Insulin: An Undeserved Bad Reputation, Part 5: Addressing the Critics

 

This series on insulin has stimulated numerous threads of discussion on various sites on the internet.  I have seen some of these discussions and some unfounded criticisms by some individuals who appear to adhere to the “carbohydrates drive insulin which drives fat storage” mantra.  However, this thinking is an example of cognitive miserliness, and I will address some of the comments of these critics here.

Some people have argued that my series on insulin only applies to healthy people and not people with glucose intolerance, obese people, or diabetics.  I briefly explained how this is not true here, but either these critics did not read that section of the article or ignored it.  To elaborate, some of the research I cited on protein and insulin secretion showed protein to be more insulinemic in obese people than lean people, yet we know that high protein intakes have been shown to be beneficial to helping obese people lose weight.  Obviously stimulation of insulin secretion is not a problem here.  Also, protein and carbohydrate tend to have a synergistic effect on insulin secretion when consumed together, creating a greater insulin response than when either one is consumed alone.  Yet, we know that a high protein, moderate-to-high carbohydrate, low-fat diet has been shown to be beneficial for weight loss.  We would expect such a diet to cause significant postprandial insulin secretion based on the combination of protein and carbohydrate, yet the diet causes significant weight loss.  Why?  Because of the effects of protein on satiety, resulting in people simply eating less.  Therefore, it comes down to a matter of energy balance.  The postprandial insulin secretion is irrelevant…insulin cannot trump the laws of physics.

To further illustrate how all of this data applies to all individuals and not just healthy people, let’s take a look at the effects of dairy on insulin.  I wrote extensively about how dairy products can be just as insulinemic, if not more insulinemic, than high carbohydrate foods, including the dreaded white bread.  If augmented postprandial insulin secretion is a problem for obese people, type 2 diabetics, or glucose intolerant people, then we would expect dairy to be a problem for these populations as well.  However, we know that they are not.  Diets high in dairy do not impair weight loss or blood sugar control in overweight people, and they improve insulin sensitivity and attenuate weight gain in animal models.  We also know that a high intake of dairy products is associated with a lower risk of metabolic syndrome and type 2 diabetes.  Thus, it is obvious that augmented postprandial insulin secretion is not the problem that some have made it out to be, even for people with health issues.

Some critics claimed that it is the combination of high postprandial insulin and high postprandial glucose that is the problem, not insulin itself.  However, if this were truly the issue, then we would still expect dairy to increase risk of weight and fat gain, since most people consume dairy along with foods that elevate glucose (most people do not consume dairy alone).  Yet, we know from a large number of studies that dairy does not increase weight gain risk, and decreases weight gain in animals.  This is despite the fact that dairy is being consumed with glucose-elevating foods.  The problem here is that the critics are taking an overly reductionistic view of insulin and body fat deposition.  Since insulin enhances glucose uptake of fat cells, and since insulin also inhibits lipolysis, these critics are concluding that the combination of high insulin and high glucose will cause fat gain.  However, this view is incorrect.  In fact, dairy products will increase the uptake of glucose into fat cells, yet result in less fat and weight gain.  Thus, things are not as simple as the critics make them out to be.

One critic pointed out how I had discussed insulin’s inhibition of lipolysis, and then insinuated that this is how insulin leads to fat gain.  Yet, on the same token, this same critic stated that it was the high insulin and high glucose that is the problem, not high insulin itself.  This was an inconsistency in this critic’s position.  Obviously the latter assertion is incorrect based on what I discussed in the previous paragraph.  Regarding the former insinuation, it again is an overly reductionistic view of insulin in the body.  Yes, insulin inhibits lipolysis, but it only takes small elevations in insulin to do this, and this does not address what happens over a 24-hour period.  It also does not address all of the other dozens of hormones and other factors simultaneously interacting on fat tissue.  Not only that, but if the former insinuation were true, then we would again expect dairy products to promote fat gain in animals and humans, yet we know that they do not.

Some critics claimed that the protein/insulin secretion studies I cited in this article mainly involved liquid and not solid foods.  However, only some of the studies involved liquids.  Other studies (such as this one and this one) involved solid foods.

Some critics created a straw man and stated that I was claiming that protein is just as insulinemic as carbohydrate.  In fact, one critic said, “I can’t believe Krieger is here trying to say that protein causes more insulin release than sugar!”  However, I only said that protein can be just as insulinemic as carbohydrate (can is the key word here).  Certainly, when you average across all foods, carbohydrate produces the greatest insulin responses, and protein comes in second.  However, when you start looking at individual foods, some protein sources can produce similar insulin responses to some carbohydrate foods (even some carbohydrate foods that create rapid rises in blood glucose).  And this is not to mention the synergistic effect that protein and carbohydrate can have on insulin secretion when consumed together.  Yet, studies that have combined the two have shown large amounts of weight and fat loss.

One particular critic that I saw created a huge load of straw men and other fallacies.   First, this individual said, “Unlike what Krieger says, insulin release actually first starts when you start to put the food in your mouth…It is wrong to say that insulin secretion starts only after the glucose is already in the blood.” This individual is referring to cephalic phase insulin secretion, and the statement is a straw man because I never claimed that cephalic phase insulin secretion does not exist or that insulin secretion starts only after glucose is already in the blood.  This individual then said that nobody claims that high carbohydrate diets lead to chronically high insulin levels.  I am not sure what this critic has been reading as I see this claim made quite often from numerous individuals all over the internet, including low carbohydrate diet gurus.  Perhaps this individual has never said this, but that does not mean that others have not.   This individual went on to make the claim that “Our argument is high insulin tends to drive fat storage.”  Again, if the statement were true, then dairy products should promote fat storage, yet they do not.  Also, if that statement were true, then that would mean that insulin levels should predict future weight gain.  However, the vast majority of prospective studies have failed to show a relationship between either basal or postprandial insulin levels and future weight gain; in fact, some studies have shown higher insulin levels to be predictive of less weight gain in overweight people.  Also, insulin levels are not predictive of weight loss.  Thus, the concept that high insulin drives fat storage is a concept not supported by the scientific data.

This individual then created a strawman out of my statement of how consuming 5000 calories worth of olive oil or table sugar is not very palatable, and tried to contradict that by claiming that it’s difficult to eat 5000 calories worth of steak but easy to eat 5000 calories worth of cake or similar high carbohydrate foods.  Well, it’s not easy to consume 5000 calories worth of steak because of the high protein content and because that would take a lot of chewing that would eventually get old.  I could easily dump 5000 calories of a full-fat dressing (Caesar salad, anyone?) and it would not be difficult at all to consume that amount.  In fact, I would find that easier to consume (due to the energy density) then 5000 calories worth of cake.  Along these lines, in the weight loss program for which I used to do research, one client was not losing weight and swore she was following the program.  Her husband eventually ratted her out and told the dietitian that she was consuming over 8 tablespoons of peanut butter per day.  That’s close to 1,000 calories per day that she was not reporting.  Eight tablespoons is a very easy way to quickly consume a large amount of calories, despite the fact that peanut butter is mostly fat and low in carbohydrate.  The ease of consuming a large number of calories of a particular food depends much more on the palatability, the protein content, the food form (solid versus liquid), the water content, the energy density, and the fiber content, then it does on the carbohydrate content.

This individual then stated that insulin “makes you hungry because it leads to insulin swings and hypoglycemia a few hours later.”  Well, insulin does not lead to insulin swings.  I think that this person was referring to carbohydrate.  There is often the claim that high glycemic carbohydrate will cause a rapid rise in blood sugar and insulin, followed by a crash which will induce hunger.  However, this concept is not fully supported by the scientific data.  High glycemic foods do not necessarily have low satiating power; in fact, one study that rated foods on their ability to create satiety found that some high glycemic carbohydrate foods, such as potatoes and white rice, were among the most satiating of all of the foods tested.  Another study found a weak relationship between the glycemic response of a breakfast and energy intake at lunch, but no relationship between the insulin response to the meal and energy intake at lunch.  In a meta-analysis of the relationship between blood glucose responses and appetite, no relationship was observed, and higher insulin levels were actually associated with decreased hunger.

As I stated in a previous blog post, human appetite control is highly complicated.  Things are not as simple as “glucose goes up, insulin goes up, glucose then crashes and hunger increases.”  Even if the latter were true (which it is not given the scientific data), most people do not consume high glycemic carbohydrates by themselves.  They generally consume them with other foods, which dramatically changes the blood sugar and insulin responses.

This critic goes on to say, “Type 2 diabetics are still often hungry even though their blood sugars are constantly high. If insulin is so good at satiating, then why do these diabetics still feel hungry?”  Type 2 diabetics have insulin resistance in the brain, which disrupts insulin’s ability to signal the brain to reduce food intake.

This critic also states that nobody said that “carbohydrates are singularly responsible for driving insulin.”  Actually Gary Taubes said it in his book, word for word.  She goes onto say that, regarding one particular study I referenced, I claimed that 75 grams of carbohydrate was “low carbohydrate.”  I never made that claim; the study labeled it as such.  I clearly addressed this with this paragraph:

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

This critic then goes on to my comments regarding how some in the low-carbohydrate community claim that the insulin response to protein is due to the gluconeogenesis from the protein.  She states, “Then he says that ‘some’ might say it is due to gluconeogenesis. Really? WHo would need to argue that when their drink has CARBOHYDRATES in it already!” This critic completely missed the point, and needs to look at the graphs of the blood insulin and glucose responses.  First, the carbohydrate in the drink was quite low (only 11 grams) and did not cause much change in blood glucose.  However, there was a very large insulin response.  This means that the insulin response was not due to the blood glucose response.  This completely contradicts the claims of some low-carbohydrate advocates that the insulin response from protein is due to the protein being converted to glucose, which would then drive up insulin.  I then supported this further by citing research showing that amino acids directly stimulate the pancreas to produce insulin.

