Where the Women Are, Nutrition Edition

I really try not to pout too much when I see lists like the one below from Jimmy Moore’s 2012 survey on “most trusted resources for the information you received about health”:

After pouring through a couple hundred names that people shared, here were the top 10 who made the list in 2012:

1. Mark Sisson (30%)
2. Robb Wolf (23%)
3. Gary Taubes (21%)
4. Chris Kresser (15%)
5. Sean Croxton (10%)
6. Dr. Mike Eades (9%)
7. Dr. Robert Atkins/Atkins.com (8%%)
8. Dr. William Davis (7%)
9. Tom Naughton (7%)
10. Diane Sanfilippo (6%)

But seriously?  ONE woman?  ONE?  That’s it?????? Good grief.

The reasons for this imbalance are another blog post.  Instead, I chose to channel my energies into introducing some women who are leading the way—in their own way—in the world of nutrition.  If there appears to be a  “bias” in that most of these women–in one way or another–suggest that the current “grains are great” approach to nutrition is an unsound approach to good health, you might ask yourself how much that has to do with the prevailing bias within our current, and highly unsuccessful, nutrition paradigm.  These women are leaders, not followers.

To me, they are the Chers, Madonnas  and Dolly Partons of the nutrition world, although with a few exceptions, you may not recognize their names (which I know is part of the problem). Most have them have been around the block a time or two, and they know how the game is played—and rigged. They’ve succeed by being entirely who they are—tough-minded broads, compassionate caretakers, and reluctant warriors in the cause for good health for all.

Some of these women I’ve met, some I know well, some I’ve only admired from a safe distance afar. I wouldn’t expect all of these women to agree with—or even like—each other, or me, for that matter. Some of them may be appalled to find themselves on this list at all. Oh well. I don’t agree with all that each of them has to say, but I embrace the diversity and the chance to recognize some women I think have shown us how to have the huevos we need for the work ahead of us.

So—without further ado, and in alphabetical order (why not?)—here they are.

Judy Barnes Baker brought us this useful meme.

Judy Barnes Baker came this close to getting the American Diabetes Association to publish and endorse her reduced-carb cookbook. When that arrangement fell through, she got her cookbook published anyway and went on to publish another. Like Dana Carpender (see below), she’s been making life easier for those folks who want a low-carb approach to life.

Dana Carpender is a force of nature. She’s been holding the toast since 1996, and with her technogeek husband, Eric, has been able to bring us that message over the web since the dawn of the internet. Her book and cookbooks have been a lifeline for many trying to figure out exactly how to put into practice a way of eating that makes them feel healthy and happy. And boy, does she ever have a mouth on her. Sometimes I think it would be fun to lock her in a padded room with Frank Sacks and see who makes it out intact. I know where my money would be.

Laurie Cagnassola

Laurie Cagnassola, dog-lover extrodinaire, was, until recently, the Director of Nutrition and Metabolism Society, a leading low-carb oriented organization. She managed to gracefully meld the work she did with NMS with her own stance as a vegetarian. While Richard Feinman lambasted the entrenched interests in science and government out front, she worked tirelessly behind the scenes to build the fledgling reduced-carbohydrate nutrition community into a full-grown movement.  I expect we’ll hear more from her in the future.

Laura Dolson’s beautiful Low-Carb Pyramid

Laura Dolson has been writing about the food, science, and politics of low-carb nutrition for over a decade.  As a person who “walks the walk,” her posts on about.com are an informative and realistic guide to carbohydrate reduction.

Mary Dan Eades MD is the beautiful half (okay, the beautiful half on the right, for all you women out there drooling over her husband) of the royal (protein) power-couple of the carb-reduction world, Drs. Mike and Mary Dan Eades. They are the authors of multiple diet and lifestyle books beginning with Protein Power, which helped me navigate my own personal path to health many years ago. She may prefer to focus on singing, traveling, and grandkids now, but her voice is what gave the brilliant biochem wonkiness of Protein Power its warmth, humanity, and accessibility.

Jackie Eberstein RN was Dr. Robert Atkins right-hand RN for many years. She’s soft-spoken, with a backbone of steel and a heart of gold. She thought Atkins was “a quack” when she interviewed for the job. Thirty years later, she was still marveling at the improvement people could make in their health following his diet. But she’s no extremist. She taught me the importance of making sure calorie levels on a low-carb diet were appropriate. She’s got her hands full with her husband, Conrad, a charmer who can seriously rock a bow tie.

Mary G. Enig PhD is co-founder with Sally Fallon Morrell of the Weston A. Price foundation. Her work on fats led her to be one of the first voices raised in warning about the dangers of trans fats—and she’s been battling the seed oil industries attempts to silence and marginalize her work ever since.

Mary Gannon PhD, has—along with her research partner, Frank Nuttall—been working quietly on the low-biologically-available-glucose (inelegantly known as the LoBAG) diet for a decade now, although her work stretches back into the 70s. She is persistent in her efforts to understand the benefits of reduced carbohydrate and increased protein in helping to reverse the symptoms of type 2 diabetes.

