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Insulin Levels and Fat Loss

Insulin is a complicated hormone, complicated further by the amount of utter nonsense and gibberish that is written about it when it comes to dieting, fat loss and fat gain.  And one of the many questions that comes up is this:

If insulin goes up when we eat, storing nutrients and inhibiting fat mobilization, how do we actually lose fat during a calorie deficit?  Does insulin eventually just drop so fat burning can resume?  How does the glycemic index (GI) impact this?  Will eating a lower GI food make a difference compared to a higher GI food?

I think you get the idea.  So let me try to address each of this by looking at the impact of insulin on fat loss along with those other issues.

Insulin is a bit Schizophrenic

This is because, in a lot of ways, insulin is a schizophrenic hormone.  Depending on what folks read (e.g. bodybuilding literature), they will be told that insulin is great, it’s the most anabolic hormone in the body, it’s key to getting big.

And if you read other stuff (a lot of mainstream dieting literature),  you’ll hear that insulin is the devil, it makes you fat and ruins your health.  Who’s right?  Well, everybody…sort of.

As the question above states, it’s best to think of insulin as a generalized storage hormone rather than being good or bad; and what it does, as always, depends on the context.   I should mention that insulin not only affects peripheral tissues such as the liver, muscle and fat cell.   Insulin also has central effects in the brain, actually decreasing hunger and appetite.

When insulin is elevated, it pushes nutrients into cells.  I’d note in this regard that carbohydrate intake is the primary determinant of insulin response.  However, protein intake also raises insulin levels.  As I’ll discuss below, the combination of protein and carbs often raises insulin even more.  Dietary fat does not raise insulin.

So insulin stimulates glycogen storage in the liver, it also enhances glycogen storage in skeletal muscle.  And while insulin isn’t that critically involved in protein synthesis per se, it does decrease protein breakdown; as discussed in The Protein Book, this is important for maximal increases in muscle mass.  So far so good.

But insulin also is involved in fat storage which is where it gets its ‘bad’ characterization.  Insulin activates an enzyme called lipoprotein lipase which is involved in breaking fatty acids off of chylomicrons for storage.  However, this isn’t the only important step in fat storage.

Insulin is not Required for Fat Storage

Contrary to popular belief (espoused by people still reading literature from the 1970’s), insulin is neither the only nor single most important hormone involved in fat storage.  Rather, a little compound called acylation stimulation protein (ASP) has been described as “the most potent stimulator of fat storage in the fat cell”.   ASP levels go up in response to eating pure dietary fat.  An increase in insulin is not required.

As another effect of insulin on body-fat levels, and this is discussed in some detail in The Stubborn Fat Solution, insulin drastically inhibits lipolysis (fat mobilization) from fat cells.

Even fasting insulin levels inhibit lipolysis by up to 50%, even small increases essentially turn off lipolysis completely.   Some could easily interpret this as meaning that “eating carbs stops fat loss” which is kind of true.  Or it might lead them to conclude that a carbohydrate based diet would make fat loss impossible which is objectively not true.

Tangentially I’d note, and one weird little study supports this, that spiking insulin (and letting it crash back down) might be superior for fat loss than the standard strategy of trying to keep insulin low but stable all day long.  The reason is that even tiny amounts of insulin block lipolysis, if you keep insulin low but stable all day, you are effectively impairing lipolysis.

But the study in question showed that blood fatty acid levels came back up much faster when insulin was spiked (which crashed blood glucose back down, lowering insulin).  The drawback, mind you, is that rapidly falling blood glucose tends to make people hungry and calorie control would be nearly impossible with this strategy.  And, as you’ll see below, in a hypocaloric situation, it probably doesn’t matter a bit.

Anyhow, despite the sometimes seen mentality that you must ‘cut carbs to get lean’, four decades of practical experience (and endless clinical research) show that that is simply not the case: bodybuilders (well, some bodybuilders) have gotten plenty lean on carb-based diets (of course, others have failed miserably) so it’s obviously not as simple as many would make it.

That’s because whether a high-carb, moderate-carb, or low-carb diet is most appropriate for someone depends on the specific circumstances.