This individual goes on to state, “The weirder thing is this study actually shows what we argue, ie that obese people have higher insulin response to the same meal compared to nonobese. This will be true of both protein AND carbs but he only talks about protein here. Thus supporting our argument that insulin drives weight gain.”  This individual is committing the cum hoc, ergo propter hoc (“with this, therefore because of this”) fallacy.  The fact that obese people present with high levels of insulin does not mean that high insulin causes the obesity; they are simply correlated.  In fact, not all obese people have high insulin levels.  High insulin is not the driver of obesity; rather, it is the result of obesity and the insulin resistance that often accompanies it.  Insulin resistance is causing the high insulin in obese people (the high insulin is the body’s way to compensate for insulin resistance).

I will continue to address other criticisms that I have seen next week, along with continuing last week’s article on how insulin regulates blood sugar.

  76 Responses to “Insulin: An Undeserved Bad Reputation, Part 5: Addressing the Critics”

  1. Keep the good information coming!

    Even I like following a lower carbohydrate diet (although I incorporate high carb days) and I find this information valuable. I never believed that a hormone can be inherently bad anyways, or else we wouldn’t have it.

    It’s just the excess of said hormone or said nutrient.

      

  2. for the longest time, i thought chronic high insulin level would cause insulin resistance. apprently, its the other way.
    gd stuff. as usual, u counter yr critics w evidence based arguments and w grt composure( how do u not seem ever to lose yr temper no matter how others insinuate stuff abt u?!?)…keep it up, looking forward to expanding ma knowledge w yr articles.

      

  3. James, I have been reading your information since Lyle Mcdonald mentioned you and I am extremely impressed with your knowledge and ability to break things down for us lay people to understand.
    Whenever someone presents a new point of view it seems everyone jumps on the bandwagon to bash it regardless of wether it is supported by science. Keep giving them hell.

    I believe you mentioned going to a paid subscription for the site. Wonderful idea I would gladly pay to read cutting edge views on nutrition because everyone else is just rehashing the same old shit.

      

  4. Good stuff as always. Working with a smart endocrinologist a few years back I learned how it is possibly the excess fat (visceral fat) that is causing the insulin resistance, and not the insulin itself. At first I was perplexed, but it all makes more sense now that we understand that visceral fat is hormonally active. Thank you for the studies!!!

      

  5. The more I examine the matter, the more I suspect that high omega-6 intake in conjunction with high carbohydrate intake drives insulin resistance. Magnesium imbalance seems to figure into the equation. Here’s a comment by Ted Hutchenson:

    “As a personal comment on the argument. I’d been following conventional health advice regarding healthy eating and because I am unable to exercise regularly or vigorously (late effects of polio) was faced with the prospect of always eating fewer calories than my appetite demanded or getting heavier year on year. As I had got to the point of being virtually unable to walk and required help with personal care I was not in a position to contemplate any further decline in mobility or muscle strength.

    After listening to the first Taubes online lecture and following a Jimmy Moore interview with Dr Dahlqvist I followed her way of eating and was able to lose weight, without extra exercise and haven’t regained it since. I don’t think it is quite as simple as just reducing carbohydrate intake. I am fairly certain correcting vitamin D3, magnesium and omega 3 status also helps. I never ate unlimited amounts of fat/protein and although I don’t think it is necessary to count every carb or calorie consumed I think you make weight loss harder if you are unreasonably greedy.”

    Response from Black57
    “This is so true. Ted, when I began re-gaining weight after losing 30 lbs., I began to speculated that I continued to somehow experience some sort of insulin reistance, somehow. I re-gained the weight while sticking strictly to my low carb regimen. I now know that I am magnesium deficient and that magnesium plays a very important part in regulating insulin and vitamin D3 works with magnesium in doing this job. Also, the longer your are deficient in magnesium, the more resistant your body becomes to magnesium which complicates its absorption. I believe that is why I am having such a hard time absorbing magnesium.”

    These comments are from this web page: http://www.livinlowcarbdiscussion.com/printthread.php?tid=5145

      

    • David,

      I am of the opinion that there is no single driving cause behind insulin resistance. There are many causes of insulin resistance, and many of these causes are interacting with each other to help drive insulin resistance in society.

        

  6. James,

    I’m not sure that you have shown unambiguously that dairy and dairy protein are not fattening.
    Some recent studies show that milk does in fact lead to weight gain. Here is a 3-year study of milk consumption in adolescent children, conducted by an all star cast including Harvard’s Walter Willett:

    Scientific version: http://www.ncbi.nlm.nih.gov/pubmed/15939853
    Popular version: http://www.washingtonpost.com/wp-dyn/content/article/2005/06/06/AR2005060601348.html

    Another study (albeit in obese rats) shows that the presence of calcium in the milk may attenuate both the weight gain and the insulin response otherwise seen with calcium-free diary proteins like whey and casein. This study suggests that one cannot draw the conclusion that the insulinogenic effect of whey protein cannot necessarily be extrapolated to dairy in general:
    http://www.nature.com/oby/journal/v18/n4/abs/oby2009300a.html

    Furthermore, the study by Johnson et al which you cite to show that dairy in the presence of glucose is not fattening is less than convincing for several reasons:

    1. The study was in mice, not humans.
    2. The dairy was “yogurt powder”, not milk.
    3. The reason given for less weight gain was “Digestive efficiency was significantly lower in the yogurt mice due to greater fecal production”; this could mean that mice had problems digesting the “yogurt powder”

    In my opinion, a 4-week study of mice fed yogurt powder that they perhaps can’t even digest is far less convincing than a 3-year longitudinal study of various levels of milk consumption in more than 12,000 chldren, with careful statistical analysis.

    Todd

      

    • Some recent studies show that milk does in fact lead to weight gain. Here is a 3-year study of milk consumption in adolescent children, conducted by an all star cast including Harvard’s Walter Willett

      First, this paper is an observational trial and cannot establish cause and effect. Second, the data in this paper is quite clear that the increased weight gain was related to increased energy intake (imagine that!) and not dairy specifically. Third, even if this paper did demonstrate an association between dairy and weight gain, you must understand what the majority of the evidence indicates, not one paper. I cited animal trials, a number of observational trials, and controlled human trials. If the vast majority of research indicates no relationship, with only a few studies showing an association, then you must go with what the majority of the evidence indicates. And in this case, it’s that dairy does not increase risk of weight gain.

      Another study (albeit in obese rats) shows that the presence of calcium in the milk may attenuate both the weight gain and the insulin response otherwise seen with calcium-free diary proteins like whey and casein.

      First, this study only showed that calcium attenuated weight gain more than whey or casein that was calcium free. However, there was no true control in this study (i.e., a group with no dairy protein at all), so one cannot claim that whey or casein have no attenuation effect in and of themselves.

      Second, this is another case where you need to look at what the majority of studies indicate. As Dr. Stephen Guyenet points out here, the majority of rodent studies (like this one) indicate calcium is not responsible for the attenuation of weight gain, indicating there is another component of the dairy that is responsible.

      Third, there is evidence of a weight-gain attenuating effect of whey protein (which is the most insulinemic of dairy proteins) in rodents, as demonstrated in this study.

      Furthermore, the study by Johnson et al which you cite to show that dairy in the presence of glucose is not fattening is less than convincing for several reasons:

      1. The study was in mice, not humans.

      Actually, the fact the study was on mice only supports my point further. Rodents have a greater capacity for de novo lipogenesis than humans. The fact that dairy did not increase weight gain, despite the fact that it is insulinemic and increased glucose uptake into fat cells, in a species that has a high capacity for de novo lipogenesis, then we certainly would expect less of an effect in humans, not more.

      2. The dairy was “yogurt powder”, not milk

      That is irrelevant. All dairy has been found to be very insulinemic, including yogurt.

      3. The reason given for less weight gain was “Digestive efficiency was significantly lower in the yogurt mice due to greater fecal production”; this could mean that mice had problems digesting the “yogurt powder

      A lower efficiency doesn’t mean “problems” digesting the powder. But regardless, this only supports my point made here that focusing on insulin is overly reductionistic. The human body is a dynamic organism regulated by a very complicated system. The individuals who demonize insulin act as if insulin operates in a vacuum, independent of all of the other important factors simultaneously acting in the system.

        

  7. Another great post, James – keep it up!

    Btw; i’ve posted a question for you in your article ‘Physical Activity and Weight Regain’, great if you could answer that.. Just posting here in case you didn’t see it, no stress!

      

  8. James,

    While not tied directly to the insulin issue, per se, your mention of potatoes and rice rating well in the satiety department got me thinking about these foods a bit more. I am wondering if you have any quick thoughts on whether it is worth the effort to prepare brown rice (as one example of a grain) in the traditional manner to reduce anti-nutrient content/impact versus simply consuming white rice with some mixe vegetables, instead. This question stems, in part from my reading of Dr. Stephan Guyenet’s (someone you’ve mentioned in the past) blog and being introduced to various preparation methods I had previously had zero exposure to. I suppose this could apply to any instance where a starchy carb source may be consumed and you can either go with the unrefined or refined option.

      

    • Giueseppe,

      I’ve heard many people talk about the anti-nutrient content of grains, and how different preparation methods can affect this content, but I have not done enough reading of the literature in this area to form an opinion. This is a good topic though that I hope to investigate some time in the future.