Zoe Harcombe has been researching obesity for a couple of decades now. A UK writer, researcher, and nutritionist, her book, The Obesity Epidemic, is giving readers on the other side of the pond a different perspective on nutrition.

hartke is online podcast

Kimberly Hartke puts the “life” in lifestyle changes as the publicist for the Weston A Price Foundation. She’s collected enough stories from being on the front lines of the nutrition revolution to write a book, which I am truly hoping she will do one day soon.

Weigh loss success story

Misty Humphrey’s warmth and humor permeate her writing and advice on diet and health.   If there was ever a way to screw up getting healthy Misty’s done it and she’s honest and funny as she tells her story and helps her readers avoid the same pitfalls.

Lierre Keith’s Vegetarian Myth is not just another story of someone who found that their favored way of eating didn’t work and—prestochango—transformed themselves and their health by discovering The Truth About Food. The power of her book lies in her examination of the beautiful myth that underlies vegetarian thinking—that we can somehow peacefully eat our way to personal and global health without any regard for ourselves as critters who—just like all other critters—must function within an ecosystem that is nothing but one expression of eat/be eaten after another. I like to put her book on the shelf next to Jonathan Safran Foer’s goofball Eating Animals, which amounts to little more than a literary snuggie for vegans (JSF considers the American Dietetic Association the very last word in science-based nutrition information <guffaw>). I expect The Vegetarian Myth to simply drain the ink off the pages of Eating Animals out of sheer proximity.

CarbSane’s Evelyn Kocur, shows us–and the rest of the world–what the focused energy of one cranky woman who thinks we’ve been fed a load of crap looks like. Although I’m not a fan of her style—after years of listening to my mother scream, even reading someone else’s raging makes me want to hide under the bed—I can nevertheless admire the no-holds-barred way she skips the warm fuzzies and goes straight for the jugular. I really wish–every now and then–that I could pull that off.  Even when she’s missed the target by a mile, I have to give her credit for sheer firepower.

Sally Fallon Morrell is the director and co-founder (along with Dr. Mary Enig) of the Weston A. Price Foundation. Sally Fallon Morrell is a mother of four and a force of nature who doesn’t mince words. She’s ticked off at least one person in the paleo movement with regard to her stance on saturated fat, but—as far as I can tell—he’s ended up changing his position on the subject; she hasn’t changed hers.

Patty Siri-Tarino, PhD, is lead author of the meta-analysis on the lack of association between saturated fat and heart disease that changed the nature of conversation about nutrition and prevention of chronic disease.

No pink fluffy weights for Krista Scott-Dixon

Krista Scott-Dixon is the first person I found on the internet who said lifting big heavy things is for women too. She taught me—and countless numbers of other women–how to squat and that feminist theory and nutrition do so go together. And she makes fart jokes. You could really just not bother reading anything else I write and just read her stuff. Case in point: a free e-book entitled, Fuck Calories. (As Krista says: Yes, this book has cuss words. Many of them. Deal with it. Hey, it’s free. You get what the fuck you pay for.) Could she get any cooler? She’s married to a rocket scientist.

Mary Vernon MD has been at the forefront of reduced-carbohydrate nutrition for many years as a leader at the American Society of Bariatric Physicians. This group has partnered with the Nutrition and Metabolism Society to encourage conversation within the scientific/academic/clinical setting about reduced-carbohydrate nutrition: its pros and cons; the science behind it; and its clinical application. When national nutrition policy eventually catches on, it will be due in no small part to the fact that Mary Vernon and ASBP have already been offering this nutrition option to patients for years.

Regina Wilshire is the inspiration for a folder on my desktop entitled, Regina Brilliance. She is full of common sense and uncommon smarts. Wife, mother, and tireless blogger, her Weight of the Evidence (now on facebook too) has been a resource for intelligent and insightful commentary on nutrition since 2005. In the midst of the PubMed duels we so often find ourselves wrapped up in, her posts on eating well on a food stamp budget bring a welcome reality check.

Daisy Zamora PhD fought battle after battle (a story she’s agreed to let me tell one day) to publish her groundbreaking research on why our one-size-fits-all diet may be especially devastating to the health of minorities. It is not difficult to imagine why the powers-that-be would not want this indictment of the failure of our dietary recommendations to be made public. But beyond being a quiet crusader for rethinking our current dietary paradigm, she recognizes the importance and centrality of food in our lives and health. You have no idea how rare it is in the world of academic nutrition experts to find someone who eats and cooks and talks about food—as opposed to nutrients in food—and, get this, appears to actually like the stuff!

Let me know who’s on your list, or who I should add.

Plus, if that’s not enough, I found that, in putting together this list, many of the women I admire in the field of nutrition are–gasp–Registered Dietitians. Since RDs catch so much crap from the rest of the alternative nutrition community about being mindless-Academy-of-Nutrition-and-Dietetics-robots, I thought I’d put together a list of RDs who have inspired me to continue to work towards better health for all, despite our own professional organization’s insistence on using USDA/HHS policy as if it is science and its wince-inducing reliance on both food and pharma funding.

Next up: Where the Women Are, RD edition.