Which brings me the long way around to the first question above.  What is happening in terms of fat loss on a diet that is hypocaloric (below maintenance levels, that is the person is burning more calories than they are consuming) but contains sufficient protein and essential fatty acids but with say 100 grams of carbohydrate? Don’t the carbs prevent fat loss by raising insulin?  What’s going on?

What’s Going On?

To understand what’s going on, I need to explain two terms which are the post-prandial and post-absorptive phases.

Post-prandial phase:
This is just a technical term for “after you’ve eaten a meal”.  In this situation, nutrients are being absorbed and digested from the gut and released into the bloodstream, a whole host of hormones are being released (depending on the macronutrient content of the meal) and the body will generally be in an anabolic state (meaning that more nutrients are being stored than are being released from storage).  How long this phase lasts depends on the size of the meal.

Post-absorptive stage
This is what happens between post-prandial phases.  Eventually what you’ve eaten has all been digested, absorbed and either burned for energy or stored in various tissues.  When this happens, hormone levels change an the body starts shifting to an overall catabolic state (I’m using this term generally here to indicate that the body is releasing more nutrients from storage than are being stored).

So throughout the day, the body is shifting between the post-prandial phase and the post-absorptive phase as you eat, that food gets digested and absorbed, and the body starts to draw on stored nutrients (hopefully stored fat in fat cells).

And when you lower caloric intake, over a 24 hour period, the body will end up spending relatively more time in the post-absorptive (remember: body burning stored nutrients) than post-prandial (remember: body storing ingested nutrients) phase.  This is simply a consequence of having less nutrients coming in relative to what’s being burned.

The Impact of Dieting

On a diet, meals are smaller (or activity is higher, or both) so any given meal will only maintain an anabolic state for so long (and that time period will be shorter than if the person were eating more) before the body shifts back to burning stored nutrients.  So even in the face of dietary carbohydrate intake, the body still will tap into stored fat; hence fat loss.

I’d note that theoretically this might mean that eating less frequently would improve fat loss, since the body would spend more time between meals in the post-absorptive stage.

But this is offset by each meal being larger and therefore taking longer to digest and I tend to doubt it matters in the long-run.  Some interesting research into intermittent fasting suggests that there is more to it than that but that’s another topic for another day.  By and large, IF’ing has not shown a superiority in fat loss at fixed calorie levels.

The Glycemic Index and Insulin

And this brings me to the second part of the above question, the Glycemic Index (GI) and insulin.  Which requires another long explanation.  The GI was developed back in the 80’s to help with diabetic meal planning.

Basically it involves feeding folks a fixed amount of a reference carbohydrate (studies have typically used either 50 grams or 100 grams of digestible carbs and while glucose was the original test food, they now use white bread) with blood glucose being measured over a several hour period.  The glucose response to the reference food is defined as having a GI of 100.

Then, whatever food was being tested (again either 50 or 100 grams of digestible carbs were given) and blood glucose was measured, researchers compared the blood glucose response of the test food to the reference food.

If the blood glucose response was say, 80% of the reference food, the test food was given a GI of 80.  If the blood glucose response was 120% of the test food, that’s a GI of 120.  You get the idea. And lower GI values basically meant that the test food was generating a smaller blood glucose response than the reference food.

GI is far from perfect, there is massive individual variability, many foods will show a different GI depending how you cook them  and, as soon as you start mixing foods or adding things like protein, fiber and fat, GI changes (almost always going down).

So GI in and of itself ends up not saying very much in the big scheme of things.    An additional confound is training.    People who are better aerobically trained show a lower GI response than those who are less well trained.

Now, it was always pretty much assumed that the GI was indicative of the insulin response and that lower GI foods caused a lower insulin response than higher GI foods.  This is part of where dieters originally got fixated on the issue.

However, it looks like it’s not quite that simple.  While there was some brief interest in an Insulin Index (II) which measured the insulin response to foods in the same way GI does, research seems to have stopped as soon as it started.

Lowering GI by Increasing Insulin

It’s also far more complex than this.  One paper actually found that the reason low GI foods were low GI was due to a FASTER initial insulin response.  This caused blood glucose to be driven out of the bloodstream so the measured blood glucose response was lower.  But the insulin response was greater.