        

  9. Well done James. I was going to comment to that “singular” person but didn’t think it worth the effort. I’ve posted on the direct stimulation of insulin by long chain free fatty acids (NEFA/FFA). Since the elevated NEFA/FFA seem to be early on in the progressing of IR/MetS/T2 due to large fat cells losing their insulin sensitivity, this seems a plausible mechanism for how obesity increases basal insulin. The obese or insulin resistant will secrete more in response to dietary stimuli, but this is because of decreased sensitivity to it. When you think about it, IF carbs –> insulin –> fat storage, the insulin resistant fat cells would not take up glucose efficiently. Taubes’ version of fat metabolism is bass-ackwards except for the occasional truth mixed in (e.g. insulin inhibits lipolysis, which it does) but then misrepresented when taken out of context.

    Your readers may be interested in the results of Shai & Diabetes. Taubes spent considerable time on this 2 year study in his latest lecture. In non-diabetics, fasting insulin went down for low carbers, in diabetics it went down the greatest in the Mediterranean group who consumed more carbs. Note also there was no significant difference in FBG for the non-diabetics while the advantage in diabetics again went to the higher carb consuming Med’n group – especially at the 2 yr mark (where weight losses were comparable between LC and Med’n).

    There have been a number of studies (don’t have onhand at this time) by Nuttal’s group looking at insulin responses to various foods in various combinations, etc. Interestingly enough, the insulin response differs with time of day, whether it’s fasted or 2nd meal of the day, etc.

    Anyway … rambling now! KUTGW James :-)

      

  10. to Todd: i checked out the study u linked. this study was evaluated based on questionnaires.i think self reporting based study should be taken w a pinch of salt as there is no way to determine how accurate te participants reportings were. also, the study concluded that the gain was as a result from the increase kcals, not because of the milk itself. i would also to suggest another possible explantion for the results of this study: there were adolescents who drank more milk. adolescents is a period where calcium absorption is high as they are growing. hence, the participants that drank 3 glass milk/day had more calcium absorbed into their bones which result to stronger (thicker and heavier) bones. this may explain their higher weight gain. (just my opinion)

      

  11. This is very interesting material.

    Speaking as a physicist, however–and I am–I have to say that I’m extremely tired of statements about calories in and calories out as a means of predicting fat gain and loss, and am especially bugged by the refrain that you “can’t trump the laws of physics.”

    Well, of course you can’t. But people’s descriptions of how calories relates to weight gain, and how weight gain relates to fat gain, tend to be vastly oversimplified.

    It isn’t just that the human body is more complicated than an engine. Most of the descriptions I read of how fat is lost or gained by caloric intake wouldn’t even be sufficient for describing a simple engine.

    This is not a criticism of you; I’m sure you have a good appreciation for the subtleties of metabolism.

    But I do wish we could declare a moratorium on the use of the phrase “the laws of physics” with respect to weight control. According to my rather unscientific survey, 99% of the time one hears that phrase, the person using it can’t tell you the difference between energy expended and work*; and 95% of the time, they can’t list the three (or four, if you include the zeroth law) of thermodynamics and explain them.

    *(Which is why so many people insist that walking a mile and running a mile burn the same number of calories. They don’t, although the work accomlished is the same.)

      

    • David, you are exactly right about the triteness of “calories in = calories out”. People say this as if to imply that every calorie of food either gets converted to body mass or gets converted to energy and expended. But there are several other “ins” and “outs” in the coupled mass and energy balances, including two major outs: (a) what gets excreted as incompletely digested; (b) what is lost in respiration. There is also at least one other “in”: the air that is breathed in, which is a source of oxidation.

      My experience is that (a) and (b) account for a lot. The efficiency of digestion of different macronutrients and specific foods can lead to major differences in how much just gets passed through as waste. I also lose about 2-3 pounds just sleeping every night. Is that all lost as “energy” or is much of the lost through transpiration of water and exhaled carbon dioxide vs. the inhaled oxygen?

      Has anyone looked into whether low carbohydrate diets might result in a smaller pecentage of calories being captured as body mass and a higher amount loss in urine, feces, water vapor and breath gases? This type of explanation would not require any special “metabolic advantage” — but rather a “stoichiometric advantage”, based on a less efficiency conversion. All still within the first law of thermodynamics!

        

      • But there are several other “ins” and “outs” in the coupled mass and energy balances, including two major outs: (a) what gets excreted as incompletely digested; (b) what is lost in respiration.

        The two major “outs” that you mention have been found to not be major outs.

        First, in regards to excretion, changes in digestive energy absorption only account for very small changes in the energy “in” side of the equation. Fractional energy absorption tends to be fairly consistent in humans at around 95% of ingested energy intake (this paper reviews the literature on this). There are small variations of 2-3%, but this would only account for 40 calories on a 2000 calorie per day diet. Thus, while fecal energy excretion is part of the “out” side of the equation, it is not a major portion of it.

        Also, calories are not “lost” in respiration, other than ketone excretion in the breath. However, ketone excretion only accounts for 100 calories per day for someone on a ketogenic diet (and that’s including ketone excretion in the urine as well as the breath); for someone who is not on a ketogenic diet, ketone excretion in the breath is negligible. You may be referring to the carbon dioxide production that occurs during oxidation of fuels in the body, but this is already captured in energy expenditure measurements (whether through indirect calorimetry or through doubly labeled water).

        There is also at least one other “in”: the air that is breathed in, which is a source of oxidation.

        Breathing in air is not a part of energy expenditure, other than through the mechanical work required for respiration. If you are referring to the oxidation of macronutrients, again, these are already captured in standard measurements of energy expenditure.

        I also lose about 2-3 pounds just sleeping every night. Is that all lost as “energy” or is much of the lost through transpiration of water and exhaled carbon dioxide vs. the inhaled oxygen?

        Overnight changes in body weight are simply due to losses of body water through respiration, urination, and perspiration. Inspired and expired gases have no relevance to it.

        Has anyone looked into whether low carbohydrate diets might result in a smaller pecentage of calories being captured as body mass and a higher amount loss in urine, feces, water vapor and breath gases?

        Low carbohydrate diets result in greater water loss than higher carbohydrate diets; this has been well established in a number of studies, including this one. This research has also established that, once water loss is accounted for, all of the weight loss can be attributed to a change in energy intake. Thus, there is no change in fecal energy excretion that is large enough to be of any significance. The loss of ketones in the breath and urine only accounts for around 100 calories per day maximum, and will diminish with time as it is difficult to remain in ketosis over time.

          

  12. thought this was interesting i regards to dairy:

    Nutr Metab (Lond). 2009 Jun 5;6:26.
    Leucine modulation of mitochondrial mass and oxygen consumption in skeletal muscle cells and adipocytes.

    Sun X, Zemel MB.

    University of Tennessee, Knoxville, Tennessee, 37996, USA . mzemel@utk.edu.
    Abstract

    ABSTRACT: BACKGROUND: The effects of dairy on energy metabolism appear to be mediated, in part, by leucine and calcium which regulate both adipocyte and skeletal muscle energy metabolism. We recently demonstrated that leucine and calcitriol regulate fatty acid oxidation in skeletal muscle cells in vitro, with leucine promoting and calcitriol suppressing fatty acid oxidation. Moreover, leucine coordinately regulated adipocyte lipid metabolism to promote flux of lipid to skeletal muscle and regulate metabolic flexibility. We have now investigated the role of mitochondrial biogenesis in mediating these effects. METHODS: We tested the effect of leucine, calcitriol and calcium in regulation of mitochondrial mass using a fluorescence method and tested mitochondrial biogenesis regulatory genes as well mitochondrial component genes using real-time PCR. We also evaluated the effect of leucine on oxygen consumption with a modified perfusion system. RESULTS: Leucine (0.5 mM) increased mitochondrial mass by 30% and 53% in C2C12 myocytes and 3T3-L1 adipocytes, respectively, while calcitriol (10 nM) decreased mitochondrial abundance by 37% and 27% (p < 0.02). Leucine also stimulated mitochondrial biogenesis genes SIRT-1, PGC-1alpha and NRF-1 as well as mitochondrial component genes UCP3, COX, and NADH expression by 3-5 fold in C2C12 cells (p < 0.003). Adipocyte-conditioned medium reduced mitochondrial abundance (p < 0.001) and decreased UCP3 but increased PGC-1alpha expression in myocytes, suggesting a feedback stimulation of mitochondrial biogenesis. Similar data were observed in C2C12 myocytes co-cultured with adipocytes, with co-culture markedly suppressing mitochondrial abundance (p < 0.02). Leucine stimulated oxygen consumption in both C2C12 cells and adipocytes compared with either control or valine-treated cells. Transfection of C2C12 myocytes with SIRT-1 siRNA resulted in parallel suppression of SIRT-1 expression and leucine-induced stimulation of PGC-1alpha and NRF-1, indicating that SIRT-1 mediates leucine induced mitochondrial biogenesis in muscle cells. CONCLUSION: These data suggest that leucine and calcitriol modulation of muscle and adipocyte energy metabolism is mediated, in part, by mitochondrial biogenesis.

      

  13. “Yes, insulin inhibits lipolysis, but it only takes small elevations in insulin to do this, and this does not address what happens over a 24-hour period.” When comparing isocaloric diets that stimulate high or low insulin secretion weight loss is the same between groups.

    “This individual then stated that insulin “makes you hungry because it leads to insulin swings and hypoglycemia a few hours later.” In reality, research has shown that insulin helps to decrease hunger. But, as James mentioned a variety of factors are involved with hunger and appetite regulation.