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Why Fat is Still a Feminist Issue

Sing along when the chorus rolls around (with apologies to Helen Reddy):

Yes I ate brown rice
And anything whole grain
Yes I’ve exercised
And look how much I’ve gained
If I have to, I won’t eat anything
I am fat
I am invisible
I am WOMAAAAAAAN!

The United Nations declared 1975 to be International Woman’s Year. Unfortunately, we haven’t really come a long way, baby, since then. Right now, I’m going to sidestep the whole media-generated body image issue, the glass labyrinth, the mommy wars, the “strong is the new sexy” idea (which somehow won out over my own personal favorite “smart is the new sexy” with campaign ads of slightly-unwashed-looking ladies without pedicures huddled over lab benches) and all the other complexities of contemporary feminist theory, and just focus on one little segment of how our national nutrition recommendations might have sucked the life out of women in general for the past 30 plus years.

We’ve been acting like the whole low-fat/low-glycemic/low-carb/paleo/whatever nutrition argument is a PubMed duel between scientists, and the fact that we are surrounded by lousy, nutrient-poor, cheap food is the fault of the Big Evil Food Industry. Let’s focus our attention regarding the current health crisis in America where it really belongs: on short-sighted, premature, poorly-designed (albeit well-intentioned) public health recommendations that were legitimized with the 1977 Dietary Goals for Americans and institutionalized as US policy beginning with the 1980 Dietary Guidelines for Americans.  Yes, fat is still a feminist issue.  But I’m not talking about body fat.

The scientific underpinnings for these recommendations came primarily from studies done with white men. And although the science conducted on these white guys was generally inconclusive, the white guys in Washington—in an attempt to prevent what they saw as a looming health crisis in America—recommended that Americans consume a diet high in carbohydrates and low in fat. And although these premature recommendations have certainly not prevented any health crises in America (the appearance seems to be just the opposite, see: Public Health Nutrition’s Epic Fail), they’ve also had serious repercussions in other respects for the rest of us, i.e. the ones of us who are not white men. [Please don’t take this as a “I hate white guys” thing; I love white guys. I gave birth to two of them.] I’m going to get into the “not white” part of the equation in another post (perhaps unimaginatively titled, Why Nutrition a Racial Issue), but let me focus just on the “not men” part.

For those of us who are not men (and mostly not poor and not part of a minority group), the 1970’s brought us Charlie’s Angels and the Bionic Woman. Women were given the message that we should be able to do and have “it all” (whatever “it all” was). The expectation was that you could “bring home the bacon, fry it up in a pan” and be thin, gorgeous, and sexy (and white) while you did it.

[circa 1980]

Only now bacon (and eggs for that matter) was forbidden, and as the eighties evolved into the nineties, breakfast became granola bars or rice cakes, nibbled virtuously while we drove the kids to school on our way to the job where we got paid less than the men with whom we worked. All the while, we were convinced that we could continue to fit into our tailored power suits by eating a diet that wasn’t designed with our health in mind.

[bacon eggs frowny face, circa 1984]

As with nearly every other aspect in the fight for equal opportunities and treatment, our health as women was based on a single shiny little myth: success would come to those who were willing to work hard, sacrifice, and follow the rules. Airbrushed media images of buns of steel and boobies of plastic sold a diet-exercise message based on an absurdly crude formula—”calories in, calories out”— with one simple rule that would guarantee success: “eat less and move more.”

So we did. We ate less and exercised more and got tired and hungry and cranky—and when all that work didn’t really work in terms of giving us the bodies we were told we should have, we bought treadmills and diet pills, Lean Cuisines and leg warmers. We got our health advice from Jane (“feel the burn”) Fonda and Marie (“I’m a little bit country”) Osmond. We flailed through three decades of frustration, culminating— unsurprisingly enough—in the self-flagellation of Spanx® and the aptly-named Insanity®.

[Jane Fonda circa 1982]

Some of us “failed” by eating more (low-fat, high-carb) food and getting fat, and some of us “succeeded” by developing full-blown eating disorders, and some of us fought the battle and won sometimes and lost other times and ended up with closets full of size 6 (“lingering illness”) to size 26 (“post pregnancy number 3”) clothes. Most of us—no matter what the result—ended up spending a great deal of time, money, and energy trying to follow the rules to good health with the deck stacked against us. If we got fat, we blamed ourselves, and if we didn’t get fat it was because we turned our lives into micromanaged, most-virtuous eater/exerciser contests. Either way, our lives were reduced, distracted, and endlessly unsatisfying.  We were hungry for more in so many ways and aching for rest in so many others, but our self-imposed denial and exhaustion allowed us to control, at least for a bit, the one thing we felt like we could control, that we’d fought to be able to control:  our bodies.

We stopped cooking and started counting. We stopped resting and playing and started exercising. We stopped seeing food as love and started seeing it as the enemy. We didn’t embrace these bodies that were finally, tenuously, ours; we fought them too.

