myth

Don’t Drink the Agave-Sweetened Kool-Aid Part I: “Natural” my foot

Mar 2 2010

UGH the subtitle. I really want Ms. Catalano to show me exactly where in "nature" she gets her agave nectar. Also, I find the use of "ultimate" to mean "exemplary" or "best" instead of "final" or "last" grating, but that's a petty battle against usage change that "Ultimate Frisbee" has clearly already won. Still, I like to think of it as "Frisbee for the End Days" Just as "wholesome" as any other hydrolyzed, refined sweetener. If you've been snarky about the Corn Refiners' Assn's recent "Sweet Surprise" marketing campaign, but have a bottle that looks like this in your cupboard, I have some delicious all-natural snake oil to sell you, good sir or madam.

This entry was nearly titled “Things That Might Not Kill You In Moderation But Certainly Won’t Make You Any Healthier Vol. I,” or “Hydrolyzed, Refined Sweeteners Masquerading as ‘Natural,’ Whole Foods,” but those seemed a little unwieldy. They do, however, capture the essence of the argument: agave is nutritionally no better than most other refined sweeteners, including high-fructose corn syrup (HFCS). If anything, it’s probably worse because it contains more fructose than table sugar or HFCS. It’s also no more or less “natural” than HFCS—it’s actually produced in a remarkably similar process that was first used on the fibrous pulp of the agave in the 1990s. While, as its proponents claim, the higher proportion of fructose has enabled people to call it a “low glycemic index sweetener,” sometimes alleged to be safer for diabetics and recommended by weight-loss programs like Weight Watchers, recent research suggests that large amounts of fructose aren’t healthy for anyone, diabetic or otherwise.

I mentioned agave nectar in passing in the HFCS post, but there’s enough conflicting information about it to merit its own post(s). A lot of the misinformation comes from agavevangelists, who can sometimes get a little sanctimonious about their avoidance of the demon HFCS and preference for “natural” sweeteners. Even this Vegfamily article that concludes “the physiological effects of all [caloric] sweeteners are similar” nonetheless claims:

Given the choice between sugar, HFCS, and agave nectar, I'll stick with organically-grown, unbleached cane sugar (evaporated cane juice) and organic raw agave nectar that are free of pesticides, herbicides, and chemical bleaching agents; not genetically engineered; and still retains some nutrients, as well as being vegan. Since HFCS is not available in organic form and is highly processed, I would never use it.

But agave nectar is just as processed as HFCS.

HFCS and Agave Nectar: One of These Things is Not Almost Exactly Like The Other

1910 magazine advertisement from http://goldcountrygirls.blogspot.com/2009/10/then-and-now-49-karo-syrup.html Like most starches, corn starch consists of large glucose polymers—70-80% the branched, non-water soluble amylopectin and 20-30% linear, soluble amylose. Normal or non-HFCS corn syrup, like Karo, is produced by breaking those polymers down into their constituent glucose molecules using acids, enzymes, and/or heat. For the history buffs: the acid hydrolysis of starch was first discovered because of the 1806 British blockade of the French West Indies. Napoleon I offered a cash reward for anyone who could come up with a replacement for cane sugar, and a Russian chemist named Konstantin Kirchhof found he could produce a sweet syrup from potato starch by adding sulfuric acid. The same process was first applied to corn in the mid-1860s, and gained popularity in the U.S. during the sugar shortages of WWI (source: The Oxford Encyclopedia of Food and Drink in America).

HFCS is produced by converting the glucose into fructose using an enzyme technology developed in Japan in the 1960s (detailed here). The resulting syrup, which contains up to 90% fructose, is then typically mixed with corn-based glucose syrup to produce HFCS-55 (the kind used in soft drinks, which has 55% fructose/45% glucose) or HFCS-45 (the kind used in baked goods, which has 45% fructose/55% glucose). Some people, like Cynthia commenting on Daily Candor, have suggested that the fructose and glucose in HFCS are absorbed into the bloodstream faster because they’re “free" instead of bound the way they are in the disacccharide sucrose, which is broken into glucose and fructose by the enzyme sucrase. Theoretically plausible, but apparently not true:

Sucrose is hydrolysed by brush-border sucrase into glucose and fructose.
The rate of absorption is identical, regardless of whether the sugar is presented to the mucosa as the disaccharide or the component monosaccharides (Gray & Ingelfinger, I 966, cited by H. B. McMichael in “Intestinal absorption of carbohydrates in man”).

