I keep doing this thing where I stand in the shower writing blog posts in my head, emerging from the suds giddy and prune-fingered, feeling strangely accomplished about the words I have not yet typed. And then I squeegee the fog off the bathroom mirror and tell myself you can do it Denise! and think about how awesome it will be to actually update my blog after so much horrible silence. And then I load WordPress and think I’m blogging, I’m blogging, I’m finally blogging, it’s really happening.

And then suddenly it’s three hours later and I’ve opened 800 new browser tabs in Firefox and have become distracted by something shiny, Facebooky, or delicious, at which point all hope is lost.

This madness must end. Today, we blog.

So now I stand before you here in Cyberland, up on my soapbox, rantin’ muscles ready to flex. In case you haven’t heard, the world just got slammed with a new “meat is bad” tsunami—and it’s a doozy. We’ve got the familiar swirl of headlines designed to strike fear in our hearts (“That chicken wing you’re eating could be as deadly as a cigarette!” – The Financial Express), and pretty much every mainstream outlet caught it on their radar (hello ABC, Fox, The Guardian, Scientific American, Washington Post, and any other big-hitters I left out). The actual study, which is decidedly less popular than the press releases heralding its existence, is available here: Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population. Go take a gander. The gist is that animal protein will (purportedly) shorten your life and increase your risk of chronic disease—at least if you’re eating a bunch of it before you turn 66. (Once you’re in your golden years, though, the study implies animal protein is a good thing. Tricky, eh?)

So what’s really going on here? Should we all go vegan until we retire?

To be honest, I get weary blogging about what seems like the same study repackaged and regurgitated every few months under a different name (and it appears I’m not the only one). Observational meat studies are a dime a dozen. The media-viral ones seem to pop up at least a few times per year (I’ve already dissected a few). Ultimately, there’s only so much you can say about a study that uses wobbly survey methods, tries to squeeze causation from correlation, and falls victim to the confounders plaguing most epidemiological projects involving food. So whenever I see a new Meat Is Gon’ Kill Ya Dead study hijacking the airwaves, I feel kind of like

except with more sadness, and less nostril flare.

But this latest study grabbed my attention for a few reasons.

For one, it doesn’t orbit around the usual meat-damning suspects—saturated fat and cholesterol—but instead looks at animal protein, which I’m rather fond of discussing due to my previous shenanigans on this blog. And two, the researchers padded their observational study with some follow-up work on mice and cells, which at least earns them an A for effort. It’s still not the sort of research that should keep you awake at night, but at least in my mind, it’s interesting enough to warrant a closer look.

And perhaps more importantly, I think there might be some truth to the researchers’ findings. Yep, I said it. Gasp shock horror!

So let’s plow into this thing, shall we?

The Study Low-Down

Here’s the gist. The study itself was a two-parter: half human, half mouse (I realize that sounds like some kind of weird centaur). The human part grabbed the most media attention, so let’s start with that.

For this leg of the study, the researchers analyzed data from NHANES III—a giant survey of the health and nutritional status of American adults and kiddos, which churns up reams of info about what the good folks of this country eat. Basically, the researchers pulled data from almost 6,400 NHANES III participants aged 50 and over, looked at their food consumption (gleaned from a 24-hour recall survey they answered two decades ago), divided them up based on reported protein intake, and followed their disease and mortality outcomes for up to 18 years. (As best I can tell, that single recall survey was the sole source of the study’s dietary data.)

Those eating less than 10 percent of their calories from protein were scooted into the “low protein” group; those eating between 10 and 19 percent of their calories from protein comprised the “moderate protein” group; and those eating at least 20 percent of their calories from protein became the “high protein” group. Simple enough.

Initially, the only visible pattern was a much higher death rate from diabetes among the moderate- and high-protein groupers—not really worth sweating, though, because the sample size was too small to draw any meaningful conclusions. Other than that, protein consumption didn’t seem to be doing anything statistically noteworthy for the group as a whole: it was unrelated to all-cause mortality, death from cancer, and death from heart disease.