Access to high quality nutrition has always been divided along gender lines [1].  There was a time–not that long ago–in our world when men, by virtue of their size, stature, place as breadwinner (i.e. because of their “man-ness”) were entitled to a larger piece of meatloaf than their sisters (a practice that persists in many cultures still).  How many of us (of a certain age) have heard, “Let you brother have the last piece of chicken, he’s a growing boy”?  Now–conveniently–women would do their own restricting.  Gloria Steinem, with a fair amount of prescience that seems to predict the epigenetic contributions of diet to obesity, noted in her 1980 essay The Politics of Food:*

“Millions of women on welfare eat a poor and starchy diet that can permanently damage the children they bear, yet their heavy bodies are supposed to signify indulgence.  Even well-to-do women buy the notion that males need more protein and more strength.  They grow heavy on sugar and weak on diets . . . Perhaps food is still the first sign of respect–or the lack of it–that we pay to each other and to our bodies.”

Dieting and exercising not only provided a massive distraction and timesuck for women, it helped maintain a social order that the feminist movement otherwise threatened to undermine, one where women were undernourished and overworked, in a word: weak.

And when the scientists finally got around to testing the whole low-fat thing on (80% white) women? The verdict, published in  2006, looked like this:

The results, published in the Journal of the American Medical Association, showed no benefits for a low-fat diet. Women assigned to this eating strategy did not appear to gain protection against breast cancer [2], colorectal cancer [3], or cardiovascular disease [4]. And after eight years, their weights were generally the same as those of women following their usual diets [5].

But it was too late. We’d raised a generation of daughters who look at us and don’t want to be us, but they don’t know how to cook and they don’t know what to believe about nutrition and they too are afraid of food. Some end up drinking the same Kool-Aid we did, except that—in the hubris of a youth that doesn’t contain hallucination-inducing sleep deprivation from babies and/or stress and/or a career on life-support, where diet and exercise and rest are, like Peter Frampton’s hair, a dim memory—they think they will succeed where we failed. Or maybe they’ve found the vegan-flavored or paleo-flavored Kool-Aid. But they are still counting and exercising and battling.

White women have been [irony alert] scientifically proven to be more likely to closely follow the high-carb, low-fat dietary ideal set forth by the Dietary Guidelines than any other demographic [6]. (Black guys—who may not be all that convinced that rules created by the US government are in their best interests, given some history lessons—are likely to have the lowest adherence.) White women apparently are really good at following rules that were not written with them in mind and which have not been shown to offer them any health benefits whatsoever (but which have proven immensely beneficial for the food and fitness—not to mention pharmaceutical—industries). The best little rule-followers of all are the dietitians of the Academy of Nutrition and Dietetics (87% white women), who heartily endorsed the 2010 Dietary Guidelines, which reinforced and reiterated 30 years of low-fat, high-carb dogma despite the Harvard-based science that demonstrated that it offered no benefits to women. (Interesting tidbit: The Academy of Nutrition and Dietetics has elected two male presidents in the past decade despite the fact that men make up only 5% of the membership. My husband thinks the organization has “daddy issues.”)

In 2010, the American Medical Association recommended that women of normal weight (that’s less than 40% of us, by the way) who wanted to stay that way “while consuming their usual diet” (i.e. low-fat, high carb) would have to exercise for an hour a day

[Other reassuring conclusions from that study: There was an overall weight gain over the 13-year time frame. Exercising for anything less than 7 hours per week was associated with weight gain over time. If a woman was already fat, increased exercise was more likely to be related to increased weight than weight loss.  If these messages don’t scream to women all over America, “GIVE UP NOW!!!” I don’t know what would. By the way, those of us who go out and skip and jump and run because we like to and it makes our hearts truly happy are not exercising. We’re playing. I love to wave at those women from my couch.**]

But let’s get back to that hour a day for just a second.

Take a look at a recent study by Dr. David Ludwig, out of Harvard. It demonstrated that people who had recently been dieting (something that would apply to almost every woman in America), and were eating a low-fat diet, had to add an hour a day of exercise in order to keep their “calories in, calories out” balanced, while those on a reduced-carbohydrate diet expended that same amount of energy just going about their business.

What is all the women in the world who have been unsuccessfully battling their bulge woke up tomorrow morning and said:

I want my hour a day back?

For those of us who do not want to exercise for an hour just to maintain our weights or for those of us for whom exercise isn’t doing a damn thing except making us hungry and cranky and tired while we gain weight, we don’t have to. Instead, we can eat fewer of those USDA/HHS/dietitian-pushed, nutritionally-pathetic, low-fat whole-grain carbohydrate foods and more truly nourishing food and do whatever we please with that extra hour.

Who knows what changes we can make to a world that desperately needs our help?  In America alone, this would mean giving around–ooh let’s just say–50 million adult women an extra hour a day. That’s an extra 365 hours a year per woman, an extra 18 billion hours of womanpower a year total.

We could stop exercising and start playing. Stop counting calories and start enjoying feeling nourished. Start putting the love back into our food and embracing the bodies we have and the bodies of the men, women, and children all around us. I know that some of us would find that hour well spent just napping. Others of us might use that hour to figure out how to dismantle the system that stole it from us in the first place.

I can bring home the bacon, fry it up in a pan. And eat it.