    “This critic also states that nobody said that “carbohydrates are singularly responsible for driving insulin.” Apparently, this critic is not well read in the area of popular nutrition info.

    “This means that the insulin response was not due to the blood glucose response. This completely contradicts the claims of some low-carbohydrate advocates that the insulin response from protein is due to the protein being converted to glucose, which would then drive up insulin.”
    From an article I wrote titled all Mighty Glucagon!:

    Amino acids are derived from a meal containing protein. They stimulate the release of both glucagon and insulin. The amount of the hormone stimulated depends on the individual amino acid and/or the group of amino acids present. A study by Kuhara and
    colleagues (1991) examined the effects of the intravenous infusion of 17 amino acids on the secretion of insulin, glucagon, and growth hormone (GH) in six castrated male sheep. Leucine was the most effective amino acid in stimulating insulin secretion but did not produce any increase in glucagon and GH secretion. Alanine, glycine, and serine induced a greater enhancement of both glucagon and insulin secretion than other amino acids. No
    amino acid was able to specifically stimulate glucagon secretion without also increasing insulin or GH secretion. Branched-chain amino acids tended to suppress glucagon secretion and enhance insulin.

      

  14. I must say I really liked this article (all of them really). Given me many ideas to writing one of my own :) I wrote an article earlier this year (in norwegian that is) about lowcarbdiets effect on weightloss and reduction of fatmass. Its actually very clear that they dont increase weightloss or reduction i fatmass. The short version is that about 70 % of the studies doesnt show any additional effect compared to traditional lowfat diets. The carbohydratecontent of the diet simply doesnt matter that much when diets er match for energy.

    If you look at studies that lasted shorter than 6 months, 11 shows better effects of lowcarb on weightloss (1-11), against 27 that showed no extra effect (12-38). Of the studies looking at fatloss only 3 show extra effect of a lowcarbdiet (3, 4, 9), against 16 that show no additional effect (13-18, 20-23, 26-28, 30, 31, 33, 34).

    If you look at studies that lasted more than 6 months, 9 showed better effects of lowcarb on weightloss (1, 3, 4, 9, 39-43), against 15 that showed no extra effect (1, 4, 5, 19, 24, 44-53). Only one studie showed extra effect after 1 year (41), against 13 that showed no additional effect (1, 4, 5, 19, 44-47, 49-53). No studies showed extra effect on fatmassreduction after 1 year (4, 50).

    When you look at all the scientific studies that are pro lowcarb, most of them have one or more of these weeknesses:

    1. Not matched for proteincontent
    2. No controll of physical activity or exercise
    3. Selfreported foodintake, make their own food and write it down.
    4. Some even have no controll of energy intake

    So, I showed that carbohydrate aint worse than fat when it comes to weightmanagement. However, people still belive in it, so the next step is to take down the insulinmyth.

    Thanks for the inspiration :)

    Iben K.

    References:
    1. Foster et al (2003) A randomized trial of a low carbohydrate diet for obesity. N Engl J Med. 348: 2082-2090.

    2. Lewis et al (1977) Effect of diet composition on metabolic adaptions to hypocaloric nutrition: comparison of high carbohydrate and high fat isocaloric diets. Am J Clin Nutr. 30: 160-170.

    3. Brehm et al (2003) A randomized trial comparing a very low carbohydrate diet and a calorie restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 88: 1617-1623.

    4. Gardner et al (2007) Comparison of the atkins, zone, ornish and LEARN diets for change in weight and related risk factors among overweight premenopausal women: The A to Z weight loss studie: Arandomized trial. JAMA 297(9): 969-977.

    5. Davis et al (2009) Comparative study of the effect of a 1-year dietary intervention of a low carbohydrate diet versus a low fat diet on weight and glycemic control in type 2 diabetes. Dia Care. 32: 1147-1152.

    6. Brehm et al (2005) The role of energy expenditure in the differential weightloss in obese women on low fat and low carbohydrate diets. Metab. 90: 1475-1482.

    7. Baron et al (1986) A randomized controlled trial of low carbohydrate and low fat/hig fiber diets for weight loss. J Public Health. 76: 1293-1296.

    8. Young et al (1971) Effect on body composition and other parameters in obese young men of carbohydrate level of reduction diet. Am J Clin Nutr. 24: 290-296.

    9. Skov et al (1999) Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for treatment of obesity. Int J Obes. 23: 528-536.

    10. Volek et al (2004) Comparison of a very low carbohydrate and low fat diet on fasting lipids, LDL subclasses, insulin resistance and postprandial lipemic responses in overweight women. J Am Coll Nutr. 23(2): 177-184.

    11. Stephen et al (2003) Effects of a low carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr. 142(3): 253-258.

    12. Volek et al (2003) An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial lipemic responses compared with a low fat diet in normal weight, normolipidemic women. J Nutr. 133: 2756-2761.

    13. Mc-Millan-Price et al (2006) Comparison of 4 dits of varyying glycemic loa don weight loss and cardiovascular risk reductions in overweight and obese young adults. A randomized controlled trial. Arch Intern Med. 166: 1466-1475.

    14. Tay et al (2008) Metabolic effects of weight loss on a very low carbohydrate diet compared with isocaloric high carbohydrate diet in abdominally obese subjects. J Am Coll Cardiol. 51(1): 59-67.

    15. Luscombe-Marsh et al (2005) Carbohydrate-restricted diets high in either monosautrated fat or protein are equally effective at promoting fat loss and improving blood lipids. Am J Clin Nutr. 81: 762-772.

    16. Noakes et al (2006) Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutr Metab. 3:7 doi:10.1186/1743-7075-3-7.

    17. Noakes et al (2005) Effect of an energy-restricted high protein low fat diet relative to a conventional high carbohydrate low fat diet on weight loss, body composition, nutritional status and markers of cardiovascular health in obese women. Am J Clin Nutr. 81: 1298-1306.

    18. Johnston et al (2006) Ketogenic low carbohydrate diets have no metabolic advantage over nonketogenic low carbohydrate diets. Am J Clin Nutr. 83: 1055-1061.

    19. Dansinger et al (2005) Comparison of the atkins, ornish, weight watchers and zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. 293(1): 43-53.

    20. Meckling et al (2004) Comparison of a low fat diet to a low carbohydrate diet on weight loss, body composition and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J Clin Endo Metab. 89: 2717-2723.

    21. Lasker et al (2008) Moderate carbohydrate, moderate protein weight loss diet reduces cardiovascular disease risk compared to high carbohydrate, low protein diet in obese adults: A randomized clinical trial. Nutr Metab. 5:30 doi:10.1186/1743-7075-5-30.

    22. Bradley et al (2009) Low fat versus low carbohydrate weight reduction diets. Effect on weightloss, insulin resistance, and cardiovascular risk: a randomized control trial. Diabetes. 58(12): 2741-2748.

    23. Golay et al (1996) Similar weight loss with low- or high carbohydrate diets. Am J Clin Nutr. 63: 174-178.

    24. Lean et al (1997) Weight loss with high and low carbohydrate 1200 kcal diets in free living women. Eur J Clin Nutr. 51: 243-248.

    25. Gerhard et al (2004) Effects of low fat diet compared with those of a high-monosaturated fat diet on body weight, plasma lipids and lipoproteins, and glycemic control in type 2 diabetes. Am J Clin Nutr. 80: 668-673.

    26. Farnsworth et al (2003) Effect of a high protein, energy-restricted diet on body composition, glycemic control and lipid concentrations in overweight and obese hyperinsulinemic men and women. Am J Clin Nutr. 78: 31-39.

    27. Rumpler (1991) Energy-intake restriction and diet composition effects on energy expenditure in men. Am J Clin Nutr. 53: 430-436.

    28. Pereira et al (2004) Effects of a low glycemic load diet on resting energy expenditure and heart disease risk factors during weight loss. JAMA. 292(20): 2482-2490.

    29. Landry et al (2003) Whole body fat oxidation rate and plasma triacylglycerol concentrations in men consuming an ad libitum high carbohydrate or low carbohydrate diet. Am J Clin Nutr. 77: 580-586.

    30. Colette (2003) Exchanging carbohydrates for monosaturated fats in energy-restricted diets: effects on metabolic profile and other cardiovascular risk factors. Int J Obes. 27: 648-656.

    31. Luscombe et al (2003) Effect of a high-protein, energy restricted diet on weight loss and energy expenditure after weight loss stabilization in hyperinsulinemic subjects. Int J Obes. 27: 582-590.

    32. Noakes & Clifton (2000) Changes in plasma lipids and other cardiovascular risk factors during 3 energy-restricted diets differing in total fat and fatty acid composition. Am J Clin Nutr. 71: 706-712.

    33. Layman et al (2003) A reduced ration of dietary carbohydrates to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr. 133: 411-417.

    34. Golay et al (1996) Weight-loss with low or high carbohydrate diet? Int J Obes Relat Metab Disord. 20(12): 1067-1072.

    35. Alford et al (1990) The effects of variations in carbohydrate, protein and fat content of the diet upon weight loss, blood values, and nutrient intake of adult obese women. J Am Diet Assoc. 90(4): 534-540.

    36. Miyashita et al (2004) Beneficial effect of low carbohydrate in low calorie diets on viceral fat reduction in type 2 diabetic patients with obesity. Diabetes Res Clin Pract. 65(3): 235-241.

    37. Hernandez et al (2010) Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high fat low carbohydrate diet. Am J Clin Nutr. 91(3): 578-585.

