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.
- Lower consumption of sugar
- Lower absolute consumption of carbohydrates
- 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.”
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 diets. Virtually 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:
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:
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:
- Continues to raise insulin levels, which inhibits fat mobilization, and
- 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.]
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:
- 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.
- They consume less total glucose, AND the glucose they consume is accompanied by less sugar (and less omega-6 PUFA, if it matters).
- 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.