The 2015 Dietary Advisory Committee Report: A Summary

Last week, the Dietary Guidelines Advisory Committee released the report containing its recommendations for the 2015 Dietary Guidelines for Americans.   The report is 572 pages long, more than 100 pages longer than the last report, released 5 years ago.  Longer than one of my blog posts, even. Despite its length, and the tortured governmentalese in which it is written, its message is pretty clear and simple. So for those of you who would like to know what the report says, but don’t want to read the whole damn thing, I present, below, its essence:

Dear America,

You are sick–and fat.  And it’s all your fault. 

Face it.  You screwed up.  Somewhere in the past few decades, you started eating too much food. Too much BAD food.  We don’t know why.  We think it is because you are stupid.

We don’t know why you are stupid.

You used to be smart–at least about food–but somewhere in the late 1970s or early 1980s, you got stupid. Before then, we didn’t have to tell you what to eat.  Somehow, you just knew. You ate food, and you didn’t get fat and sick.

But NOW, every five years we have to get together and rack our brains to try and figure out a way to tell you how to eat–AGAIN.  Because no matter what we tell you, it doesn’t work. 

The more we tell you how to eat, the worse your eating habits get. And the worse your eating habits get, the fatter and sicker you are.  And the fatter and sicker you are, the more we have to tell you how to eat. 

DGA - Length & Obesity 1980-2010

Look. You know we have no real way to measure your eating habits.  Mostly because fat people lie about what they eat and most of you are now, technically speaking, fat.  But we still know that your eating habits have gotten worse. How?  Because you’re fat.  And, y’know, sick.  And the only real reason people get fat and sick is because they have poor eating habits.  That much we do know for sure.

And because, for decades now,  we have been telling you exactly what to eat so you don’t get fat and sick, we also know the only real reason people have poor eating habits is because they are stupid.  So you must be stupid.

Let’s make this as clear as possible for you:

sick fat stupid people

And though it makes our hearts heavy to say this, unfortunately, and through no fault of their own, people who don’t have much money are particularly stupid.  We know this because they are sicker than people who have money.  Of course, money has nothing to do with whether or not you are sick.  It’s the food, stupid.

We’ll admit that some of the responsibility for this rests on our shoulders.  When we started out telling you how to eat, we didn’t realize how stupid you were.  That was our fault.

In 1977, a bunch of us got together to figure out how to make sure you would not get fat and sick.  You weren’t fat and sick at the time, so we knew you needed our help.

We told you to eat more carbohydrates–a.k.a., sugars and starches–and less sugar.  How simple is that?  But could you follow this advice?  Nooooooo.  You’re too stupid.

We told you to eat food with less fat. We meant for you to buy a copy of the Moosewood Cookbook and eat kale and lentils and quinoa.  But no, you were too stupid for that too.  Instead, you started eating PRODUCTS  that said “low-fat” and “fat-free.”  What were you thinking?

We told you to eat less animal fat. Obviously, we meant JUST DON’T EAT ANIMALS.  But you didn’t get it.  Instead, you quit eating cows and started eating chickens.  Hellooooo?  Chickens are ANIMALS.

After more than three decades of us telling you how to eat, it is obvious you are too stupid to figure out how to eat.  So we are here to make it perfectly clear, once and for all.

FIRST:  Don’t eat food with salt in it.

Even though food with salt in it doesn’t make you fat, it does raise your blood pressure.  Maybe.  Sometimes.  And, yes, we know that your blood pressure has been going down for a few decades now, but it isn’t because you are eating less salt, because you’re not.  And it’s true that we really have no idea whether or not reducing your intake of salt prevents disease. But all of that is beside the point.

Here’s the deal:  Salt makes food taste good.  And when food tastes good, you eat it.  We’re opposed to that.  But since you are too stupid to actually stop eating food, we are going to insist that food manufacturers stop putting salt in their products.  That way, their products will grow weird microorganisms and spoil rapidly–and will taste like poop.

This will force everyone to stop eating food products and get kale from the farmer’s market (NO SALT ADDED) and lentils and quinoa in bulk from the food co-op (NO SALT ADDED).  Got it?

Also, we are working on ways to make salt shakers illegal. 

