April 18, 2012

Nutritional biochemistry

How do some cultures stay lean while still consuming high amounts of carbohydrates?

Read Time 8 minutes

Many of you have asked this question over the past few months, and I’m sure many more of you have at least contemplated this question at some point.  I know I did.

For the sake of this discussion, let’s ignore the fact that the “historically” lean countries (e.g., France, Italy, Japan) are catching up to our levels of obesity and metabolic syndrome, especially in certain affluent subsets.  After all, we did get a 40 year head start on how to eat poorly.   So, let’s ask the question this way:

How does the average person living in, say, Japan stay leaner and healthier than the average American while still consuming >70% of their caloric intake in the form of carbohydrates?  

I don’t claim to know the answer this question, but I’ve got a few ideas.

Before getting to this question I want to mention that I have reorganized a page on the blog, Media, which now has a lot of videos and interviews.  A lot of the questions I get asked are addressed in these videos and interviews (both of me and others), so please check there for answers to your questions. Last week I was interviewed by Ben Greenfield. Ben asked a lot of great questions which many of you have also asked over the past few months. Take a look here and see the questions Ben posed.  If you’re interested in hearing my thoughts, listen to the audio clip from the interview.

Back to the question at hand

These data are a bit dated, but you can see the point: the United States is leading the way in the obesity race, while other countries (including those eating at least as high a total percent of their intake from carbohydrates) are not.  How is this possible if insulin – stimulated by carbohydrate intake – is an important hormone in the body’s drive to accumulate fat?  

This problem has many layers to it, but for the purpose of simplicity (always a danger when aspiring to explain complex phenomena) I’ll limit the discussion to three main points – think of them as the “higher order terms” – in their order of importance.

  1. Lower consumption of sugar
  2. Lower absolute consumption of carbohydrates
  3. More favorable consumption of polyunsaturated fatty acids (PUFA)

These reasons are not independent.  In other words, they are highly correlated and linked to each other, which actually amplifies their effects.

One other point to keep in mind: There is no definitive experiment I will point to that can prove my assertion beyond a reasonable doubt – for that I would need a prospective, well-controlled experiment comparing the eating habits of these countries over decades.  Many things I’m discussing are observational in nature, so you’ll have to really scrutinize my thesis on your own.


Reason #1 — Sugar intake

There is a great disparity between U.S. sugar consumption and the sugar consumption of countries like France, Italy, and Japan (and most countries, actually).  When I say “sugar,” of course, I mean sucrose, high fructose corn syrup, beet sugar, cane sugar, and liquid fructose (e.g., fruit juice) to name just a few forms.  Why does this matter?  If you’re not currently up on the why-sugar-is-bad-for-you data, it’s worth reading this post, and watching the lecture by Dr. Lustig.  For a quicker answer, watch this video from 60 Minutes.

Think of sugar as a “metabolic bully” or the proverbial Trojan Horse of metabolic syndrome – you let sugar in, and before you know it, you have diabetes, heart disease, and cancer.  Consumption of sugar makes us metabolically inflexible as part of a vicious cycle I’ve diagrammed below.  The more sugar you eat, the more insulin resistant you become.  The more resistant you are to the effects of insulin, the more insulin your pancreas needs to secrete in response to all carbohydrates, including the not-so-bad “non-sugar” ones. The more insulin your pancreas needs to secrete to manage your glycemic load, the higher your average insulin levels, which is manifested by higher levels of circulating insulin at all times – fed and not fed. Higher levels of insulin lead to less fat oxidation and more fat storage (from both ingested fats AND ingested carbohydrates – de novo lipogenesis).  This, not surprisingly, leads to greater insulin resistance, and so the cycle continues.  There is a reason “vicious cycles” are called “vicious.”

Vicious cycle



Reason #2 — Total glycemic load

It’s important to keep in mind that the percent of carbohydrate consumed is nowhere near as important as the absolute amount of carbohydrate consumed. Failure to understand this point may be one of the most significant reasons for the calories-are-everything-argument.  Recall my post on why Weight Watchers and most commercial diets are actually low-carb dietsVirtually any diet that reduces caloric intake also reduces glycemic load.  Worth repeating: Virtually any diet that reduces caloric intake also reduces glycemic load. That is, cutting calories almost always means cutting carbohydrates, cutting insulin, and cutting fat storage.  So what does this have to do with folks in Japan eating rice?  While these cultures may consume a higher percentage of their intake from carbohydrates, their actual glycemic load is lower. In other words, they actually consume fewer total carbohydrates in most cases than a typical Westerner (and in the presence of much less sugar!).  Contrast “typical” carbohydrates consumed by these “high” carbohydrate societies:

Photo by plusstory1 (http://plusstory1.tistory.com/28) [CC BY 4.0], via Wikimedia Commons
Photo by Liene Vitamante on Unsplash


Photo by Jonathan Pielmayer on Unsplash

Sure, they eat rice and bread and pasta.  But how much at one time?  And what are they eating it with?