But here’s where it gets interesting. Instead of keeping all the participants lumped together, the researchers tried stratifying folks based on age—with the 50 to 65 year olds ushered into one group and the 66+ folks into another. The goal was to test for an age interaction, where a variable behaves differently depending on how old the participants are.

And it turned out “age interaction” was there in spades. Suddenly, a whole slew of diet-disease links cropped up—highlighting a trend for high protein to be bad news for middle-aged adults (50 to 65 years) but a boon for anyone older than that. Weird, right? It’s why protein didn’t have many meaningful correlations for the participant pool as a whole: its positive effects in the older crowd were canceled out by the negative effects in the younger crowd, creating the illusion of neutrality.

Anyway, the most interesting findings of that age stratification included:

The 50 to 65 crowd had a 74 percent greater risk of death from all causes for the high-protein group compared to the low-protein group (hazard ratio: 1.74), and a 433 percent greater risk of dying from cancer (hazard ratio: 4.33).

Folks aged 66 and older had a 60 percent lower risk of cancer mortality for the high-protein group compared to the low-protein group (hazard ratio: 0.40), and a 28 percent decrease in deaths from all causes (hazard ratio: 0.72).

In other words, the middle-aged adults eating the most protein faced higher rates of cancer mortality and deadness in general. Meanwhile, the 66-and-older crowd was apparently benefiting from all things proteinaceous, and those eating the most were living longer and more cancer-freely. And because I can’t not: here’s a friendly reminder that this is an observational study, and we can’t slap a cause-and-effect label on any of these relationships.

* Important caveat: both in the media hoopla and throughout the text of the Cell Metabolism paper, the results are reported as relative risk (e.g., “five-fold greater chance of getting heart disease”) rather than absolute risk (e.g., “3 percent died of heart disease”)—a great way to make findings seem wildly more dramatic and scary than they really are. For instance, this study found that among the NHANES III participants who were diabetes-free at the study’s onset, those eating the most protein were 73 times more likely to die of diabetes (yikes!). But if we look at the absolute numbers, which are tucked away in a little PDF supplement accompanying the study, we’d see that 0.2 percent of the low-protein group died of diabetes (one person) versus 2.0 percent of the high-protein group. That’s an absolute difference of 1.8 percent, which no longer sounds quite as horrifying.

The researchers also added another layer to their analysis: percent of calories from animal protein and percent of calories from plant protein. Here’s where the plot thickens. When adjusting for animal protein, all those links between protein intake, cancer mortality, and all-cause mortality went poof into the abyss—with the protein-cancer connection significantly diminishing, and the protein-total-mortality connection disappearing entirely. But when the researchers tried adjusting for plant protein in the same way, nothing happened.

So what does that mean? In a nutshell, that animal protein specifically was driving those disease links, whereas plant protein didn’t elicit an effect one way or another. (That rules out the possibility that plant protein had special mortality-slaying superpowers that made animal protein look bad by comparison.)

Should You Freak Out?

To figure out how seriously we should take this, let’s look at the study’s lifeblood: its dietary intake data. Although the Cell Metabolism paper is strangely silent about how people’s food intakes were gauged (a bit unnerving, considering how heavily this study depends on that data being sound), we know that NHANES collects its information via 24-hour recalls. The CDC website has a file discussing the whole process. Basically, participants get phoned by an interviewer, are asked to name everything they ate from midnight to midnight of the previous day, get prodded to make sure they didn’t forget any snacks or butter pats or late-night cookie nibbles, and then receive some follow-up questions about tap water and salt and other fun things. According to the CDC file, the participants also answer a short questionnaire “to ascertain whether the person’s intake on the previous day was usual or unusual.”