Ban Salt Shakers

 

NEXT:  Don’t eat animals. At all.  EVER.

We told you not to eat animals because meat has lots of fat, and fat makes you fat.  Then you just started eating skinny animals. So we’re scrapping the whole fat thing.  Eat all the fat you want.  Just don’t eat fat from animals, because that is the same thing as eating animals, stupid.

We told you not to eat animals because meat has lots of cholesterol, and dietary cholesterol makes your blood cholesterol go up.  Now our cardiologist friends who work for pharmaceutical companies and our buds over at the American Heart Association have told us that avoiding dietary cholesterol won’t actually make your blood cholesterol go down.  They say:  If you want your blood cholesterol to go down, take a statin.  Statins, in case you are wondering, are not made from animals, so you can have all you want.  

Eggs? you ask.  We’ve ditched the cholesterol limits, so now you think you can eat eggs?  Helloooo?  Eggs are just baby chickens and baby chickens are animals and you are NOT ALLOWED TO EAT ANIMALS.  Geez.

Yes, we are still hanging onto that “don’t eat animals because of saturated fat” thing, but we know it can’t last forever since we can’t actually prove that saturated fat is the evil dietary villain we’ve been saying it is.  So …

Here’s the deal:  Eating animals doesn’t just kill animals.  It kills the planet.  If you keep killing animals and eating them WE ARE ALL GOING TO DIE.  And it’s going to be your fault, stupid.

And especially don’t eat red meat.  C’mon.  Do we have to spell this out for you?  RED meat? 

RED meat = COMMUNIST meat.  Does Vladimir Putin look like a vegan?  We thought not. 

 

 If you really must eat dead rotting flesh, we think it is okay to eat dead rotting fish flesh, as long as it is from salmon raised on ecologically sustainable fish farms by friendly people with college educations. 

FINALLY:  Stop eating–and drinking–sugar.

Okay, we know we told you to eat more carbohydrate food.  And, yes, we know sugar is a carbohydrate. But did you really think we were telling you to eat more sugar?  Look, if you must have sugar, eat some starchy grains and cereals. The only difference between sugar and starch is about 15 minutes in your digestive tract.  But …

Here’s the deal:  Sugar makes food taste good.  And when food tastes good, you eat it.  Like we said, we’re opposed to that.  But since you are too stupid to actually stop eating food, we are going to insist that food manufacturers stop putting sugar in their products.  That way, their products will grow weird microorganisms and spoil rapidly–and will taste like poop.

This will force everyone to stop eating food products and get kale from the farmer’s market (NO SUGAR ADDED) and lentils and quinoa in bulk from the food co-op (NO SUGAR ADDED).  Got it?

Ban cupcakes

 

Hey, we know what you’re thinking.  You’re thinking “Oh, I’ll just use artificial sweeteners instead of sugar.”  Oh NOOOO you don’t.  No sugar-filled soda.  No diet soda.  Water only. Capiche?

 So, to spell it all out for you once and for all:

DO NOT EAT food that has salt or sugar in it, i.e. food that tastes good.  Also don’t eat animals.

DO EAT kale from your local farmers’ market, lentils and quinoa from your local food co-op,  plus salmon. Drink water.  That’s it. 

And, since we graciously recognize the diversity of this great nation, we must remind you that you can adapt the above dietary pattern to meet the your own health needs, dietary preferences and cultural traditions. Just as long as you don’t add salt, sugar, or dead animals.

Because we have absolutely zero faith you are smart enough to follow even this simple advice, we are asking for additional research to be done on your child-raising habits (Do you let your children eat food that tastes good?  BAAAAD parent!) and your sleep habits (Do you dream about cheeseburgers?  We KNOW you do and that must stop!  No DEAD IMAGINARY ANIMALS!)

And–because we recognize your deeply ingrained stupidity when it come to all things food, and because we know that food is the only thing that really matters when it comes to health, we are proposing  America create a national “culture of health” where healthy lifestyles are easier to achieve and normative.

“Normative” is a big fancy word that means if you eat what we tell you to eat, you are a good person and if you eat food that tastes good, you are a bad person. We will know  you are bad person because you will be sick. Or fat. Because that’s what happens to bad people who eat bad food.

