Insulin, An Undeserved Bad Reputation: The Finale

Last week I addressed some criticisms of this series that I had seen at various places on the internet.  This article represents some of my final thoughts on insulin and body weight regulation.

Are You a Cognitive Miser?

Consider this problem.  Jack is looking at Anne, but Anne is looking at George.  Jack is married, but George is not.  Is a married person looking at an unmarried person?

  1. Yes
  2. No
  3. Cannot be determined

This problem is from an article in Scientific American about dysrationalia, a concept that describes where intelligent people think irrationally.  The article also discusses a concept known as cognitive miserliness, which refers to people's tendencies to take short cuts in their thinking.  These short cuts can then often lead to incorrect conclusions since the conclusions are based on incomplete information.  In fact, cognitive miserliness can often lead to the phenomena of dysrationalia described in the article.

Have you determined your answer for the above problem yet?  About 80% of people will choose the third option ("Cannot be determined").  However, that is not the correct answer.  The correct answer is the first option ("Yes").  The puzzle doesn't say whether Anne is married or not; either she is, or she isn't.  If Anne is married, she's looking at George, so the answer is "yes".  If Anne is not married, Jack is still looking at her, so the answer is still "yes".  Most people get this problem wrong because they don't take the time to go through all of the possibilities.  Instead, they choose the easiest inference.

The Carbohydrate/Insulin Hypothesis: An Example of Cognitive Miserliness

The "carbohydrates drive insulin which drives fat storage" mantra is a perfect example of cognitive miserliness.  It is a concept that is based on incomplete information regarding insulin, carbohydrate, and body weight regulation.  Many people are drawn to this hypothesis because of its simplicity.  However, its simplicity is exactly what makes it incorrect, because it does not address all the available data.  It is a shortcut in thinking, based on a narrow view of insulin's effects on lipolysis and glucose.

One of the big problems with the carbohydrate/insulin hypothesis of obesity is that it does not address what happens over a 24 hour period.  I briefly alluded to this in the first part of this series, and will expand upon it here.

Let's take alcohol as an example.  Alcohol, when ingested, is known to suppress fat burning.  This is because the metabolism of alcohol takes precedence over the metabolism of protein, carbohydrate, and fat.  If one just looks at the suppression of fat burning, then one might predict that alcohol will cause weight and fat gain.

However, it is erroneous to make this prediction, because you need to address what happens over a 24 hour period, and what is happening in regards to overall energy balance.  One study looked at the effects of alcohol on fat storage.  The researchers compared two conditions.  In one condition, alcohol was consumed in addition to meals, so that the subjects were consuming more calories than they were expending.  In another condition, alcohol replaced some carbohydrate in the meals, so that the subjects remained in energy balance.

In both conditions, alcohol suppressed fat burning over the 6 hours that it was actively metabolized.  When the subjects consumed alcohol in addition to their meals, fat balance over the day was positive, meaning the subjects gained fat.  However, when the subjects consumed alcohol in place of some carbohydrate, there was no increase in fat balance over a 24-hour period.  Although the alcohol suppressed fat burning over the 6 hours that it was metabolized, fat burning increased over the remainder of the day.  This canceled out the suppressive effect of alcohol on fat burning.  The authors stated,

Short term studies that fail to account for later readjustments of macronutrient balance can be misleading.  We conclude that alcohol has a fat-sparing effect similar to that of carbohydrate and will only cause fat gain when consumed in excess of normal energy needs.

Just like with alcohol, one cannot simply look at the fact that carbohydrate ingestion will suppress fat burning during the time that carbohydrate is metabolized.  Unfortunately, proponents of the "carbohydrates drive insulin which drives fat storage" mantra do exactly that.  You have to consider the big picture and what is happening over a 24 hour period.

The other reasons why the carbohydrate/insulin hypothesis is an example of cognitive miserliness is due to all of the factors discussed in this series.  There are numerous scientific observations that are inconsistent with the hypothesis.  Also, the hypothesis, with its narrow focus on insulin, fails to address the myriad of other hormones and factors that are all interacting simultaneously to regulate body weight.

The Finale

The bottom line is that insulin does not deserve the bad reputation that it has been given, and the "carbohydrates drive insulin which drives fat storage" mantra is wrong.  To summarize:

  • Insulin suppresses appetite; it does not increase it
  • A high carbohydrate diet does not cause chronically high insulin levels
  • Protein is insulinemic, and in certain cases, can be just as insulinemic as carbohydrate
  • Contrary to popular belief, glucagon does not "cancel out" the suppression of lipolysis by insulin when protein is ingested
  • The insulinemic effects of protein are due to a direct stimulatory effect on the pancreas, and not because the protein is converted to glucose
  • The combination of protein and carbohydrate can produce greater insulin secretion than either one alone, yet high protein, moderate-to-high carbohydrate diets are very effective for weight loss
  • Very high carbohydrate diets have been demonstrated to produce weight loss when people are in an energy deficit
  • Dairy is extremely insulinemic, just as insulinemic as white bread, yet does not promote weight gain in the absence of an energy surplus.  This is supported by a very large number of studies, including animal studies, observational studies, and randomized controlled trials.
  • Insulin is not required for fat storage
  • Insulin levels are not predictive of weight gain or weight loss in the majority of prospective studies
  • Exenatide restores rapid phase insulin release in diabetics, yet causes weight loss
  • The effects of insulin injection cannot be compared to normal physiological insulin release, since amylin is co-secreted with insulin from the pancreas
  • Insulin mainly functions as an inhibitory hormone rather than a storage hormone, acting as a brake on many important physiologic processes
  • A type I diabetic without insulin becomes hyperglycemic because of overproduction of glucose by the liver, not because insulin can't get into cells
  • Insulin enhances the uptake of glucose into cells, but is not required for it
  • Insulin regulates blood sugar after a meal both by stopping the liver from producing glucose and enhancing glucose uptake into cells.
  • In a fasted state, insulin regulates blood sugar by controlling glucose production of the liver, not by affecting the uptake of glucose into cells
  • You cannot simply look at the temporary effects of insulin on lipolysis and glucose storage.  You have to address what is happening over a 24-hour period; body fat will not increase if there is no overall energy surplus.

Don't be a cognitive miser.  Insulin is not the bad guy.

55 Responses to “Insulin, An Undeserved Bad Reputation: The Finale

  • Thank you for taking the time to write these articles. I enjoyed learning that insulin reduces blood sugar mainly by inhibit glucose production in the liver when the blood glucose is high.