Compare the figure above with that below, showing “typical” American carbohydrate consumptive patterns:


American eating

Are we eating the same amount of pasta per meal as the folks in Italy?  Perhaps, though I don’t think so.  Furthermore, while they make their own pasta sauce out of home-grown tomatoes, garlic, and olive oil, we dump a pound of Prego on ours (the second or third ingredient is nearly always sugar).  While the French are eating baguettes, we’re eating sugar-filled bread.  While the Japanese are eating a small bowl of rice, we’re stuffing our face with a plate of fries and breaded onion rings.

Why does consuming more glucose matter, notwithstanding the point that the glucose we consume is virtually always linked to sugar?  The human body can only store a finite amount glycogen, so any excess glucose we ingest actually does 2 harmful things:

  1. Continues to raise insulin levels, which inhibits fat mobilization,  and
  2. Gets stored as fatty acid, and ultimately ends up as triglyceride in fat cells.  Remember, this is a one-way metabolic street.  When your body turns glucose into fat (technically, we turn acetyl-CoA into malonyl-CoA into palmitate), you can’t turn that fat back into glycogen.

More absolute glucose, regardless of the relative percent, still leads to more fat accumulation.


Reason #3 — Inflammation

While insulin is certainly near the top of the list of pro-inflammatory factors in our bodies, it’s important to keep in mind the role of some other factors whose balance plays a role in inflammation such as eicosapentaenic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA) to name a few.  I will, in a separate dedicated post, compose a thorough discussion on the metabolism of omega-3 and omega-6 fatty acids. To be clear, the science around this is not fully worked out, and much of what we speculate is based on indirect cause-and-effect inference, coupled with “sound” mechanistic reasoning and, of course, strong observation.  In other words, this is not close to bulletproof logic.

What is known is that diets high in omega-6 polyunsaturated fatty acid (PUFA) (e.g., mostly plant oils like sunflower, canola, safflower, and corn oil) relative to omega-3 PUFA (e.g., fish and fish oils) create a disproportionate ratio of AA to EPA and DHA. When I go through the biochemistry of this (which is super-cool!) it will be obvious why this is true: Eat a huge excess of omega-6 PUFA relative to omega-3 PUFA and your blood and tissues will show a lot of AA relative to EPA and DHA.  Same logic holds in reverse.

What does this mean?

Here’s where the story goes from being “clear” to “less clear,” at least to me. There is reasonable evidence that too little EPA and DHA (omega-3) predisposes us to certain diseases, in particular, cardiovascular disease.  There is some evidence that the relative amounts of EPA to AA and DHA to AA matter, too (i.e., what happens when you eat too much omega-6 PUFA relative to omega-3 PUFA).  What is not clear is if too much AA relative to EPA and DHA (i.e., much more omega-6 than omega-3) leads to clinically significant inflammation in the body that fosters other disease states.  In fact, a case can be made that high amounts of omega-3 PUFA are outright protective from many diseases including the disease spectrum of metabolic syndrome (e.g., diabetes, heart disease, cancer, Alzheimer’s disease), independent of omega-6 PUFA intake.

Observationally, this seems “clear” – societies whose ratio of omega-6 to omega-3 consumption are lowest (e.g., 3-to-1 or better) have far less disease than societies whose ratio is much higher in favor of omega-6 (e.g., 30-to-1).  Of course, this does not prove anything, since uncontrolled observations are just that.  This is how folks like Ancel Keys and Colin Campbell have caused so much trouble and confusion in the field of nutrition.  It is possible that some other factor, beyond this, is resulting in the differential disease pattern.   In other words, it is not clear if this observation is correct because of the relative amounts of omega-3 and omega-6, OR if it is true because of the absolute amount of omega-3, OR if it is true for some other reason? I don’t know (yet), but will continue to work on this.

That said, there is some indirect evidence linking differential consumption of PUFA (i.e., relative differences in omega-3 versus omega-6) with actual disease states.  A paper published in 1993 in the New England Journal of Medicine showed that patients with more EPA/DHA precursors than AA precursors in cell membranes had greater insulin sensitivity and less heart disease (though, obviously, these are linked).  I will review this in much greater detail in a dedicated omega-3/omega-6 post, but I want to point out that there is some evidence beyond just the observational data suggesting more omega-3 and less omega-6 in your diet leads to better insulin sensitivity:

Eating more omega-3 and less omega-6 may lead to more EPA/DHA precursors in cell membranes than AA precursors, which is correlated [not causally linked] with less insulin resistance.