After looking over that questionnaire, I’ve got to say the word “ascertain” seems a bit optimistic to me. Keep in mind, the 24-hour recall is the sole source of dietary data in this study—so it darn well better strive for accuracy. And indeed, the NHANES survey employs a five-step strategy to help participants remember every bite they ate, described in “Nutrition in the Prevention and Treatment of Disease” (PDF) as follows:

An initial “quick list,” in which the respondent reports all the foods and beverages consumed, without interruption from the interviewer; A forgotten foods list of nine food categories commonly omitted in 24-hour recall reporting; Time and occasion, in which the time each eating occasion began and what the respondent would call it are reported; A detail pass, in which probing questions ask for more detailed information about the food and portion size, in addition to review of the eating occasions and times between the eating occasions; and Final review, in which any other item not already reported is asked.

As far as boosting reporting accuracy, that’s all a great help. But it appears the interviewers only asked one question to gauge how typical each participant’s reported diet was, relative to what they generally eat: “Was the amount of food that you ate yesterday much more than usual, usual, or much less than usual?”

That’s it. No qualifier for what “much more” or “much less” actually meant; no queries about specific foods; no prodding to see whether yesterday happened to feature a birthday barbeque, thus skewing the day’s frankfurter-to-kale ratio in a meatier direction than usual. Just one vague question about total food quantity, whose answer could only ever be subjective. (After the diet recall, each person’s reported intake was converted into food codes and nutrient components—so any flaws in that initial reporting trickled upstream to the final statistical analysis.)

And it gets worse. While it’d be nice to suspend disbelief and pretend the NHANES III recall data still manages to be solid, that’s apparently not the case. A 2013 study took NHANES to task and tested how accurate its “caloric intake” data was, as calculated from those 24-hour recall surveys. The results? Across the board, NHANES participants did a remarkable job of being wrong. Nearly everyone under-reported how many calories they were consuming—with obese folks underestimating their intake by an average of 716 calories per day for men and 856 calories for women. That’s kind of a lot. The study’s researchers concluded that throughout the NHANES’ 40-year existence, “energy intake data on the majority of respondents … was not physiologically plausible.” D’oh. If such a thing is possible, the 24-hour recall rests at an even higher tier of suckitude than does its cousin, the loathesome food frequency questionnaire.

(And in case that’s not enough to make your blood boil: the NHANES data is what the US government uses to determine what the country is eating, formulate dietary guidelines, and divvy up funding. Your tax dollars hard at work!)

If it’s that bad with calories, can we really expect the protein data to be much better?

In case you’re wondering why anyone uses such a destined-for-failure way of determining food intake, the answer is simple: it’s a heck of a lot cheaper (and easier) to ask people what they’re eating than to hellicopterishly stalk them all day long, weighing and measuring every morsel of food headed for their lips. When it comes to massive surveys like NHANES that track thousands of enrollees, affordability and convenience reign supreme. And sometimes that means cutting corners with precision.

Bottom line, it’s almost a given that the recall data here is less than stellar. And despite all the magical things math can do, no amount of statistical wizardry will heal numbers that are wrong from the start.

And to add insult to injury, keep in mind that this was the only diet information collected for each participant over the course of 18 whoppin’ years. Even if the recall managed to be accurate for the time it was recorded, there’s no way to know whether the participants’ diets evolved over the next two decades, and how any changes in their noshing habits impacted mortality outcomes.

That’s a lot of trust to put in one day’s worth of self-reported eating!

Diamonds Among Coals?

Now that I’ve bashed the NHANES diet survey to the moon and back, let’s look at why it might actually have some legitimacy. Bear with me!

While combing through the Cell Metabolism paper, one thought kept tickling my brain. Typically, if we dig into an observational study about meat, we see the heavy meat eaters—particularly those daredevils mowing down on red and processed varieties—engaging in a variety of lifestyle practices that spell I AM NOT HEALTH CONSCIOUS loud and clear: more smoking and drinking, less exercise, higher calorie intake, fewer fruits and vegetables each day, the works.

In turn, all those health-defeating behaviors tend to confound the true relationship between meat and various diseases and mortality. It’s hard to decipher whether meat itself is increasing cancer and heart disease and early death, or if reckless-with-their-health folks—already on a crash course towards chronic illness—just eat more of it because they don’t heed any conventional advice about diet and lifestyle.

