N of 1 Nutrition Part 3: The Love Song of Walter C. Willett

I didn’t want you all to have to wait all weekend for the truth:  Walter Willet didn’t really say, “I’ve never met a statistical person I didn’t like,” but he is sort of the Will Rogers of nutrition.

The Will Rogers of nutrition?

Everybody likes him, me included. Like Will Rogers was about politics, Willett is a staunch nutrition middle-of-the-roader who thinks fat it not so bad after all, but hey now, let’s not go any kind of crazy here, because saturated fat will still kill you in a New York minute probably maybe. 

I spent a lot of time with him earlier this year—okay, really just his book, but his book is so sweet and personal that I felt just like I was sitting at the master’s feet—which were clad in my imagination in the most sensible of shoes—as he unfolded for me the saga of nutritional epidemiology.

What I’m about to say is said with all due respect to the man himself (he’s basically created a whole freekin’ discipline for goodness sake). This is simply my reading of a particular text located within a particular context, i.e. this is what happens when they let English majors into science programs.

There are many reasons why nutritional epidemiology may not be up to the task of giving us a sound basis for nutrition policy. But why take my word for it? If you want to understand the heart of nutritional epidemiology—the driving force behind our bold 40-year march in the misguided direction of one-size-fits-all dietary recommendations—you must read Walter Willett’s Nutritional Epidemiology. It is a book I love more every time I read it, and I say this in all sincerity.

The exciting cover graphics merely hint at the fabulousness that awaits inside!

While I suppose it was written as a sort of textbook, and it is certainly used as one, it doesn’t really read like a textbook. It is part apology and part defense, and is much more about “why” than “how.” And the “why?” that it tries to answer to is “Why apply the techniques of epidemiology to nutrition and chronic disease?”

In this regard, it is a touching masterpiece. Walter Willett, MD, DrPH is a professor at the Harvard School of Public Health and at Harvard Medical School. He is considered by many to be the father of nutritional epidemiology. To stretch the analogy, you can think of nutritional epidemiology as his child. Reading the book this way, it almost moves me to tears (again, not joking*), for I find this book to be a father’s sweet and sad paean to a beautiful prince full of promise, who has grown into a spoiled, churlish, and lazy adult, unfit to rule the kingdom, but with too much of the dreams of many poured into him to banish altogether. And the dreams of the father are the most poignant of all.

Apparently, to Willett’s eternal dismay, the whole field got started off on the wrong foot by focusing on dietary cholesterol (as a cause) and serum cholesterol (as an outcome), associations—as we now know—that turned out to be weak, inconsistent, nonexistent, or even the inverse of what was expected (pp. 5-6, 417-418) . We now know that sub-fractions of serum cholesterol affect heart disease risk differently (LDL-C vs HDL-C, for instance) and that different foods affect different aspects of serum cholesterol differently, making the relationship to overall heart disease risk even more obscure, which seems to be par for the course in this field, as Willett readily admits.

Here, according to Willett, is what we don’t know and can’t do in nutritional epidemiology:

  • We don’t know any given individual’s true intake. It can only be estimated with greater or lesser degrees of error. (p. 65)
  • We don’t know any given individual’s true status for a nutrient. Ditto above. (p. 174)
  • We don’t know the true nutrient content of any given food that a person might eat. Double ditto. (pp. 23-24)
  • We don’t know what factors/nutrients in a food may operate together to prevent/cause disease. Similarly, we don’t how foods commonly found together in dietary patterns may operate together to prevent/cause disease. (pp. 15, 21-22, 327-328)
  • We have a really hard time separating calorie intake from nutrient intake (Ch. 11). Ditto nutrients and food patterns, food patterns and lifestyle patterns, etc. (pp. 10, 15, 22)
  • We can’t separate metabolic consequences of food intake patterns from the food itself, i.e. what we are looking at in any given data set is really metabolism of food, not food. (p. 15)
  • We don’t know what really causes the chronic diseases we study in nutrition epidemiology (p. 12); age, genetics, education, income, and lifestyle factors may influence, modify, or be more important than any dietary factor in the origins of these diseases (pp. 10, 15).
  • We can’t distinguish between causal and coincidental associations. Furthermore, weak associations could be causal; strong associations can be coincidental (p. 12).
  • Associations we do find are likely to be weak; we will often find no associations at all. Even if we do find statistically significant associations between nutrients and disease, they may be clinically or practically irrelevant and should not necessarily be used to make public health recommendations. (pp. 12-14, 21).