    38. Kogon et al (1994) Psychological and metabolic effects of dietary carbohydrates and dexfenfluramine during a low energy diet in obese women. Am J Clin Nutr. 60: 488-493.

    39. Samaha et al (2003) A low carbohydrate as compared with a low fat diet in severe obesity. N Engl J Med. 348: 2074-2081.

    40. McAuley et al (2005) Comparison of high fat and high protein diets with a high carbohydrate diet in insulin-resistant obese women. Diabet. 48: 8-16.

    41. Shai et al (2008) Weight loss with a low carbohydrate, mediterranean or low fat diet. N Engl J Med. 359: 229-241.

    42. Yancy et al (2004) A low carbohydrate, ketonic diet versus a low fat diet to treat obesity and hyperlipidemia. Ann Intern Med. 140:769-777.

    43. Westman et al (2008) The effect of a low carbohydrate, ketonic diet versus a low glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab. 5:36 doi:10.1186/1743-7075-5-36.

    44. Elhayany et al (2010) A low carbohydrate Mediterranean diet improves cardivascular risk factors and diabetes control among overweight patients with type 2 diabetes mellitus: a 1-year prospective randomized intervention study. Diabe Obes Metab. 12: 204-209.

    45. Wycherley et al (2010) Long term effects of weight loss with a very low carbohydrate and low fat diet on vascular function in overweight and obese patients. Intern Med. Doi.10.1111/j.1365-2796.2009.02174.x.

    46. Brinkworth et la (2009) Long term effects of a very low carbohydrate diet and a low fat diet on mood and cognitive function. Arch Intern Med. 169(20): 1873-1880.

    47. Stern et al (2004) The effects of low carbohydrate versus conventional weight loss diets in severely obese adults: one year follow up of a randomized trial. Ann Intern Med. 140: 778-785.

    48. Yancy et al (2010) A randomized trial of low carbohydrate diet vs orlistat plus a low fat diet for weight loss. Arch Intern Med. 170(2): 136-145.

    49. Sacks et al (2009) Comparison of weight loss diets with different compositions of fat protein and carbohydrates. N Engl J Med. 360: 859-873.

    50. Frisch et al (2009) A randomized controlled trial on the efficacy of carbohydrate-reduced or fat-reduced diets in patients attending a telemedically guided weightloss program. Cardiovas Diabetolo. 8:36 doi:101186/1475-2840-8-36.

    51. Vetter et al (2010) Long term effects of low carbohydrate versus low fat diets in obese persons. Ann Intern Med. 152(5): 334-335 Letter.

    52. Lim et al (2009) Long-term effects of a low carbohydrate, low fat or high unsatureted fat diet compared to a no-intervention control. Nutr Med Cardiovasc Dis. Aug 17 (Epud ahead of print).

    53. Brinkworth et al (2010) Renal function following long term weight loss in individuals with abdominal obesity on a very low carbohydrate diet vs high carbohydrate diet. J Am Diet Assoc. 110(4): 633-638.

      

    • Iben,

      This is an excellent compilation of work that you have done here.

        

    • You make the common error of conflating efficacy with effectiveness. The majority of the studies you cite describe a low-carb arm which, upon close examination, turns out to be anyting but. Researchers unfamiliar with the nuances of administering carbohydrate restricted diets make common mistakes that reduce compliance. Then, an intention-to-treat analysis is done which tends to wash out the evidence of the diet’s efficacy by including the results of those who were not compliant. Then, what are essentially effectiveness data are interpreted as though they were efficacy data. To understand the efficacy of a low-carb diet you must look at case studies or trials with high compliance rates. The studies conducted by Volek et al generally have high compliance rates and will give a better assessment of the diet’s efficacy. When you examine their results you will find that the diet delivers more weight loss and better outcomes for a range of cardiometabolic risk markers including abdominal fat loss, lipid profile, inflammation, insulin and leptin resistance, and vascular regulation. This is what we find in the clinical setting, as well, when patients comply with the diet.

        

      • Hey Wortman!

        Well, I guess it all comes down to your defenition of lowcarb. In the original article I used both the definition of Wilkinson & McCargar (2) and the team of Volek (1). However, excluding the definition of Wilkinson and McCargar stating that a low carbohydrate diet has less than 45 % of the energy consumed from carbohydrates, some of the studies I sited must be excluded. Volek and his coworkers (Feinman, Westman, Wortman (related?), Yancy, Phiney, Mavropoulos, Sharman) define a lowcarb diet as getting 50-150 gram of carbohydrates daily. < 50 gram carbohydrate a day they define as a ketogenic diet. Using only the definition of Volek and coworkers the evidence is still not dooming carbohydrate as a fat fuel from hell. Looking at studies with less than 6 month duration, 8 studies shows better results using lowcarb diets (3-10) compared to 16 studies showing no better effect from reducing carbohydrates in the diet (11-26). Comparing those studies of 6 months or longer 6 studies shows better effect of low carbohydrate diets (3, 5, 27-30) at 6 months. After 6 months the evidence shows that low carbohydrate diets have no advantage over others in reducing bodyweight (5, 6, 31-34).

        Of all the evidence pro low carbohydrate, most of them have weaknesses. Some of them are not matched for protein content (3, 5, 7, 8, 10, 27, 29, 30), some have no control over energy expenditure (3, 5-9, 28) and most of them prepared their own food (3, 5-9, 27-30) being subject to the possibility of false report. Samaha et al (27) isn’t even matched for energy intake.

        I’m not saying that low carbohydrate diets won’t work. I’m just saying they don’t give better weightloss and fatloss results when matched for energy and protein intake. There isn’t something magical about reducing carbohydrates that makes your fat vanish from your body. If you replace the calories with fat, you will stay fat. I personally like to separate the results of fatloss from other health issues. A lot of healthy people with no other illness then a few pounds too much choose low carbohydrate diets because they heard someone talk about insulin and how bad this is for you. Mr Krieger here showed how that simply isn’t the case. Even though insulin can increase fat storage and reduce fat mobilization doesn’t mean it will override all other hormones and signaling enzymes.

        So, the short version, carbohydrates doesn’t make you more fat then dietary fat. However, in some cases I have met people who preferred less carbohydraterich food, and thus had more success with those types of diets.

        PS: I have not looked at the newest studies, publish after my article, maybe there are some new information there?

        References
        1. Westman et al (2007) Low-carbohydrate nutrition and metabolism. Am J Clin Nutr. 86: 276-284.
        2. Wilkinson & McCargar (2004) Is there an optimal macronutrient mix for weight loss and weight maintenance? Best Prac Res Clin Gastro. 18(6): 1031-1047
        3. Brehm et al (2003) A randomized trial comparing a very low carbohydrate diet and a calorie restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 88: 1617-1623.
        4. Lewis et al (1977) Effect of diet composition on metabolic adaptions to hypocaloric nutrition: comparison of high carbohydrate and high fat isocaloric diets. Am J Clin Nutr. 30: 160-170.
        5. Gardner et al (2007) Comparison of the atkins, zone, ornish and LEARN diets for change in weight and related risk factors among overweight premenopausal women: The A to Z weight loss studie: Arandomized trial. JAMA 297(9): 969-977.
        6. Davis et al (2009) Comparative study of the effect of a 1-year dietary intervention of a low carbohydrate diet versus a low fat diet on weight and glycemic control in type 2 diabetes. Dia Care. 32: 1147-1152.
        7. Brehm et al (2005) The role of energy expenditure in the differential weightloss in obese women on low fat and low carbohydrate diets. Metab. 90: 1475-1482.
        8. Volek et al (2004) Comparison of energy-restricted very low carbohydrate and low fat diets on weight loss and body composition in overweight men and women. Nutr Metab. 1:13 doi:10.1186/1743-7075-1-13.
        9. Volek et al (2004) Comparison of a very low carbohydrate and low fat diet on fasting lipids, LDL subclasses, insulin resistance and postprandial lipemic responses in overweight women. J Am Coll Nutr. 23(2): 177-184.
        10. Stephen et al (2003) Effects of a low carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr. 142(3): 253-258.
        11. Mc-Millan-Price et al (2006) Comparison of 4 dits of varyying glycemic loa don weight loss and cardiovascular risk reductions in overweight and obese young adults. A randomized controlled trial. Arch Intern Med. 166: 1466-1475.
        12. Tay et al (2008) Metabolic effects of weight loss on a very low carbohydrate diet compared with isocaloric high carbohydrate diet in abdominally obese subjects. J Am Coll Cardiol. 51(1): 59-67.
        13. Noakes et al (2006) Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk. Nutr Metab. 3:7 doi:10.1186/1743-7075-3-7.
        14. Noakes et al (2005) Effect of an energy-restricted high protein low fat diet relative to a conventional high carbohydrate low fat diet on weight loss, body composition, nutritional status and markers of cardiovascular health in obese women. Am J Clin Nutr. 81: 1298-1306.
        15. Johnston et al (2006) Ketogenic low carbohydrate diets have no metabolic advantage over nonketogenic low carbohydrate diets. Am J Clin Nutr. 83: 1055-1061.
        16. Meckling et al (2004) Comparison of a low fat diet to a low carbohydrate diet on weight loss, body composition and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J Clin Endo Metab. 89: 2717-2723.
        17. Bradley et al (2009) Low fat versus low carbohydrate weight reduction diets. Effect on weightloss, insulin resistance, and cardiovascular risk: a randomized control trial. Diabetes. 58(12): 2741-2748.
        18. Golay et al (1996) Similar weight loss with low- or high carbohydrate diets. Am J Clin Nutr. 63: 174-178.
        19. Volek et al (2004) Comparison of energy-restricted very low carbohydrate and low fat diets on weight loss and body composition in overweight men and women. Nutr Metab. 1:13 doi:10.1186/1743-7075-1-13.
        20. Volek et al (2003) An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial lipemic responses compared with a low fat diet in normal weight, normolipidemic women. J Nutr. 133: 2756-2761.
        21. Colette (2003) Exchanging carbohydrates for monosaturated fats in energy-restricted diets: effects on metabolic profile and other cardiovascular risk factors. Int J Obes. 27: 648-656.
        22. Golay et al (1996) Weight-loss with low or high carbohydrate diet? Int J Obes Relat Metab Disord. 20(12): 1067-1072.
        23. Alford et al (1990) The effects of variations in carbohydrate, protein and fat content of the diet upon weight loss, blood values, and nutrient intake of adult obese women. J Am Diet Assoc. 90(4): 534-540.
        24. Miyashita et al (2004) Beneficial effect of low carbohydrate in low calorie diets on viceral fat reduction in type 2 diabetic patients with obesity. Diabetes Res Clin Pract. 65(3): 235-241.
        25. Hernandez et al (2010) Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high fat low carbohydrate diet. Am J Clin Nutr. 91(3): 578-585.
        26. Kogon et al (1994) Psychological and metabolic effects of dietary carbohydrates and dexfenfluramine during a low energy diet in obese women. Am J Clin Nutr. 60: 488-493.
        27. Samaha et al (2003) A low carbohydrate as compared with a low fat diet in severe obesity. N Engl J Med. 348: 2074-2081.
        28. Yancy et al (2004) A low carbohydrate, ketonic diet versus a low fat diet to treat obesity and hyperlipidemia. Ann Intern Med. 140:769-777.
        29. Westman et al (2008) The effect of a low carbohydrate, ketonic diet versus a low glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab. 5:36 doi:10.1186/1743-7075-5-36.
        30. McAuley et al (2005) Comparison of high fat and high protein diets with a high carbohydrate diet in insulin-resistant obese women. Diabet. 48: 8-16.
        31. Wycherley et al (2010) Long term effects of weight loss with a very low carbohydrate and low fat diet on vascular function in overweight and obese patients. Intern Med. Doi.10.1111/j.1365-2796.2009.02174.x.
        32. Stern et al (2004) The effects of low carbohydrate versus conventional weight loss diets in severely obese adults: one year follow up of a randomized trial. Ann Intern Med. 140: 778-785.
        33. Yancy et al (2010) A randomized trial of low carbohydrate diet vs orlistat plus a low fat diet for weight loss. Arch Intern Med. 170(2): 136-145.
        34. Brinkworth et al (2010) Renal function following long term weight loss in individuals with abdominal obesity on a very low carbohydrate diet vs high carbohydrate diet. J Am Diet Assoc. 110(4): 633-638.