We will kick-off this “culture of health” by creating an Office of Dietary Wisdom that will make the healthy choice–kale, lentils, quinoa, salmon, and water–the easy choice for all you stupid Americans.  We will establish a Food Czar to run the Office of Dietary Wisdom, because nothing says “America, home of freedom and democracy” like the title of a 19th century Russian monarch.*

The primary goal of the “culture of health” will be to enforce your right to eat what we’ve determined is good for you. 

This approach will combine the draconian government overreach we all love with the lack of improvements we expect, resulting in a continued demand for our services as the only people smart enough to tell the stupid people how to eat.**

 Look.  We know we’ve been a little unclear in the past.  And we know we’ve reversed our position on a number of things. Hey, our bad.  And when, five years from now, you stupid Americans are as sick and fat as ever, we may have to change up our advice again based, y’know, on whatever evidence we can find that supports the conclusions we’ve already reached.

But rest assured, America.

No matter what the evidence says, we are never ever going to tell you it’s okay to eat salt, sugar, or animals.  And, no matter what the evidence says, we are never ever going to tell you that it’s not okay to eat grains, cereals, or vegetable oils.  And you can take that to the bank.  We did.

Love and kisses,

Committee for Government Approved Information on Nutrition (Code name: G.A.I.N.)

***********************************************************************************

*Thank you, Steve Wiley.

**Thank you, Jon Stewart, for at least part of this line.

 

TMAO? LMAO.

Move over saturated fat and cholesterol. There’s a new kid on the heart disease block: TMAO.

TMAO is not, as I first suspected, a new internet acronym that I was going to have to get my kids to decipher for me, while they snickered under their collective breaths. Rather, TMAO stands for Trimethylamine N-oxide, and it is set to become the reigning king of the “why meat is bad for you” argument. Former contenders, cholesterol and saturated fat, have apparently lost their mojo. After years of dominating the heart disease-diet debate, it turns out they were mere poseurs, only pretending to cause heart disease, the whole time distracting us from the true evils of TMAO.

The news is, the cholesterol and saturated fat in red meat can no longer be held responsible for clogging up your arteries. TMAO, which is produced by gut bacteria that digest the carnitine found in meat, is going to gum them up instead. This may be difficult to believe, especially in light of the fact that, while red meat intake has declined precipitously in the past 40 years, prevalence of heart disease has continued to climb. However, this is easily accounted for by the increase in consumption of Red Bull—which also contains carnitine—even though it is not, as some may suspect, made from real bulls (thank you, BW).

Here to explain once again why we should all be afraid of eating a food our ancestors ignorantly consumed in scandalous quantities (see what happened to them?  they are mostly dead!) is the Medical Media Circus! Ringleader for today is the New York Times’ Gina Kolata, who never met a half-baked nutrition theory she didn’t like (apparently Gary Taubes’ theory regarding carbohydrates was not half-baked enough for her).

Step right up folks and meet TMAO, the star of “a surprising new explanation of why red meat may contribute to heart disease” (because, frankly, the old explanations aren’t looking too good these days).

We know that red meat maybe almost probably for sure contributes to heart disease, because that wild bunch at Harvard just keeps cranking out studies like this one, Eat Red Meat and You Will Die Soon.

This study and others just like it definitely prove that if you are a white, well-educated, middle/upper-middle class health professional born between 1920 and 1946 and you smoke and drink, but you don’t exercise, watch your weight, or take a multivitamin, then eating red meat will maybe almost probably for sure increase your risk of heart disease. With evidence like that, who needs evidence?

Flying like the Wallenda family in the face of decades of concrete and well-proven assumptions that the reason we should avoid red meat is because of its saturated fat and cholesterol content, the daring young scientists who discovered the relationship between TMAO and heart disease “suspected that saturated fat and cholesterol made only a minor contribution to the increased amount of heart disease seen in red-meat eaters” [meaning that is, the red-meat eaters that are white, well-educated, middle/upper-middle class health professionals, who smoke and drink and don’t exercise, watch their weight, or take a multivitamin; emphasis mine].

Perhaps their suspicions were alerted by studies such as this one, that found that, in randomized, controlled trials, with over 65 thousand participants, people who reduced or changed their dietary fat intake didn’t actually live any longer than the people who just kept eating and enjoying the same artery-clogging, saturated fat- and cholesterol-laden foods that they always had. (However, this research was able to determine that a steady diet of broiled chicken breasts does in fact make the years crawl by more slowly.)