I'm going to start refering to packaging like this as granola-washingJust like HFCS, agave nectar is produced by breaking down a plant-based polymer into its constituent sugars. In the case of agave, the relevant molecule is inulin, a fiber composed mostly of fructose units with a terminal glucose. Just like with corn and potato starch, there are different methods of hydrolyzing the sugars in inulin.  Blue Agave Nectar uses a thermic process. Madhava uses an enzyme process, just like HFCS.

Agavevangelists like to claim that agave nectar is a traditional sweetener used by native peoples, which appeals to the popular notion that the foodways of the past were generally healthier (e.g. Michael Pollan’s advice not to eat anything your great-grandmother wouldn’t recognize as food). Some, like Lynn Stephens of Shake Off the Sugar, merely note that the agave plant itself “has long been cultivated in hilly, semi-arid soils of Mexico.” That’s true, although it’s about as relevant as the long history of corn cultivation. Others claim that agave nectar itself has an ancient history. Flickr user Health Guy says of agave nectar: “It is 1-1/4 times sweeter than sugar, so you need less, and it has been consumed by ancient civilizations for over 5,000 years.”

Wrong. According to the website for Madhava Honey:

Agave nectar is a newly created sweetener, having been developed during the 1990's. Originally, the blue agave variety was used. This is the same plant used in the manufacture of tequila. During the late 90's, a shortage of blue agave resulted in huge increases in cost and a sweetener based on this plant became uneconomical. Further research was done and a method using wild agave was developed. Overcoming the language barrier between the Indians able to supply the nectar from the wild agave on their land and the Spanish speaking local manufacturer was the key that finally unlocked a supply of raw material and has led to our bringing this wonderful new product to market.

Still doing some native-washing (wild agave harvested by Indians who don’t speak Spanish—can’t you just feel the virtue?), but here’s what happens to the agave sap after harvesting, as described in the abstract of the 1998 patent issued for the production of fructose syrup from the agave plant:

A pulp of milled agave plant heads are liquified during centrifugation and a polyfructose solution is removed and then concentrated to produce a polyfructose concentrate. Small particulates are removed by centrifugation and/or filtration and colloids are removed using termic coagulation techniques to produce a partially purified polyfructose extract substantially free of suspended solids. The polyfructose extract is treated with activated charcoal and cationic and anionic resins to produce a demineralized, partially hydrolyzed polyfructose extract. This partially hydrolyzed polyfructose extract is then hydrolyzed with inulin enzymes to produce a hydrolyzed fructose extract. Concentration of the fructose extract yields a fructose syrup. (via Patentstorm)

Probably the healthiest sweetener pictured here and the one most shoppers in the market for a "natural sweetener" would be least likely to purchaseIt’s true that the corn used in HFCS is less likely than agave to be organically-grown, but you can get organic-certified corn syrup from the same manufacturer as the blue agave nectar pictured above and nutritionally, the main difference between that, the HFCS used in most processed foods, and agave nectar is the ratio of glucose: fructose. The regular corn syrup is 100% glucose, HFCS is usually 55/45 glucose/fructose, and agave nectar 56-90% fructose, depending on the plant and the process.