Hence, Western diets, where we don’t consume much omega-3 PUFA, and it is very difficult to avoid omega-6 PUFA (they show up in virtually every processed and packaged food we touch, not to mention all sauces and dressing, and even our grain-fed meat), may predispose us to greater insulin resistance and inflammation.  As you can see in the figure below, a (historically) typical Japanese diet was nearly equal in omega-6 to omega-3, while our diets are typically much higher in omega-6 than omega-3 – BOTH because we don’t eat much omega-3 AND because we eat much more omega-6.  The same is true of a traditional Mediterranean diet.

Let me reiterate: I do not know if the relevant issue is the denominator (i.e., absolute amount of omega-3 consumed) or the ratio (i.e., relative amount of omega-6 to omega-3).

[Personal note: Pending resolution, I do both: I maximize my omega-3 intake and minimize my omega-6 intake to a ratio of about 1:1 with lots of EPA and DHA and little omega-6.  What is not clear to me yet from current data is if I should be minimizing my omega-6 intake.]

Omega-3 vs. Omega-6



What can we learn from this?

I alluded to how multifactorial this issue was, but I hope it’s clearer to you now.  Let me try to summarize why some cultures have historically been able to consume rice and pasta and baguettes but stay leaner and healthier than Americans:

  1. They consume a fraction of the sugar we do.  More sugar consumption leads to greater insulin resistance, more fat creation, less fat breakdown, and more fat accumulation.
  2. They consume less total glucose, AND the glucose they consume is accompanied by less sugar (and less omega-6 PUFA, if it matters).
  3. They consume a ratio of omega-6 to omega-3 PUFA that is much lower than we do.  This may further reduce any insulin resistance brought on by the glucose they do consume (in smaller doses and with less sugar).

Let me close with one personal and anecdote.  When I began my nutritional journey, for over 18 months I still consumed a modest amount of carbohydrate, probably on the order of what a typical person in Japan would consume.  The biggest elimination in my diet was sucrose, HFCS, and “junk” carbohydrates. The results were impressive.  I went from being about 200 pounds at 25% body fat to being 177 pounds at 10% body fat while still consuming some carbohydrates (by that point I was down to maybe 100-150 gm per day).   However, I was able to get leaner (170 pounds, 7.5% body fat) and further improve my risk profile for disease by going below 50 gm per day (i.e., entering nutritional ketosis).  Was this last step of nutritional ketosis necessary? Of course not, but it was a nice way to experience the full spectrum of carbohydrate restriction.  Will I ever go back to eating 100-150 gm per day of the “right” carbohydrates at some point? Probably, provided I don’t go back to eating sugar and stuffing my face with carbohydrates.  It will depend on what I’m optimizing for.

My point is this: Just modifying your diet by the 3 factors I mention in this post — elimination of sugar, less total glucose load, and improved omega-3/omega-6 profile — even if you are not genetically programmed to be lean, will probably deliver 80% of the value in terms of disease risk and body composition.

Photo by Jorge Zapata on Unsplash

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  1. Peter,
    I came across your blog while researching for a talk I am giving next week. Nice job. What a tremendous amount of research and review distilled into easily digestible bites. Thanks for your effort.

    I am an obstetrician/gynecologist and about three years ago we (8 partners in a suburban practice) decided to offer our patients a healthy eating plan. The design was not exactly a ketogenic diet but it stressed the low glycemic load carbohydrates and modest protein and fat. We have had tremendous results with weight loss, improvement in insulin levels and lipids. Our diet is about conscious eating and changes for a lifetime. Not just lose the weight and gain it back. We do not use pills and shots which are so popular. Enough about our program. I have a question.

    Do you have any thoughts on why the obesity epidemic in this country (evidenced by the percentage of the population is overweight and obese and the percentage of diabetics) started in the Mississippi valley and spread east and west? Interesting in this is the fact that Nevada was years behind the rest of the country in achieving the same diabetes and obesity rates. If you look at a map over time it looks like an infectious disease.

    Was there something in the environment? Bacteria in the food? Something is (was) going on that has not been addressed.

    Please keep up the good work.


    • Very interesting question, Phillip. It could be a cultural difference (e.g., cultural affinity for certain foods), a socioeconomic difference, or a genetic predisposition. Those would be my starting guess.

  2. At this point, it’s hard for me to feel that any analysis that doesn’t include looking at gut microbiota is going to be incomplete, and find things that can’t be explained. (Not to say that the kinds of studies you’re doing aren’t valuable!)