If a situation like that was at play in this study, and protein intake was a surrogate for health-unconsciousness the same way meat tends to be, we’d expect to see the folks in the high-protein group fitting a similar anti-health profile—poorer diets overall, more risky behaviors. In turn, that would mean the study’s results could’ve been biased against the high-protein consumers due to all that residual confounding.

So was that the case?

Unfortunately, the paper doesn’t make it very easy to answer that question. There’s no data for biggies like drinking or exercise in the paper’s “participant characteristic” list. But we can see that the high-protein group actually had relatively fewer smokers than the low-protein group (18.2 percent versus 21.8 percent for current smokers; 37.8 percent versus 39.8 percent for former smokers), and that the high-protein group reported a lower calorie intake than the low-protein group (though heaven knows if that’s accurate). In addition, more people in the high-protein group than the low-protein group reported trying to lose weight during the past year (43.9 percent versus 37.5 percent), as well as changing their diet for health reasons (29.3 percent versus 15 percent). But it’s hard to say whether that’s a reflection of greater health awareness or poorer health when the study started.

What can we piece together from that?

Here’s my take. Contrary to what we might assume, the deck probably wasn’t stacked against the high-protein eaters from the start. If anything, the study’s confounders should have given them an advantage in their health outcomes. And I think that possibility is supported by more than just the (admittedly sparse) participant characteristics.

Here’s why. When the researchers took their protein correlations and adjusted for fat and carbohydrate intake (as percent of total calories), the numbers didn’t budge. That’s pretty interesting, because this batch of NHANES III surveys happened at the height of the nation’s fat-phobia, when mainstream thought was that all fat was bad—regardless of whether it came from something hooved, winged, or rooted in the dirt. Since adjusting for fat intake didn’t dissolve the links between protein and mortality, it reduces the likelihood that fat was acting as a confounder here.

Likewise, protein—at least until this study came out and ignited terror in omnivorous hearts near and far—has been the only macronutrient not demonized by any popular diets or mainstream health authorities. Fat and carbs have received more than their fair share of bashing over the years, but protein, as far as conventional thought goes, has clung tightly to its health halo—emerging unscathed from even the bloodiest of diet wars. (And the perception of “good protein” certainly includes that from animal sources, thanks in large part to the USDA’s push to consume our meat and dairy lean. How many egg-white omelets and and skinless chicken breasts have been choked down in the name of health?)

So again, if we were going to find any bias in the survey data, it’d probably lean towards protein being a good thing—at least in the eyes of the health-conscious crowd. The fact that a non-stigmatized macronutrient had such defined links with mortality cranks up its relevance, in my mind.

Of Mice and Rodent Chow (And Growth Factors and Protein)



Is your brain full yet? Save room, because there’s still another piece of the study to run through our wringer—and this one’s a lot more rambunctious and furry. To understand why protein might be linked to cancer and overall mortality as their human study suggested, the researchers conducted a series of experiments on mice, feeding them a range of protein levels mirroring that of the NHANES III participants—4 percent to 18 percent of calories. The prime goal was to see whether tweaking those protein levels would impact levels of insulin-like growth factor 1 (IGF-1) circulating in the mice’s bodies, as well as cancer incidence and progression.

But first, lets back up for a moment and get some context on this whole IGF-1 thing and why it’s so relevant.

As you might’ve seen in some of the news reports, the lead researcher of this study was Valter Longo—the director of the University of Southern California’s Longevity Institute, who already has a scroll of really cool studies under his belt (mostly on fasting and cancer). And he was profiled on “Through the Wormhole” with Morgan Freeman, which ups his awesomeness quotient considerably. Because science.

And in the world of aging research, IGF-1 is a bona-fide spotlight stealer. As its name implies, insulin-like growth factor 1 is a hormone molecularly similar to insulin, with its modus operandi being “grow, grow, grow!” It promotes growth for nearly every cell in your body—building muscle, making young’uns get taller, creating new brain cells, repairing nerve damage, and doing other awesome things that keep your body cranking like the fabulous machine it is. But IGF-1 is kind of a double-edged sword. And the bad-slicey side plunges right through the heart of longevity.