You can almost ALWAYS catch something on a fishing expedition.

Our brave scientists knew they couldn’t just throw up their hands and say “Let them eat meat!” That would undermine decades of consistent public health nutrition messaging and those poor stupid Americans might get CONFUSED—and we wouldn’t want that! So, instead the scientists went on a “scientific fishing expedition” (Ms. Kolata’s words, not mine) and hauled in a “little-studied chemical called TMAO that gets into the blood and increases the risk of heart disease.” Luckily, TMAO has something to do with meat. [As Chris Masterjohn points out, it also has something to do with fish, peas, and cauliflower, but–as I’m sure these scientists noticed immediately–those things do not contain meat.] Ta-da! Problemo solved.

Exactly how TMAO increases the risk of heart disease, nobody knows. But, good scientists that they are, the scientists have a theory. (Just to clarify, in some situations the word theory means: a coherent group of tested general propositions, commonly regarded as correct. This is not one of those situations.) The researcher’s think that TMAO enables cholesterol to “get into” artery walls and prevents the body from excreting “excess” cholesterol. At least that’s how it works in mice. Although mice don’t normally eat red meat, it should be noted that mice are exactly like people except they don’t have Twitter accounts. We know this because earlier mouse studies allowed scientists to prove beyond the shadow of a doubt that dietary cholesterol and saturated fat cause heart disease mice definitely do not have Twitter accounts.

Look, just because the scientists can’t explain how TMAO does all the bad stuff it does, doesn’t mean it’s not in there doing, you know, bad stuff. Remember, we are talking about molecules that are VERY VERY small and really small things can be hard to find–unless of course you are on a scientific fishing expedition.

What will happen to the American Heart Association’s seal of approval now that saturated fat and cholesterol are no longer to be feared?

Frankly, I’m relieved that we FINALLY know exactly what has been causing all this heart disease. Okay, so it’s not the saturated fat and cholesterol that we’ve been avoiding for 35 years. Heck, everybody makes mistakes. Even though Frank Sacks and Robert Eckel, two scientists from the American Heart Association, told us for decades that eating saturated fat and cholesterol was just greasing the rails on the fast track to death-by-clogged-arteries, they have no reason to doubt this new theory. And even though they apparently had no reason to doubt the now-doubtful old theory, at least not until just now—as a nation, we can rest assured that THIS time, they got it right.

Now that saturated fat and cholesterol are no longer Public Enemies Number One and Two, whole milk, cheese, eggs, and butter—which do not contain red meat—MUST BE OKAY! I guess there’s no more need for the AHA’s dietary limits on saturated fat, or for the USDA Guidelines restrictions on cholesterol intake, or for those new Front of Package labels identifying foods with too much saturated fat. Schools can start serving whole milk again, butter will once again be legal in California, and fat-free cheese can go back to being the substance that mouse pads are made out of. Halla-freaking- looyah! A new day has dawned.

But—amidst the rejoicing–don’t forget: Whether we blame saturated fat or cholesterol or TMAO, meat is exactly as bad for you now as it was 50 years ago.

N of 1 Nutrition Part 2: Biochemistry and Nutrition Policy – The Great Divorce

Full disclosure: I happen to love biochemistry. I have a favorite transcription factor (ChREBP) and a favorite neurotrophic factor (BDNF). I think proteins are beautiful. If I were a biochemist who had discovered a novel protein, I would carry a picture of it around with me in my wallet.

An absolutely fabulous (looking) protein.

The animal and cells models used in biochemistry are great for looking at genetics, epigenetics, at biological mechanisms, and how these things interact. We can manipulate these models in ways that we can’t with humans, and this has given us some crucial insights into mechanisms, especially neural and epigenetic ones—critical to understanding the effects of nutrition—that would be virtually impossible to study in humans.

Nutritional biochemistry can also wear the mantle of “objective-er than thou” when it comes to science. As one of the biochem profs at UNC noted: If you have to use statistics to discuss the results of your experiment, you need to redesign your experiment. Sure, the questions asked, the interpretation of results, and what gets published in biochem are influenced by funding sources, social/scientific contexts and dominant paradigms. But unless you are a truly bad scientist, you can’t make the experimental results come out in a way that supports your hypothesis.