I’ve already talked a little about fructose vs. glucose here and here, but more coming soon in Agave-rant Part II concerning:

1) whether the fructose in agave is somehow better than, or indeed, different in any way from the fructose in HFCS

2) whether the fact that it’s sweeter than sugar makes it a lower-calorie alternative to sugar

3) whether its “low glycemic index” rating makes less likely to produce insulin resistance than table sugar and

4) whether it’s safer for diabetics

All of which people have claimed. I won’t keep you in suspense, especially given how long it may take me to put all of that together. The short answers are:

1) not in any nutritionally meaningful way

2) perhaps very slightly, but a <10 calorie/serving difference likely doesn’t make up for the increased risk of fatty liver syndrome and insulin resistance

3) no, it’s actually more likely to produce insulin resistance and

4) in miniscule amounts, perhaps, but recent trials involving diabetics and agave nectar were halted because of severe side effects.

Things That Won't Kill You Volume 4: Saturated Fat Part II: Cholesterol Myths

Feb 5 2010

image In retrospect, this probably could have been an entirely separate article in the "things that won't kill you" series, as many people still believe that dietary cholesterol (i.e. cholesterol in food) is a bad thing. For example, the article that image was taken from claims:

If you get too much dietary cholesterol (over 300mg a day) the extra cholesterol will accumulate in the walls of the blood vessels, making your LDL (bad) blood cholesterol levels rise. Over time, your arteries will become narrower, which can cut off the blood supply to your heart (causing a heart attack), or your brain (causing a stroke).

However, that's pretty easily dismissed—even Ancel Keys, "Monsieur Cholesterol" himself, never argued that dietary cholesterol was related to serum cholesterol or heart disease. In a 1952 article in Circulation, the journal of the American Heart Association, Keys noted that although rabbits and chickens that eat high-cholesterol diets will develop high cholesterol and atherosclerosis, or hardening of the arteries:

No animal species close to man in metabolic habitus has been shown to be susceptible to the induction of atherosclerosis by cholesterol feeding…. Moreover, even in the favorite species for such  experimentation, the herbivorous rabbit, the necessary concentration of cholesterol in the diet is fantastically high in comparison with actual human diets. Moreover, there is reason to believe that man has a greater power of cholesterol regulation than does the rabbit or the chicken. From the animal experiments alone the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis.

Two "moreovers" in one paragraph, people! “Most reasonable conclusion”! Moreover, five decades of subsequent research haven't given anyone any reason to think differently. In 1997, Keys was even more direct:

There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter unless you happen to be a chicken or a rabbit.

Research done in the interim on the relationship between diet and heart disease in humans like the Framingham and Tecumseh studies showed no relationship between cholesterol consumption and blood cholesterol or heart disease. I'm not even going to modify this with "probably" or "as far as we know": There is no reason to believe that how much cholesterol you eat has any effect on your health.

But that doesn’t stop the AHA from recommending that “most people…limit cholesterol intake to less than 300 mg per day” and claiming that “an egg can fit within heart-healthy guidelines for those people only if cholesterol from other sources — such as meats, poultry and dairy products — is limited.” Despite repeated studies showing that egg consumption is not associated with higher serum cholesterol, myocardial infarction, cardiovascular disease, or all-cause mortality.Read more

Salt Headlines That Make The Vein In My Forehead Throb

Jan 27 2010

Salt has been all over the news this week because of a study just published in The New England Journal of Medicine claiming that if everyone in the U.S. reduced their sodium consumption by 3 grams/day, there would be 32,000 fewer strokes, 54,000 fewer heart attacks, and 44,000 fewer deaths every year. The story that got my attention was:

Remaining Arctic Ice Seen Melting Away Completely! (...on a computer screen)

That’s surprising, I thought. Everything I’ve read suggests that the relationship between salt consumption and cardiovascular disease is weak, inconsistent, and probably only valid for 20-30% of the population. So I expected the article to refer to some new research where, you know, “big benefits” were “seen.” As in observed. Like, in the world. And, given the claim about the magnitude, probably also measured.

To their credit, the authors of the study claim no such thing. The numbers are projections based on the application of several assumed effects of salt reduction, adjusted for different demographics and then applied to a model of the entire U.S. population. Thus, the title of the study: “Projected Effect of Dietary Salt Reductions on Future Cardiovascular Disease.”

