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

 

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

Insulin Is Not Required for Cells To Take Up Glucose

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

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

A Man Ahead of His Time

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

The results of  pancreas extirpation and pancreas grafting are best explained by supposing that the islet tissue produce an Autacoid which passes into the blood stream and effects carbohydrate metabolism and carbohydrate storage in such a manner that there is no undue accumulation of glucose in the blood.  Provisionally it will be convenient to refer to this hypothetical substance as insuline.

Insulin would go onto be discovered 8 years later.  Schafer also hypothesized that insulin was created from an inactive precursor:

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

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

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

The Black Age of Endocrinology

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

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

Glucose Transport is Not Insulin Dependent

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

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

What Really Happens in a Type I Diabetic

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

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

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

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

Insulin…More of a Traffic Cop Than a Storage Hormone

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

Of course, this research only tells us what happens when insulin is present versus when it is not present.  What about the normal situation of a healthy person, who ingests a meal and sees a rise in blood glucose?  What is happening to bring glucose back to normal?  And what happens in a type II diabetic in this situation?  Learn the answers to these questions by reading part 6 of the series.  Also click here to read part 5 where I address comments made by some of the critics of this series.

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

  62 Responses to “Insulin: An Undeserved Bad Reputation, Part 4: The Biggest Insulin Myth of Them All”

  1. Great article! I read read the original Sonksen and Sonksen article before when you are someone else (CarbSane?) posted it, but it is good to have a concise summary. Jeremy

      

  2. wow

    First time a science article made me feel like I had taken some good psychoative mushrooms.

      

  3. “Taubes even stated around the 31 minute mark in this interview that he doesn’t pay attention to modern research because “all of this should have been obvious decades ago.” This is a surprising stance for a science writer;” Sounds like a science writer who doesn’t understand science. Which is not an uncommon characteristic in popular science writers.

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

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

      

  4. Great stuff, James. I’m impressed by the amount of time, effort, and insight you bring to these blog posts. :-)

      

  5. Great just great!

      

  6. Thanks, Jordan & Murffi!

      

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

      

  8. KD says: September 8, 2010 at 2:06 pm
    Me thinks you are giving a very incomplete picture focusing solely on weight loss. Carbohydrate restriction significantly improves glycemic control in people with IGT/IFG/T2 even with
    __________________________
    In this context, you’ve posted a non-sequitur.

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

      

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

        

      • Actually, what he’s doing is presenting a very lawyer like argument against a very narrow set of “myths” of his own choosing

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

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

          

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

            

          • KD,

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

              

          • It sounds to me like you are asserting that glut4 fusion/translocation is irrelevant in vivo. If you have studies in human beings I would be most interested, and eagerly await your next article.

              

          • No, that’s not what I’m saying; that would be a strawman. Glut-4 translocation is not irrelevant in vivo; it’s simply not required for glucose entry into cells, and it is not the reason a type I diabetic is hyperglycemic when insulin is not present.

              

  9. KD says: September 9, 2010 at 1:54 pm

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

    _____________________
    You really have the shoe on the wrong horse.

    You’ve confused “James Krieger” who I’ve seen regularly correct himself, applying the heuristic “am I choosing only the evidence that supports my view, or am I considering all the available evidence”

    with either “David Gillespie” or

    “Gary Taubes”, who seemingly regularly introspects “what evidence should I exclude to make my case?”. Doubly labeled water being the most egregious omission.

      

  10. As long as we’re going to talk about cherry picking, how about cherry ignoring, case in point:

    ” However, there are plenty of glucose transporters on the cell surface, even when there is no insulin. In fact, there are enough transporters on the cell surface to allow the cell to get enough glucose to sustain its energy needs. Thus, glucose transport into cells is never truly dependent upon insulin. Insulin enhances the uptake of glucose into cells, but it is not required for it. ”

    What exactly are you arguing with, KD? that this is not a biochem textbook? In case you haven’t noticed, it’s not and is not pretending to be. This statement covers just about everything you’ve complained about.

    “Insulin enhances the uptake of glucose into cells, but it is not required for it. ”

      

  11. Interesting set of articles.

    I’d like to know your thoughts on keto diets; I’ve tried them, and all it did was give me a headache from the lack of glucose.

      

  12. Really great article James, I’m really glad Alan Aragon linked to your site so I found it :)

      

  13. Awesome and very important series of articles! Keep up the great work!

      

  14. Ok so the lack of insulin does not cause hyperglycemia in type 1 diabetic, because extra glucose is produced in the liver.

