A Heaping Dish of Humility and a Side of Caution

This was not on the menu at the “Is Nutrition Research Keeping Pace with Policy and Consumers” panel at the Consumer Federation of America’s National Food Policy Conference.

I’m not sure what I expected, but I was encouraged by the fact that during other presentations at the conference, I had heard murmurs that perhaps we don’t really know what we mean what we say “healthy food” and that the public has some real concerns about what they are being told about nutrition.  So I was manifestly disappointed to hear just another rallying cry for the status quo from the academics and policymakers on this panel.

A panelist from the National Cancer Institute asserted–despite those rumors heard elsewhere in the conference–that we “do have consensus” about what constitutes a healthy diet: “lean meat, whole grains, more fresh fruits and vegetables, and reduced saturated fat, sugar, trans-fats, and sodium.”  Linda Van Horn, who chaired the 2010 Dietary Guidelines Advisory Committee, told the audience that:  “We know what the problem is in obesity.  It’s the calories.  The calories.”  She went on to let us all know that if we just had policies that would help Americans follow the recommendations that are already in place, we could reverse the obesity crisis.  Sigh.  Make the healthy choice the easy choice for poor stupid fat Americans?  Again?  Already?

And–yes–in case you are wondering, I was quivering with rage by the time the panel finished talking (yogic breathing sadly not helping).  When my turn to ask a question arrived, I reminded the panel of the changes that we’ve already made in our diets–reduced red meat and egg consumption, increased whole grains and fresh fruits and vegetables, switched whole milk for low fat milk–and yet obesity and chronic disease continue to rise.  My question to them was, “When are nutrition experts and policymakers going to quit blaming the consumer for not following the food rules and start thinking about whether or not the advice we’ve been given is truly effective?”

After the panel, the gentleman next to me said “Good question.”  Yeah, I thought so too, but I got a truly lousy response from Dr. Van Horn:  “We may have reduced red meat, but we’ve increased sugar.”  Have we? Why might that have happened–if indeed it has?*  “No one is blaming the consumer; the fault lies with the food industry.”  This, at a conference devoted to showing consumers how their choices have driven the actions of industry. To blame industry is to blame the consumer; it’s just a sneaky and, frankly, dishonest way of doing it.

Ironically, the next day BMJ published an editorial with a completely different perspective. In it, Gary Taubes  (science writer and champion for the return of common-sense and intellectual rigor in the world of nutrition science)** suggests that instead of yet another round of “making the healthy choice the easy choice” for poor stupid fat Americans who haven’t the good sense to lose weight and stay healthy the way they’ve been told to for the past 35 years, perhaps nutrition experts might try a different tact:

“We believe that ultimately three conditions are necessary to make progress in the struggle against obesity and its related chronic diseases—type 2 diabetes, most notably. First is the acceptance of the existence of an alternative hypothesis of obesity, or even multiple alternative hypotheses, with the understanding that these, too, adhere to the laws of physics and must be tested rigorously.

Second is a refusal to accept substandard science as sufficient to establish reliable knowledge, let alone for public health guidelines. When the results of studies are published, the authors must be brutally honest about the possible shortcomings and all reasonable alternative explanations for what they observed.

Finally, if the best we’ve done so far isn’t good enough—if uncontrolled experiments and observational studies are unreliable, which should be undeniable—then we have to find the willingness and the resources to do better. “

While I find plenty to disagree with here (high glycemic grains?  really?), Taubes outlines some fascinating aspects of the history of obesity research and sheds some light on why the calories in-calories out hypothesis won out over the endocrinological (say it 5 times fast) one—and what nutritional mayhem has ensued since.  (Read the whole thing.  You’ll be glad you did.  I’ll wait here.)

His editorial reminds us that when it comes to the question of what dietary pattern will prevent obesity and chronic disease, we really don’t know much.  And it makes clear that what is needed now is a view toward a future where we will approach this question with much more humility and caution than we have in the past.