    Given that studies show when we transfer fecal bacteria from lean mice into obese mice, the obese mice get lean. And given studies showing that foods high in resistant starch (which influence gut bacteria balances) decrease glucose response from meals containing carbohydrates, I have to hypothesize some aspects or tranches of the obesity epidemic has something to do with changes in gut bacteria. And I’ve been basically LCHF for 40+ years, since the 60s, so I’m not anit-carb-hypothesis.

    You asked above what might have changed the gut microbiota. I’d note that you can also correlate the rise of obesity and diabetes, etc. with the rise of antibiotic use, especially if you factor in a generation delay between the introduction of antibiotics into meat. As that rose, the next generation was the generation that started to see obesity levels rise. Why might that be? Because you get your initial set of gut bacteria from your mother at birth, and if the mothers’ guts started to become bacteria-deficient, that would be passed on.

    And certainly the fact that we started eating more simple and processed carbohydrates rather than more complex carbohydrates (with more soluble fiber), would change gut bacteria, and probably not for the better considering that adding resistant starch seems to improve the health of gut microbiota. It also seems to significantly improve satiety signaling, and there are a couple of potential reasons for that. I would bet you a dollar or two that carbohydrate resistant people like your wife (and some other friend of mine that drive me crazy for the same reason) have very different gut biomes than carb-sensitive people.

    And I bet we’re going to find industrial oils and sugars damage the balance of gut bacteria, possibly beyond the fact that we lose important nutrients by substituting them for good fats and safe carbs. (Though maybe the latter is more significant in the long run.)

    Again, I’m not arguing against the value of the carb-insulin hypothesis, only to say it might be a big part, but only part of the answer. I’ve often said that there isn’t one reason we get fat, and carb-sensitivity can be intrinsic or acquired. And without taking into account a system containing 99% of the DNA in your body, where 90% of the neurotransmitters in your body are produced among other things, it’s going to be hard to get a complete picture.

    Here’s an interesting article I just found that seems to speak to this: “Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/

    And this one: “The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43.” http://www.ncbi.nlm.nih.gov/pubmed/23652017

    • I agree that gut balance is key….and that the microbiome is an under-appreciated and very confusing issue, and imbalances can be dreadful to treat. I have been diagnosed with SIBO (Small Intestinal Bacterial Overgrowth) and Leaky Gut, and have been in various treatments for over a year….with many starts and stops, various restrictive diets, special antibiotics, various other drugs, and now about to try low dose naltrexone (LDN). The only thing besides food that I obsess about is information about food. One point about carb craving that I have been told: overpopulation of “bad” gut bacteria, who crave “their” kind of food, sends a message that goes directly to the human brain, overriding all human motivation to control dietary intake. Thus, gut balance must come before any effort to control the human diet. Astonishing as this sounds, I believe it must be true. Thanks for your wonderful web site and blog. Eagerly reading onward…

  3. Dr.Attia, I have seen you use the term “absolute” amount of carbs in this webpage and others however I do not understand what is meant by the term “absolute”? I have searched your blog but could not turn up anything. I am assuming it means the grams of carbs after the grams of fiber are subtracted, Im sure this is incorrect but i don’t understand the meaning, forgive my ignorance. Any explanation would be greatly appreciated.

  4. Have there been any really good analyses comparing diets of different populations, wrt macronutrients, types of macronutrients, and health? This seems like an obvious thing to do.

    Similarly — and even more interesting to me — have there been any good studies comparing diets of indigenous populations that were found to be healthy on contact, then whose health declined on adapting to a Western diet?

    These seems like potentially rich sources of epidemiological evidence about what constitutes a healthy diet. Shouldn’t we rigorously and carefully study what is proven to ‘work’ as diets historically and internationally?

    I haven’t turned up much on Google, so I wonder whether this research has been done.

    For one fascinating experiment based on an indigenous Native American diet, see http://michiganradio.org/post/year-eating-indigenous-diet .

  5. Hi, Peter. I’m a regular reader of your blog for a while now. Couldn’t congratulate you enough.

    I noticed you still don’t have any post on the economics and natural resources use that influence our actual eating patterns and the challenges we would have to face for a change towards a less carbs dependent diet. I understand you’re a scientist, not a historian or economist, but these topics are so deeply related to your described goals i don’t think they can be ignored on your personal blog. I’m sure you have already given thought to it, i’m just stimulating you to put on a new item on your to write list.

    I thought i would also recommend you this: http://www.vaclavsmil.com/japans-dietary-transition-and-its-impacts-food-health-and-the-environment/ . I haven’t read it yet, but Vaclav Smil is an assured read.

    Keep with the good work! Cheers.