    Then, there must be (barely) the same amount of glucose entering the cell with and without insulin. The rate of entrance should barely be the same, and it would just be the total production that skyrockets.
    Has it ever been mesured? Type 1 diabetic vs healthy on cell’s glucose intake? Paper?

    Thank you James for the great articles!

      

  15. I thought having high circulating insulin during the day means insulin insensitivity (i.e. diabetes type 2)… is that not a case against insulin?

    So putting aside whether or not a diet high in proteins/fats are preferable to one in carbs/sugars, if everything can lead to fat gain equally (based on energy expenditure only), what is *your* diet for fat loss?

    Does it include any fructose? wheat gluten? oats? rice? legumes?

      

  16. @snoop

    I think the point is that insulin does leads to weight gain, with excess protein, just as much as excess carbs… plus, muscle can consume glucose from the blood without insulin. Insulin is only for pancreas/liver&bodyfat communication. As for diet, keep carbs/grains to <20g a day. High adiponectin levels leads to insulin sensitivity.

    Since Fructose is the preferred form of sugar for the liver.. any food with a high fructose/glucose ratio can cause you to get fat, and then develop a fatty liver when consumed in excess. (the liver can only hold 100g of glucose!!). There is still much research (and debate) in this area though. Many swear that "High Fructose Corn Syrup" (i.e. plain ol' fructose), is any just as good (and bad) as regular table sugar (sucrose).

    Wheat Gluten may cause inflammation in some people (due to lectin), but in general is a healthy source of in/soluble fiber. You can also omit fiber carbs, from your dietary carb quota. Nuts/Seeds/Rice/Legumes (if soaked), are fine.

    Hope this help,
    James

      

    • James said “I think the point is that insulin does leads to weight gain, with excess protein, just as much as excess carbs.

      In response to that point. If there is high levels of dietary fat in conjunction with the excess dietary protein, will the liver go through gluconeogenesis?

        

  17. Chuck:

    The liver is always “going through” gluconeogenesis. However, gluconeogenesis from dietary protein will increase in conditions of low exogenous carbohydrate availability.

    James:

    My point is that excess calories of any kind will lead to weight gain, through different mechanisms. People need to stop pointing fingers at insulin, because insulin will not cause weight gain in the absence of positive energy balance. Even foods with a high fructose/glucose ratio will not cause you to get fat if you are in an energy deficit.

    Snoop:

    Insulin insensitivity is not a case against insulin….it’s a case against insulin insensitivity. Insulin is not “the bad guy”. The “bad guy” (well, one of the bad guys among many) is when your body does not respond to insulin like it should. I also don’t have any specific diet for fat loss. I favor an individualized approach, although I tend to favor high protein intakes (for satiety) and relying primarily on whole, unprocessed foods. The overall macronutrient distribution is not all that important. But I have stated in many of my articles/blog posts that I favor highly individualized approaches to nutrition, and the optimal approach for one person will not be the same as for another. You need to address each person’s needs/sensitivities/tastes/history.

    Nico:

    You’re bringing up the concept of metabolic clearance rate (MCR), which is the rate of glucose uptake into peripheral tissues. Insulin does increase MCR in healthy people, which I will address in a future part of this series.

    Scott and Fredrik:

    Thanks for your comments!

    Max:

    Ketogenic diets aren’t for everyone, but certainly can be effective for some people. It really depends upon how you respond, as well as your individual needs (for example, are you sedentary or active?).

      

    • James:

      I can see that insulin doesn’t seem to be a problem. Is chronically elevated blood sugar (in non diabetics) something we should be concerned with?

      Chuck

        

      • Chuck,

        Chronically elevated blood sugar in a non-diabetic is called glucose intolerance, and is generally a sign of insulin insensitivity. This definitely is something to be concerned with. But this is a different beast then concerning yourself whether a food raises insulin levels or not.

          

        • I guess what I mean is should we be concerned with constantly elevating our blood glucose via the food choices we make. Elevated insulin does not seem to be a problem but is elevated blood glucose a problem?

            

          • Elevated glucose can be a problem, but only when that elevated glucose is secondary to insulin resistance (i.e., the insulin resistance is causing the elevated glucose, which then becomes chronic). Simply elevating blood glucose through meals, even when done on a very high carbohydrate diet, will not cause a problem as long as one remains in energy balance (unless you are already diabetic or have glucose intolerance, where then you need to be more concerned about how much blood glucose is elevating).