Part of the problem is that, while fulfilling its growth-promoting duties, IGF-1 doesn’t distinguish between healthy cells and damaged ones—potentially spurring cancer proliferation and contributing to tumor growth, if the conditions are right. High levels of IGF-1 have been linked to breast cancer, prostate cancer, bladder cancer, colorectal cancer, endometrial cancer, and lung cancer (though most of that research is observational, so there’s always the possibility of tumors increasing IGF-1 levels instead of the other way around, or a third unmeasured variable raising both). On the flip side, folks with a genetic deficiency in IGF-1 appear nearly immune to cancer—a phenomenon Longo himself has investigated.

Apart from the potential cancer connection, IGF-1 plays a huge role in the aging process. After all, the cycle of cells growing, dividing, and repairing is just a fancy way of explaining that they’re aging—so IGF-1 is pretty much orchestrating how rapidly that happens.

And the evidence comes from more than just the usual rat and test-tube studies. As far as human data goes, there’s some interesting research showing a connection between IGF-1 levels and lifespan when we look at the oldest of the old. A disproportionate number of centenarians have mutations affecting their IGF-1 receptor activity, which probably plays a role in their long-livedness. Likewise, the offspring of centenarians have lower IGF-1 levels than others of their age, gender, and BMI—suggesting the hereditary component of longevity could be due to reduced IGF-1 tricking through a family’s bloodline. (It’s less useful to look at IGF-1 levels in centenarians themselves, since the hormone naturally declines with age and will be pretty low in anyone who reaches the century mark.)

For longevity researchers, there’s an ongoing quest to “hack” all this life-extending genetic stuff and help us average Joe Shmoes reap the same benefits. Quite a few things can influence your body’s levels of IGF-1 beyond genes—everything from your stress level to your ethnicity to your estrogen status to the time of day—but diet is a huge determinant, and perhaps the easiest to tweak and control. So it’s not too surprising that food gets so much attention in this field. And as Longo was keenly aware of, protein is chief among the IGF-1 governors we consume.

But the life-extension hunt is still a work in progress. For at least 60 years, the darling of longevity seekers was calorie restriction (CR)—with the first case of its life-extension properties appearing in 1935, when an experiment showed that rats lived longer if their energy intake was reduced. Ditto for mice, flies, crustaceans, and yeast, more studies revealed. And subsequent research showed the same longevity effect in calorie-restricted ringworms, who idled in their larva’s “dauer” stage instead of catapulting towards maturity like usual. (Which made their lives longer, but not necessarily more enjoyable: the dauer stage consists mostly of not eating, not reproducing, and sitting like a lump on a bump until food supply becomes abundant. Even if we humans had a dauer stage, I can’t imagine wanting to stay there for very long. It sounds too much like high school.)

The reasons behind calorie restriction’s perks? A biggie was thought to be its suppressive effect on growth hormone and IGF-1—essentially slowing down aging and age-related diseases. Calorie-restricted organisms had much lower levels of IGF-1 than their more abundantly fed counterparts, at least in the creatures and fungi that’d been studied up to that point. And those reduced IGF-1 levels seemed to help protect cells from DNA damage—a boon for warding off cancer. It made sense: there’s a huge evolutionary and survival advantage to halting growth in times of food scarcity.

Although there wasn’t controlled data available for humans (we live too darn long to make lifespan studies an easy feat), the benefits of calorie restriction were expected to be universal. And thus emerged an era of books, gurus, theories, and research funding all pouring towards the promising new field of “CR.”

But soon cracks in the calorie-restriction theory started appearing. More comprehensive rodent studies, including one looking at 41 different strains of mice, found that calorie restriction shortened the lifespan in more strains than it extended. Likewise, in wild mice opposed to massively lab-domesticated ones, a lower energy intake did nada for average life expectancy (though it did curtail cancer rates). A 25-year rhesus monkey study—which the longevity world had waited with baited breath for completion—failed to show any life-extension benefit from feeding them less. And while studies on calorie-restricted humans weren’t far enough along to offer mortality data, the existing numbers showed their IGF-1 levels were pretty much the same as everyone else’s, casting doubt on the hope those earlier rodent and yeast and worm studies would be translatable to humans.