  6. Hello, i just wanted thank Peter Attia for this great blog. I am german and found about the possible benefits of a low carb diet almost 3 years ago when i was 21 years old reading some blogs and finally discovering Martin Berkhan’s leangains page. I started intermittent fasting weight training fasted (precisely: with eating 2 egg whites pre-workout after 15 hours fasting) and having a huge carb meal post-workout. On my non-training days i basically ate low-carb (~ 30-50g) while not being in ketosis because my protein consumption was too high. I lost 10kg and built muscle on the same time with this approach and it worked really well because it enables you to still have high amounts of carbs 3 times per week (sweet potatoes, rice, LOTS of berries and rarely some ice cream post-workout. So basically it’s good maintainable approach for a lot of people that want lose weight and still have their carbs and social life to be more “normal” (normal in the way that carbs are everywhere today and it’s certainly harder to avoid them in social circumstances). So, while i had great results with this technique, as i started to inform myself better over the years i started to think if it really is an optimal approach for me. Because i wondered about how well i am adapted to fat considering this 3 big carbs meals in the week, certainly i handled fat really well, felt energetic and could train basically fasted without any problems (expect sometimes when i experienced fuzziness in my head while going fast from a sitting to a standing position [e.g. deadlifting] and i concluded after testing some things out that the cause was most likely an exaggerated adrenalin-noradrenalin response because of my depleted liver glycogen, eating 2 egg whites has surprassed this effect (i prefer it to 2 whole eggs cause calories would increase and i am not sure if this could decrease HGH, so i just eat the 2 egg yolks priot to my training). But after some time i wondered if this is an “optimal” approach because i was thinking that i can’t be that well fat adapted with eating 3 big carb meals per week (ofc some of this carbs replenish glycogen stores while others will still be used for the brain so i thought i could maybe build more muscle just taking as much carbs as needed to replenish my stores and focussing more on fat as my “general” energy source cause i thought the better adapted i am fo fat the less likely protein from my muscles will be converted to sugar to fuel different energy needs. Ofc it is not that simple but this were just my starting ideas. And i what i should say too is eating high carb on the workout day always correlates with eating low fat on that day too for “obvious” reasons, but i questioned this tactic cause of the benefits of fats (saturated for testosterone and EPA/DHA for lots of other reasons especially fat loss). Another reasons I questioned my approaach because i knew i dont need this huge amounts of carbs to replenish my stores so i thought while i got way better at metabolizing fat i am still “adapted” to carbs as my main energy source (on my rest days my high protein consumption would supply quite an amount of sugar too and while fasting i wondered how much my muscles actually contribute to my sugar need with converting my muscle protein). While i was looking good and feeling fine i didn’t think that i had optimized the whole process (because i know there are even vegan bodybuilders etc but being just “in shape” and having optimized the muscle building process is certainly another frame of reference). So i rougly calculated how much my glycogen stores would be depleted (this took some time cause i need consider not only excercise but fasting too) and replenished only that while eating 24/7 LCHF or better to say “required carb” and high fat (while not being in ketosis cause my protein intake i still too high but in some time i will probably test training in ketosis to determine how good for muscle building it is considering the lower protein intake (protein higher than 120g has certainly an effect on protein synthesis and muscle building in my self-observation. And there are some people that believe in the benefits of a high insulin spike after training, which i know is not needed cause post-workout protein and other factors will take care of that (and i am highly insulin sensitive in this circumstance anyways). But it doesnt mean an insulin spike post-workout is a disadvantage, logic tells me that replenish carbs after a workout is a good thing, and carbs drive insulin, so higher insulin levels post-workout are a natural consequence and science shows some benefits of that while it still didn’t answer how much is perfect and how much is too much. But yea, i don’t have enough knowledge and understanding for now to determine this things and there are not that many informations in german that i could understand better, so for now i need stay with my self-observational data 🙂 I experience really good results with my “required carb, high fat” diet and i realized eating a high amound of carbs prior to workout (did this when i had no chance training fasted) actually decreased my performance. I don’t know it it’s only for the carbs or just cause i was not training fasted or maybe even for both or something else…but i will continue to play around with the things. I just know that i forgot what i wanted to say and why i even wrote all this half-baked stuff, but maybe it can help some people can relate to it. Anyways, i just wanted thank Dr Attia for doing all his great work and being such a sharp thinker questioning even the most basic things (or things that we consider basic now because we got used to them). That’s the only way to reach new levels of understanding. Best regards! 🙂

  7. Reason #4 – Individual Differences in AMY1 Gene Copy Number

    While there is a considerable range of variation in dietary starch intake among human populations, a distinction can be made between “high-starch” populations for which starchy food resources comprise a substantial portion of the diet, and the small fraction of “low-starch” populations with traditional diets that incorporate relatively few starchy foods. Such diets instead emphasize proteinaceous resources (e.g., meats and blood) and simple saccharides (e.g., from fruit, honey and milk).