The article seems to grasp the essentially speculative nature of the findings. The very first sentence uses the conditional tense:

…scientists writing in The New England Journal of Medicine conclude that lowering the amount of salt people eat by even a small amount could reduce cases of heart disease, stroke and heart attacks as much as reductions in smoking, obesity, and cholesterol levels.

The headline, on the other hand, seems to have confused the “scientists” with clairvoyants. Never mind doing any checking into the validity of their assumptions.

And the claim about how the benefits compare to smoking and obesity reduction led to a few headlines like this:

webmd salt

This crazypants idea initially sounds a lot like what the study’s lead author claims:

"The cardiovascular benefits of reduced salt intake are on par with the benefits of population-wide reductions in tobacco use, obesity, and cholesterol levels."

But the logic behind the claim is that a small improvement in the health of every single American would be as significant as a large health improvement in the health of every single smoker:

Dr. Bibbins-Domingo said that for many people the decrease in blood pressure would be modest, which is why, she said, “many physicians have thrown up their hands and said, ‘I’m not going to advise my patients to reduce salt because it’s too hard for patients and the benefits for any individual are small.’

“But small incremental changes in salt, such as lowering salt in tomato sauce or breads and cereals by a small amount, would achieve small changes in blood pressure that would have a measurable effect across the whole population,” she said. “That’s the reason why this intervention works better than just targeting smokers.”

For any given individual, there is no question about whether cutting salt is even close to “as good” as quitting smoking. The evidence for the link between smoking and lung cancer and death is strong, reliable, consistent, and has a clear causal mechanism (carcinogens). The link between salt and cardiovascular disease and death is weak, inconsistent, and still poorly understood.

That latter point starts to get at the problems with the study itself, and not just the headlines it inspired. A number of the assumptions the projection was based on are either demonstrably false or simply unsubstantiated. More on this some other time; for now, a few quotes and links to the essays they come from in Esquire and the medical journal Hypertension:

In a more recent statement, the founder of the American Society of Hypertension, Dr. John Laragh, goes further: "Is there any proven reason for us to grossly modify our salt intake or systematically avoid table salt? Generally speaking the answer is either a resounding no, or at that, at best, there is not any positive direct evidence to support such recommendations."

Studies show that 30 percent of the Americans who have high blood pressure would greatly benefit from a low-sodium diet. But that's about 10 percent of the overall population -- the rest of us are fine with sodium. And drastically cutting out sodium may actually hurt some people. ( "Go Ahead, Salt Your Food")

And:

The available data suggest that the association of sodium intake to health outcomes reflected in morbidity and mortality rates is modest and inconsistent. Therefore, on the basis of the existing evidence, it seems highly unlikely that any single dietary sodium intake will be appropriate or desirable for each member of an entire population.... The decision to adopt a low sodium diet should be made with awareness that there is no evidence that this approach to blood pressure reduction is either safe, in terms of ultimate health impact, or that it is as effective in producing cardioprotection as has been proven for some drug therapies. (Salt, Blood Pressure, and Human Health)

Things That Won't Kill You Volume 4: Saturated Fat, Part I

Dec 14 2009

I know this is misleading because lard is mostly unsaturated, but it's been one of the major icons of "bad" fat and also, how graet is this image? from http://www.npnworldwide.com/lard

This is probably going to be an even harder sell than MSG, but I swear I'm not just trying to be contrary. It's true that all the major sources of public health and nutrition advice, including the Harvard School of Public Health, Mayo Clinic, CDC, and American Heart Association continue to refer to saturated fats as "bad fats" and suggest that people avoid them as much as possible, limit them to <7-8% of their total caloric intake, and replace them with "good," i.e. unsaturated fats, whenever possible. It's also true that there are a few studies that suggest that increased saturated fat consumption is correlated (albeit weakly) with cardiovascular disease (CVD).

However, many other studies have found no increase in CVD associated with saturated fat consumption. And several recent review articles have concluded that the evidence for a connection between saturated fat consumption and CVD is inconsistent, insufficient or nonexistent.