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

In my own personal celebration of Asskicking Women of Food, I think (I hope) my next post will be:  The Grande Dames (Goddesses? Queens?) of Nutrition

*Thanks to Gingerzingi for bringing this to my attention.  What a great essay–look for it in a collection entitled Outrageous Acts and Everyday Rebellions.

**I have absolutely nothing against activities that bring inner/outer strength and happiness.  But exercise in the 80s and 90s was not about being happy or strong–it was about punishing ourselves (feel the burn? seriously?) in order to win at a game–being in total control of everything in our lives from babies to bodies to boardrooms–whose rules were created within the very social construct we were trying to defeat.

References:

1.  Bentley, Amy (1996) Islands of Serenity: Gender, Race, and Ordered Meals during World War II. Food and Foodways 6(2):131-156.

2. Prentice RL, Caan B, Chlebowski RT, et al. Low-fat dietary pattern and risk of invasive breast cancer: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006; 295:629-42.

3. Beresford SA, Johnson KC, Ritenbaugh C, et al. Low-fat dietary pattern and risk of colorectal cancer: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006; 295:643-54.

4. Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006; 295:655-66.

5. Howard BV, Manson JE, Stefanick ML, et al. Low-fat dietary pattern and weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. JAMA. 2006; 295:39-49.

6.  Sijtsma FP, Meyer KA, Steffen LM et al.  Longitudinal trends in diet and effects of sex, race, and education on dietary quality score change: the Coronary Artery Risk Development in Young Adults study. Am J Clin Nutr. 2012 Mar;95(3):580-6. Epub 2012 Feb 1.

N of 1 Part 5: A Different Question

The magic formula

My friend, Andrew Abrahams, puts the current “diet wars” situation this way:

1.  the n of 1 view:  what works for you is what works, this is all that matters, end of story.

2.  the Platonic view: this is how your body/metabolism works, and so this is what you should do and if it isn’t working you probably are not doing right.

I think many of us start off being interested in nutrition because we like to know stuff, and knowing stuff about how to be healthy and fit is really cool because then you get to look better in your bathing suit than most or you can solve health problems that others can’t or any number of other minor acts of smug superiority masquerading as an objective search for knowledge. When we start out, we usually are completely immersed in perspective #2, that there is a “right” way to eat and exercise. We figure out what the “right” way is through various forms of scientific investigation/reporting brought to us by experts and/or the media; we apply that magic formula to ourselves, and we wait for the magic results to happen. If we are young and unencumbered by reality, they usually do—no matter what formula for fitness and health we’ve chosen from the ones offered by the experts—and we congratulate ourselves for our hard work and strength of character.

Enter reality. Crying babies. Crazy work hours. Demoralizing paychecks. Chronic injuries. Insane parents. Needy friends. Crying, crazy, demoralizing, chronically insane, needy life partners (No, my dear sweet rockstar hubby, I certainly couldn’t have had you in mind when I wrote this.)

A little reality can drop-kick your magic fitness formula into outer space.

For many of us, somewhere along the line, the magic formula stops working, or we stop working at the magic formula, or a little (or a lot) of both.

Some of us respond to this by looking for the next—better, easier, quicker, more doable—magic formula. Some of us respond by working even harder at the magic formula we haven’t given up on—yet. Some of us give up looking and trying because life is hard enough already.

But that doesn’t mean we’ve given up on the idea that there is a “right” way to go about being healthy. I was a low-fat vegetarian eater for 16 years because I thought it was the “right” way to eat. I’ve been a (mostly) low-carb, animal eater for 13 years, during most of which I thought I’d—finally—found the really “right” way to eat.

What I’d really found was a new and different way to be wrong.

I wasn’t wrong about the diet plan–for me. It helped me lose 60 pounds that I’ve kept off for 13 years without hunger, without a calculator, and without having to exercise more than I want to. What I was wrong about was being right. I was wrong about the magic formula—any magic formula.

[In blog posts yet to come, I’ll tell you all the story of the woman who changed my perspective on everything.]

I hate being wrong (although goodness knows I’m really good at it, from years of practice). I really want there to be a formula, magic or otherwise. I like order, routine, facts, and answers. Gray areas make me woozy. That’s why I love biochemistry. It’s a game with nothing but rules that, literally, every body has to follow.

But, to quote Andrew Abrahams again, a detailed understanding of the minutiae of biochemical mechanisms doesn’t really help us in the big messy world of real people. Although everyone is subject to the same biochemical rules, how those rules play out in any given individual is difficult—perhaps impossible—to predict.

I salute the work that Gary Taubes and Peter Attia are doing with NuSI, which will focus on providing randomized controlled experimental evidence regarding nutritional interventions. The idea is to have both highly controlled experiments and more “real world” ones. Hooray for both. These experiments may help us understand how well certain nutrition interventions work—in experimental situations with a selected group of individuals. As awesome as this might be for a scientific pursuit, this science still may not be of much help for you personally, depending on how closely matched you feel your life and your self are to the experimental conditions—and it won’t provide any easy answers for the hardest issue of all, public health policy.