(This is in marked contrast to observational studies in nutrition epidemiology where the whole point of the data analysis “experiment” is to find results that support your hypothesis. Sometimes you don’t find them, and those findings should be reported, although they may not be because who’s to know?  Just you and your SAS files. My point is that you are actively seeking results that confirm a particular idea, and this just might influence what “results” are found. More on this in another post.)

But beyond the utility and elegance of nutritional biochemistry, the problems with regard to health policy are two-fold.

The first problem: In many ways, nutrition policy has become almost completely divorced from the basic science investigations done in biochemistry. The Dietary Guidelines Advisory Committee (DGAC)—the committee of scientists that, at least theoretically, reviews the science upon which the US Dietary Guidelines are based—started in 1985 as mostly MDs and biochemistry professors. As time went on, the DGAC became more heavily populated with epidemiologists. This would be fine if epidemiology was meant to generate conclusive (or even semi-conclusive) results. It isn’t. Epidemiology gives us associations and relationships that are meant to be understood through a reasonably plausible, preferably known, biological mechanism. Note these interesting conclusions from the 2010 DGAC Report and the 2010 Dietary Guidelines policy document with regard to dietary cholesterol:

Here’s our mechanism: Exogenous, or dietary, cholesterol down-regulates cholesterol synthesis in the liver to maintain cholesterol balance.”
[D3-1, Reference 1, emphasis mine]

Here’s our epidemiology: Traditionally, because dietary cholesterol has been shown to raise LDL cholesterol and high intakes induce atherosclerosis in observational studies, the prevailing recommendation has been to restrict dietary cholesterol intake, including otherwise healthy foods such as eggs.”
[D3-2, Reference 1, emphasis mine, “induce”? really? how does one “observe” that cholesterol “induces” atherosclerosis? I’m assuming committee fatigue had set in at this point because that word should have been “are associated with”]

Here’s our policy recommendation: Consume less than 300 mg per day of dietary cholesterol.”
[Ch. 3, p. 21, Reference 2]

See, wasn’t that easy?

This brings me to the second problem, which is sort of the flip-side of the first: Biochemical processes that are understood primarily through mouse or cell models only work as the basis for dietary recommendations for chronic disease if you’re making them for cells or mice.

As one of my favorite professors in the Nutrition department likes to quip, “We know how to cure obesity—in mice. We know how to cure diabetes—in mice. We have all the knowledge we need to keep our rodent population quite healthy.” Obviously this knowledge has not been translatable to humans. In some ways, basic nutrition biochemistry should be divorced from public health policy.

The reason for this is that the equivalency of animal models to humans is limited in ways that go beyond simple biological comparisons—although the biological differences are significant.

Mouse large intestinal tract, courtesy of Comparative Anatomy and Histology: A Mouse and Human Atlas, edited by Piper M. Treuting, Suzanne M. Dintzis

My knowledge of comparative physiology is limited at best, but my understanding is that most rodents used in nutrition biochemistry work (rats included) have a cecum (an intestinal pouch that facilitates the breakdown of cellulose), an adaptation that would be necessary in a diet composed of hard-to-digest plant material such as seeds and grains. Because this process is not terribly efficient, many rodents also recycle nutrients by eating their feces. Humans don’t have a functional cecum for fermentation; we don’t tend to reingest our own poops (or anyone else’s poop, unless you’re starring in a John Waters film) in order to extract further nutrition from them as our bodies are already very efficient at this during the first go-round.

Furthermore, due to inherent difference in physiology, animals may not accurately model the physiological conditions that produce disease in humans. For example, in some species of rodents, a high fat diet will induce insulin resistance, but there is no definitive evidence that higher fat intake per se impairs insulin sensitivity in humans [3]. Why this is so is not entirely clear, but likely has something to do with the diet each species has consumed throughout its evolution. In a natural setting, rodents may do well on a diet of mostly grains. On the other hand, humans in a natural setting would do okay on a diet of mostly rodents.