That is, it’s important to realize that the blood glucose response of a food is determined by both its rate of digestion and entry into the bloodstream as well as the rate of glucose storage in tissues such as muscle.

And it looks like low GI foods are not necessarily digesting more slowly but that a fast initial insulin response is clearing more blood glucose.  To quote from the summary of that research article:

“Bran cereal has a low GI because a more rapid insulin-mediated increase in tissue glucose uptake attenuates the increase in blood glucose concentration, despite a similar rate of glucose entry into the blood.”

In this regards, I’d note that adding protein to carbs has been known to lower the GI for a couple of decades.  However, it’s also been established that adding protein to carbs increases the insulin response.   Which is consistent with the conclusions of the paper above, by increasing insulin, protein lowers blood glucose levels giving a lower effective GI.

It’s just not for the reason that most people think.  And I daresay that most of the ‘insulin is evil’ people are going to argue that eating more protein hurts fat loss, yes protein increases the insulin response to carbs.  While increasing the insulin response.  Go figure.

Which is a long way of saying that I don’t think the GI and insulin response matter much (although see my final comments below).  If there is much effect of GI on fat loss, it’s more likely to be mediated through food intake and fullness as lower GI foods generally make people feel fuller and often cause decreased food intake.

This is always a source of confounds in debates over whether or not a calorie is a calorie.  Certain food types often make people spontaneously eat less, causing fat and weight loss and people confuse the food itself with the reduction in food intake that it causes.

It’s also worth noting that a 2006 review paper titled Glycaemix Index Effects on Fuel Partitioning in Humans examined this issue and concluded that:

“Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fuel oxidation.”

Basically, at least outside of the absolute extremes (where it’s possible that some of this stuff might matter), it just doesn’t really seem to matter much outside of any influence on food intake (e.g. if a certain food keeps you fuller and you eat less, it’s good for fat loss; if it doesn’t, it’s not).

As I said above, even basal insulin levels will inhibit FFA release by about 50% below maximum.  Just about any increase in insulin above that will inhibit it by 100%.  How much it goes up just doesn’t seem to matter in the big picture.

The GI doesn’t truly indicate the insulin response in the first place, if it does it appears that low-GI foods may be generating a faster initial insulin response in the first place, and none of this seems to meaningfully impact on fuel utilization anyhow.  Certainly any tiny differences in GI between brown and white rice are going to be utterly irrelevant for 99% of cases.

Wrapping Insulin Up

Now, to wrap this up, I’d note that most studies done on this topic are drawing conclusions from average responses and emerging evidence suggests that it’s a bit more complicated than this.   Some research suggests that the degree of insulin sensitivity, or baseline insulin levels determines how someone will respond to a given diet.

The punchline of that article is that individuals who are insulin resistant (and/or show a pronounced early insulin response to food intake) seem to get superior results from a lower GI/lower-carbohydrate diet.

In contrast, individuals with high insulin sensitivity show superior results on a carb-based diet.  Which is something  I’ve observed for the last 15 years since writing my first book The Ketogenic Diet.

Ok, I know that was long but, as noted initially, there’s a lot of confusion over insulin and I have a lot to say on the topic.  Hopefully I answered your question.

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21 thoughts on “Insulin Levels and Fat Loss

  1. Lyle – I’m really surprised you failed to mention anything about protein’s effect on hormonal production of glucogon, which significantly negates insulin’s ability to drive calories into fat tissue.

    Moreover, both in this article and others, you seem to contradict your opinion on insulin’s affect on fat loss. You seem to hold in this article that it is not as important as ASP, yet in your “How Many Carbohydrates Do You Need?” article, it seems that insulin (as a result of carb intake) is the most important factor in fat gain/loss.

    I’d be very interested to read your thoughts on these points. I’m also wondering if you’ve taken a look at any of Gary Taubes work, specifically “Good Calories, Bad Calories” ( or his essay “What If Its All Been A Big Fat Lie?” (

  2. Three things

    1. Glucagon only affects liver metabolism in humans, hence the increase in glucagon from protein is irrelevant to insulin’s effects in fat cells. This is something that has been known for several decades but individuals such as Sears, etc. continue to rely on rat/animal research to talk (incorrectly) about glucagon.