One big long experiment

Is there a way to round up our messy, individual realities into comprehensible information that will eventually translate into meaningful policy? Maybe. Andrew Abrahams and others in the ancestral health community have been tossing around the idea of “n of 1” nutrition for a while. The basis for this approach is the idea that we all experiment. In fact, life is one big long experiment.

But how do we conduct these “n of 1” experiments in a manner that

  • helps the person doing the experiment learn the right lessons (rather than be distracted by coincidences or random events)?
  • helps the clinician give better nutrition guidance, not of the “one size fits all” variety?
  • helps the field of nutrition science develop more meaningful methods of investigation, especially with regard to long-term health and prevention of chronic disease?
  • helps us renegotiate the top-down, one-size-fits-all framework of current public health nutrition policy?

Andrew Abrahams had the brainchild of setting up a community for n of 1 nutritional experimentation to do exactly this.

As Andrew says, and I agree, individual characteristics, circumstances, and history are tremendously important as far as choosing food and activity that works for you. His idea is to create a way to help people with this n of 1 experimentation so they can evaluate how their body will respond to changes and find what’s right for them.

The purpose of this community would be to capture the wide variety of attributes that may contribute to the outcomes for any individual, and provide modeling tools that can help people make the right decisions about what changes to make.

From a participant’s perspective, it would:

  • provide a way for you to observe and analyze personal health in an organized and (more or less) objective fashion
  • give direction, support, and structure to your own n of 1 experimentation
  • create a community of fellow experimenters with whom you could compare/contrast results

From a health professional’s perspective, it would:

  • provide a way to assist clients/patients in find what works best for them without a superimposing “it’s supposed to work this way for everyone” bias
  • create a set of algorithms for adapting common patterns to individualized recommendations and further experimentation
    • For example: A postmenopausal female who wants to lose weight may start one way and experiment in a series of steps that is different from, say, a 30-year old marathoner who wants to have a healthy pregnancy.

From a researcher’s perspective, it would:

  • create a way to structure and conduct experiments across a variety of nutritional (and other) factors
  • allow sharing and analysis of both pooled results and case studies/series of relevant community members or subpopulations with common characteristics
  • develop tools allowing one to interpret the community results in an individual context, make predictions and suggest “next steps”
  • contribute to the development of modeling systems for complex and interrelated inputs and outputs

A different question means a different approach to public health

I see the value of n=1 as a scientific pursuit because it will teach us to ask a very different question than the one we’ve been asking.  We’ve been asking, “What way of eating will prevent chronic disease in most/all Americans?” Typically, nutrition epidemiology is recruited to try to answer that question with the idea that there is some factor or factors (like smoking and lung cancer) that can be included/eliminated to reach this goal.  We’ve been so phenomenally unsuccessful at chronic disease prevention with our current population-wide model that I think a new framework of investigation is needed. Thus, n of 1 investigation changes the question to something more like: “What way of eating will bring improved health to you now?”

As people make incremental changes toward shorter-term personal health goals, modeling tools can be used to map out “nearest neighbor” communities. These communities may be similar in terms of personal characteristics and health history, but also attributes relating to culture, region, lifestyle, ethnic and family background, education, income, etc. Over time, this information will reflect long-term health outcomes built on a background of complex human traits interacting with complex human environments.

The complexity of n of 1 nutrition seems to be the very opposite of public health nutrition. And it would be naïve to think that the concept of n of 1 will not be at least partially co-opted by the food, drug, and research industries (“Try new Methylation Carbonation –for PEMT polymorphisms!”).  But by its very nature, n of 1 nutrition resists being turned into yet another “magic formula.”  More importantly, it reframes our current approach to public health nutrition along two very important lines:

First, it weakens the current public health message that a one-size-fits-all dietary recommendation is appropriate. This is especially important because it has been assumed for 30+ years that dietary recommendations that are normed on one population are equally applicable to other populations. 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 [1].

DQI stands for Diet Quality Index. Blacks with a higher DQI had more weight gain over time than blacks with a lower DQI. From [1]



Second, n of 1 nutrition emphasizes the need to return to a focus on the provision of basic nutritional needs rather than prevention of chronic disease.  Balancing the complexity of the n of 1 concept (i.e. each human is radically different from another) with the simplicity of promoting/understanding essential nutrition (i.e. but each human shares these same basic needs provided by food) moves us away from the prevention model to the provision model. And the literature is pretty straightforward about what our basic nutritional needs are:

  • essential amino acids
  • essential fatty acids
  • vitamins and minerals
  • sufficient energy

Notice anything missing on that list of essentials? As the Institute of Medicine’s Food and Nutrition Board says: The lower limit of dietary carbohydrate compatible with life is apparently zero” (DRI, Ch. 6, 275) [2]. This doesn’t mean you can’t or shouldn’t eat carbohydrate foods, or that some carbohydrate foods aren’t beneficial for some people or even many people. Indeed, some of my best friends are carbs. But dietary carbohydrate is not an essential component of our nutritional needs and never has been (although it is a fine source of energy if energy is what is you need and you aren’t wearing a 6-month supply on your backside like I am). Rather, carbohydrate has been recommended as the source of the majority of our calories as a means of replacing the fat, saturated fat, and cholesterol that we’ve been told cause chronic disease.* This recommendation seems to have conveniently upsized the market for the industrialized and heavily marketed foods—made mostly from corn, wheat, and soy—that take up most of the space on our grocery store shelves.