There are basically three things that have convinced me that saturated fat isn't independently responsible for heart disease or death:

1) groups of people who eat vastly more saturated fat than most Americans frequently have lower rates of CVD—or no apparent CVD at all

2) the study that first inspired many people to think saturated fat was a bad thing had a lot of obvious flaws and has been thoroughly discredited

3) there's no good evidence that the proposed mechanism actually works—briefly: saturated fat supposedly causes heart disease by raising serum cholesterol levels because cholesterol is what clogs arteries and causes heart attacks and strokes, but serum cholesterol turns out to be a really poor predictor of CVD 

1) The French (and Polynesian and Melanesian and Masai and Fulani and Sri Lankan) Paradox 

photo by Arun Ganesh http://en.wikipedia.org/wiki/User:PlaneMadThe most confounding phenomenon for the theory that saturated fat consumption causes heart disease (sometimes called the lipid hypothesis or lipid-heart hypothesis or diet-heart hypothesis) is the virtual non-existence of CVD in multiple populations that eat way more saturated fat than most Americans. This has primarily been documented in the Pacific islands where coconuts, which are very high in saturated fat, are a staple food. For example, before the 1970s, the inhabitants of the island Tokelau got an estimated 55% of their calories from saturated fat, but heart disease was virtually unknown (according to Gary Taubes and Stephen Guyenet; notably, since their diet has shifted to include less saturated fat but more sugars and refined carbohydrates, many health indicators have worsened). Read more

Things That Won't Kill You Volume 3: MSG

Oct 14 2009

From Flickr user "The Other Dan" taken in Corktown, Toronto 

Unlike juice, which has sort of a mixed reputation even among contemporary nutritionists and doctors, MSG has been consistently demonized. Most people can't tell you why, they just know that it's bad. If pressed, they might tell you that it's "unnatural," that food manufacturers put it in processed foods to con people into eating "junk," that it's basically salt (which I'll address in a future post in this series), or that it gives some people headaches. Or they might just gesture to the fact that it's common knowledge that MSG is basically some kind of poison—after all, why would Chinese restaurants be so eager to reassure you that they don't use it if it were completely benign?

A recent commercial for Campbell's New Select Harvest Light (which is the sort of self-satirizing product name I'd expect to find in David Foster Wallace's fiction) suggests that even if people don't know what MSG stands for, they know that it's bad—potentially bad enough to deter people from buying a particular brand. Reading from a Progresso Light can, blonde #1 gets through "monosodium" but stumbles on "glutamate"—fortunately, the rainbow coalition includes an Asian woman who can translate that jargon into something we all understand: "That's MSG."

Although people may still associate it primarily with Chinese restaurant cooking, the Campbell's ad hints at its broader prevalence—MSG and other forms of glutamic acid are omnipresent in processed foods. They're especially likely to be found in foods designed to taste like things that have a lot of naturally-occurring glutamate (or similar molecules like inosinate or guanylate). Stock, broth, and bouillon often contain MSG, as does anything cheese-flavored or ranch-flavored, like Doritos, which actually contain five different forms of glutamate. I taste it the most in instant ramen and Chex Mix, but even though I know what it tastes like on its own, I can't always tell when something contains it or not. When used sparingly, it may not even be possible to discern because whether the glutamate in a dish comes from a mushroom or a salt, once it's dissolved in liquid or on your tongue, it's the exact same molecule:

from Wikipedia, showing up weirdly gray here

So even people who think it's "bad" and expect to feel bad after eating it probably eat MSG, at least from time to time, without even knowing it, and without suffering any negative effects.Read more

Things that won't kill you Vol. 1: High-fructose corn syrup

Sep 7 2009

Confession: I not only avoided high-fructose corn syrup (hfcs) until about a year ago, I was actually skittish about fresh corn for a while after my first encounter with Michael Pollan in The New York Times Magazine (or it might have been this article). I stopped eating corn tortillas and frozen corn kernels and felt vaguely panicky about the possibility that I was consuming hfcs in condiments and sandwich bread when I ate out, even if it would have only been tiny amounts.