          

  15. 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?

      

    • Mallory; For the first and second question; Visit your doctor, or buy yourself a blood glucose tester. You can find the classifications for resistance vs. sensitivity on Wikipedia.

        

    • 1) glucose intolerance= prediabetes. test for fasted glucose level. above normal but below diabetic level=glucose intolerance.
      3)poor insulin sensitivity=prediabetes. v poor insulin sensitivity=diabetes=insulin resistance. normal insulin sensitivity= no diabetes. so, similarly, test for fasted blood glucose levels. insulin sensitivity and insulin resistance are not completely 2 seperate things

        

  16. Ahmed, imee, Todd, Fredrik, Jamie, everyone else who I may have missed…thank you for your comments, and I’m glad you are getting value out of these articles. I will try to address some of your individual comments soon.

      

  17. James Krieger….you are an absolute certified nutritional badass and an excellent debater! Keep up the great work you kick ass!

      

  18. It is really beautiful work I read here. But I can’t find an answer on the question how type 1 diabetics should match their insulin administration to their diet. When administering too much insulin (on a high protein meal) they become hypoglycemic. I really want to understand that mechanism.

      

  19. According to Dr. Lustig,
    http://www.thelivinlowcarbshow.com/shownotes/2112/dr-robert-lustig-episode/ (1st 15min are all about insulin)

    the evidence against insulin is pretty good… not just a traffic cop…

      

    • There is actually no evidence against insulin, people lose weight on an hypocaloric diet of candy bars if needed. Insulin make no different and serious isocaloric controlled studies have proved this over and over.

        

      • Bull. Type II diabetics will starve to death on a high sugar diet while their fat mass grows.

          

        • Mike, I suggest you provide some evidence that type II diabetics will “starve to death while their fat mass grows.”

            

        • According to Gary Taubes from Why we get fat and what to do about it in chapter 9 the laws of adiposity. The only reference I cant find is the one by Greenwood, M. R et al, called Adipose tissue metabolism and genetic obesity published in Recent Advances in Obesity Research 1981 which appears to be a book.
          I think it might be a bit of a stretch to claim obese rats died from starvation still obese as they were genetically obese rats anyway. would be good to see if there is any more research out there that supports this.

            

  20. James, what do you say to Rob Wolff’s column disputing your claims that insulin is anorexigenic? He says you are confusing acute and chronic effects?
    http://robbwolf.com/2010/02/04/insulin-anorexic/

      

  21. All I can say is truly brilliant, when I saw your first article I almost couldn’t believe the notion of insulin not causing weight gain, but I read through all your articles so far, went through the studies and I’m to say I’ve had a paradigm shift and I’m just glad I came across your website and the great resources you give.

      

  22. Thank you for what you have posted – I have found your articles very interesting having read so much about why I am fat. Not a believer in the zone diet or the atkins after reading about them, I hoped there was another explanation about carbs/protein/fat and insulin.I knew protein decreases hunger and complex vegetable carbs (low glycaemic) are better for slow release of sugar and insulin but I didnt know how to get rid of my 2kg a year increases. If I was to increase my exercise alone to compensate, I would be exercising for about 10 hours a day by the time I get to 50. I research pubmed all the time looking for information and I agree with what you have written and it is logical..and it is backed up by the published data. As a PhD student now in the field of nutrition coming out of a purely microbiological degree I find the whole human health thing really interesting particularly the balance between healthy and not and how the body modulates the release of its chemicals to maintain well being.

    PS the type II mice that starve to death and die fat by Mike back in November is from the book “why we get fat and what to do about it” by Gary Taubes. Its on page 103 by the way. What Gary was saying was that the rodents have insulin sensitive fat cells that lock in their fat when insulin rises in the blood then the liver has to dump glycogen till it runs out then the muscles do the same until they run out then because they cant access the fatty acids locked up in the fat cells the liver has to do gluconeogenesis or break down protein for energy. Gary does have the citations at the back but its hard to tell which one it is only that in his book he says most of the work was done in 1981
    1981
    may as well have been 1901 as I am sure there are much better publications out in the public domain now.

      

  23. James – given the studies you’ve quoted on whole dairy protein, indicating that the leucine content is a possible driver of the insulin response, do you feel that protein-induced (or rather, leucine-induced) insulin spike would provide little to no interruption to lipolysis?

    Could this provide the basis for an argument for someone looking to gain muscle to use amino acid or protein pulsing with a fast-digesting protein 3-4 times per day to spike protein synthesis without interrupting fat-burning?

    Would love to know your thoughts. Thanks in advance.

    PS – Haters gonna hate on your articles, don’t take it personally.

      

    • Hi, PF,

      Leucine isn’t just a possible driver of the insulin response…it IS a driver of the insulin response. More research has been coming out demonstrating this. There is also evidence that a combination of branched-chain amino acids has a synergistic effect, causing more insulin release than leucine alone.

      Any elevation in insulin, whether from protein or carbohydrate, is going to inhibit lipolysis. But it’s irrelevant, because lipolysis is not the same thing as fat oxidation. When it comes to fat loss, we’re concerned with fat oxidation, not lipolysis. Lipolysis just refers to the breakdown of triglycerides into free fatty acids. However, if those free fatty acids are not oxidized, they will simply be repackaged back into triglycerides. This is why energy balance ultimately reigns supreme.

      Thanks for the comment!

        

      • Thanks for the response, very interesting – in that case using a combination of MCTs, Leucine and BCAA (or hydrolysed casein) strategically, we could promote blood free fatty acid content while elevating protein synthesis and not inhibiting overall fat loss.

        The annoying thing about reading your series on insulin is that I’ve come away feeling like I know less than I did before I started, you’ve just shattered so many assumptions.

          

  24. So, this is an honest question… In your opinion, do you believe it to be true that I will “burn more fat” by going for a steady-state cardio run in a fasted state vs. the same run after a meal? That’s what I have been lead to believe and what I am picking up from the “insulin inhibits lipolysis” comments. Am I wrong?…

      

    • Jeremy, you will burn more fat running in a fasted state, but it’s irrelevant over a 24-hour period, because your body will make up for it at other time points in the day. Likewise, you might burn less fat after a meal, but you’ll burn more at a later time point in the day, as long as you are in a calorie deficit.

        

  25. cialis effet secondaire $rn6435# viagra naturel

      

  26. What would explain my weight gain on a low-carb low-fat diet? (80lbs.) Why did I become diabetic on this diet?

      

    • I think you meant high-carb, low fat. Simple…you overate on the high-carb, low-fat diet…most likely because of inadequate protein intake and lack of fiber, contributing to lack of satiation. This is also not to mention that some high-carb, low fat foods are quite energy dense (especially processed ones). If you were inactive this would have exacerbated the problem, as inactivity results in insulin resistance, which impairs appetite regulation. Then it was the weight gain that eventually led to the diabetes.