      

  • Jonatan Bording
    7 years ago

    “A type I diabetic without insulin becomes hyperglycemic because of overproduction of glucose by the liver, not because insulin can’t get into cells”

    I think i meant to write:
    “… not because glucose can’t get into cells”

      

    • Jonatan Bording
      7 years ago

      sorry. “I think YOU meant to write” of course.

        

  • Nice…. Looking forward to the paid subscription!

      

  • Thank you for the comments, everyone. Glad you find the articles of value

      

  • until reading this article, i had assumed since alcohol prevents fat oxidation so it would cause reduced fat loss. thks for clearing that up. also, the summary helps to collate everything u covered, which is grt because i’m still trying to absorb n understand all these information.

      

  • Great series. I love learning about this. I look forward to your upcoming posts, free or paid subscription (the latter will be worth it!)

      

  • Insulin suppresses appetite; it does not increase it

    This conclusion was based on a faulty inference from the isolated fact that central administration of insulin (i.e. direct injection into the brain) suppresses appetite. This, however, occurs only late in the action. In normal metabolism, insulin first enters the peripheral tissues, where it rapidly inhibits release of glucose and fatty acids in the liver, muscles, fat cells, etc. and facilitates glucose uptake to the cells. The resulting transient hypoglycemia undeniably increases appetite and helps initiate eating. Eventually insulin does reach the brain’s appetite centers where it suppresses appetite. But this occurs well into the meal. This has been proven again and again, from Le Magnen to the present, both by peripheral additional references on my previous posts to support this, but you never responded to them.

    So insulin induces hypoglycemia, which induces hunger. You earlier denied this by saying the cause of the hunger was the hypoglycemia, not the insulin. But a cause does not have to be a proximate cause in order to still be a cause. If I light a fuse that explodes a bomb that sets off a fire, do we deny that the lighting the fuse caused the fire, just because the bomb explosion was the proximate cause?

      

    • This conclusion was based on a faulty inference from the isolated fact that central administration of insulin (i.e. direct injection into the brain) suppresses appetite.

      The direct demonstration of cause/effect is not a “faulty inference.” If one injects insulin centrally and it suppresses appetite, versus no suppression when only the vehicle is injected, then this is direct evidence that insulin suppresses appetite. When you add the evidence that knocking out insulin receptors in the brain results in hyperphagia, as well as the removal of insulin in type I diabetics results in hyperphagia, then you really cannot get better evidence that insulin is an appetite suppressant.

      This, however, occurs only late in the action.

      Do you have any evidence to support this assertion?

      In normal metabolism, insulin first enters the peripheral tissues, where it rapidly inhibits release of glucose and fatty acids in the liver, muscles, fat cells, etc. and facilitates glucose uptake to the cells.

      There is no evidence that insulin “enters” peripheral tissues first. Insulin is present throughout the entire bloodstream and will simultaneously affect a variety of tissues, including the brain.

      The resulting transient hypoglycemia undeniably increases appetite and helps initiate eating

      The scientific evidence does not support this statement. If this was true, then there would be a relationship between postprandial insulin secretion and subsequent energy intake (with greater secretion correlating with greater intake). However, as I cited here, there is no relationship between the two. In fact, higher insulin levels were associated with greater fullness. This research even showed a very weak relationship between the glycemic response and subsequent energy intake. The authors stated, “The current study does not support the contention that the postprandial glycemic response has an important effect on short-term appetite sensations.” This is also not to mention this research which demonstrated that some of the foods with the highest glycemic and insulinemic responses were among the most satiating of the foods tested.

      Eventually insulin does reach the brain’s appetite centers where it suppresses appetite. But this occurs well into the meal. This has been proven again and again, from Le Magnen to the present, both by peripheral additional references on my previous posts to support this, but you never responded to them

      First, I have not responded because I have not had the time to respond as of yet, and I noted to you that I would respond to your comments at a later date.

      Second, I browsed through your older comments and I do not see where you referenced Le Magnen. Please point out the comment. Second, I do not see where you have provided any evidence to support your assertion that insulin acts on the brain later. If I missed it, please point out the correct comment.

      So insulin induces hypoglycemia, which induces hunger. You earlier denied this by saying the cause of the hunger was the hypoglycemia, not the insulin.

      Because insulin injection in someone who is fasted is not relevant to physiological insulin secretion due to feeding.

        

      • James,

        Here is what you wrote:

        If one injects insulin centrally and it suppresses appetite, versus no suppression when only the vehicle is injected, then this is direct evidence that insulin suppresses appetite…There is no evidence that insulin “enters” peripheral tissues first. Insulin is present throughout the entire bloodstream and will simultaneously affect a variety of tissues, including the brain.

        Is that so? According to Woods (http://jcem.endojournals.org/cgi/reprint/93/11_Supplement_1/s37), there is a major difference between the action of insulin administered “systemically” (also called “peripherally”) and insulin administered “centrally” (i.e. directly into the brain). In discussing the appetite suppressive effect of insulin and leptin in the brain (which I do not deny ) Woods notes:

        A key question therefore is whether agonists for the leptin and/or insulin receptor would be viable targets for the pharmaceutical industry. One obstacle is that to be effective, any compound would have to gain access to key receptors in the brain, yet any such compound would most likely have to be administered systemically. Administering insulin systemically elicits hypoglycemia and other side effects, and hypoglycemia per se increases food intake, thus working against the therapeutic intent. Systemically administered insulin does result in reduced food intake when plasma glucose is prevented from decreasing in animal models, but this would be difficult to achieve therapeutically. Alternatively, there are reports that some formulations of nasally administered insulin elicit reduced food intake and body weight in humans without altering plasma glucose.

        This is exactly my point: the fact that insulin suppresses appetite when directly administered to the brain is not relevant to the situation that occurs in real life physiology, where insulin is secreted “systemically” in response to food cues (preprandially) or food (postprandially). The studies you cite to support the appetite suppressive effect of insulin resemble the studies Woods cites where “plasma glucose is prevented from decreasing in animal models, but this would be difficult to achieve therapeutically.” In other words, these experiments are designed to isolate a single variable (the central effect of insulin) out of its usual total context on the system. Scientifically interesting, perhaps. But focusing only on that part of the picture, out of the total context, makes it less applicable to real world situations (where glucose is not constantly being administered).

        I browsed through your older comments and I do not see where you referenced Le Magnen. Please point out the comment. Second, I do not see where you have provided any evidence to support your assertion that insulin acts on the brain later. If I missed it, please point out the correct comment.