What the heck was going on?

Eventually it emerged that calorie restriction, for most species, was only effective if it also restricted protein intake. And as the study gods breathed more and more research into being, it seemed all that deliberate hunger might be for naught. Protein restriction alone could push down IGF-1 levels and spark a cascade of longevity-enhancing changes. (In case you’re wondering, neither fat restriction nor carbohydrate restriction seemed to increase lifespan, at least in rodent models.)

But it didn’t end there! A new wave of studies zeroed in on methionine, a sulfur-containing amino acid abundant in muscle meat and eggs. In mice, restricting methionine—without reducing calories—was enough to increase lifespan and induce health perks like slowing down immune aging, improving blood glucose, reducing IGF-1 and insulin levels, and protecting organ cells from oxidative damage. The reason? It appeared to be twofold: methionine tends to generate toxic byproducts—

And then the plot turned once more! Seriously, this saga had more twists than a pretzel factory. A fascinating but woefully little-known study in 2011 showed that in mice, supplementing with glycine—an amino acid found abundantly in connective tissue and gelatin and bone broth—had the exact same life-extending effect as restricting methionine. Without reducing calories or other amino acids, glycine supplementation increased the rodents’ lifespan, reduced fasting glucose and insulin, decreased IGF-1 levels, and nearly halved their triglycerides—the very perks that’ve variously been attributed to calorie restriction, protein restriction, and methionine restriction.

Let me make it abundantly clear: THIS IS HUGE. If the glycine finding translates over to humans (which I strongly suspect it does), life-extension-seekers may be barking up the wrong tree—or at least an unnecessarily complicated one—by trying to selectively reduce animal protein in order to live longer, as Longo seems to support. A wiser method could be simply getting a more “biologically appropriate” balance of amino acids than the standard Western diet typically provides. That means eating more of the glycine-rich foods that’ve been gradually stripped from our menus—things like skin, bones, tendons, tripe, feet, hooves, ears, connective tissue, and some organ meats—and less of the muscle meat typically dominating our fridges and freezers.

So to put all that in a Reader’s Digest version, the history of life-extension research went something like this:

“Calorie restriction extends rats’ lifespans. We must eat less to live longer!”

“Wait… reducing protein without reducing calories does the same thing. We must eat less protein to live longer!”

“Well I’ll be darned! The whole ‘life extension’ thing works just by limiting methionine. Methionine bad. Other amino acids okay! Down with meat!”

And now, it seems we’re at yet another crossroads—one where methionine intake may become less important than its balance and interaction with other nutrients, especially glycine.

*Note: This is deliberately oversimplified and lots of other really interesting discoveries happened. But heaven knows this blog post doesn’t need to be even longer than it already is.

Now back to Longo’s mice.

In a nutshell, the researchers put groups of mice on different experimental diets: one relatively high protein (18 percent of total calories) and one very low (4 to 7 percent of total calories). Then the mice were injected with cancer cells—melanoma for one experiment, breast cancer for another—in order to kick off the tumor-growing process.

Now brace yourself for some China Study déjà-vu. Fifteen days after getting their melanoma implants, all of the mice on the high-protein diets had developed measurable tumors—compared to only 80 percent of the low-protein group. (Over the course of the experiment, that number rose to 90 percent, but never got any higher.) What’s more, the low-protein group’s tumors seemed to grow at a much slower rate: by the final day of the experiment, the average tumor size in the high-protein group was 78 percent bigger than in the low protein group.

When that experiment was repeated with breast cancer cells, the results were pretty similar—except the tumor rate of the low-protein group maxed out at 70 percent of the mice, while the high-protein group was universally tumor-stricken.

And to tie IGF-1 back into the picture, the low-protein mice—as we might expect—had significantly lower levels than their protein-gorging brethren.

So there’s the gist. Is it a legitimate strike against eating lots of protein?