    2. Please read Insulin Sensitivity and Fat Loss on the site or Comparing the Diets and several other articles on the site to understand my stance on what affects fat loss/fat gain, etc. How carbs affect weight gain/loss interacts with insulin sensitivity more than absolutely. There is no contradiction that I see. Whether carbs or fat are relatively more of a problem depends on the individual.

    Insulin sensitive individuals tend to handle carbs very well, insuiln resistant frequently don’t. Individuals who can upregulate fat oxidation well (e.g. the high-fat phenotype of Rolls et. al.) can handle increases in dietary fat well; those that can’t can’t. Frankly, the carb article isn’t really dealing with fat loss/fat gain in the first place so I’m not sure I understand your comment.

    3. Taube’s book is filled with half-truths, cherry picked data and is mostly crap. I will do a long review at some point but he starts with an incorrect starting point (The obese don’t eat any more than the lean, an old data set now known to be incorrect) and therefore draws totally incorrect conclusions (it’s not calories but insulin that are the culprit).

  3. Hi Lyle, I think I got this research reference from you in the past…

    J Physiol. 2003 May 1;548(Pt 3):919-27. Epub 2003 Mar 21. Links
    Skeletal muscle fat and carbohydrate metabolism during recovery from glycogen-depleting exercise in humans.

    * Kimber NE,
    * Heigenhauser GJ,
    * Spriet LL,
    * Dyck DJ.

    Fat oxidation in the presence of elevated insulin during muscle glycogen replenishment after exercise? If the body is able to use its IMTG stores in this way, are these intramuscular fats likely to be replaced from other fat stores when a low-fat, balanced-carb (iso-carb??) diet is followed? Perhaps during sleep when insulin drops and GH increases? Or has it been shown that IMTG stores need to be restocked via digested fats only?

    Also, I read somewhere that somatostatin is released in response to mixed meals, which allegedly blunts the insulin response and slows gastric emptying? If fat burning is poor outside near zero insulin I’d guess this too helps little, however the slowed gastric emptying must help to reduce eating frequency and therefore helps reduce the likelyhood of overeating?

  4. As I recall, in that study, it wasn’t indicated that the fat oxidation was IMTG but blood fatty acids; I’d have to check to be 100% sure. But post-training is a slightly different situation (biochemically) to the rest of the day. And outside of the main thrust of this question and my answer (which had to do with meal consumption during dieting or whatever).

    And you need to read the article again. Even with basal insulin (insulin is NEVER zero except in type i diabetics) levels, fat oxidation is blunted by 50%. Eating basically turns it down to zero and calories are always being net stored in the post-prandial state (and note that dietary fat can affect this even with no increase in insulin). I have no idea where you’re going with the comments about somatostatin.

  5. Wasn’t going anywhere with comments Lyle, just picking your brains for more info

  6. Is Taubes not speaking the same words as Mcdonald??

    I have been reading Taubes g c b c book and have lost 35lbs and am not hungry.
    cut out sugar and white flour, eat lots of meat and eggs along with green vegtables and that keeps insulin low resulting in fat loss.

    I will buy The Ketogenic Diet book and see how it differs from what Taubes says .

    all this talk of dieting has me wanting a 6pack and a bag of chips but wait!! bad calories….

  7. Taubes is saying that calories don’t matter, only insulin.

    McDonald says that calories always matter because they do.

    That’s the difference

  8. Your links in this are wonderful I went through all this and I really appreciate it thanks for your articles.

  9. Is a calorie a calorie, is THE question that we must answer now. Just done reading your article conserning this issue… what do you think about the work of Hugo Rony and Alfred Pennington which are the skelleton of Taube’s work? Richard Feynman holds a very different view on this subject than you. Michael Eades too. Charles Poliquin, who has trained several elite athlete, swear mostly only but cutting carbs to get them lean (under 10%). You said it, it probably all has to do with metabolic difference. So i guess that you don’t beleive in the metabolic advantage. I’m a kinesiologist workin with people to lose fat-gain muscle. From my own experience,low-carb has always been the best way to do this. And Taubes also talks about alot of Insulin health’s others issues, such as oxydative and hypertensive.
    I think it is quite sad that you said such a thing about Taube’s work. He has done the nicest job that anyone had done yet. His book is very important.
    I find it really hard to know what to believe, after all.
    So many great people differing so much in their opinion. Oh well. It is always, in the end, about what works no?
    Thanks for the article, and maybe, for the answer.