What is more critical is that animal and cell life can’t imitate the complex environmental inputs that humans encounter throughout their lives and during each day. Animals and cells only get to consume what they are given. If you’ve ever been at a conference where the breakfast is low-fat muffins, whole grain bagels, fat-free yogurt, orange juice, and fruit, you know what that feels like. But typically our food choices are influenced by a multitude of factors. Mice, unlike humans, cannot be adversely affected by labeling information on a box of Lucky Charms.

Mice don’t know that whole grains are supposed to be good for you.
Bad on them.

Does that matter? You bet it does.

Where do most Americans get their nutrition information these days? From media sources including the internet, from their grocery stores, from the packages holding the food they buy. People who have never read a nutrition book, much less the actual Dietary Guidelines, still “know” fat is bad and whole grain is good [4, 5]. These environmental exposures affect food choices. Whether or not the person still decides to consume food with a high fat content depends on another set of cultural factors that might include socioeconomic status, education, race or ethnicity, age, gender—in other words, things we can’t even begin to replicate in animal or cell models.

Human biochemistry is unique and complex, as are our social and cultural conditions, making it very difficult to study how these primary contributors to health and food choices are related to each other.

Can we do a better job with nutritional epidemiology? I know you’re on the edge of your seat waiting for the next episode in the unfolding drama, N of 1 Nutrition, when we get to hear Walter Willett say:

“I never met a statistical man I didn’t like.”

Stay tuned.

References:

1. U.S. Department of Agriculture. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans 2010. Accessed July 15, 2010. http://www.cnpp.usda.gov/DGAs2010-DGACReport.htm

2. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2010. http://www.cnpp.usda.gov/DGAs2010-PolicyDocument.htm Accessed January 31, 2010

3. Report of the Panel on Macronutrients, Subcommittees on Upper Reference Levels of Nutrients and Interpretation and Uses of Dietary Reference Intakes, and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary Reference 4. Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). Washington, DC: The National Academies Press; 2005.

4. Eckel RH, Kris-Etherton P, Lichtenstein AH, Wylie-Rosett J, Groom A, Stitzel KF, Yin-Piazza S. Americans’ awareness, knowledge, and behaviors regarding fats: 2006-2007. J Am Diet Assoc. 2009 Feb;109(2):288-96.

5. Marquart L, Pham AT, Lautenschlager L, Croy M, Sobal J. Beliefs about whole-grain foods by food and nutrition professionals, health club members, and special supplemental nutrition program for women, infants, and children participants/State fair attendees. J Am Diet Assoc. 2006 Nov;106(11):1856-60.

N of 1 Nutrition Part 1: Same Old Tools

I’ve been thinking a lot about tools lately.  This actually has nothing to with the ongoing fascinating-in-a-train-wreck-sort-of-way paleo soap opera, although I have been reading Audre Lorde’s essay “The Master’s Tools will Never Dismantle the Master’s House” and loving it.  I have all kinds of things to say about feminism and nutrition (yeah, I’m going to go there), but there are all kinds of tools and we’re going to have to talk about all of them eventually.  Today, I’ll start with the scientific kind.  

At Ancestral Health Symposium 2012 there was, among other things, a great deal of discussion about what diet works “best:” primal, paleo, neopaleo (my friend Andrea invented that one), safe starch, low-carb, no-carb, etc. The reality is that, in terms of being able to make sweeping generalizations about which dietary pattern will work best for everyone, we as nutrition scientists and clinicians actually sorta suck. Other than describing very general recommendations for essential nutrition—amino acids, fatty acids, vitamins and minerals, and even these have a wide variability in individual requirements—we simply do not have the skills, the tools, or the knowledge to make sweeping dietary recommendations that do not come with the very real possibility of unintended negative consequences for an individual who might follow them.

Choline is a great example of what happens when you mix individual variation with universal recommendations:

Although our body makes some choline, we still require a dietary supply of this important nutrient.* Eggs are a primary source of dietary choline. The past 30 years of Dietary Guidelines have frightened us into reducing egg consumption and/or using egg substitutes that replace the yolk (where the choline is) with soybean oil in order to prevent heart disease, even though dietary cholesterol has little effect on serum cholesterol [1] and our average cholesterol intake is below recommended levels and has been for 40 years [2]. Nevertheless, egg yolks, a recent headline screamed, are as bad for you as cigarettes.