    Recent study found that mean diploid AMY1 copy number is greater in high-starch populations. Strikingly, the proportion of individuals from the combined high-starch sample with at least 6 AMY1 copies (70%) was nearly 2 times greater than that for low-starch populations (37%). To visualize the allele-specific number and orientation of AMY1 gene copies, the authors performed high-resolution fluorescence in situ hybridization on stretched DNA fibers (fiber FISH); these results were consistent with diploid AMY1 copy number estimates from our qPCR experiments.
    Read more: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2377015/

    Personally I think, that increased risk of obesity in persons with low amylase can be explained by a reduced responsiveness of the islet B-cells to incretins. Incretins are insulinotropic factors of the gut released by nutrients and stimulating insulin secretion in physiological concentrations in the presence of elevated blood glucose levels. The incretin effect refers to the phenomenon of oral glucose eliciting a higher insulin response than intravenous glucose at identical plasma glucose profiles. It is conveyed by the two insulinotropic incretin hormones: glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Type 2 diabetes mellitus (T2DM) has been shown to be characterised by an almost abolished incretin effect.

    The incretin effect was shown to be affected in subjects who had impaired glucose tolerance and who were therefore at high risk for developing type 2 diabetes. This observation could imply a primary role for the reduced incretin effect in type 2 diabetes, but on the other hand, the finding could also represent an early consequence of the chronic mild hyperglycemia of impaired glucose tolerance. However, recent study suggests that reduced incretin effect in type 2 diabetes is a consequence of the diabetic state rather than a primary event leading to type 2 diabetes. (http://www.medscape.com/viewarticle/562484_4)

    Nevertheless primary role of reduced increting effect due to low amylase cannot be excluded. This assumption is supported by the fact, that proper assimilation of nutrients stimulates secretion of GIP and GLP.1. (http://www.ncbi.nlm.nih.gov/pubmed/20591345) Importantly, there is also evidence that genetic variants may influence the incretin effect and possibly also the responsiveness to incretin-based therapy in some patients. (http://care.diabetesjournals.org/content/34/Supplement_2/S251.full)

  8. Good morning Dr. Attia,

    I am a health care professional who is also skeptical of traditional nutrition. I would love to know what you think about the idea that different people metabolize food differently; many authors have posited that different people should have different diets depending on their “metabolic type”(Wolcott, The Metabolic Typing Diet), “blood type”(D’Adamo, Eat Right for Your Type), or “acid/alkaline type”(Wiley, Biobalance).



    • I think there is definitely something to this, though I’m not sure which phenotype is the best differentiator. To date, I think the best predictor of dietary response is hyperinsulinemia.

  9. Two other things: exercise and portion size.

    Most Japanese use public transportation and that involves walking/biking to the train station and taking the stairs to and from platforms. It’s not rigorous exercise, but it’s more than many Americans get.

    The McDonald’s size L in Japan is a small in the US. A Japanese proverb goes, “eight parts of a full stomach sustain the man; the other two sustain the doctor”. When I eat at McDonald’s in the US, I get the larger Happy Meal to mimic Japanese portion sizes. Also, when I worked in Japan, my coworkers didn’t snack at their desks. Vending machines are ubiquitous in Japan, but most sell beverages and I never saw one that sold chips or candy bars.

  10. Neither sugar nor fat consumption seems to be a good indicator of obesity — not at least among those countries that eat the most fat and sugar. Sure, Americans are both eating way too much sugar and outpacing the rest of the world in waistline. But outside of that, there doesn’t seem to be much of a suggestion that an affinity for either is associated with higher rates of obesity in these countries.

    The average Swiss citizen eats 12 kg of chocolate per capita and this mean each person eats about 240 bars per year. Similarly, other countries, including Belgium, the Netherlands, Finland and Sweden, are both near the top in sugar, fat and dairy intake, and near the bottom in obesity rates.

    The country with the largest per capita consumption of bread is Turkey with 199.6 kg (440 lb) per person. Turkish people eat more than three times their own body weight in bread annually. 101 million loaves of bread are produced daily in Turkey. Obesity in Turkey is much smaller than in USA.

    All healthy civilizations throughout history thrived on a primarily complex carb diet. Even the Neanderthals have been proven to have grains as a main dietary staple, despite what the book-selling low carb and paleo propaganda would like us to believe.

    Sugar is currently the popular scape goat for all our problems (rivaled only by grains and gluten). Claims that sugar makes people fat are just ridiculous. While I eat a lot of sugar every day for over 50 years and I am skinny with perfect blood pressure and normal blood sugar level they are having troubles loosing weight yet they would still argue that it will make me fat.