  10. The problem I have with Taube’s book is this: after criticizing folks for cherry picking their data, he does the exact same damn thing.

    He starts with an incorrect/out of date 1980 paper (suggesting that the obese eat the same as the lean) and then goes looking for reasons why this is the case, concluding that it’s insulin.

    He then carefully ignores all data that doesn’t agree with him including an enormous amount of data showing that the obese under-report their true food intake (which is why the 1980 survey is garbage

    For someone who ‘spent 5 years raiding the research’, he mainly just selected data that agreed with his pre-formed conclusion, ignoring a tremendous amount of current research that did not.

    And that a lot of people keep insisting on a metabolic advantage that NO study has ever been able to measure doesn’t change the fact that NO study has ever been able to measure it. I’d point you to the study by Brehm for example:

    “The role of energy expenditure in the differential weight loss in obese women on low-fat and low-carbohydrate diets. J Clin Endocrinol Metab. 2005 Mar;90(3):1475-82.”

    Which directly measured both resting energy expenditure and thermic effect of food after a low- and high-carb meal. Results? No difference in resting energy expenditure and a higher TEF after the carb-based test meal. If the metabolic advantage exists, it should be measurable with current technology. And no study has been able to find it EVER (it’s always inferred by changes in weight).

    And bodybuilders have gotten to sub 10% for a couple of decades with carb-based diets so what Poliquin says doesn’t seem to be that relevant here.

    Which isn’t to say that lowcarb diets don’t work for a lot of people. But they work because people eat less, not because of any metabolic magic.

    Understand? I’m not anti-lowcarb diets (my first book is about nothing but them), but I am against people preaching magic voodoo that doesn’t exist.


  11. Thanks a lot for the answer. I’ve been reading anything that I could and seriously, i’m just more lost than I have ever been. I mean, obviously Taubes and you are both very bright guys. But how the hell is one supposed to know if any of you is right or wrong. One can back up about anything with cherry picking study (I’m not taling about Met. Adv. because I know there are no study out there proving it to be right – but i’m talking in a general way). And I don’t think that you hold any personnal interest (such as money or fame) in proving that your are right (both of you – I mean, one has to pay for his living, but I don’t think you/he truly believe this could make you/him rich). So it makes one wonder how can two bright men trying to help the nutrition feild quitting it’s non-sens can hold such opposite view (tho, saying that, I believe Taubes was more hypothizing and bringing new… hypotizes to think upon troughout his book rather than trying to settle a new ”truth”). But you’re also doing a pretty important work here so i’m thanking you for that, and I know you probably will but please, keep it up!

    Oh yeah, and as far as I know Poliquin was saying this because it’s the fastest way to burn off fat while keeping muscle.



  12. So how can I tell if I am insulin resistant. I feel like hell when I eat too much sugar that is for sure, I am 32 and have now had a baby. Feel like when I eat carbs I just want more a few hours later……

    I would love not only to be lean but also to look very young and healthy and have a lot of energy taboot.

    but how can I tell if I handle carbs well or not.

  13. Read the article on the sight “Insulin Sensitivity and Fat Loss” as it gives some rough ways of estimating insulin sensitivity vs. resistance.

  14. Thank you for this. I’m a fairly lean male, and tried to lose fat on a low carb diet with HIIT. All it did was leave me feeling light headed. In fact, I gained a few pounds, despite being hypocaloric. I kept cutting carbs, and boosted my fat intake to compensate for the lack of energy, and it left me feeling more lethargic, light-headed, and weak post workouts. I also had these periodic cravings for carbs, which I tried to suppress.

    I switched to a low fat, moderate carb diet with cardio, and it’s been night and day. I can see the fat coming off, recovery is less of an issue as well. The carb cravings went away entirely; I guess my body was trying to tell me something. I didn’t understand why until I read this. Great stuff.