But wait! Willett cries. Don’t give up! This book is also a defense of those shortcomings—although one blinkered by what I must assume is Willett’s love for the field. I am always a little touched and frustrated by the section on why we find so many instances of lack of association between an ostensible nutritional cause and a disease outcome in nutrition epidemiology. Willett meticulously lists the possible reasons one by one as to why we may not be able to “observe a statistically significant association when such an association truly exists” (pp. 12-14). At no time does he venture to offer up the possibility that perhaps—and how would we know one way or the other?—no such association does truly exist.

A new edition of the book is coming out; this should make the old edition cheap in comparison. I won’t read the new edition because I’m afraid it would ruin my romance with the old edition, which is the one I recommend to you.

If you think Gary Taubes is “a poisonous pea in an ideological pod” (as I’ve heard him called), read this book (especially Ch 17 on “Diet and Coronary Heart Disease”). On the other hand, if you think population studies investigating nutrition and chronic disease are basically a gigantic undifferentiated crock of malarkey, read this book. Why? Because there are no clear answers and no real heroes. If you want to know the strengths and weakness of nutritional epidemiology, best to hear them outlined in excruciating and loving detail by Willett himself.

You don’t have to read it cover to cover. Skip around. You’ll learn in passing some methodology behind the folly of trying to forge links between specific nutrients in food to long-term chronic diseases that have multiple and complex origins (just the sections on how we collect information about what we think people are eating are eye-opening in that regard—Ch. 4-8). But I think (I hope) you’ll also hear the voice of a father wise enough to know that children are—must be—brought into this world on grand faith, one that hopes that they will make the world a better place than before, and that his child—nutritional epidemiology—is no different. Willett believes in this child and the book is a statement of that faith.

Please draw your own conclusions, here’s mine: Faith is not science.

Any parent out there knows this: you seem at first to have a child of your own, but you end up sending an adult out into the world who is no longer yours and never really was. The mistakes, limitations, failures, shortcomings belong only to that grown child, not to the parent. But still. It may be hard to acknowledge the fact that your precious one is no better than the other kids and probably won’t save the world. Sometimes, when I’m reading this book—when I’m supposedly studying for an exam—I am caught unawares by the sighs of disappointment, the rally of excuses, and finally the prickly justifications: The prince must be allowed to rule; the king knows he’s a weak little louse, but he’s all we’ve got.

I know—and any of us who are students of literature know—that this is the king’s tragic flaw. The prince can’t save the kingdom; the empire must crumble. But here is the king, holding brick and mortar together through sheer force of will, somehow acknowledging and somehow—at the same time—unaware, that this particular castle was built on sand in the first place. In this book, I hear Willett’s love for a hopelessly flawed field, a touching declaration of blind optimism, and I love this book, and I deeply respect the man himself, for showing that to me.

Note: I don’t expect anybody but dweeby English majors to get the title of this post, but for dweeby wanna-bees, see T. S. Eliot’s “The Love Song of J. Alfred Prufrock.”   It just makes my heart sing with joy that Willett refers to his diet of preference as the “prudent” diet.

Stay tuned for N of 1 Nutrition: Part 4, when you’ll hear Dr. Roger J. Williams say:

“Nutrition is for real people. Statistical humans are of little interest.”

*Admittedly, it could be eye strain.  I am OLD.