In response to these scare tactics, Americans have dramatically reduced their egg consumption [3]. As a result, average choline consumption does not meet current recommended standards; less than 4% of women even reach adequate intake levels [4, 5].

This is bad enough, but these adequate intake levels were based on a small study done on adult white males; standards for everyone else, including children, were extrapolated from those results [6]. Post-menopausal females, pregnant women, children, and people with certain genetic polymorphisms (which may exist in more than 50% of the population) may actually have increased needs for choline above and beyond the adequate intake level [7].

It’s hard to say exactly how large the gap between intake and actual needs are for these subpopulations, but I can hazard a guess that as long as whole eggs are discouraged as part of our diets, it will only continue to widen. The fact that dietary choline is needed for the development of  brain cells seems rather ironic in the face of such goofiness.

Brain food? Or death by cholesterol?

When dietary guidance shifted from being about provision of basic nutrition to prevention of chronic disease, we found ourselves using tools that were designed to examine diseases of nutrition deficiency (i.e. diseases with one fairly straightforward cause), to now make recommendations about chronic diseases with long, complex, multi-factorial origins [8]. Everyone deprived of Vitamin C will eventually develop scurvy, but not everyone who avoids cholesterol will also avoid heart disease.  Chronic diseases that result from a complex interplay between the individual and environment are difficult—if not impossible—to examine using our current tools and methods, and assessing an individual’s risk of heart disease and tailoring dietary guidance accordingly is much different from making population-wide recommendations to avoid a food–in this case, eggs–that is a primary source of an essential nutrient.

Our current approach takes the complex reality that is one individual human living his/her life and

  • dials into a discrete mechanism within this complex unit using cell cultures and animal models that can’t even begin to describe the physiological, psychological, and cultural context of a whole complicated individual (nutritional biochemistry), or
  • lumps a complicated individual into a pile with a lot of other complicated individuals and uses a fancy schmantzy computer program or a highly-controlled artificial experimental protocol to paint an simplified, homogenized broad brush stroke of a picture that bears little resemblance to the reality of any of the specific individuals it is supposed to describe (nutrition epidemiology), and then
  • turns these overly-simplified, homogenized descriptions into one-size-fits-all nutrition policy that has never actually been shown to work.

From reality to policy: Four perspectives on nutrition

Everyone is subject to the same biochemical rules—and it’s great to learn more about how these rules work on a mechanistic level—but how those rules play out in any given individual is difficult to predict. Is there a way to use the focus of an experimental intervention without losing the environmental influences present in observational studies, and still create something that will eventually translate into meaningful policy?

Maybe. In next few posts, I take on some of the shortcomings in our current methodology and explore an approach that may help move nutrition science, and thus nutrition policy, into the 21st century.

*Choline acts as a methyl donor in pathways involving gene expression and other metabolic functions; as an important contributor to structural integrity and signaling function in cell membranes, especially those involved in nervous tissue and brain development; as a necessary constituent of lipid metabolism and transport, including VLDL required for the export of fat from the liver; and as the precursor to the neurotransmitter, acetylcholine.

References:

1. Willett, Walter. Nutrition Epidemiology, 2nd edition. 1988.

2. U.S. Department of Agriculture. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans 2010. Accessed July 15, 2010. http://www.cnpp.usda.gov/DGAs2010-DGACReport.htm

3. U.S. Dept. of Agriculture, Office of Communications. 2001-2002 Agriculture Fact Book. Washington, DC:2003.

4. Jensen H. Choline in the diets of the US population: NHANES, 2003-2004. The FASEB journal: official publication of the Federation of American Societies for Experimental Biology. 2007;21(Meeting Abstract Supplement):lb219.

5. Moshfegh A. Usual Nutrient Intakes of Americans. USDA Whitten Building; 2009.

6. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline [Internet]. [cited 2012 May 21]. Available from: http://books.nap.edu/openbook.php?record_id=6015

7. Zeisel SH, da Costa K-A. Choline: An Essential Nutrient for Public Health. Nutr Rev. 2009 Nov;67(11):615–23.

8. Harper AE. Killer French Fries. Sciences 1988, 28 (Jan/Feb): 21-27.