But I think the most significant ramification of the history of our Dietary Guidelines is not its effect on diet so much as the acceptance of the notion that something as intimately and intricately related to our health, culture, personality, lifestyle, family, and history as food can and should be directed—in a most comprehensive manner—from a place exceedingly remote from the places where we actually get fed.

Focus on community

While the ostensible focus of n of 1 nutrition is the individual, the real focus is the community. Advances in both biological and social sciences are increasingly focused on what are now considered to be the primary determinants of health status for an individual: that person’s genetic community and that person’s present community. What health behaviors you as an individual think you “choose” have already been largely determined by social factors: culture, socioeconomic status, education, etc. Those behaviors interact with genetic and epigenetic mechanisms that you didn’t have much choice about either. Although every individual has some control over his/her health behaviors, many of the health outcomes that we think of as being a result of “individual choice” are already largely predetermined.

One of the enduring myths of healthcare in the US is that there are some folks out there who “choose” poor health. Maybe there are, but I’ve met a lot of people in poor health, and I’ve never met anyone who deliberately chose it.

As we find virtual “nearest neighbor” communities in our n of 1 nutrition database, we may be able to use this information to assist real communities to develop their own appropriate food-health systems. Despite our increasing diversity, much of America still clusters itself in communities that reflect shared characteristics which play leading roles in health and health behavior. Culturally-influenced food preferences and nutrition beliefs may be part of that community formation and/or may reinforce those communities. With scientific tools that embrace complexity and diversity, we can honor those characteristics that make one community (real or virtual) different from the next, rather than ignore them.

N of 1 nutritional approaches will give us a new way to think about public health nutrition and the individuals and communities most affected by nutrition policy. I’m proud to say that Healthy Nation Coalition will be supporting the project.

Up next:  My take on why nutrition is a feminist issue, or “I am Woman, hear my stomach growl.”

*While on a field trip to Washington, DC in January of 2010, I met Linda Meyers, one of the authors of reference #2 below. I asked her why carbohydrates were recommended as such a large part of our diet if there is no essential requirement for them. Her response was that the recommendation was based on prevention of chronic disease. I’m still not sure I get that.

References:

1. 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.

2. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients) (2005)

N of 1 Nutrition Part 4: The Elephant in the Room

“Nutrition is for real people. Statistical humans are of little interest.”
Roger J. Williams, PhD

Nutritional epidemiology has many shortcomings when it comes to acting as a basis for public health nutrition policy.   But you don’t have to take Walter Willett’s word for it.  Apart from the weaknesses in the methodology, there is one great big elephant in the nutrition epidemiology room that no one really wants to talk about:  our current culture-wide “health prescription.”

(Thanks to Utopia Theory!)

You don’t have to care about or read about nutrition to know that “fat is bad” and “whole grains are good” [1,2]. Whether or not you follow the nutrition part of the current  “health prescription” is likely to depend on a host of other factors related to general “health prescription” adherence, which in turn may have a much larger impact on your health than your actual nutritional choices. This is especially true because variation in intake and/or variation in risk related to intake are frequently quite small.

For example, in a study relating French fry consumption to type 2 diabetes, the women who ate the least amount of French fries ate 0 servings per day while the women who ate the most ate 0.14 servings per day or about 5 French fries per day (i.e. not a big difference in intake) [3]. The risk of developing type 2 diabetes among 5-fries a day piggies was observed to be .21 times greater than the risk among the no-fry zone ladies (i.e. not a big variation in risk).

Okay, everyone knows that French fries are “bad for you.” But these ladies ate them anyway. Were there other factors related to general “health prescription” adherence which may have had an impact on their risk of diabetes?

The French fry eaters also “tended to have a higher dietary glycemic load and higher intakes of red meat, refined grain, and total calories. They were more likely to smoke but were less likely to take multivitamins and postmenopausal hormone therapy.” (They also exercised less.) In other words, the French fry eaters, within a context of a known “health prescription” had chosen to ignore a number of healthy lifestyle recommendations, not just the ones related to French fries.

“As a general rule, noncompliant patients will usually have worse outcomes than compliant patients. In fact, there is solid evidence that patients who fail to comply with a placebo have worse outcomes than patients who comply with a placebo [4, 5] . . . . Patients who comply poorly with a placebo probably have other poor self-care habits.”

[Also, see Gary Taubes’ characteristically exhaustive discussion of the compliance effect. Pack a lunch.]

If you think of our current default diet recommendation as the “placebo” (although its effects may not be exactly benign), it is clear that people who fail to comply with dietary prohibitions against red meat, saturated fats, and “junk” food like French fries may also be more likely to have other poor self-care habits, like smoking and not exercising. That poor health care habits are related to poor health is of no surprise to anyone.

Statistical people

In their statistical manipulation of a dataset, nutritional epidemiologists attempt to “control” for confounding variables (confounders), such as differences in health behavior. A confounder is something that may be related to both the hypothesized cause under investigation (i.e. French fry eating) and the outcome (i.e. type 2 diabetes).  As such, it muddies the water when you are trying to figure out exactly what causes what.