        Sorry, I did not actually provide a reference for Le Magnen, I only referred to him. The Le Magnen reference is in Taubes, Good Calories, Bad Calories, p. 432, and in eight Taubes references in Taubes’ bibliography.

        Regarding the evidence that insulin reaches the brain later than the liver and digestive tract, I base this on the location of the pancreas in the body, the kinetics of a peptide crossing the blood-brain barrier, and the fact that glucose can readily enter the brain without insulin (more so than in other body tissues). However, my point would still stand if insulin reached the brain at the same time as it reached the liver and digestive organs, because one needs to consider the integrated effect of hypoglycemia and hyperinsulinemia acting on the brain, not just hyperinsulinemia and euglycermia (constant glucose) as in the animal studies you cite. The two effects act against each other. I would argue that insulin spikes often lead to an “overshoot” in hypoglycemia (especially from high carb meals in people who are prediabetic and have chronic hyperinsulinemia) leading to a hypoglycemia induced hunger.

        You cite a study by Flint et al which concludes “The current study does not support the contention that the postprandial glycemic response has an important effect on short-term appetite sensations.” Unfortunately, I only have access to the abstract you linked, since I cannot get PubMed articles without significant cost. So I can’t evaluate the research (and I don’t think one should rely on conclusions without studying the study design and reading all the caveats). But that conclusion flies in the face of the majority of other studies I’ve seen which DO show a relationship between blood glucose levels and hunger. It also flies in the face of blood glucose experiments I’ve performed on myself.

        In short, I remain unconvinced that the NET effect of insulin, acting only the total metabolism is to suppress appetite. My considered opinion is that insulin frequently increases appetite via hypoglycemia, particularly for meals of simple carbs or large meals, especially when consumed by people with poorly controlled blood sugar, e.g. pre-diabetics with some degree of insulin resistance. The fact that some degree of appetite suppression will also occur at some point during the meal, due to central effects of insulin on the brain, does not take away from these facts.

        Todd

          

  • This is a great series, I learned a lot – and I’m going to refer to these for a long time… 🙂

      

  • Great point about the cognitive miser! Glad to see a fitness expert who can read science.

      

  • Thanks again everyone for your comments!

      

  • Martin Levac
    7 years ago

    Hey James, you’re wrong. Alcohol acts exactly like fructose in the liver. I’ll give you a few minutes to figure this one out.

      

    • Hey James, you’re wrong. Alcohol acts exactly like fructose in the liver.

      And, like fructose, the adverse effects (increases in triglycerides, fatty liver accumulation, etc) only occur at high doses beyond a certain threshold. The threshold for fructose is estimated to be anywhere from 60 grams to 100 grams per day in humans. And even these effects are not completely independent of energy expenditure. For example, a 50% fructose diet (which is a very high fructose intake) does not impair exercise-induced body fat loss in rodents (who have a much higher capacity for de novo lipogenesis from fructose than humans). As Alan Aragon points out in this blog post, one must consider the dose and context when discussing the effects of fructose, and the same holds true with alcohol. In fact, when it comes to alcohol, moderate intakes are known to have beneficial effects on blood lipids, while high intakes are known to have adverse effects on blood lipids. Again, it comes down to dose and context. And you also have to clarify what you are discussing. For example, increased hepatic lipogenesis and triglyceride production is not equivalent to increased body fat gain….you seem to be treating the two concepts as equivalent.

        

      • Martin Levac
        7 years ago

        I’m sorry I wasn’t clear enough. Please try to refute your own argument instead of trying to confirm it all the time. Maybe then you’ll understand why I said that alcohol acts exactly like fructose in the liver.

          

        • Martin,

          Claiming that alcohol behaves like fructose in the liver (in which they are similar) is not refutation of my argument. Given your tendencies to produce straw men, non-sequiturs, and other fallacies as shown in your other comments, I have my doubts that your thinking regarding alcohol and fructose is sound as well.

            

          • Martin Levac
            7 years ago

            Just think it through will you instead of refusing to play. Why is it relevant that fructose acts exactly like alcohol in the liver? I’ll give you a hint, it has to do with fat burning suppression.

              

          • Just think it through will you instead of refusing to play. Why is it relevant that fructose acts exactly like alcohol in the liver? I’ll give you a hint, it has to do with fat burning suppression.

            Martin, you are providing an example of the “cognitive miserliness” that I discussed in this article. Yes, fructose, like alcohol, takes precedence in oxidative pathways. But, as I stated in the article, this fails to address what is happening over a 24-hour period. It also does not consider the energy status of the body or liver glycogen status. As I stated in the previous comment (which you appeared to ignore), fructose metabolism changes when energy balance changes. Your thinking is erroneous because you assume fructose has the same biological effects under all conditions (which it clearly does not). Fructose has multiple pathways in the liver through which it can be metabolized, and the pathway that predominates depends on a myriad of factors that you are not addressing. Even if fructose is converted to fat, this still does not address what is happening over a 24-hour period. You have a very narrow (and incorrect) focus on what is happening when the fructose is being metabolized.

            This cognitive miserliness that you continue to show is also displayed in your thinking regarding insulin and its effects on lipolysis and energy balance. I will address your other comments in regards to this later on today or this evening.

              

          • Martin Levac
            7 years ago

            In the mean time, here’s another question regarding that study.

            Did they isolate insulin? What I mean is did they compare two diets of equal calories but of different insulin load? No, they merely compared two diets of differing calories and differing insulin load. How then can we conclude that it was all about calories and not all about insulin? In order to conclude anything, we have to isolate both insulin and calories. So, we have to compare two diets of equal calories but of differing insulin load, and two diets of equal insulin load but of differing calories. Otherwise that study can show that it was all about calories, and that it was all about insulin. In other words, it does not actually support your position. And considering that the only data you provided to support your last installment is this study, we can safely dismiss it outright.

              

          • What study are you referring to? I referenced a study on alcohol and total fat balance to illustrate that alcohol, despite the fact that it inhibits fat oxidation, does not result in positive fat balance if participants are in energy balance. Whether insulin was measured is irrelevant. This study was to show that, when considering the effects of a particular macronutrient on fat oxidation, you have to consider what is happening over a 24 hour period and not just during the time the macronutrient is being oxidized. I then compared this to how people view insulin. People blame insulin for fat gain because it inhibits lipolysis. But, like with alcohol, you have to consider what is happening over a 24-hour period, not what is happening during the postprandial period when insulin is elevated.