I’m going to suggest now–and you dear readers help me remember–that this time next year, we need to take Consumer Federation’s Food Policy Conference by storm.  It isn’t expensive (I think registration is $90, cheaper still if you are a student).  We are, after all, consumers.   The meeting is full of industry reps, policymakers, journalists, as well as academics.  It’s a small enough venue that I believe we can make our voices heard.  We can let them know that the current definition of “healthy food” doesn’t work for all of us & we, as consumers, want different choices and different information.

I get the impression that the current crop of nutrition experts and academics isn’t interested in trying this new dish–humility with a side of caution.  Since these folks seem to want to persist in keeping the public’s health on a trajectory where they can be the solution to the problems they have caused, perhaps we can find some ways to  “make the reasonable choice the easy choice” for them.

I’ll rent the hotel room & anybody who wants to can bring a sleeping bag–paleo sleepers can spread their bearskins on the floor.  Let’s do it.

*The truth is we don’t really know how sugar intake has changed.  Dietary data and food availability data offering conflicting views.  A mean of 15.8% of consumed calories was from added sugars in this study; data from 2010.  This study estimated that 26% of calories were from added sugar; data from 1977-1978.

**Full disclosure:  I know, and usually actually like, Gary Taubes.  But he does not pay me to say nice things about him & I disagree with him as much as I agree.


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

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

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

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

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

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

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

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

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

You can almost ALWAYS catch something on a fishing expedition.

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

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

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

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

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

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

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

“Broccoli has more protein than steak”—and other crap

Of all the asinine things that I read about nutrition—and let me tell you, I read a lot of them—this one has got to be the asininniest: Broccoli has more protein than steak.

I’ve seen this idiotic meme repeated many times, but the primary source of this stupid—see also: delusional, ludicrous, and absurd—notion seems to be Dr. Joel Furhman. My mom—bless her little osteoporotic soul—keeps his books down at the beach cottage. I don’t think she does it to taunt me, but you never know. I was a bad kid, and payback may be in order. My family has forbidden me to read Dr. Furhman’s books, to pick them up, or to even glance at the covers because the resulting full-on nutrition-rant kills everybody’s beach buzz.

However, as of last week, I have officially maxed out my tolerance for just ignoring this nonsense. So, note to my family: Read no further, it will kill your beach buzz.

According the Dr. Furhman’s book, Eat to Live, a 100-calorie portion of sirloin steak has 5.4 grams of protein, and a 100-calorie portion of broccoli has 11.2 grams of protein. This is rubbish. According to the USDA’s Agricultural Research Service’s Nutrient Data Laboratory database, 100 calories of broiled beef, top sirloin steak has exactly 11.08 grams of protein and 100 calories of chopped, raw broccoli has exactly 8.29. I’m not sure what universe Dr. Furhman lives in, but in my universe, 8.29 is less than 11.08.

I can explain the discrepancy in numbers by the simple fact that Dr. Furhman and I used different sources for our information. Dr. Furham wrote his book—the one that contains the piece of drivel under consideration—in 2005, but he chose to reference a nutrition book written in 1986 (Adams, C. 1986. Handbook of the Nutritional Value of Foods in Common Units, New York: Dover Publications). Just to put things in perspective, in 1986, the internet and DVDs had not yet been invented, no one knew who Bart Simpson was, and it would be another couple of years before Taylor Swift even draws her first ex-boyfriend-bashing breath.

Here’s what I can’t explain: Why, oh why did he dig up a reference nearly two decades old and not just use the USDA internet database, which is—and has been since the 1990s—available to anyone with a library card and a half a brain? While I do not wish to speculate on exactly which of these tools Dr. Furhman might be lacking, suffice it to say that it would take less than 10 minutes for any blogger interested in the truth of the matter to find a more recent source of information—assuming of course that bloggers who perpetuate this particular fiction are interested in the truth.

But wait—before you foam at the mouth too much, Adele—8.29 grams of protein is fair bit of protein.  There is only a difference of a couple of grams of protein between broccoli and steak.  Yes, I would agree, those numbers are a lot closer than you might expect, and this might actually be nutritionally important, if—Big If—all protein were created equal. Which it isn’t.