Now that I'm over it, I sometimes have a hard time remembering what was so scary about the idea that there was corn in everything I was eating, an idea that was obviously ludicrous anyway because I was a vegetarian who mostly ate food prepared at home from whole, fresh, non-corn ingredients. But looking back at the articles linked above, they are pretty ominous. Even though Pollan notes that a corn-based diet has been the norm in Mexico for centuries without any apparent ill effects, and the story he tells about the "cornification" of the American diet is too complex to be a nefarious plot designed to kill us all, it's clear that he thinks the amount of corn Americans eat on average is a Bad Thing. Sure, it may rely on innocent accidents of nature, like the uniquely efficient way corn fixes carbon during photosynthesis and and the great distance corn pollen has to travel to reach the style, but it's also reliant on much more insidious developments: synthetic pesticides and fertilizers, an arcane federal farm subsidy systems that turned corn into "a welfare queen," agribusiness giants with seed patents on genetically-modified strains, giant livestock feeding operations that use antibiotics to keep cows alive because eating corn makes them sick, and food manufacturers who profit from getting people to buy cheap food in ever-increasing quantities. Eating corn in any form may seem like a way of giving in to all of that or even supporting it.

So although I did a fair bit of eye-rolling when I read about people avoiding sweet corn at their farmer's markets this summer or feeling "corn guilt" when they eat popcorn, it's worth remembering that I was one of them not so long ago.

HFCS paranoia is not primarily an issue of ethical consumption

It's not that many of those concerns are invalid—it's true that most corn relies on a lot of synthetic fertilizers and pesticides, that much of it is grown using genetically modified seeds with patents held by huge corporations that have been known to sue farmers when corn with their patented genes end up in their fields, that cows fed diets of corn get sick and are more susceptible to diseases like e coli that can threaten humans. But it's also far from clear that refusing to eat ketchup containing high fructose corn syrup is an effective means of changing any of that or even primarily motivated by the desire to change those things.

Although people like Pollan have made a big deal about corn sweeteners being artificially cheap due to farm subsidies, the actual farm cost of hfcs in the food products we buy is so minimal that even if subsidies were eliminated entirely, it might not affect portion sizes or consumer demand at all. Even in soft drinks, which are by far the most demonized hfcs delivery system, hfcs represents just 3.5% of the total cost of manufacturing. The corn content, the only part actually affected by farm subsidies, is only 1.6 percent of the price (based on US Department of Commerce data). A comparison between the U.S., Australia, the UK, and France, all of which have different sugar policies but similar consumer prices, show no pattern in the relationships between how cheap sugar is, how much of it people eat, or how fat on average they are (which most people wrongly assume is a reliable measure of health outcomes, but I'll tackle some other time).

Pollan's formal case against hfcs relies primarily on arguments about price and prevalence, but that doesn't really explain the kind of paranoia his books and articles have helped inspire about eating corn and/or hfcs. Not buying and eating something because it's too cheap just isn't the kind of consumer behavior that spreads the way hfcs-phobia has. Nor is this some sort of mass avoidance of all added or refined sugars, or brands like Snapple and Pepsi wouldn't be running huge campaigns to advertise soft drinks containing only "natural sugar."

Instead, people have latched on to the implication, which isn't supported by any data I can find, that hfcs is nutritionally worse than other sugars. The hfcs paranoia isn't caused by the idea that hfcs might be unwisely or unfairly subsidized or that pesticides used to produce corn are poisoning waterways or anything related to feeding corn to cows. The fear is that hfcs might be some kind of demon poison that makes people fat.

The confusing part: "high fructose" isn't actually high fructose

The idea that hfcs is worse than other sugars seems to be primarily reinforced by research about how fructose is metabolized. Just last April, an article about a study comparing drinks sweetened with fructose and  glucose in the New York Times began:

Some research has suggested that consumption of high-fructose corn syrup, used as a sweetener in a wide variety of foods, may increase the risk of obesity and heart disease. Now, a controlled and randomized study has found that drinks sweetened with fructose led to higher blood levels of L.D.L, or "bad" cholesterol, and triglycerides in overweight test subjects, while drinks sweetened with another sugar, glucose, did not.