              

  • Martin Levac
    7 years ago

    James, you said that removal of insulin in type 1 diabetics results in hyperphagia. Your argument about calories stops making sense here. That’s because in addition to the hyperphagia, there’s emaciation. And the addition of insulin causes fat accumulation. How can hyperphagia cause emaciation? And how can the reversal of condition, i.e. the addition of insulin, cause fat accumulation? You use evidence that refutes your own arguments. And you expect us to pay for that stuff in the future?

    I guess everybody’s got pay his rent.

      

    • James, you said that removal of insulin in type 1 diabetics results in hyperphagia. Your argument about calories stops making sense here. That’s because in addition to the hyperphagia, there’s emaciation.

      Actually, it makes perfect sense. The removal of insulin removes insulin’s inhibitory functions on appetite, which results in hyperphagia (the same effect is created in rodents when you block central insulin receptors in the brain). However, the removal of insulin also removes insulin’s inhibitory functions on proteolysis and lipolysis. You get “runaway” proteolysis and lipolysis, which results in the emaciation. No amount of food intake is able to make up for the runaway proteolysis and lipolysis. Blood glucose climbs to dangerously high levels due to runaway gluconeogenesis by the liver (which itself is rapidly breaking down amino acids from muscle tissue to supply the glucose…hence the loss of muscle tissue). Ketones also climb to dangerously high levels due to runaway ketogenesis (from the liver breaking down the massive amount of fatty acids released due to runaway lipolysis…hence the loss of fat tissue).

      How can hyperphagia cause emaciation?

      Hyperphagia doesn’t cause the emaciation. In the uncontrolled type I diabetic, they are simply occuring at the same time. Correlation does not imply causation.

      And how can the reversal of condition, i.e. the addition of insulin, cause fat accumulation?

      Are you referring to administering insulin to a previously uncontrolled diabetic without insulin? If so, it doesn’t cause “fat accumulation.” It simply stops the runaway ketogenesis, lipolysis, and proteolysis that occurs in the absence of insulin. It simply corrects the emaciation that you were referring to earlier.

      You use evidence that refutes your own arguments.

      No, you are creating a strawman of my arguments, and it appears you do not have a clear understanding of insulin physiology and diabetes.

        

      • Martin Levac
        7 years ago

        Indeed. You said “the removal of insulin also removes insulin’s inhibitory functions on proteolysis and lipolysis. You get “runaway” proteolysis and lipolysis”. Yet you claim that “Insulin is not required for fat storage”. By which mechanism, prey tell, can fat accumulation, let alone excess fat accumulation, is made possible without the action of insulin? Do I need to remind you that you said “No amount of food intake is able to make up for the runaway proteolysis and lipolysis.”

        You said “Hyperphagia doesn’t cause the emaciation.” Of course it does not. What you claim is that hyperphagia causes obesity. But there’s a problem with this. If hyperphagia causes obesity, and if removing insulin causes hyperphagia, then removing insulin should cause obesity. It does not. Removing insulin causes emaciation as you so eloquently pointed out.

        Would you say that emaciation is the result of a caloric deficit? Would you say that emaciation is the result of the removal of insulin? Then you would also say that a caloric deficit is the result of the removal of insulin.

          

        • You said “Hyperphagia doesn’t cause the emaciation.” Of course it does not. What you claim is that hyperphagia causes obesity. But there’s a problem with this. If hyperphagia causes obesity, and if removing insulin causes hyperphagia, then removing insulin should cause obesity.

          Martin, once again you have created a straw man. Nowhere have I claimed that hyperphagia causes obesity under all conditions. Hyperphagia is defined as an abnormal appetite and increased consumption of food. If this increased consumption/appetite is met by an increased energy expenditure (or a dramatically increased excretion of glucose/ketones in the urine as in the uncontrolled type I diabetic), then it will not cause obesity.

          Would you say that emaciation is the result of a caloric deficit? Would you say that emaciation is the result of the removal of insulin? Then you would also say that a caloric deficit is the result of the removal of insulin.

          The caloric deficit due to the removal of insulin is due to the massive excretion of glucose and ketones in the urine. There is also an increased metabolic rate due to the rapid catabolism of protein and muscle tissue. The increased metabolic rate is actually due to hyperglucagonemia and not the removal of insulin.

          Another problem with your thought process is that you are trying to take one condition (the effects of the complete absence of a hormone versus its presence), and are extrapolating that to a different condition (the effects of variation of a hormone within physiological levels). This is an erroneous extrapolation.

            

          • Martin Levac
            7 years ago

            Let me remind you of what you said:
            “The direct demonstration of cause/effect is not a “faulty inference.” If one injects insulin centrally and it suppresses appetite, versus no suppression when only the vehicle is injected, then this is direct evidence that insulin suppresses appetite. When you add the evidence that knocking out insulin receptors in the brain results in hyperphagia, as well as the removal of insulin in type I diabetics results in hyperphagia, then you really cannot get better evidence that insulin is an appetite suppressant.”

            If the rule you established is good enough to determine cause and effect with hyperphagia, it’s good enough to determine cause and effect with a caloric deficit. So what’s the cause of our caloric deficit? That’s right, the removal of insulin. Just like with our hyperphagia.

            So what’s the problem with your though process then?

              

          • If the rule you established is good enough to determine cause and effect with hyperphagia, it’s good enough to determine cause and effect with a caloric deficit. So what’s the cause of our caloric deficit? That’s right, the removal of insulin. Just like with our hyperphagia.

            Martin, this is third strawman that you have constructed. Yes, the removal of insulin causes a caloric deficit, because it results in massive excretion of glucose and ketones in the urine, along with elevated energy expenditure due to hyperglucagonemia and massive protein oxidation. I thoroughly explained this in my last comment; why you ignore it is baffling. Such a condition is not equivalent to variations of insulin in a normal physiological range, nor does it mean that less insulin secretion will automatically lead to an elevation of energy expenditure. In fact, when you lower carbohydrate intake to zero, there is actually a slight non-significant reduction in energy expenditure, not an increase.

            Why you continue to think that the removal of insulin is somehow equivalent to the dietary modification of insulin is baffling. In fact, if we were to use your logic, then that would imply that lowering carbohydrate intake would result in massive proteolysis and muscle loss (because the removal of insulin results in this).

              

          • Martin Levac
            7 years ago

            The complete lack of insulin, or chronic hypoinsulinemia as it’s technically called, is merely one end of the spectrum of insulin. The other end is chronic hyperinsulinemia. Everything in between is merely a variation on this theme. Indeed, correcting hypoinsulinemia only a little will result in only a little correction of the emaciation. Accordingly, correcting hypoinsulinemia too much will result in an exaggerated correction of emaciation, i.e. they’ll grow fatter than normal.