There’s one major reason I’m reluctant to draw any conclusions from all this (apart from the whole we aren’t mice thing). And that reason is called “AIN-93G standard chow.” That’s the name of the lab diet used for the high-protein mice, according to some notes in the paper’s supplement. You can download the AIN-93G specs here, but if you’d like to save yourself the effort (and hard drive space), here are the top six ingredients:

Corn starch (397 g)

Casein (200 g)

Maltodextrin (132 g)

Sucrose (100 g)

Soybean oil (70 g)

Cellulose (50 g)

Yum?

A lot of things are wrong with this picture, such as “where are the food things?”—but for the sake of brevity, I’m just going to focus on that second ingredient: casein. It’s one of the major proteins in milk, and it’s got an awful track record for promoting tumor growth more than other types of protein, including its dairy-derived cousin whey.

I’ve already written tomes on casein, cancer, and rodents in previous blog entries—including my Fork’s Over Knives critique and China Study critique—so I won’t torture you by rehashing it all here. Chris Masterjohn also has some awesomesauce posts on the subject, so hop on over there if you’re insatiably curious about it all. The bottom line is that when we look at the mice-and-protein studies outlined in Longo’s paper, this is what we’re dealing with: a cocktail of purified ingredients, with the protein component being a well-known promoter of cancer in rodents. It’s not at all surprising that the mice eating the most of it sprouted tumors like mad. But it’s impossible to say how much of that’s due to protein per se, or to casein—especially casein that’s been stripped of all the other goodies in dairy and tossed into a party bag of refined junk.

Putting It All Together

For those of us in the ancestral, paleo, “real food,” low carb, and other related communities, there’s a tendency to see a study like this and be like RAAWRRR KILL IT BEFORE IT BREEDS at the first whiff of its correlation-is-causation tone. And as someone who generally places epidemiology in the ninth circle of Research Hell, I’ve certainly been guilty of that myself. But one of the biggest gifts of observational studies like this one is the opportunity to explore new hypotheses and test out perspectives that challenge what we believe.

I think that’s definitely the case here.

Think of it this way. For most of human history, dietary consistency was a fairy tale. Famines struck. Periods of scarcity tangoed with those of abundance. We gorged on energy-dense foods like meat when they became available, knowing full well we might not be so lucky the next day or week. And to be sure, we ate the whole freakin’ animal after a kill—not just the skeletal muscle.

Constant abundance and pickiness is absolutely new to our bodies, even for those of us eating foods we deem ancient or ancestral. So it’s really not all that far-fetched to think that America’s animal protein habits—heavy on the methionine-rich muscle meats, scant on the glycine, swimming in ceaseless surplus instead of punctuated with scarcity—could be a problem for our health.

Perhaps it’s not a coincidence that many of the world’s longest-living populations eat fairly low-methionine diets or periodically abstain from protein-rich foods (like in Ikaria, where the predominantly Orthodox Christian residents cyclically fast from animal products). And perhaps just as relevant as the types of foods we eat is the manner in which we eat them—nose-to-tail for animals, with some plant-only days thrown in for good measure.

That doesn’t mean the solution is to go vegan. Nor is it necessarily to eat a low-animal-protein diet. But perhaps it’s time to seriously explore options like protein cycling, periodic fasting, or just cooking up heaps o’ bone broth to get that glycine down our gullets.

Just to be clear, nothing I’ve written here—even my moments of quasi-defending this study—changes the fact that the NHANES III data is observational and the diet recalls are basically handicapped from the start, thanks to the history-revising sinkhole that is the human mind. As always, correlation isn’t causation. It’s pretty disappointing that the study’s own researchers seemed to forget that. The reason I’m not sliding this study straight into the slush pile is because regardless of its validity, it at least opens the door to some important discussion. The bigger point is that the trends it excavated and hypotheses it explored could feasibly be real—evolutionarily, biologically, logically. In my opinion, the greatest value of this study, then, is its role as a springboard for breaking out of the comfort zone of what we think—and want—to be true.

Otherwise, I guess it could make a nice doorstop.