        

      • I was active.
        I also was hungry, although I ate quite a bit of protein.
        I just look at carbs, even plain boiled potatoes and I cannot stop eating.
        If I eat lettuce, for example, I eat at least two heads, or I am not full.
        I cannot function if I have to be hypoglycemic.
        I also had to eat all the time, even at night.

        Not any more, thanks to a hypercaloric ketogenic diet.

          

        • First, you need to define “active”. Research shows that people dramatically overestimate their activity.

          You also claim you ate “quite a bit of protein.” But that can’t be true because you claimed you were on a high carb diet. You can only consume so much protein if the majority of your diet is made up of carbs. Either that, or you were overeating in the first place and some of that overeating consisted of extra protein. Most people who think they eat quite a bit of protein don’t really consume as much as they think, especially enough to have appetite suppressant effects.

          You say that if you eat two heads of lettuce, you are not full. Of course you are not full, because lettuce has no energy value. Fullness is partly a response to calorie intake. Lettuce has almost no calories.

          You state “I cannot function if I have to be hypoglycemic.” True hypoglycemia is extremely rare in people without diabetes.

          You now claim to be on a “hypercaloric ketogenic diet.” But it cannot be hypercaloric if you are not gaining weight. As I said before, you have to explain what is happening to all those extra carbon and hydrogen atoms if you think you are hypercaloric and not gaining weight.

            

  27. Although I do not agree with everything you are concluding, I appreciate this discussion.
    We still do not understand everything in great detail, and I wish we did.
    However, for practical reasons, staying away from sugars and other carbs (and avoiding the corresponding insulin releases from those carbs) has been saving lives, including my own.

      

    • That link is not relevant to my posts regarding insulin. That link compares cream to casein. Cream has very little casein, which is why it doesn’t cause much of an insulin response. The reason dairy foods (other than butter and cream) cause high insulin responses is because of the casein and whey protein in the dairy. Yet, foods that are high in casein and whey have been found to be beneficial for weight loss. This alone is a major hole in the “carb/insulin” hypothesis, because all of that insulin from the dairy protein should be making you gain fat…but it’s not. Thus, if carbs make you fat (which they don’t), it is certainly NOT through the action of insulin.

        

    • This is an observational study which cannot establish cause/effect. It is more likely that overweight kids consume low-fat dairy BECAUSE they are overweight and are trying to reduce calorie intake, rather than the low fat dairy CAUSING them to be overweight. This is especially true when you look at randomized controlled trials on dairy and body weight, which I cover extensively in this post.

        

  28. https://www.google.ca/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CDsQFjAB&url=http%3A%2F%2Fwww.mdpi.com%2F2072-6643%2F5%2F1%2F23%2Fpdf&ei=f3dOUe3bL6KnigK6kYGoAw&usg=AFQjCNH_pP2mHZl8eal-NUGtvQM_WQIv8g&sig2=g3ftkVjERtVR1zA9Uw53oQ&bvm=bv.44158598,d.cGE

    You probably know this one, as you read every study out there.

    http://www.nutritionj.com/content/pdf/1475-2891-11-83.pdf

    Traditionally, people used to eat high fat dairy. They gave the rest to their pigs, to fatten them up! (I would not touch skim milk.)

    The next one is about the effect of fermentation, presumably.
    http://ajcn.nutrition.org/content/74/1/96.full

    http://nutricore.com.br/app/webroot/img/bibliotecas/LEITE%20E%20ELEVA+%E7+%E2O%20P+%F4S%20PRANDIAL%20DE%20INSULINA.pdf

    You probably know this one too.

    http://ajcn.nutrition.org/content/74/1/96.full.pdf

    And this: Favour highfat and fermented dairy with no added sugar:
    http://www.lipidworld.com/content/6/1/25

    http://ajcn.nutrition.org/content/82/1/69.full (milk proteins suppress glycemia according to their interpretation)???<For how long? But, as they said, the blood sugars were suppressed way into the day after a whey breakfast.

    Chris Masterjohn points out, milk proteins mostly appear harmful only when separated from their natural fat. (He should probably add other adulterations as being hazardous to our health).

    I am not in favour of frankenfoods like whey protein isolate etc…even if a lot of people recommend them. I like my milk products whole, and fatty.

    http://www.drbriffa.com/2011/07/26/dairy-products-can-assist-weight-loss/
    Although, I cannot eat regular full fat yoghurt now (6%), I could when I was younger. Now I definitely need higher fat contents in order to be metabolically stable. (I was never a milk drinker.)

    I am still looking for this graph, comparing insulin levels post carb compared with milk-product ingestion.

    And I know what happens to a person on a high protein low fat diet (as opposed to the high-carb relatively high protein low-fat diet I once ate, probably too much carb according to you).
    I have seen it with my own eyes, this is better proof than any studies. It is called RABBIT STARVATION, lots of diarrhea, cachexia……..and if nobody intervenes…death.
    You can read John Yudkin on this topic, but you probably know that already, you read a lot. (Other people read too.)

    You are probably very knowledgeable about differences between milk products from different animals: Holsteins versus Jerseys, goats, sheep…..
    Milk is NOT milk!

    Another one in favour of Whey (supposedly reduces insulin resistance): http://www.12340000.com/medicine-health/endocrine-and-systemic-disease/39686.html

    How about doing a real study, in a controlled setting for a longer term?

    And, I have to get back to work now, again.

    The flaw of your logic question in paper #6 is that there are only two options, married or not married, black and white.
    This does not apply to what you are discussing.
    If Gary Taubes is 80% right with his hypothesis (as he calls it), then this is pretty darn fantastic in comparison to whatever else is being proposed out there, and it seems to work too. Isn't that worth something?
    Of course, if you can explain things in greater detail with different shades of grey, we will all be happy to learn more and understand the issue better. No reason to look down upon those who came before you, trying to do the same as you: Helping others and furthering deeper insights into the issues of diet, insulin, diabetes,obesity…….
    I expect that you yourself will keep modifying what you are currently believing, the world does not stand still, and new things come to light all the time.

    Thank you for your time, and hopefully you can do some good by further researching (which seems to be your passion) and keeping an open mind.

      

    • I’ve read all these studies you have presented, and they STILL don’t refute anything that I’ve claimed.

      So far, this is what you’ve presented to me:

      1. A study comparing the insulin response between protein-free cream and casein. Of course this would happen because it is the milk protein component of dairy that is responsible for insulinemia. Doesn’t refute anything that I’ve stated in my insulin series.

      2. An observational study showing greater BMI in preschoolers consuming low fat dairy compared to high fat diary. This study cannot establish cause effect and is also contradicted by many of the adult observational studies showing beneficial or neutral impacts of low fat diary on weight.

      3. A study showing a negative correlation between high fat dairy and BMI. So what? This does not refute anything in my insulin article series. In fact, this study more contradicts the “carbohydrate/insulin” hypothesis as full fat milk is just as insulinemic as low fat milk.

      4.

      You probably know this one, as you read every study out there.

      http://www.nutritionj.com/content/pdf/1475-2891-11-83.pdf

      Yes, another study I’ve read, and another study that does not refute anything that I’ve stated. Do you read the studies you are referencing? This study showed equivalent insulin responses when white bread was compared to equi-carbohydrate dairy (and in fact was highest with whey), which refutes the carbohydrate/insulin hypothesis; it does not support it.

      5.

      You probably know this one too.

      http://ajcn.nutrition.org/content/74/1/96.full.pdf

      Yes, I do know about that one, and once again, this study actually refutes the carb/insulin hypothesis. I again have to ask…do you read these studies you are referencing? This study showed fermented milk products to produce insulin responses that were equivalent to white bread…which has exactly been my point in this post.

      You probably know this one too.

      http://ajcn.nutrition.org/content/74/1/96.full.pdf

      That’s the same study you linked to in #5.

      6.

      http://www.lipidworld.com/content/6/1/25

      Says nothing about insulin. And again refutes the carb/insulin hypothesis because dairy produces high insulin responses yet has been found to be beneficial for appetite regulation.

      7.

      http://ajcn.nutrition.org/content/82/1/69.full (milk proteins suppress glycemia according to their interpretation)??

      Yes, I’ve read this study too, and it again REFUTES the carb/insulin hypothesis. Insulinemia was HIGHER in the whey condition, and this HIGHER insulinemia was BENEFICIAL to the glycemic response. Kind of messes up the whole carb/insulin thing, doesn’t it?

      Chris Masterjohn points out, milk proteins mostly appear harmful only when separated from their natural fat.

      Where is the evidence that separated milk proteins are harmful? Or are you taking Chris’s word for it without question?

      (He should probably add other adulterations as being hazardous to our health).

      I take alarmist “hazardous to health” claims with a grain of salt. “Hazardous to health” is a very bold claim, and such bold claims require bold evidence. Smoking is hazardous to health because the evidence overwhelmingly tells us so. But claims about milk? I have my doubts that strong evidence for such claims exist.

      And I know what happens to a person on a high protein low fat diet (as opposed to the high-carb relatively high protein low-fat diet I once ate, probably too much carb according to you).
      I have seen it with my own eyes, this is better proof than any studies. It is called RABBIT STARVATION, lots of diarrhea, cachexia……..and if nobody intervenes…death.
      You can read John Yudkin on this topic, but you probably know that already, you read a lot. (Other people read too.)