            Indeed, insulin is used in bodybuilding for its anabolic qualities, on top of MGF, IGF, growth hormone, testosterone, etc. In other words, it’s just one end of the spectrum of insulin. The other end being emaciation. And would you believe it, more insulin means more growth, and less insulin means less growth. All this in a dose response fashion. And would you believe it further, bodybuilders know that injecting too much insulin makes you fat. And why would they know that unless it was true? What, are they injecting a different substance mistakenly believing it’s insulin? Surely, in a domain where results are all that matter, the wrong substance would quickly be found and corrected.

            But seriously, it’s your thought process that is lacking. You advance that the condition chronic hypoinsulinemia is irrelevant to fat accumulation but then you also advance that the same condition is now relevant to satiety. If you’re not logical, at least be consistent my good man.

              

          • And would you believe it, more insulin means more growth, and less insulin means less growth.

            This is where you are incorrect. The effects of insulin are not linear across its concentrations. This is perfectly illustrated where the absence of insulin results in an increase in energy expenditure in vivo, yet reducing insulin by reducing carbohydrate does not increase energy expenditure in vivo.

            And would you believe it further, bodybuilders know that injecting too much insulin makes you fat. And why would they know that unless it was true? What, are they injecting a different substance mistakenly believing it’s insulin?

            The injections of supraphysiological doses of insulin are not relevant to variations of insulin within a normal physiological range. Not only that, but given that the pancreas cosecretes amylin with insulin, the effects of insulin injection are not the same as the effects of pancreatic insulin secretion.

              

  • Martin Levac
    7 years ago

    Linearity is not required for a dose response to occur. Furthermore, the variation in insulin resistance across various tissues changes insulin’s perceived effects accordingly. The linearity could very well be affected by this mechanism. For example, we could perceive an increase in plasma insulin merely because certain cells have suddenly become resistant in response to a non-insulinogenic stimuli. Butter would be such a stimuli. The point is that we have here a perceived effect of insulin without the direct action of insulin itself or of an insulinogenic agent.

    Further, ignoring insulin when talking about calories is like ignoring physiological mechanisms to prove that it has nothing to do with the physiological mechanisms you are ignoring. In other words, you close your eyes and try real hard to believe what you imagine. The study you cited ignored insulin. You try to convince us that we don’t need to look at insulin. I point out that you must look at the very thing you are trying to argue against. The alternative is that you argue against a non-measured entity. Excuse me while I consider the practicality of such an endeavor.

    It reminds me of a joke. There’s this guy on the train throwing magic powder out the window every now and then. Another man asks him why he does that. The first man explains that it’s to keep the pink elephants away. The other man replies that there aren’t any pink elephants. The first man triumphantly exclaims “Of course there ain’t no pink elephants, this magic powder works.”

    If you don’t measure it, it might as well not exist.

      

    • Linearity is not required for a dose response to occur.

      Of course it doesn’t. But the problem is that in your simplistic argument comparing one extreme (no insulin) to the other extreme (supraphysiological doses of insulin), a linear or near-linear relationship is assumed.

      Dose-response relationships are quite complex. For example, with some substances, there are U shaped relationships where you see certain effects up to a certain dose, and then attenuated effects at higher doses. In other cases (like the health effects of alcohol), there are benefits to moderate doses and deteriments to high doses. There are also logarithmic relationships, where there is a rapid increase at low doses, followed by a plateau at higher doses.

      Further, ignoring insulin when talking about calories is like ignoring physiological mechanisms to prove that it has nothing to do with the physiological mechanisms you are ignoring.

      No, this is another non-sequitur on your part. One can study the outputs and inputs of a system without necessarily knowing the mechanisms inside the system. This is particularly true when the system has multiple pathways through which the outcome can still be the same. What you fail to understand is that the body always “finds a way.” There are numerous biochemical pathways through which the body regulates energy balance and weight. Insulin is only one component among a complex interaction of many components. Your comment over on the low carb forum that you do not think that someone can get fat on purely fat feeding is a perfect example of how you fail to understand this. In terms of fat overfeeding, the body has mechanisms to deposit fat that are not related to insulin. For you to argue that one cannot get fat on purely fat feeding, you would need to be able to explain what happens to the carbon and hydrogen atoms that are consumed if one consumes 5000 calories of fat yet expends only 2000 calories per day. And one cannot argue that energy expenditure is upregulated, because it has already been experimentally demonstrated that the removal of carbohydrate in the diet does not result in an upregulation in energy expenditure in humans.

      Dr. Kevin Hall, a biophysicist, has created complex computational models that accurately predict changes in body weight and composition due to changes in diet. He has tested the model against the results of a number of dietary intervention trials, including low carbohydrate trials, and has found it to be very accurate. Yet, with all the variables in the model (including fat, protein, and carbohydrate oxidation rates), insulin is not included among these. Obviously he has demonstrated that one can model changes in body weight and energy balance without including insulin (or any other hormone) in the model. According to your reasoning, this is not possible…but he has obviously demonstrated that it is.

      The study you cited ignored insulin.

      It doesn’t matter, because the input (alcohol) and the outcome (fat balance) is all we care about. The mechanism behind how fat balance was affected is not relevant.

      If I press the accelerator pedal on my car (the input), and my car goes faster (the outcome), I do not need to know the internal mechanisms of how the engine works to know that pushing the accelerator pedal will make my car go faster. I can demonstrate this in experiments without having a clue what’s under the hood.

      The alternative is that you argue against a non-measured entity.

      Using this reasoning, that would mean that I cannot know that pressing the accelerator on my car will make my car go faster, because I do not know the internal mechanisms of how the engine works. The problem with this logic is quite obvious.

      Applying this same reasoning to the human body, that would mean Dr. Kevin Hall could not build the models he did without including insulin. Yet he did. Or, to apply your same reasoning to a drug study, your reasoning would imply that I can’t measure pain relief of a COX-2 inhibitor without measuring COX-2 activity. Yet we can.

      The absurdity of your logic is also illustrated when you consider the following. You claim that one must measure insulin because you must measure the physiological mechanisms. If that’s the case, then that would also imply that we not only need to measure insulin, but also leptin, growth hormone, catecholamines, IGF-I, glucagon, cortisol, ASP, IL-6, amylin, and every other factor that is related to fat metabolism. That also means we need to look at not only hormones, but what is happening on a cellular and molecular level, including changes in gene transcription and translation. According to your reasoning, any study that does not measure all of these physiological mechanisms must be useless for determining the effects of an input on an outcome. Of course this is absurd.