    Too often people say only one way works, but people don’t realize everyone’s body is different. People just need to stick to what works for them, and the industry needs to propose options, as you are doing, rather than pushing all these fads and singular ideas.

  15. Hiya Lyle!

    Fantastic website and i very much appreciate the rigour in your approach.

    As a medical student i have exposed to dubious dietary dictates on the course which have no substantion in the literature – at least as far as i can tell!

    I was very much hoping on tips on how to search pubmed when performing a review of the field – unfortunately my body packed around the time we did literature reviews a few years back 🙁

    An idea of the framework you utilise for literature searches and some examples of the search terms you may use if you were to perform a search for the metabolic effects of insulin and relevance to much propounded idea that insulin levels are a major determinant of adiposity.

    pleeeeeeeeeeeeease 🙂

  16. I believe Taube’s main contention was merely to debunk modern low-fat dogma and to point out that there was no actual scientific backing to many of the current recommendations. The theory “calorie in, calorie out” ignores too many other physiological truths to be of any use at all, as a theory by itself. Nearly 40 years of worsening health and failure by the medical establishment to reliably help people is showing this to be true – and Taubes was one of the early heralds to this.

    I have yet to see any research in any way bolstering the original claim from the 40’s and 50’s claiming total dietary fat was to blame for obesity and heart disease.

    When it came clear that total fat wasn’t the answer, they started zeroing in on dietary saturated fat – again, without ANY research to back it up. The only citation i have seen from the era showed the results of feeding lab rats artificially saturated fats (and vegetable fats, irony of ironies) .. and this has been the only literature anyone has ever come up with, from that era, justifying the hysteria. Bad science!! The only tangible result of this fat phobia – several decades putting Americans on trans-fat laden margerine and oils – has had huge, sweeping ill effects upon the population at large (pun intended).

    The general population grew obese, and in a way that outpaced dramatically the reduction in exercise. Reviews showing the lessening of exercise for people do NOT mirror the rise in obesity and disease. No-one disputes exercise being good for you, and everyone agrees it is a part of healthy living. But it is demonstrably NOT the main causative factor in the meteoric rise of morbidity that hit the people of North America with exponential growth …

    However, if you chart the growth (proportionately) of the increase in processed carbs and altered vegatable oils over time, you WILL see exactly the same trend as seen for the increased obesity and illness.

    Taubes was one of the more lucid earlier skeptics on this topic, and I have enjoyed his writings immensely. I myself am only in the infant stages of researching this topic, and it is a daunting task. The sheer hype and emotion that abounds on all sides is suffocating! One of the things I liked about Taubes is the style of his writing, it’s calm … one does tend to cringe when criticism say it’s “mostly crap” and “cherry picked” and “half-truths” … I dare say there will be lucid rebuttals of some of his theories, and they are very welcome as part of the debate. I have yet to see any OTHER work that contains as balanced a bibliography as his GCBC book, it includes the works he dislikes as well as the works he favors.

    To those who react viscerally and call him “crap” I will say this .. I’m fairly sure you are reacting to one, small aspect of what he spoke of, namely the “exercise won’t make you slim”. It is perhaps one of the more controversial theses in his book. And it does indeed seem like you don’t understand at all what he is saying. It does take a calm bias-free read to ‘get it’. I recommend you take the time, it is well worth it.

    He recommends moderate exercise for health, throughout the book. At no time does he say “don’t exercise at all”.

    What he says is, from a scientific point of view, a review of all studies and work to date very strongly points to “diet and exercise” (i.e. calorie in / calorie out, a calorie is a calorie no matter what) fails. If you review all the attempts and documentations overall, and are an unbiased scientists, you will conclude the same (remember, conclusion has to be based on OUTCOME, on actual results ..not what your heart wishes it to be). He postulates several reasons for all this poor outcome for exercise in dieting, including rebound-hunger as well as poor nutritional support .. as well as poor long-term compliance. Whatever the reason, it fails the vast majority of the time. Critics of Taubes return to the phrase “well, the obese are lazy and they lie about their intake”, something that fails to resolve the situation or further the debate. Taubes refused to endorse the widespread believe that “suddenly 25-50% of Americans are fat, lazy liars” (does this imply that up until the 70’s, mostly everyone was NOT lazy and without motivation?). He proposed real theories on the actual CAUSE of the problem. And he has proposed true and population-wide remedies, even if implementing them will be a tremendous challenge.