    Your cells most important job is to create energy. Glucose is needed to fuel this cellular energy production and help meet the demands put on your body every day. When your intake is not sufficient your body starts the inflammatory process of breaking down fat and proteins to MAKE glucose. While your body CAN make energy from proteins and fats, it’s less efficient, and puts added stress on your body. Stress is not healthy.

    When our cells don’t have enough glucose to do their job they find alternative means by which to get their energy, particularly through either Lipolysis (fat breakdown) and Gluconeogenesis (new sugar creation from our own body tissue).
    These processes require the release of adrenaline and cortisol—our “fight or flight” hormonal responses.
    This is why so many people have sensations of clarity, easy weight loss, and boundless energy when turning to a no-sugar or low-carb diet. Their bodies are “thriving” off of adrenaline and cortisol. And while these positive effects can last many months or longer, ultimately the body is not designed to live off of these stress hormones. The long term results are bad. Ditching sugar can destroy metabolism and lead to a weakened immune system, poor digestion, impaired sexual/reproductive function, depression and accelerated aging.

    Health is about balance, moderation. Let’s stop blaming fat, sugar, or any other “one” thing. Throughout most of human history, calories were relatively scarce and hard to get, and physical activity was unavoidable. We are well adapted to that, but it’s a daily challenge and inconvenience. So we devoted our large Homo sapien brains to the task of fixing it — and overshot, devising a modern world in which physical activity is scarce and and calories are plentiful. We devised world full of harmful chemical polutions, pesticides, hormones, antibiotics, stresess… and desperatelly look for antidotum in form of restricting what we eat… first fat, later salt, cholesterol, red meat, gluten, dairy, sugar and pretty soon we limit everything we happily consumed over many centuries….but restrictive diet is not good solution even if it give us quick result in a form of loosing weight. You can also loose weight by getting sick…

  11. Awesome!!! Great info!!!

    I was in Sweden and read through their PDR on Insulin. Insulin is what causes Atherosclerosis!
    I know that increased Carbs causes an increase in Insulin production, but it is the Insulin that causes the damage to our vessels. Our American PDR will not come out and place the blame on Insulin; it places the blame on increased blood sugar, and states the high glucose causes the Metabolic Syndrome. But basic physiology will show you that it is Insulin that is actually doing the damage.

    Also, eating cholesterol will not increase the LDH. Basic physiology shows that after eating cholesterol, say an egg yoke, our bodies stop producing the LDH, and start to produce the HDH. This HDH attaches itself to the cholesterol (from said egg yoke) and escorts it throughout our bodies to be deposited (into cell membranes etc…).

    Basis physiology says one thing, but the media says another. Thank God for people like you who will stick with physiology.

  12. What does someone do if they’re on a low residue diet, meaning they can’t eat complex carbohydrates, nuts, and high fiber food?

    • Why cant you eat a complex carb diet. Do you have an proven enzyme deficiency in one of the di-saccharide metabolic pathways?

  13. Possibly one of the dumbest things I have ever read.

    Sugar is broken down into the same basic form: glucose. Carbs are broken down into glucose.

    Sugar and carbs have the same immediate affect on the body.

    The point is: if you consume more energy than you burn, you’ll get fat. Regardless of what you eat. So, no, sugar isn’t relevant.

    • Before calling something “one of the dumbest things” you’ve ever read, it would help you know a thing or two about biochemistry. Sugar is actually broken down into fructose and glucose, not glucose alone. Big difference. Get it right and get in the arena.

    • Hi Brandon,

      “The point is: if you consume more energy than you burn, you’ll get fat. Regardless of what you eat.”

      Why would you consume more energy than burn? Or why would you burn less than consumed?

    • I love mean comments. On my blog, I check out their IP address and then just imagine how miserable their life is to take time out of their day to be an idiot.

      Dr. Attia, you are awesome and I appreciate the fact that you try to answer everyone… Even this guy.

      P.S. I learn so much from you just in reading what you respond to in comments. Appreciate you paying it forward with your knowledge and humility.

  14. Why is sugar worse than starch? Have you seen some of the new studies about people with low AMY1 (salivary amylase) whose blood sugar spikes higher from starch than sugar?

  15. I’m certainly not an expert when it comes to nutrition, but I do have an opinion when it comes to healthy diet. I think the main reason why people on a traditional Asian diet tend to be leaner is that the body relies on carbohydrates not just for vitamins and minerals, but primarily for energy. Glucose is the body’s energy source and the body cannot function effectively without it. Carbohydrates are converted very easily into glucose. When this happens the body becomes fueled with energy so that it can perform it’s daily functions at work, at home and in other situations as well.