      If you don’t measure it, it might as well not exist

      So if I don’t measure gene transcription and translation in adipose tissue, does that mean it might as well not exist?

        

      • Riddle me this.

        y1 = x1 + x2 + x3
        y2 = 3×1 +2×2+ x3
        y3 = x1 + x2 – x3

        z = 6×1 + 4×2 – x3

        Does x1 have an effect on z if it can be independent controlled? Does it cease to have an effect on z if it cannot be independently controlled?

        I’m clearly oversimplifying here, but just because a biophysicist can model body composition based off feeding habits does not mean that insulin does not play a role in fat storage.

        What kind of argument is that?

          

        • “What type of argument is that?” It’s not an argument that I ever made.

          I never claimed that insulin does not play a role in fat storage. There are numerous hormones that play a role in fat storage. But that does not mean that you need to account for the effects of insulin (or any other hormone) when modeling body fat change. You do not need to know the inner workings of a black box to be able to accurately model its inputs and outputs.

          Genes also play a role in fat storage. So does that mean I would need to model the impact all the way down to the effects of individual genes to accurately model body weight? Of course not.

            

    • You try to convince us that we don’t need to look at insulin.

      I need to add one more comment to this, because again you are constructing a strawman. The purpose of my entire series is to show that the carbohydrate/insulin hypothesis simply fails to explain a large number of scientific observations, from the effects of dairy on body weight to the fact that insulin levels do not predict changes in body weight. This is not “ignoring” insulin…it’s showing that trying to structure a diet based on its effects on insulin is misguided because the underlying hypothesis is simply wrong.

        

  • Martin Levac
    7 years ago

    James, you keep calling “straw man” and “that’s irrelevant” as if doing so will win you arguments. It doesn’t. It merely changes the goal posts continuously so that your arguments are now made valid. Like you’re both a player and the referee and you’ve thrown out every other player so you’re the only player left that can score a point. You’ve thrown me out James. You win. Congratulations James, for what that’s worth.

    You are now the sole member of a very exclusive club. Others who agree with you are just standing on the sidelines not trying very much to score points because it is obvious to them that they just can’t do that what with you being the referee as well as the opposing player and all. Some of those people try to score points with me elsewhere but fail miserably when I point out the glaring flaws in their thinking. That’s because with them, the field is not theirs like this field is yours. That’s right James. You are referee, player, and field owner. How can anybody score points when playing against you here?

    If you truly want to discuss the subject, you will do so on a public field where you are not the owner and not the referee either but are simply a player just like every other player playing this great game of boost yar ego. But maybe you don’t think that your ideas are ready for amateur night.

    Granted, this last post of mine is utterly irrelevant. But don’t you think it’s a pretty good approximation of what you’ve been doing all this time? It’s not possible for me, or anybody else for that matter, to score points if you remain where you are. But that doesn’t deter me from trying to discuss with you though so I invite you to come to my domain where I’m not the field owner nor a referee but simply just another player. Come play with me James. You’ll see, it’s so much more fun when you win arguments on their own merit and not through some arbitrary decision.

    Until next time James.

      

    • James, you keep calling “straw man” and “that’s irrelevant” as if doing so will win you arguments.

      The purpose of a debate is not to “win.” If your intent is to win this, that is more indicative of a dogmatic position rather than an evidence-based position.

      Calling something a strawman is extremely relevant to the conversation. If you are going to construct faux arguments that I never made, in the interest of giving yourself something that you can easily dismantle (never mind that it is not the position I held), then I will call you out on it. Being able to identify strawmen is critical to providing rational arguments. If you have to resort to such strawmen and other tactics, then it is clear that you do not have a rational, evidence-based position on this issue.

      It merely changes the goal posts continuously so that your arguments are now made valid.

      Calling something a straw man is not shifting the goal posts. When it is clear that you attribute an argument to me that I never made, then that dictates that you are the one in error, and I will point this out to you.

      Like you’re both a player and the referee and you’ve thrown out every other player so you’re the only player left that can score a point. You’ve thrown me out James. You win. Congratulations James, for what that’s worth.

      You are now the sole member of a very exclusive club. Others who agree with you are just standing on the sidelines not trying very much to score points because it is obvious to them that they just can’t do that what with you being the referee as well as the opposing player and all. Some of those people try to score points with me elsewhere but fail miserably when I point out the glaring flaws in their thinking. That’s because with them, the field is not theirs like this field is yours. That’s right James. You are referee, player, and field owner. How can anybody score points when playing against you here?

      This isn’t a game, Martin. Apparently you view it as such, which tells me that you are tied deep in dogma rather than seeking truth based on evidence. I have seen you post other places, and your penchant for clinging to low carbohydrate dogma, ignoring errors in your logic, and ignoring facts and evidence that clearly show you to be incorrect, is rivaled by few others in the low carbohydate arena. For example, many people showed you that you were incorrect on a number of even basic physiological facts in this post by Martin Berkhan, yet you simply ignored it and kept repeating yourself.

      This behavior is even apparent in this discussion. On the low carb forum, you stated, “If we want an accurate prediction model, we can’t just look at insulin in the blood, we must also look at insulin resistance.” I showed you how you were wrong about this; I gave you models by Dr. Kevin Hall that accurately predict weight change, without the need to include either insulin or insulin resistance in the models. Yet, you ignored that and continue to repeat the same statements. This is the hallmark of someone deep in dogma. It’s like you arguing that the color of the sky is green, and then someone shows you that it is blue, and you continue to state that it is green.

      In fact, throughout this discussion, you have yet to provide a single piece of evidence for anything. No studies, no references…just assertions that you have been shown to be wrong about.

      If you truly want to discuss the subject, you will do so on a public field where you are not the owner and not the referee either but are simply a player just like every other player playing this great game of boost yar ego

      This forum is a public field. I have not censored any of your comments. Every comment has gone through without me touching them. They are freely available to view by all.

      Your comment here is absurd. You are complaining that I have control of this blog, despite the fact you have never been censored from it. No one is stopping you from saying what you want to say.

      The fact that I have control of this blog does not invalidate any of my arguments. For you to invalidate my arguments, you need to actually provide evidence…something that you still have not brought to the table.

      You’ll see, it’s so much more fun when you win arguments on their own merit and not through some arbitrary decision.

