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How do some cultures stay lean while still

consuming high amounts of carbohydrates?

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.

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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

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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.”

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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:

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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:

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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

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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.

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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

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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.]

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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).

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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.

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About the Author:

Peter Attia, M.D., is the co-founder and President of the Nutrition Science Initiative (NuSI),

a non-profit based in San Diego, CA. He received his B.Sc. from Queen's University in

Canada and his M.D. from Stanford Medical School in California. After his surgical

residency in general surgery at Johns Hopkins he worked as a consultant at McKinsey &

Company. He founded NuSI with scientific journalist Gary Taubes in 2012.