    I say this because I actually tried the low carb diet back when it was starting to become popular in the mid 1990’s. What I discovered was that though I did lose weight initially, my energy level dropped significantly. I became tired and irritable and I wasn’t thinking very clearly. I couldn’t maintain any kind of aerobic activity. I would get worn out as soon as I started. Eventually I started gaining the weight back. See, I think what happens is that when we switch to a low carbohydrate diet our body simply cannot metabolize foods like fatty meats, dairy and eggs very efficiently and so our metabolism drops. Not only do we become sluggish, irritable and unhealthy but we actually end up gaining the weight back.

    This is why I think people on a high carb diet tend to be leaner. They just have more energy. I think it’s a much healthier diet in the long run.

    • “This is why I think people on a high carb diet tend to be leaner. They just have more energy. I think it’s a much healthier diet in the long run.”

      Your not considering the EFFECTS of the insulin required to convert those carbs into fuel. Rather than the ‘fuel’ that dictates individual activity levels… I would suggest genetics AND life circumstances influence activity levels primarily.

      CONSIDER.. the body appearance of carb eaters later in life… almost ALL have the spare tire, some degree of insulin resistance ABOVE the ideal range and the loss of lean tissue. Higher insulin levels simply advance body aging more rapidly than lower insulin levels.

      Thin active people are NOT immune to heart attacks… WHY? A combination of genetic factors… with high carb/insulin levels a main driver of these events.

      This quote above clearly illustrates the ‘human condition’…. ‘ I do not like the idea’…hence they find a reason to pan it… always in emotional ways… heck with the BRAIN.. the ability to THINK and ANALYZE…………….

  16. I’m thinking the more you work and burn it off, the better the chances of one staying thin. I may be of a small number but in my family, we eat heavy meals frequently and often. Those who knows this scoths at the fact we stay thin. I may eat five meals (being modest) and what leftovers are remaining, I eat those too. We have a hobby farm that’s probably helping on exercise and extremely competitive. It may all be in if its burned off.

  17. Not to over simplify, but you really over analyze. Those cultures stay lean because they are not as spoiled and not as lazy as Americans. Simple.
    You take away all the blue collar jobs in America, and send them overseas.
    You increase the white collar jobs in USA, and then increase porductivity by “metrics” to measure a workers perfomance, thereby chaining to a boring desk job and the only “break” is food. They are too burnt out to exercise after work.
    You increase the number of indoor activities( INTERNET is greatest offender). Give a person a laptop and a TV set to watch.
    You take away activities such a yard mowing and maintenance and pay someone to do it for you. ( You give them your health in the process)
    You take away washing your car as back in the 60s, act like it s odd if someone washes their own car! Heaven forbid!
    You air condition ALL houses with modern central air, hence, nobody goes outside to cool off and tlak to their neighbors.
    Any questions oh modern world thinkers?

    This world, this mess, must be re-activated. If all those things were taken away, then if people were naturally inclined to be heatlthy then we would all be like Arnold Schwarzenegger with ALL the FREE time we have and perfect climate workout areas!

    But, as the Bible says, the flesh seeks to please itself. Hence Ahh…comfort and another soda please! Done

  18. I’m in the process of changing my diet based on your book Grain Brain, but I have a problem. I’m already quite thin, and eating this way is making me lose weight I can’t afford to lose. What is the best way to NOT lose weight while getting the greatest benefit from this diet? (I did a search on this website for info about thin people and couldn’t find anything based on my search term “too thin.”)

    I’m 63, have a history of 4 heart events (SCAD), I exercise most days and lead a pretty healthy lifestyle.

  19. I eat over 600g of carbs a day, and 250g sugar, all from whole foods vegan diet, low/no oil. My total cholesterol has gone from 115 when I first started vegan diet to 99 last week when tested. Glucose is 86 mg/dL (literally unchanged from when I was eating high protein high fat omnivore diet). I’m 5’11” 180lbs. All my vitamins and minerals are nominal as well as I get about 200%-400% of all of them from eating nutrient dense plant foods…
    I think this issue is made more complicated then it needs to be. Fatty foods being more calorically dense are easier to get into caloric surplus. I don’t quite understand the low carb thing because the US has always been low carb and high fat.

    • Andrew,

      One of Peter’s main goals is to deconstruct the idea of “calories in, calories out.” Fat is more dense in calories than the other macronutrients, yes. That says absolutely nothing about the hormonal impact that any of the macronutrients have on metabolism.

      Most Americans are on a predominantly carbohydrate based diet. You couldn’t possibly get a quarter of the population with metabolic syndrome if “the US has always been low carb high fat.” Congratulations on having a diet base on whole foods. Your diet is almost assuredly better than the standard American diet. But I think you should take a look at the data on what the standard American diet looks like.

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