      Your decision to leave is yours and yours alone; there was never any “arbitrary” decision on my part. Again, I have not censored a single comment of yours, nor have I prevented you from posting your disagreement.

        

  • Martin Levac
    7 years ago

    Straw man.

    Did you or did you not say:
    “The removal of insulin causes hyperphagia.”
    What this means is that hyperphagia is an effect.

    Did you or did you not say:
    “Nowhere have I claimed that hyperphagia causes obesity under all conditions.”
    What this means is that you did say that hyperphagia causes obesity under certain conditions.
    What this further means is that hyperphagia is a cause.

    Did you or did you not say:
    “In fact, higher insulin levels were associated with greater fullness.”
    This means satiety and thus cessation of eating is an effect.

    Did you or did you not say:
    “The direct demonstration of cause/effect is not a “faulty inference.” Etc…
    This means you know precisely what the concept of cause and effect is.

    Did you or did you not say:
    “Another problem with your thought process is that you are trying to take one condition (the effects of the complete absence of a hormone versus its presence), and are extrapolating that to a different condition (the effects of variation of a hormone within physiological levels). This is an erroneous extrapolation.”
    This means you know that you yourself did such a thing when you used the type 1 diabetics data and “the removal of insulin…” to support your argument about insulin and satiety.

    Straw man? There is no straw man. You said these things.

    Considering that we have now established that there is no straw man in anything in this post, how can you rationalize that hyperphagia is an effect at one end of the spectrum of insulin, a cause in the middle, and an effect at the other end of the same spectrum? Why is it not an effect in all instances? Why is it not a cause in all instances? What makes hyperphagia so special that its nature so easily changes as it changes position in the spectrum of insulin?

    I’m not here.

      

    • Martin Levac
      7 years ago

      Addendum. With your argument that when insulin is associated with satiety, you mean to say that insulin is an anorexiant. Anorexia is the opposite of hyperphagia (polyphagia in wiki). Effects, not causes.

        

    • Martin, your logic in this discussion is highly distorted and flawed. For example,

      Did you or did you not say:
      “In fact, higher insulin levels were associated with greater fullness.”
      This means satiety and thus cessation of eating is an effect.

      No, I said that higher insulin levels were associated with greater fullness in that particular study. Correlation does not equal causation. Please read this post on the cum hoc, ergo propter hoc fallacy.

      Did you or did you not say:
      “The direct demonstration of cause/effect is not a “faulty inference.” Etc…
      This means you know precisely what the concept of cause and effect is.

      And, judging by your comment on insulin and fullness, apparently you do not understand the concept of cause and effect. Remember, the word associated does not mean cause and effect.

      This means you know that you yourself did such a thing when you used the type 1 diabetics data and “the removal of insulin…” to support your argument about insulin and satiety.

      Another strawman. I never claimed that variation of insulin within a physiological range will affect satiety. My claim that insulin suppresses appetite was never meant to mean that more insulin automatically causes greater appetite suppression. I’m able to understand the difference between the two concepts; I don’t assume a linear relationship between insulin and appetite suppression. It appears that you are struggling to understand the difference between the two (like your assumed linearity when discussing the extremes of insulin concentrations). You seem to have trouble understanding gray areas and subtleties in terms of physiology (like your earlier comments regarding fructose…you appear to believe that fructose is lipogenic under all conditions, which it is not).

      It is clear that insulin is absolutely needed for appetite suppression (and the ability of the brain to respond to that insulin…some evidence suggests that type II diabetics are hyperphagic partly due to insulin resistance in the brain). However, once a certain basal level is achieved, the data on its relationship with satiety within a normal physiological range (from the low end of the physiological range to the high end) is not as clear. There are a number of studies showing higher insulin to be associated with greater satiety, but the few controlled studies that have manipulated insulin and glucose using clamps have not been able to support this relationship as causal.

        

      • Martin Levac
        7 years ago

        Did you or did you not write:
        “direct evidence that insulin suppresses appetite.”
        If that’s not equivalent to “causes satiety”, shoot me and call me crazy.

        Yet did you or did you not say:
        “No, I said that higher insulin levels were associated with greater fullness in that particular study.”
        That looks like denial.

        James, you said it. It’s not my fault if it doesn’t fit, it’s your fault: You said it.

        You said:
        “I never claimed that variation of insulin within a physiological range will affect satiety.”
        I never said you did.

        Here’s what I tried to show you but apparently failed.

        You said:
        “The removal of insulin causes hyperphagia”
        In support of your argument that insulin causes satiety. (I have already established that you meant “caused” and not “associated”)
        The above is the extrapolation of one condition to a different condition.
        You said:
        “Another problem with your thought process is that you are trying to take one condition (the effects of the complete absence of a hormone versus its presence), and are extrapolating that to a different condition (the effects of variation of a hormone within physiological levels). This is an erroneous extrapolation.”

        You established the rules yet when you break them it doesn’t seem to trigger any alarm. I’m not making this up, you said the things you said. How many times do I have to remind you of what you said before you admit that maybe you said them? And when will you even consider that maybe what you said contradicts itself and doesn’t actually make any sense?

        It just occurred to me, do you think it’s a question of proof reading what you write? I’m just guessing here but maybe if you had somebody else proof read what you write, it wouldn’t contain so many contradictions and we wouldn’t have this little back and forth that’s pretty much absurd all things considered. Who knows, maybe if somebody real that was sitting besides you told you the same things I told you, you wouldn’t just dismiss it like you dismissed everything I told you to date. It’s like “straw man this, and irrelevant that and this Martin dude is just crazy and here’s why”. You’re not even considering for one second that it might just be you, not even for a single little word you wrote.

          

        • Martin, there is no point in continuing this discussion with you, and here’s why.

          First, you continue to take quotes out of context and create contradictions where there are none. This is your style of argumentation:

          James: When you press on the accelerator pedal and the car engine is on and the gear is in Drive, the engine will rev and the car will move forward.
          James: When you press on the accelerator pedal and the car engine is on and the gear is in Park, the engine will rev and the car will not move forward.
          James: When you press on the accelerator pedal and the car engine is off and the gear is in Park, the engine will not rev and the car will not move forward.

          Martin: You said that pressing the accelerator pedal will move the car forward, and then you turn around and said that pressing the accelerator pedal will not move the car forward. You have contradicted yourself!

          James: No, Martin, its just that the effects of pressing the accelerator pedal are different under different conditions.