            Insulin resistance is key here. What healthy people need to worry about are the factors that cause insulin resistance, not necessarily whether food is elevating blood glucose. And there are numerous contributors to insulin resistance, including, but not limited to, inactivity, lack of sleep, stress, diet high in trans fatty acids, excessive caloric intake (of any kind) in relation to expenditure, etc.

              

          • I have learned SOOO much from this series I cannot even begin to word it right…. but….

            how does one know is he/she is glucose intolerant?
            how does one know if glucose/insulin is matched in a good way to promote muscle vs fat?
            how do you test for insulin resistance vs insulin sensitivity?

            i would guess checking blood sugar, but if a spike is expected with food then how do you know if it is a good or bad spike?

              

          • I am very grateful for all the info I have found in this series. Thanks James! My question then has to do with the claim that many low-carbers make with regards to beta-cell destruction or decline in function over time when dealing with the constant blood glucose peaks associated with a high-carb diet. Is this a valid concern? Or, if everything you mention is kept in check (i.e. activity level, transfats, stress, sleep, excess calories, etc.), this simply a strawman?

              

          • Eric,

            I think it’s a strawman. There’s absolutely no scientific evidence that the blood sugar swings of a high-carb diet play any causal role in the decline in beta cells over time.

              

  18. Great article. But how do u explain hypoglycemia symptoms when diabetics take high insulin doses?

    Thanks!

      

  19. Just, really, thanks!

      

  20. Really interesting stuff, but how do you explain Bisschop et al. who found an low carb diet cut HGP in both healthy and diabetic people ?

    In a study of six healthy men, Dr Peter Bisschop compared the effects of diets containing 85%, 44% and 2% carbohydrate; there was no difference between the two higher carbohydrate diets, but the low-carbohydrate diet made a dramatic change. After a few days, their livers made more glycogen, the storage form of blood sugar, and cut back glucose output: “dietary carbohydrate content affects the rate of postabsorptive [fasting] glucose production mainly by modulation of glycogenolysis [the making of blood sugar by breaking down glycogen].” On the low carbohydrate diet, glucose made from glycogen was cut by 56% compared to the high carbohydrate diet (http://jcem.endojournals.org/cgi/content/full/85/5/1963).

    A similar study of seven diabetics compared an 89% carbohydrate diet with a diet without any carbohydrate, and found the no-carbohydrate diet produced a similar 45% reduction in the breakdown of glycogen (http://jcem.endojournals.org/cgi/content/full/89/12/6193). Furthermore, their HOMA IR insulin resistance fell by 31%,

      

  21. Could it be that: low-carb -> low glycogen -> less glycogenolysis -> less fasting hyperglycemia in the diabetics if their livers converted a larger proportion of the smaller amount of available glucose to glycogen resulting in less glycogen

    ( “Furthermore, their HOMA IR insulin resistance fell by 31%” should refer to the healthy people, not the diabetics whose IR didn’t change )

    BTW, I’m Type I, and my HbA1c on Dr Bernstein’s 6% -carb high-fat diet is 5.5% – I can’t exchange protein for fat without my blood sugar going out of control as it does if I add any more carb – nevertheless, my HDL is 53 and my TGs are 80 so I’m likely expressing large fluffy LDL and at low risk of heart trouble. No many may advocate such a dietary pattern, but it works for me

      

  22. “the correction of hyperglycemia comes primarily from inhibiting gluconeogenesis of the liver…not from stimulating glucose uptake into cells.”

    “Inhibition of hepatic gluconeogenesis means that the liver is not synthesizing glucose from amino acids or glycerol. After consuming a meal, how does the body remove the excess glucose in the blood and achieve homeostasis? ”

    “Metabolic tracer studies have shown that insulin regulates blood sugar primarily by inhibiting hepatic gluconeogenesis, so that the rate of appearance of glucose in the blood drops significantly.”

    I’m interested in this part:

    After consuming a meal, how does the body remove the excess glucose in the blood and achieve homeostasis?

    Thanks!
    p.s. love your site and posts James, it’s great to have an expert who is not afraid to jump into discussions!

    [quote=infernooo;842241]I would be interested to hear your response to the unanswered part of his question:

    As your answer only restated what you wrote in your last post, i.e.:

    I’m interested in this part:

    After consuming a meal, how does the body remove the excess glucose in the blood and achieve homeostasis?