References:

Page numbers and chapters refer to the following edition:

Willett, W. Nutrition Epidemiology, 2nd ed. New York: Oxford University Press, 1998.

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.


The REAL Paleo Challenge: How NOT to be Just Another Elitist Fad for Skinny White People Wearing Goofy Shoes

The blogsphere is beginning to rattle with commentary on the recent Ancestral Health Symposium 2012 events. Some folks who don’t necessarily “look the paleo part” have voiced concern about feeling excluded or marginalized as the conversation/social activities/celebrity parade seemed dominated by:

  • white people
  • young people
  • thin/athletic/fit people
  • men
  • well-educated, upper-middle class socioeconomic status people
  • people wearing goofy-looking shoes

You can read my take on why that might be the case here: AHS 2012 and the BIG BUTT: Lessons in Nutritional Literacy.

I understand that an NPR reporter was at the event, interviewing some of the movers and shakers. There was some concern that the reporter seemed to think that the paleo movement is a bit of an elitist fad. I understand this perspective, and on many levels, I agree.

As a “fad,” the paleo movement is a bunch of highly enthusiastic people with a lot of disposable income and time who are deeply committed to a particular way of being fit and healthy. It has its leaders, it controversies, its “passwords” (can you say “coconut oil” or “adrenal burnout”?), and its stereotypical paleo dude or dudette. As a fad, it would be destined to go the way of all of other diet and health fads—including Ornish and Atkins, Pritikin and Scarsdale, extending all the way back to the “Physical Culture” movement of the earlier part of this century (Hamilton Stapell spoke about this at AHS2012).

The original paleo chick – no high heels on this lady

Is it elitist? Well, there are some ways that it is possible that the paleo movement may marginalize the very folks who might benefit most from its efforts. Maybe an African-American guy still sensitive to the fact that his grandfather was consider “primitive” might not want to get his full cavemen on. Maybe a Mexican-American woman who remembers her abuela telling her stories about being too poor to have shoes doesn’t really want to go back to being barefoot just yet. Maybe an older, heavier person simply feels intimidated by all the young healthy fit people swarming to the front of the food line.

But the paleo movement does not have to be an elitist fad unless insists on limiting itself to its current form, and I believe the people at the Ancestral Health Society  are working hard to make sure that doesn’t happen. This is why I really love these folks. I don’t mean the paleo leaders like Mark Sisson or Robb Wolf, although I’m sure they’re good people; I’ve just only met them briefly. I mean those somewhat geeky-looking-in-an-adorable-sort-of-way folks in the brown T-shirts who hung in the background and made it all happen for us last week. Notice that they don’t call themselves the Paleo Health Society, right? I love them because they ask good questions, they question themselves, they think long-term, and they’ve created a community that allows these conversations to take place.

So, what do we do to transform this paleo-led, AHS-supported community into the public health, human rights revolution it could be?

According to Doug Imig at the University of Memphis, a protest becomes a movement when:

1) It defines and proclaims widely shared cultural norms.

2) It creates dense social networks.

3) It gives everybody something to do.

Each of these deserves its own blog post, so let’s look at the first—and most important—item: widely shared cultural norms. This is where the “elitist fad” part of paleo falls short, but not really. Because in all my encounters with paleo folks and people from AHS, I find norms and values that the culture as a whole can embrace. Here’s the weird thing, I’ve spend the past couple of years also talking to mainstream scientists, from one end of the diet spectrum to another, including Joanne Slavin, a down-to-earth, warm, wonderful lady who was on the most recent Dietary Guidelines Advisory Committee and Henry Blackburn, who is a delightful gentleman and a protégé of Ancel Keys. Guess what? We all have some values in common.

Here are some concepts that I think may unite us all, from vegan to primal, from slow food to open government, from “mainstream” scientist to “fringe scientists” like Gary Taubes (yes, one of my UNC instructors referred to GT as a “fringe scientist,” although another found his views “very convincing”—go figure):

We must create an open, transparent, and sustainable food-health system.