    There are not many researchers, in the last 5-10 years, who disagree that the traditional ‘calorie in / calorie out’ model has failed. Just that Taubes got there much earlier 🙂

    He puts forth some theories to explain why, and he for sure doesn’t cover all of the bases. He misses out by and large on the emergence of huge injections of dietary artificial fructose into our daily diets. However, his book has been an eye opener for me and many others. I look forward to anything he writes in the future as a welcome addition to the debate.

    Bet he doesn’t include the word “crap”in there anywhere, either 😉

  17. Blah, blah, blah, blah. Yes, I’ve seen and heard it all before but here’s the problem. A major part of Taube’s entire premise is based on a 1980 study that is incorrect.

    I’ll simply quote Bray from his review of Taube’s book and then ask you the following question: How come Taubes, in his ‘5 years of research’ wasn’t able to realize that the self-reported food data in 1980 was wrong?

    It’s 2009 and we know factually that the obese eat more than the lean. Yet somehow Taubes was unable to come across that data point. And refuses to acknowledge it even now. What does that tell you about him and his agenda?

    This quote comes from the following paper.

    Bray, GA. Good Calories by Gary Taubes. Obesity Reviews (2008) 9:251-263.

    Bray says:
    “In developing his ideas about calories and obesity in Good Calories, Bad Calories, Taubes argues that obese individuals do not eat more than lean ones do. The data for his belief come from the Diet and Health Report (16) prepared by the National Academy of Sciences. This report said ‘Most studies comparing normal and overweight people suggest that those who are overweight eat fewer calories than those of normal weight’.calories more per day. To maintain this extra weight the women have to eat enough food to provide this extra energy.

    We now know that the data used in the Diet and Health Report were wrong and that obese people eat more food energy than do lean ones. The data showed that normal-weight people underreport what they eat by 10–30%. This means that dietary food-intake records underestimate energy expendi- ture by nearly a quarter. For overweight people, the degree of underreporting is higher, varying from 30% to 50%.”

    Bottom line, it’s still calories in vs. calories out.

  18. Have you read GCBC? Because it doesn’t sound like you have.

    You keep focusing on something that is hardly even present in the book and that has essentially no bearings about what Taubes’ actual message is. There is one line causally mentioned about obese people eating the same amount as lean. He does not delve into this topic and this is not anywhere near the focus of the book. He does not mention the words ‘metabolic advantage’ anywhere.

    The main three points of the book is that previous studies and analysis on the fat/cholesterol hypothesis are poorly done, that excess consumption of refined CHO are most likely the causes of disease and that insulin is the main regulator of fat storage.

    Of course its more complicated than that but the bottom line is refined carbs drive hunger. Hunger drives excess calorie consumption.

    I don’t get why you are trashing this book completely. There surely must be lots of it you agree with. It doesn’t seem like you’ve given it a fair chance.

    Calories in = calories out is an oversimplification and a pointless statement and ignores all other aspects of health besides weight.

    Im still waiting for your critical analysis.

  19. Yes I’ve read it and that is a fundamental aspect of his argument and when you start from a moronic assupmtion you reach moronic conclusions.

    Not to mention that he’s simply WRONG about everything else (e.g. exercise is ineffective since it raises hunger). I realize that Taubes tells people what you want to hear but he’s simply full of shit about EVERYTHING.

    Every aspect of his hypothesis is disproven by research but he so carefuly cherry picks his data that he makes a convincing sounding argument that is just wrong. James Krieger points this out here

    Bottom line: Taubes is wrong about everything he claims. Yet in his ‘5 years of research’ he seemed to never find the contradictory data. He pushed his agenda just as he claimed the saturated fat people did. And you people can’t see it for one simple reason: he tells you what you want to hear.

    And with that I’m closing comments on this thread. Everything that need be said has been said. Those of you who want to believe Taubes message and make excuses, feel free to do so. I’ll keep providing correct information and solutions. When you decide that you’re tired of looking for excuses and want solutions, you know where to come.

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