When statisticians “control” or “adjust” for these confounders in a data set, they essentially “pretend” (that’s the exact word my biostats professor used) that the other qualities that any given individual brings to a data set are now equalized and that the specific factor under investigation—diet—has been isolated. Well, it has and it hasn’t. The “statistical humans” created by computer programs that now have equalized risk factors are a mirage; these people do not exist. The people who contributed the data that ostensibly demonstrates that “French fries increase risk of type 2 diabetes” are the exact same people who had other behaviors that may also contribute to increased risk of diabetes. (Please note: I chose this example, rather than “red meat causes heart disease” because there are many plausible explanations for French fries causing type 2 diabetes, it is just that you aren’t going to find evidence for them using this approach.)

If nutrition epidemiologists were clinicians.

(Thanks and apologies to Baloocartoons.com.)

Most nutritional epidemiology articles contain some version the following statement in their conclusions:

“We cannot rule out the possibility of unknown or residual confounding.”

Meaning: We can not rule out the possibility that our results can be explained by factors that we failed to fully take into account. Like the elephant in the room.

That this is actually the case becomes apparent when hypotheses that seem iron-clad in observational studies are put to the test in experimental conditions.

Lack of experimental confirmation

If ever there was a field about which you could say “for every study there is an equal and opposite study,” it is nutritional epidemiology–although experimental results are generally considered “more equal” than observational data. Associations that link specific nutrients to the prevention of specific diseases can be (relatively) strong and consistent in the context of nutritional epidemiology observational data, but absent in experimental situations. Epidemiological studies suggested that beta carotene could prevent cancer; experimental evidence suggested just the opposite and in fact, smokers given beta carotene supplements had increased risk of cancer [6]. Epidemiological studies suggest that low-fat, high-carb diets are related to a healthy weight. This may be the case, but experimental evidence shows that reducing carbs and increasing fat is more effective for weight loss [7, 8]. In one study, when experiment participants added carbs back into their diet (the increase in calories from 2 months to 12 months is entirely accounted for–and then some–by carbohydrate), they regained the weight they had lost.*

Data from [7]

Kenneth Rothman, in his book Epidemiology: An Introduction, emphasizes the importance of applying Karl Popper’s philosophy of refutationism to epidemiology:

“The refutationist philosophy postulates that all scientific knowledge is tentative in that it may one day need to be refined or even discarded. Under this philosophy, what we call scientific knowledge is a body of as yet unrefuted hypotheses that appear to explain existing observations.” [9]

Rothman makes the point that there is an asymmetry when it comes to refuting hypotheses based on observations: a single contrary observation carries more weight in judging whether or not a hypothesis is false than a hundred observations that suggest that it is true.

In the case of the current “low fat, whole grain diets will prevent chronic disease” hypothesis, there is not just one contrary observation, but scores of them, including the results of applying this hypothesis in a 30-year, population-wide experiment in the US.

If the current nutrition paradigm needs to be “refined or even discarded,” how will we acquire the knowledge we need to create a better system? How can we move away from “statistical people” towards a perspective that encompasses the individual variations in genetics, culture, and lifestyle that have such a tremendous impact on health?

Tune in next time for the final episode of N of 1 nutrition when I ask the all-important question: What the heck does n of 1 nutrition have to do with public health?

*This doesn’t mean that carbs are evil–some of my best friends are carbs–but that the conditions in a population that are associated with a healthy weight and the conditions in an experiment to that lead to increased weight loss are very different.

References:

1. 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.

2. 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.

3. Halton TL, Willett WC, Liu S, et al. Potato and french fry consumption and the risk of type 2 diabetes in women. Am J Clin Nutr. 2006 Feb;83(2):284-90.

4. Coronary Drug Project Research Group. Influence of adherence to treatment and response of cholesterol on mortality in the coronary drug project. N Engl J Med. 1980 Oct 30;303(18):1038-41.

5. Horwitz RI, Viscoli CM, Berkman L et al. Treatment adherence and risk of death after a myocardial infarction. Lancet. 1990 Sep 1;336(8714):542-5.

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

7. Gardner C, Kiazand A, Alhassan, et al. Weight Loss Study: A Randomized Trial Among Overweight Premenopausal Women: The A TO Z Diets for Change in Weight and Related Risk Factors .Comparison of the Atkins, Zone, Ornish, and LEARN. Journal of the American Medical Association. 2007;297(9):969-977

8. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, et al; Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008 Jul 17;359(3):229-41.

9. Rothman, K. Epidemiology: An Introduction. New York: Oxford University Press, 2002.


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.

Just Asking the Question

 

 

So wouldn’t it be cool if we could ask folks on the street what they think caused the obesity crisis, and then show them this and ask them again?

Now back to your regularly scheduled blob.

Data from:  Centers for Disease Control and Prevention (CDC).  National Center for Health Statistics, Division of National Health and Nutrition Examination Surveys.  Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1976–1980 Through 2007–2008. 

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.

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