    Thanks!
    p.s. love your site and posts James, it’s great to have an expert who is not afraid to jump into discussions![/quote]

      

  23. As someone who lives with and externally manages Insulin for a young Type 1 Diabetic, and has done so for a number of years, your summary theory does not concord with my reality and I would like you to explain if you can my reality compared to your theory.

    You say “This is why hyperglycemia and ketoacidosis occur simultaneously.”

    My experience is this is false. My Diabetic child can have Blood Glucose levels of 20 to 30 mmol/l and when we read using an abbott diabetic meter that measures ketones, we always read < 0.5 mmol/l. Which means, he has hyperglycemia but not ketoacidosis. They do not occur simultaneously, in fact it takes extended elevated levels for ketoacidosis to be measurable in the blood. And we never normally let his elevated blood glucose levels (hyperglycemia) last long enough. Further, even if he has high BGLs for long periods (sick days), provided we are providing enough insulin to compensate, which may not effect BGL's < 12mmol/l, ketoacidosis is avoidable for long periods (days).

    It may have seemed that way to the researcher you cite, in 1978 when the research you reference was published, but I probably have more advanced diagnostic tools available in my kitchen than these scientists dreamed of in 1978. In 1978 they weren't even doing (or recommending) diabetics do blood glucose readings at home (even if they could afford the machines). Diabetics shouldn't self diagnose doncha know.

    Pretty much everything else you conclude with is a crock of sh*t for anyone who deals with the realities of type 1 diabetes on a daily basis and knows the results of low carb food and high carb food and the metabolism of their child AS MEASURED with blood glucose and ketone measurement devices. A Diabetic can be successful and live healthily on either type of diet, one is hard to manage than the other however, and I believe a diabetic is much more likely to get fat on one than the other.

    As per the rest of your article.

    I love the way you cite research, but the research wasn't looking for the answer you said it proved, genius.

    I also laughed at the graphs where you compare things against themselves, with no reference to a control. Whey protein is high, compared to what??? Metabolism is complex. http://www.ajcn.org/content/80/5/1246.full.pdf+html shows that fat and protein and water play a regulating role in insulin response to glucose. Thats not a surprise. But it is key, its as the study says "The relation between protein contents and ISs was negative but not significant". If you care to, look at the table showing GI vs IS, there is a commensurate IS per GI, its just not an exact match, depending on the other macros present in the food.

    I particularly loved the stating of a Myth and then presenting something which is supposed to be proof, but it doesn't disprove the "Myth" it shows something else in its entirety. For example, it is 2 completely different propositions to say "Carbohydrate Drives Insulin, Which Drives Fat Storage" and then show that "blood fat prevents fat cells releasing fat into the blood stream". The two concepts are not even related, one does not prove or disprove the other.

    You are just as guilty as everyone else that blogs about diet of having a pet horse and riding that. You will selectively quote studies, quote them out of context and ignore information that counters your pet hypothesis.

    Oh and if your hypothesis is that its "all about the calories" then in future you should make sure your studies normalize their result to calorie content, or at least you should normalize the result. Otherwise the results are nonsense in the terms of your argument.

      

  24. It might be worth your while to bone up on the latest research on the role of fructose in all this. A lot of the mysteries are now explained. Eg why do th Atkins died and the Okinawa diet both work? What on earth do they have in common (low fructose). See

    Watch “sugar the bitter truth”
    http://www.youtube.com/watch?v=dBnniua6-oM
    short version
    http://www.youtube.com/watch?v=tdMjKEncojQ
    Slides
    http://www.mendosa.com/lustig_fructose.pdf
    or
    http://www.ucsfcme.com/2009/slides/MPD09001/14LustigSugar.pdf
    In relentless detail
    http://edrv.endojournals.org/cgi/reprint/30/1/96.pdf
    Hypothesis: Could Excessive Fructose Intake and Uric Acid Cause Type 2 Diabetes? by Richard J. Johnson, Santos E. Perez-Pozo, Yuri Y. Sautin, Jacek Manitius, Laura Gabriela Sanchez-Lozada, Daniel I. Feig, Mohamed Shafiu, Mark Segal, Richard J. Glassock, Michiko Shimada, Carlos Roncal, and Takahiko Nakagawa doi: 10.1210/er.2008-0033 Full text available http://edrv.endojournals.org/cgi/content/short/30/1/96
    Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease by Richard J Johnson, Mark S Segal, Yuri Sautin, Takahiko Nakagawa, Daniel I Feig, Duk-Hee Kang, Michael S Gersch, Steven Benner, and Laura G Sanchez-Lozada Am J Clin Nutr 2007;86:899 –906 Full text available via http://www.ncbi.nlm.nih.gov/pubmed/17921363
    Fructose, insulin resistance, and metabolic dyslipidemia by Heather Basciano, Lisa Federico and Khosrow Adeli Full text at http://www.nutritionandmetabolism.com/content/2/1/5