      Rabbit starvation only occurs under very extreme conditions (EXTREMELY high protein and EXTREMELY low fat). Rabbit meat is 85% protein and 15% fat. This represents the extreme of the extreme and is not representative of the vast, vast majority of high protein, low fat diets.

      Still don’t know what this has to do with insulin or the carb/insulin hypothesis.

      And the fact that you think an anecdote is better proof than any study tells me that your standards of evidence are quite low, which then doesn’t suprise me why you buy into Gary Taubes.

      You are probably very knowledgeable about differences between milk products from different animals: Holsteins versus Jerseys, goats, sheep…..
      Milk is NOT milk!

      What’s that got to do with insulin? You are going off on tangents here.

      The flaw of your logic question in paper #6 is that there are only two options, married or not married, black and white.

      What do you mean by “paper #6″? It is not even clear what you are referring to.

      If Gary Taubes is 80% right with his hypothesis (as he calls it), then this is pretty darn fantastic in comparison to whatever else is being proposed out there, and it seems to work too. Isn’t that worth something?

      It’s not worth anything because Gary is not even 80% right. He’s not even 20% right. He is so far wrong that that is why no one in the scientific community takes him seriously (he will claim that the “establishment” is against him and is wrong, but any objective examination of the evidence says otherwise). He has ignored HUGE amounts of literature that strongly contradicts his “hypothesis” (and I use that term loosely because the evidence against him is quite powerful). You can’t be 80% right when you willfully ignore 80% of the literature that contradicts what you believe. In fact, I reviewed one chapter in his book and it was so full of misinformation that it was absolutely dumbfounding. Gary’s own references in his book don’t even support his claims; perhaps he was hoping no one would notice since most people never take the time to investigate the references. I also suggest you take a look at CarbSane’s “Gary Taubes reference check” blog posts where she exposes serious errors in Taubes’s “scholarship.”

      Thank you for your time, and hopefully you can do some good by further researching (which seems to be your passion) and keeping an open mind.

      I have an open mind to what the evidence tells me. And the evidence is pretty damning that the “carb/insulin” hypothesis is completely and utterly wrong. This insulin blog post series only touches on some of the things that are wrong with it. I also suggest you read Dr. Stephen Guyenet’s critical examination of the carb hypothesis and why it is incorrect.

        

      • Sigh! I am sorry to not have the time to continue with this discussion. I find that the issues are being treated in a very reductionist manner when it is a complex issue. It does not suffice to destroy someone else’s hypothesis, you then have to go on to explain what is happening in all its complexity.
        Our “diabetes genes” get turned on by starvation/malnutrition (ours, our parents’, our grandparents’, our great-grandparents’).
        Social injustice, environmental degradation, political unrest, and other factors are at play here. They need to be addressed to address some of the roots of the problem. (This is one major reason we all have different carb sensitivities.)
        I congratulate Gary on making some connections there.

        Into this genetic background we are forced to eat exactly the things that will exacerbate our metabolic situation further, because they are cheap and all we can afford.

        And what does this have to do with milk?

        And why did I cite those studies?

        Because you can invest your time and efforts into things that are worthwhile. Debating like a lawyer is not a worthwhile use of time if you wish to help other people, those with metabolic problems. Instead, you can research the problem in all its complexity, come up with your own interpretation and documentation (with no need to show others that they are wrong), and devise your own plan showing how to eradicate the problem at its roots.

        I quoted all these studies, because some of them are observational. as you noticed, some of them do only deal with short-term effects and do not tell me anything about twenty years of milk (milk in children, teens, in old age?), they investigate one little thing only (and if you don’t integrate it into everything else and see the big picture, the exercise was a useless waste of money and time)…..

        Like it is often stated: There is more money and time being spent on developing hair growth products than solving the real problems in this world.

        Oh, drinking milk gives us a short acting incretin rush. Well that’s not going to solve anything, and so is this whole debate, at least so far…….

        I am still hoping, that something real will come out of this.

        And, Sigh!!!, The lady sitting in between the two men is either married or unmarried, and even worse, no matter if she is married or unmarried, the outcome will be the same (some unmarried person will look at a married person).

        Could this wisely chosen analogy also apply in this case? We will eventually end up with the same conclusion?
        (Just, it is a little more complex.)

        I will not post on this any more, I am busy with real work.
        I will read what you have suggested though, when I have time for it.

          

        • I find that the issues are being treated in a very reductionist manner when it is a complex issue.

          Then it surprises me why you find Taubes so convincing. His hypothesis is the ultimate in simplicity, which is also why it is an easy hypothesis to refute.

          It does not suffice to destroy someone else’s hypothesis, you then have to go on to explain what is happening in all its complexity.

          Yes, obesity is a complex issue, and various aspects of it have already been addressed by numerous scientists all over the world. Taubes, in his interest to sell books, create something that the layperson can buy into, and go “against the establishment”, has created a giant strawman (the “gluttony/sloth” hypothesis), and then created his own hypothesis based on inaccurate data to refute this strawman. This is why the average person, who is not familiar with the vast amount of research out there, finds Taubes so easily convincing.

          There is no “single” hypothesis of obesity, which is also why Taubes is wrong. Taubes appeals to the mindset of people who want to find one thing to blame on obesity. But the fact is that obesity is a multifactorial problem with numerous variables contributing to it.

          Our “diabetes genes” get turned on by starvation/malnutrition

          Evidence please.

          Debating like a lawyer is not a worthwhile use of time if you wish to help other people,

          It is not debating like a lawyer, it is debating like a scientist. And good scientists make their case based on the evidence, and also ask other people making claims to support those claims with evidence. And debating like a scientist DOES help other people because it helps to sort out factual information from misinformation.

          I quoted all these studies, because some of them are observational. as you noticed, some of them do only deal with short-term effects and do not tell me anything about twenty years of milk (milk in children, teens, in old age?), they investigate one little thing only (and if you don’t integrate it into everything else and see the big picture, the exercise was a useless waste of money and time)…..

          Huh? Now you make no sense. I asked you to provide evidence to refute claims in my insulin articles, and you presented these studies. I pointed out how these studies don’t refute anything, and now you say that “they aren’t integrated into the big picture.” What you fail to understand is that Taubes has presented a hypothesis of obesity along with a mechanism. If basic scientific observations are not consistent with his proposed mechanism, then his proposed mechanism is wrong…period. It has nothing to do with complexity and everything to do with a concept known as hypothesis testing. In fact, the studies you reference help to refute Taubes, not support him, because they refute the mechanism.

          Hypothesis testing means seeing if basic observations are consistent with your hypothesis. If basic observations are not consistent with it, either the hypothesis needs to be modified, or the hypothesis needs to be thrown out. Taubes has done neither, despite a huge body of basic scientific observations that are inconsistent with his hypothesis.

          There is more money and time being spent on developing hair growth products than solving the real problems in this world.

          My client have lost an average of 40 pounds in 3 months. So are you saying that I’m not solving real problems in this world?

          I will read what you have suggested though, when I have time for it.

          If you have time to read Taubes and anything that remotely supports him, then you should have time to read all of the cases against him before evaluating whether his hypothesis has any merit.

            

  29. I have hypoglycemia, and I learned alot from your articles. I understand the high blood sugar article. But, I have hypoglycemia, how does insulin affect this? I don’t understand. Is to much insulin not allowing a hypoglycemic to store sugar, or is it not allowing the liver to make glucose? If I eat fruit, I get shaky not long after. What’s going on in this situation? Please help !

      

    • Vik,

      Has a doctor told you what the cause of your hypoglycemia is?

        

      • I have hyperparathyroidism, which my blood calcium levels are going really high because one of my parathyroids has an adenoma. I’m not sure if the calcium is causing insulin resistance, or to much insulin. It’s really hard and all the doctors pass me around because its hard to find a specialist of the parathyroids. Tough times. By the way, I’d like to thank you for putting this info out there. I’m learning alot about the body !

          

  30. Minor editing issue.

    Where you write that “Another study found a weak relationship between the glycemic response of a breakfast and energy intake and lunch, but no relationship between the…” I suspect you meant to write ” Another study found a weak relationship between the glycemic response of a breakfast and energy intake at lunch, but no relationship between the…”

      

  31. I loved as much as you’ll receive carried out right here.

    The sketch is tasteful, your authored material stylish.
    nonetheless, you command get got an nervousness over that you
    wish be delivering the following. unwell unquestionably come further formerly again as exactly the same nearly a lot often inside case you
    shield this hike.

      

  32. Hi there, always i used to check weblog posts here in the early hours in the break of day, for the reason that i enjoy to find
    out more and more.

    my weblog: ab bench

      

  33. Hey I know this is off topic but I was wondering if you knew of any widgets
    I could add to my blog that automatically tweet my
    newest twitter updates. I’ve been looking for a plug-in like this for quite some time
    and was hoping maybe you would have some experience with
    something like this. Please let me know if you run into anything.
    I truly enjoy reading your blog and I look forward to
    your new updates.

    Feel free to visit my web page … dumbbells for sale cheap

      

  34. What’s Taking place i am new to this, I stumbled upon this I have discovered It positively useful and it has helped
    me out loads. I’m hoping to give a contribution & help other users
    like its helped me. Great job.

      

  35. The Atlanta Luxury Lifestyle Examiner strives to explore all aspects of the luxury lifestyle
    as it relates to products, hotels, fashion, cars, restaurants, etc.
    So where’s the best place to start if Luxury Travel is
    top of the list on your holiday spec this year. Sure you enjoy the
    luxury everyday but the initial excitement you felt will tend to
    reduce as you get familiar with the car and get used to it.

    Feel free to surf to my web blog – luxury rental

      

 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>