The RD that inspired me to take an internship at the American Dietetic Association for a semester, Mary Pat Raimondi, said: “We need a food system to match our health system.” And whatever shape either of those systems may take, she is absolutely right. Conversations about food must encompass health; conversations about health must encompass food.

Right now our food-health system is closed. Directives come from the top down, public participation is limited to commentary. The people who are most affected by our nutrition policies are the farthest removed from their creation. We need to change that.

Right now our food-health system lacks transparency. USDA and HHS create nutrition policy behind doors that only seem to be transparent. Healthy Nation Coalition spent a year filing Freedom of Information Acts in order to get the USDA to reveal the name of a previously-anonymous “Independent Scientific Panel” whose task, at least as it was recognized in the Acknowledgments of the Dietary Guidelines, was to peer-review “the recommendations of the document to ensure they were based on a preponderance of scientific evidence.” You can read more about this here, but the reality is that this panel appears to not be a number of the things it is said to be. This is not their fault (i.e. the members of the panel), but an artifact of a system that has no checks and balances, no system of evaluation, and answers to no outside standards of process or product. This must change.

Our food-health system must be sustainable. And Pete Ballerstedt would say, yes, Adele, but what do you mean by “sustainable”? And to that I say—I mean it all:

Environmental sustainability – Nobody wants dead zones in the Gulf or hog lagoons poisoning the air. But environmental sustainability can’t be approached from the perspective of just one nutritional paradigm, because a food-health system must also have:

Cultural sustainability – We are not all going to become vegans or paleo eaters. Our food-health system must support a diversity of dietary approaches in ways that meet other criteria of sustainability.

Economic sustainability – Our food-health system must recognize the realities of both producers and consumers and address the economic engines that make our food-health system go around.

Political and scientific sustainability – Our food-health system must become a policy dialogue and a scientific dialogue. Think of how civil rights evolved: an equal rights law was passed, then overturned, a Jim Crow law was passed, then overturned, an equal right law was passed, then upheld, etc. etc. This dialogue reflected changing social norms and resistance to those changes. But we have no way to have a similar sort dialogue in our food-health system.

What would the world look like if, in 1980, an imaginary Department of Technology was given oversight of the development of all knowledge and production associated with technology? Production of food and knowledge about food (i.e. nutrition) became centralized within the USDA/HHS in 1977-1980 and there have been no policy levers built into the system to continue the conversation, as it were, since then. The Dietary Guidelines have remained virtually unchanged since 1977; our underlying assumptions about nutrition science have remained virtually unchanged since 1977. That’s like being stuck in the age of microwaves the size of Volkswagens, mainframe computers with punchcards, and “Pong.” We need a way for our food-health system to reflect changing social and scientific norms.

One of the primary shifts in understanding that has taken hold since 1977 is that:

There is no one-size-fits-all diet that works for everyone.

In 1979, Dr. William Weil Jr at the Department of Human Development at Michigan State University, voiced concern about “the frequent use of cross-national and cross-ethnic inferences” [Weil WB Jr. National dietary goals. Are they justified at this time? Am J Dis Child. 1979 Apr;133(4):368-70.]  He went on to day that we cannot assume that “because ‘a’ and ‘b’ are correlated in one population group that they will also be correlated in another group” yet our one-size-fits-all dietary recommendations make just that assumption.

There were more scientific articles generated from the Nurses’ Health Study–composed of 97% white women–in 2009 alone, than in the entire 10+ year history of the Black Women’s Health Study. Those large epidemiological studies done with a mostly white dataset are what drive our policy making, even though evidence also points to fact that we should not be making the assumptions to which Dr. Weil referred. A landmark study published in 2010 shows that African-Americans who consumed a “healthier” diet according to Dietary Guidelines standards actually gained more weight over time than African-Americans who ate a “less healthy” diet [Zamora D, Gordon-Larsen P, Jacobs DR Jr, Popkin BM. Diet quality and weight gain among black and white young adults: the Coronary Artery Risk Development in Young Adults (CARDIA) Study (1985-2005). American Journal of Clinical Nutrition. 2010 Oct;92(4):784-93].