      

  25. Thank you James for the great info.

      

  26. Thanks for the great synthesis. It is great food for thought, or sugar for brain, if you will! I think perhaps your title is a little misleading, since it is clear that insulin is beneficial for muscle uptake of glucose, and it delegates away from tissues the role of sensing glucose. However, it is necessary to look at all research and the Okamoto article you link to may suggest an essential triad of brain-liver-pancreas as key. One thing that is lately coming into the limelight is glucagon. For readers, it is made by alpha cells, the neighbours of the insulin-producing beta cells. Please correct me if I am wrong, I am still catching up with the scientific literature. Glucagon does the opposite of insulin, it stimulates the liver to dump glucose into the bloodstream. Some reports show that insulin from beta cells normally quietens alpha cells. In fact, when insulin is up, glucagon is down, and when insulin is down, glucagon is up. Glucagon is the hormore that allows us to still get up in the morning after a long sleep without food. It may be that glucagon (in the absence of insulin’s inhibition) is keeping the liver actively maintaining the blood glucose high, but since the brain can only use glucose as its only source of energy, it is a little dangerous to be thinking of lowering glucagon as a therapy without being cautious of hypoglycemia. Thanks.

      

  27. Thanks for the info, I am not at all educated in the medical/science field but I could understand your writing, THANKS!!! Your info helped me not to be so hung up on insulin rather to be more aware of what I eat. You are more helpful than you know.
    Cindy in Ohio

      

  28. I know I’m really late to the party on this one, but hopefully you’re still alerted of new comments and reply to them. I started reading this series because I found it during a search of why dairy is bad (something people keep trying to sell me on lately), and kept reading because I was interested.

    Anyway, I’m also an ICU nurse who sees DKA patients regularly, and it’s kinda blowing my mind to hear stuff like: “However, there are plenty of glucose transporters on the cell surface, even when there is no insulin. In fact, there are enough transporters on the cell surface to allow the cell to get enough glucose to sustain its energy needs. Thus, glucose transport into cells is never truly dependent upon insulin.” You’re saying that even in the absence of insulin, the high blood sugars seen in Type I diabetics in DKA are caused by glucagon coming from the liver.

    But what about the fact that patients who have had total pancreatectomies, and therefore no pancreatic glucagon, will also develop DKA?

    Just trying to understand!

      

  29. I think diabetes is very much a mystery and needs to be approached with an open mindset. If we can all work together for the cure, (and better management) we may find that there is truth in nearly every blog that has been written. We aren’t looking for one person to be right. Diabetes is very complicated and unique for every person, and therefore, needs to be approached without prejudgement.

    I am always searching for new information about diabetes and am grateful to have found this blog to confirm a recent experience. My daughter (Type 1) was continually having high blood sugars because unknown to us, we were over medicating her and therefore, the liver would overcompensate. This overcompensation of the liver would cause the blood sugar readings to always look high. In reality she was dropping to major lows shortly after receiving fast acting insulin so then the liver would come to the rescue.

    It makes sense to consider that the insulin did such a fine job in up taking the glucose into the cells there was not enough insulin to be the traffic cop to tell the liver to stop dumping. Without a doubt, the liver produced a high blood sugar not the food. Most doctors would quickly prescribe more units of fast acting insulin. Fortunately, we happened to catch a reading when my daughter dropped to 39 and the endo agreed not to raise her meds. We are working on a treatment plan that keeps in mind the interactive roles of both the pancreas and the liver. It is learning process even for the doctors.

    Keep up the great work – all of you – and keep sharing!

      

  30. Is your daughter low-carb? I’ve been insulin dependent for 30 years, my HbA1c is 5% on Dr Bernstein’s Diabetes Diet. I haven’t had a serious hypo since I switched fifteen years ago, and my coronary artery calcium score is zero.

      

  31. My brother recommended I might like this blog. He was totally right.

    This post actually made my day. You cann’t imagine just how much time I had spent for this info!
    Thanks!

      

 Leave a Reply

(required)

(required)

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>