kcal and it doesn’t matter what macros you eat for weightloss? I have to say this is counter to my experience. I ate 2,500 kcal a day, weighed and measured, food-pyramid recommendation and lost 10lbs in 6 months. I dropped my carb to 75-100g a day with no wheat and a single serving of berries and dropped 90lbs in 6 months. I think you have an axe to grind and are misrepresenting the facts. Why? I don’t know. I just know what you are saying is wrong.

          

        • So you are maintaining that any calories controlled diet will work equally well?

          This is a strawman. I never made such an assertion.

          I ate 2,500 kcal a day, weighed and measured, food-pyramid recommendation and lost 10lbs in 6 months. I dropped my carb to 75-100g a day with no wheat and a single serving of berries and dropped 90lbs in 6 months.

          Unless you are simultaneously measuring your energy expenditure using doubly labeled water, and your food intake is tightly controlled under research conditions, your personal anecdote can hardly be constituted as evidence.

          I think you have an axe to grind and are misrepresenting the facts. Why? I don’t know. I just know what you are saying is wrong.

          You know what I’m saying is wrong and I’m misrepresenting facts, yet you don’t have a shred of evidence to contradict anything I’ve said. All you have to offer is a personal rant. It sounds like you are the one who has an axe to grind here.

            

  14. Olanzapine (Zyprexa) causes insulin levels to increase dramatically. Healthy adults experience big weight gain as a side effect of Zyprexa. How do you explain this?

      

  15. Thank your for the great information. I wonder why you not allow to copy your article, as Id like to save them on my pc.

      

  16. In your article why do you use research that is focused on the acute response of insulin?

    It seems like a bit of sophistry on your part.

    What is relevant is the chronic level of insulin in the body and hunger, not an acute response.

      

    • Someone left the following over at Robb Wolf’s blog that more pointedly describes what I tried to say:

      “It seems to me that saying insulin has an ‘acute anorexigenic effect’ is like saying cocaine has an acute positive psychological effect. Technically true but missing the point.”

      I would take it a step further and say that you are intentionally misleading.

      I am greatly disappointed, because I was looking for a detractor of Taubes and Low Carb that seemed to have some legitimacy. I read what the low carb diet promoters had to say and wanted a second contrarian opinion before I made up my mind. First I found Carb Sanes’ blog, but she is just bat shit crazy. You seemed better, at least intelligent and rational in you analysis. But, if you are going to use misleading tactics embedded in your arguments it suddenly throws all of what you have to say into doubt.

        

    • Insulin in the above studies was measured before, during and after the meal.
      At what other time did you want to have it measured?
      The “chronic” level would be the fasted level after meals.

      Good luck in your quest to live without insulin!

        

  17. Do you mind if I quote a couple of your posts as long as I provide credit and sources back to your website? My blog is in the very same area of interest as yours and my users would genuinely benefit from a lot of the information you present here. Please let me know if this ok with you. Appreciate it!

      

  18. Hi, I definitely agree with you and laud the citations you make.

    It seems insulin is just doing important tasks just right and is not to be blamed for fat gain, and its high blood sugar that is bad.

    But here is the deal – even if high blood sugar is bad, the carbblame circle is still intact – it just doesnt have the insulin link in it now thanks to your articles.

    To be specific, from [ excessive carbs > sugars > insulin > lipogenesis ], we can go to [ excessive carbs > sugars > insulin > lipogenesis ].

    So that does lead to a low-carb solution for fat loss. Not 100% of Protein or Fat will turn into sugars, but 100% of carbs will turn into Sugars, to be stored as bodyfat.

    Am I understanding this correctly? I really hope you answer this for us. Thanks.

      

  19. Just started to read this. It is interesting, and I have not finished, so I have not made up my mind yet about this article.
    Yes, you are right: Gary has a CARB/insulin hypothesis NOT a PROTEIN/insulin hypothesis. You are right in blaming the carbs.

      

    • Sabine, Gary implicates insulin as the mechanism behind which carbs are supposedly fattening. But if this was true, any food that is insulinemic should be fattening. Yet we know this is not the case.

      On top of that, there are controlled studies using high carbohydrate diets (including high sugar intake) that show weight loss.

      The “carb/insulin” hypothesis is a failed hypothesis. It fails on so many levels that it’s impossible to count. The fact that Taubes continues to promote such nonsense in the face of overwhelming evidence against him is quite telling.

        

  20. Thank you for this. I’ve always been underweight (hereditary), using carbs well without weight gain or inflammation. I understand you to be saying that it is the excess (whatever that means for you) of carb intake over energy expenditure that causes problems, not carbs themselves.
    This past summer I had a DCIS lesion removed and was warned to limit insulin spikes, as they can contribute to tumor recurrence. I “went paleo” and felt ok, but dropped too much weight. I also developed joint pain. So I slowly re-introduced carbs/sugars and it has helped. But my paleo endo tells me the carbs are causing the inflammation, ironically. I think it is estrogen loss (age 52, 6 mos since last period). He ordered blood tests to check CRP and insulin levels.
    Question: if CRP is up but insulin levels ok, does it mean it’s not dietary? Thank you so much?

      

    • Hi, Kay,

      I really don’t see how the carbs would be contributing to inflammation. There could be a myriad of reasons why CRP is up, and it may have nothing to do with your diet. I would not be surprised that menopause may be playing a role.

        

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