While I am a big fan of coming at nutrition from an individualized perspective, and I am aware that nutrition scientists don’t have any monopoly on truth, we have managed to nail down a few essential things that human must acquire from the food that they eat. In terms of essentiality, after calories and fluid comes protein—or more specifically, essential amino acids (there are more essentials, but they are not the topic of this particular rant). Because these amino acid requirements are so important (a particular form of starvation, kwashiorkor, involves not overall calorie deprivation, but protein deficit in the context of adequate or near-adequate calories), the World Health Organization has established specific daily requirements of the essential amino acids that are necessary for health.

Let’s see how similar caloric intakes of steak and broccoli stack up when comparing how these two foods provide for essential amino acid requirements. A 275-calorie portion of steak (4 ounces) has 30.5 grams of protein and comes very close to meeting all the daily essential amino acid requirements for a 70 kg adult. A 277-calorie portion of broccoli is not only way more food—you’ll be chewing for a long time as you try to make it through 9 ¼ cups of broccoli—exactly NONE of the daily essential amino acid requirements for an adult are met:

EssentialAmino acids (g) Daily requirement 70 kg adult (g) Essential amino acids (g) in 275 calories of steak (4 oz or 113.33 g) Essential amino acids (g) in 277 calories of chopped, raw broccoli (9.25 cups)
histidine 0.70 0.975 ( +0.275) 0.48 (-0.22)
isoleucine 1.400 1.391 (-0.009) 0.643 (-0.757)
leucine 2.730 2.431 (-0.299) 1.05 (-1.68)
lysine 2.100 2.583 (+0.483) 1.099 (-1.001)
methionine 0.70 0.796 (+0.096) 0.309 (-0.391)
cysteine 0.28 0.394 (+ 0.114) 0.228 (-0.052)
threonine 1.050 1.221 (+0.171) 0.716 (-0.334)
tryptophan 0.280 0.201 (-0.079) 0.269 (-0.011)
valine 1.82 1.516 (-0.304) 1.018 (-0.802)

In reality, it takes twice that much broccoli, or over 18 cups, containing nearly twice as many calories, in order to get anywhere near meeting all essential amino acid requirements.  While I’m willing to concede that individual amino acid requirements may vary considerably, I am not willing to concede that similar caloric amounts of steak and broccoli provide a similar supply of those requirements.  I’m no broccoli basher (it’s sooo yummy baked with cheese & a little bacon on top), but as a protein source, even a lot leaves a lot to be desired.

Oh yeah? Well then, “how on earth do animals like elephants, gorillas and oxen get so big and strong eating only plants? A diverse plant-based diet can obviously support a big, powerful body.” Sure it can. If you’re an elephant or a gorilla or an ox.

In general, human bodies don’t work very efficiently without a regular dietary supply of all essential amino acids: “It would be difficult to find a protein that did not have at least one residue of each of the common 20 amino acids. Half of these amino acids are essential, and if the diet is lacking or low in even one of these essential amino acids, then protein synthesis is not possible” [Emphasis mine; reference: Campbell & Farrell’s Biochemistry, 6th edition]. Protein synthesis allows us to grow, heal, reproduce, and function in general. One of the specific outcomes of protein deficiency in humans is stunting, i.e. where humans who would otherwise grow bigger, don’t.

Dr. Furhman seems to think that those of us who “believe” that food from animals provides a more biologically complete source of protein than food from plants “never thought too much about how a rhinoceros, hippopotamus, gorilla, giraffe, or elephant became so big eating only vegetables.” Hmmm. I have to say, I’m thinking the same thing about Dr. Furhman. Maybe he is unaware that humans aren’t really all that much like rhinoceroses, hippos, gorillas, giraffes, or elephants. But then maybe he just hangs out with a different crowd than I do.

Once again, armed with a library card and half a brain, it is not too difficult to figure out—assuming you did think about how those animals got so big eating only plants and didn’t just mindlessly parrot Dr. Furham’s poorly-researched blather—that, as Gomer Pyle would say, surprise! surprise! Humans and other large mammals ARE different.