.

DQI stands for Diet Quality Index. Blacks with a higher DQI had more weight gain over time than blacks with a lower DQI. From Zamora et al.

Even with a more homogenous population, this issue applies. Remember all those discussions about “safe starches” you heard at AHS2012?

This concept also captures the emerging knowledge of how genetic variability affects nutrition needs and health, i.e. individualized nutrition, a very useful buzzword. I have lots to say about n of 1 nutrition coming up soon. But, most of all, not trying to cram everyone into the same nutritional paradigm captures reality of our own lives and choices about food. Which brings me to:

Food is not just about nutrition, and nutrition is not just about science.*

When we all begin to question our own assumptions about food and nutrition, we will be better able to reach across communities, create common ground, and be humble about our way forward.

We need to understand and help others understand that all nutrition messages are constructed and contain embedded values and points of view.

We need to learn to ask and teach others to ask: Who made the message and why? Who may benefit or be harmed? How might people interpret this message differently?

We need to think and help others to think about income and funding models, industry, and the framing of dietary problems by scientist, bloggers, and the media (and I don’t just mean “the other guys”—apply these critical thinking skills to your own nutrition/food community).

Nothing about our food and nutrition thinking was born in a vacuum. Food is a part of our cultural and social fabric. It allows us to belong; it allows us to define ourselves. Even as we strive to find better science and to shift our current diet-nutrition paradigm, we must approach this with the understanding that there is no truly objective science. How science gets used, especially in the policy arena moves us even farther from that non-existent ideal. Even as we strive to improve public health, we must understand that we don’t always know what “health” and “healthy food” means to the people we think we are trying to serve.

If these points sound remarkably like the mission statement for Healthy Nation Coalition, my non-profit, then you’ve been paying attention. But it is not my plan for HNC to “lead” any nutrition reform movement as much as it is for us to get behind everyone else and shove them in the same direction. There is very much a herding kittens aspect to this (as Jorge of VidaPaleo.com pointed out), but as a former high school teacher and mother of three, this is not new territory to me.

So, yes, I have an agenda. Everyone has an agenda. I’ll spell mine out for you:

Somewhere out there in America, today, there is a young African-American girl being born into a country where many—if not most—of the forces in her world will propel her towards a future where she will gain weight, get sick, have both of her legs amputated, get dialysis three times a week, be unemployed and unemployable, on disability and welfare, and—this is what gets me out of bed in the morning and drags my weary ass to one more round of getting punched in the face by those very forces arrayed against her—she will, somewhere underneath it all, blame herself for her situation. I’m an old white lady, in a position of relative power and knowledge. I don’t know this young lady, and she doesn’t know me. She doesn’t owe me anything because she’s not asking for my help. But it is my job in this life to begin—at the very least—to shift those forces so that she has a better opportunity to choose a different life if she wants to. That’s all I care about. I don’t care who gets credit or who gets the cushy book deal.  I just want it to happen.  I would want the world to do the same for my children if they had not had the privilege of birthright that they do. That child is my child as sure as the three that live here and drive me crazy are. All I ask of the paleo community is that she be your child too. And if, as a community, you decide to adopt this child, well then, don’t worry about becoming an elitist fad made up of goofy-shoe wearing white people destined to fade into obscurity. Instead, you all will change the world.

Next Up: What makes a movement? (and I mean a social change one, not the bowel-y kind)

*Much of what follows borrows liberally from the work of Charlotte Biltekoff at UC-Davis, a wonderfully warm and intelligent woman who has been working on and thinking about this issue for—believe it or not—longer than Gary Taubes. She has a book coming out next summer which, IMHO, will be the social/cultural partner to Good Calories, Bad Calories.