          The bottom line, Martin, is that you argue like a politician. You take quotes out of context and string them together to create apparent contradictions where there are none. This is why you are creating strawmen. This tactic is nothing new to you….Valtor pointed out how you were taking his quotes out of context and from different discussions as well.

          Another reason there is no point in discussing with you is that you blatantly ignore it when you have been shown to be incorrect, and then will repeat the same statements. In Martin Berkhan’s thread, it was pointed out to you that glucose is not needed to produce glycerol, and that fat cells can obtain glycerol through glyceroneogenesis. However, despite the fact that this was pointed out to you, you continue to make the same erroneous statement that glucose is needed to produce glycerol.

          Finally, when one cannot seem to understand what even a basic word like “associated” means, there really is no use in engaging in discussion with that individual.

          This is why I will no longer engage in discussion with you; it is a waste of my time to discuss with someone who engages in such tactics. You are simply too entrenched in low-carb dogma to have any productive discussion.

            

  • Josh Dale
    7 years ago

    Hi James,

    Excellent series on insulin! If insulin’s major role in lowering hyperglycemia is turning down hepatic glucose production where does that leave peripheral insulin resistance? For example in hyperinsulinemic clamp studies they will typically tout increased glucose uptake in the muscles as a measure of improved skeletal muscle insulin sensitivity. Is this a faulty or insignificant metric or are skeletal muscle insulin sensitivity and peripheral insulin resistance not related? My understanding after reading Sonksen’s piece was that the unchecked lipolysis was the real problem with peripheral insulin resistance?

    Also, Sonksen mentions that ketosis can prevent glucose from entering the cells, which makes sense, but my question, what triggers the ketosis in the first place? In other words, why is the body making ketones when their is glucose available and free to move into the cells. Is it because we lose a minimum amount of ketones in the urine vs. glucose, and so they get preference? I feel like I’m in the chicken or the egg argument. Help!

    Thanks,

    Josh

      

  • James, I think you insulin is a straw man you’ve setup. While you statements seem mostly consistent (except where pointed out otherwise by Todd and Martin), you don’t actually come out and state a thesis. Saying insulin is not bad for you is a worthless statement.

    There is pretty compelling evidence as admitted by yourself that insulin plays a role in regulating lipolysis and fat oxidation. Thus for someone who wants maximal weight loss would it not behoove themselves to maximize their insulin sensitivity via diet? Signaling mechanism in the body, particularly one such as insulin, affects multiple things at the same time.

    Its also pretty much established that caloric restriction, particularly extreme caloric restriction, is actually counterproductive to weightloss. For most people regulating their caloric intake and eating better foods is enough. For some people (http://www.marksdailyapple.com/the-unconquerable-dave/) a more dramatic shift is necessary.

    I can tell you from personal experience that I’ve tried caloric restriction for weightloss and I will actually gain wait. Particuarly, one time where I eating whole grains, fruits, and vegetables. I went from 200 -> 220 in a month on 2000 calories a day, while training every day in the gym and measuring portions with a scale.

    If insulin doesn’t play a role in fat loss, then I’m still looking for an explanation for my continued weight loss and body recomposition eating 5000 calories a day of mostly fat. I’ve dropped from a 43 along the widest part of the waist to a 40.

    Just because insulin plays a critical role in the functioning of the body and suppressing appetite does not rule it out as playing a critical role in the dysfunction of the body. It’s like saying people who are fat eat more calories than they burn.

    How is that useful?

      

  • I might want to add that it was not muscle I gained. I looked puffy, inflammed, and was tired all the time and was constantly sore even taking protein powder (which I was accounting for in my calories).

    I did better when I tried the milk only diet (where I only consumed whole milk and multi-vitamins). Which got me to my lowest weight ever of 195, but I was constantly hungry (I’m guessing something was missing from the diet).

      

  • James any ideas on how I’m still losing weight by raising my energy consumption to 5000 calories a day? I’ve increased my energy intake, but I’m still losing weight. I’d like to know how this fits in with your models.

      

  • 423546566
    4 years ago

    Did Martin finally shut up? He must be that stalker/troll that harasses all the nutrition blogs. Another dumb lonely old man that should run on out and eat a bullet for being such a ****ing loser.

    He should have simply stated a question and stated his thoughts in his very first post rather than playing word games. Worthless POS. Hey Martin Levac, do us a favor and stop wasting internet badwidth you **** for brains.

      

    • I blocked Martin from being able to post on the site a long time ago. He’s only one of 3 people I’ve blocked. Fred Hahn and Razwell are the other two.

        

  • I forgot to mention, I eat hypercaloric, and I am skinny and healthy again, just by cutting carbs.
    I do eat high-fat dairy with negligible lactose-content.
    I will search for the dairy study if I have time.

      

    • If you’re not gaining weight, then you are not hypercaloric. You might *think* you are, but you’re not. Otherwise, you would need to explain where all those additional carbon and hydrogen atoms you are consuming are going. They can’t just disappear.

        

  • James Badger
    3 years ago

    Hey James, great articles!

    I’m a personal trainer and have played around with low carb for about 3 months. I felt crap, my energy was low and my muscles looked flat! I did lose weight but still carried fat around my sub-scapular, which according to gurus like poliquin, means my insulin is high due to high carb intake, which is bogus because I had eliminated all carbs apart from veg! So for me it only proves that the dogmatic carbs = high insulin = fat storage just doesn’t stand up! I now practice a more free dieting approach keeping in a deficit of 10% under maintenance cals for when I am cutting! I have noticed better fat loss and energy levels! As long as my protein is high enough my muscle mass remains! I know it’s simple but it really is, as long as you burn off more than what you take in you will loose fat! Try it!

      

  • What I find interesting in low-carb debates is the tacit assumption that insulin resistance arises from repetitively activating the insulin-receptor system, as though through mechanical wear. More recent research suggests there is actually an effect from fat accumulation in the target tissues (e.g. liver and muscle). Certain accumulated lipids, possibly including diacylglycerol or sphingolipids, then interfere with insulin signal transduction. This mechanism would account for the fact that moderate fat loss (with fat lost preferentially from liver and muscle rather than adipose tissue) can improve insulin sensitivity. It would also make sense of the effects of high-fat diets on insulin resistance in rats.

    The idea that sugar causes diabetes is actually specifically mentioned in Taubes’ “The Case Against Sugar” ( a book in which he inadvertently reveals he does not know that measured “blood sugar” is glucose, not fructose). It seems obvious–diabetics have sugar in their urine, which comes from too much sugar in their blood, which must be from eating too much sugar. But this is not science. It is sympathetic magic.

      

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