While non-ruminants (like humans) must get their essential amino acids from their diet, ruminants (like giraffes) “may also acquire substantial amounts of these amino acids through the digestion of microbial protein synthesized in the rumen” (see: Amino Acids in Animal Nutrition, edited by J.P. Felix D’Mello). This may come as a bit of a shock to Dr. Furhman and his readership, but humans don’t actually have rumens and utilizing this particular approach to the acquisition of essential amino acids from plant matter ain’t gonna work for us.

You can get plenty of protein from a plants-only diet by eating like a hippo.

Other non-ruminant grazers—see elephants, rhinos, and hippos—have a different eating strategy. They “eat for volume and low extraction.” In other words, the relatively low availability of protein in the food is overcome by the high volume consumed. In that regard—assuming you aspire to an elephant-like, rhino-like, or hippo-like bod—it may be possible to get sufficient protein from a strictly plant-based diet. If you don’t mind eating all the time. And pooping. Less than half of what is consumed by the high-volume grazers is utilized by the body; the rest—like a handsome stranger—is just passin’ through (see: Nutritional Ecology of the Ruminant, by Peter J. van Soest). If the idea of literally flushing over half of what you eat down the toilet doesn’t bother you, then this strategy actually might work.

ooooh! Can we? Please?

So what about gorillas? This particular primate-to-primate comparison has been tossed all around the internet. Why can’t we just eat plants like gorillas do? Gorillas, although not so good at Jeopardy, are big and strong and they’re vegans, so we should all be vegans too, right? Aside from the fact that we don’t really know exactly what gorillas are eating much of the time, it does seem that they eat a lot of bugs along with their plants. So unless you have a particularly fastidious gorilla, some dietary protein won’t be vegan. Compared to humans, gorillas also have a much larger proportion of the gut devoted to fermentation—again, another source for microbes to contribute to the nutritional completeness of a plants-only diet. And, again, a high volume of food is consumed to compensate for the low nutritional value of it. You won’t have to worry about half your food going down the toilet, though. Those who want to live like gorillas can just eat that poop instead of flushing it. This provides the body with another opportunity to extract nutrition from the substance formerly known as food and may also help explain the willingness of Dr. Furhman’s readers to swallow what he’s shoveling.

I have nothing against a plants-only diet—in whatever form it takes—if that’s what a person want to do and it makes him/her happy. I have no more interest in converting a vegan to omnivory than I do in having a vegan attempt to convert me to swearing off bacon. I am also aware that there is more—much more—to food choices than the nutritional content of the food chosen.

But I’m afraid this is just one of those situations where ideology has been sent to do the work of science. Ideology has its place, and science has its flaws. Truth, facts, and beliefs can be hard to define and harder still to separate. I get all that. But – to quote Neil deGrasse Tyson – “The good thing about science is that it’s true whether or not you believe in it.” Unfortunately, for all those gorilla-wannabees out there, the reverse also applies: Believing in something doesn’t make it true. You can believe all you want that broccoli is a better source of protein than steak, but your ribosomes don’t have access to a keyboard and they might vote differently.

Now, dear readers, if you ever run across some library-card-challenged blogger out there perpetuating Dr. Furhman’s little myth, you have a link to help spill some sunshine on the matter.

A beautifully-written summary by Emily Contois regarding the recent Critical Nutrition Symposium held at UC-Santa Cruz. Organized by Julie Guthman, author of Weighing In, this symposium brought together food scholars from around the country (plus me) and invited us and the audience to participate in a thought-provoking and nuanced conversation about food, nutrition, culture, and ways of knowing.

Emily Contois

On March 8, 2013, I had the pleasure of attending the Critical Nutrition Symposium at UC Santa Cruz, organized by Julie Guthman, author of Weighing In. The event was spawned from a roundtable discussion at last year’s Association for the Study of Food and Society conference. The symposium brought together an interdisciplinary group of scholars to critically examine what is missing from conventional nutrition science research and practice, discuss why it matters, and brainstorm how to move forward in an informed and balanced way. What follows are a few of my favorite key ideas from the day’s discussions.

Adele Hite, a registered dietitian and public health advocate who is not afraid to ask big and delightfully confrontational questions regarding nutrition science, began the day by dissecting Michael Pollan’s now famous aphorism—Eat food. Not too much. Mostly plants. Step by step, she revealed the decades of revisionist myth…

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