Things like this get reported all the time. However, the very last sentence of the article quotes another biochemist:

The study did not test high-fructose corn syrup, he said, and judgments should not be made about it from the findings.

Not that that stopped the author from leading with the useless, ambiguous claim about a supposed link between hfcs and obesity, but surely this deserves a little more attention: yes, fructose alone seems to cause more insulin resistance and weight gain in both rats and people than glucose alone. But high fructose corn syrup is only "high fructose" relative to normal corn syrup, which is 100% glucose.

The kind of hfcs used in most food processing, including soft drinks, is hfcs-55, which is approximately 55% fructose and 45% glucose, or almost identical to sucrose, which is about 50/50. Another kind, hfcs-42, is used in the manufacture of some baked goods, and if fructose is really worse, that would make that kind of hfcs healthier than cane sugar. Indeed, studies comparing the consumption of hfcs to sucrose have shown no differences in metabolic responses (or energy or macronutrient intake) at all.

The argument that hfcs is somehow responsible for the obesity epidemic relies entirely on correlations between the rise of hfcs in food manufacturing in the 1980s and the rise in national rates of overweight/obesity (and the exponential rise in concern about fatness). Pollan's case against hfcs amounts to a gut suspicion that:

It's probably no coincidence that the wholesale switch to corn sweeteners in the 1980's marks the beginning of the epidemic of obesity and Type 2 diabetes in this country.

Of course, this fails to account for the simultaneous increases in obesity in many other countries, perhaps most notably Australia, where obesity rates rival or even exceed those in the U.S., but sugar is the primary sweetener. It's not that he's totally wrong; it does seem probable that U.S. farm subsidies and the cheap price of highly-palatable, nutrient-poor, calorie-rich, primarily carbohydrate-based foods is one factor driving the relatively small increases in the average American's weight since the 1970s. And the history of corn cultivation and agricultural policy has something to do with that. But there's no reason to think that hfcs is uniquely responsible for the "obesity epidemic." After all, if it weren't for subsidies and tariffs that keep the price of sugar artificially inflated, which are the result of a different set of biological, historical, and political contingencies, it would be just as cheap. 

Ultimately, hfcs is just another source of sugar, nutritionally no different from cane sugar, and way better than agave nectar if you're concerned about fructose. It might be slightly worse than things like honey (esp. raw) and maple syrup (esp. grade B or lower) if you're interested in vitamins and minerals. (This is all assuming the hfcs in question contains mercury, but that's sort of another story altogether).

That doesn't mean hfcs is  "natural," a word which has virtually no meaning when it comes to food labeling anyhow, but then, if "natural" is the alternative to "processed," no sweeteners are. Agave nectar must be filtered, hydrolyzed, re-filtered, and concentrated before it can be used as a sweetener. Refined cane sugar is purified with phosphoric acid and calcium hydroxide, and sometimes whitened using bone char which is why some vegetarians and vegans refuse to eat it.

The upshot is there's no reason to believe that hfcs is any worse for you than sugar or much worse for you than any other sweeteners, and there's certainly no reason to believe that a little bit here and there in a favorite condiment or even the occasional soda is going to hurt you.

Later in this series: I've gotten a request to weigh in on fruit juice, and will try to do that soon. And someday I'll get around to msg, as promised before.

Feeling "umami": On taste, subjectivity, and metaphor

Sep 1 2009

The Modern Four Taste Orthodoxy

The idea that there are four basic tastes—sour, salty, bitter, and sweet—was widely taken to be gospel truth until 2002, when the taste receptors for glutamate were identified. Glutamate, and the "umami" flavor it imparts to foods like seaweed, bacon, parmesan cheese, and Doritos, was first identified and isolated by a Japanese chemist named Kikunae Ikeda in 1908. But the four-taste model was so dominant that umami's status as a distinct taste was considered "controversial" until its molecular basis was confirmed almost a century later. Here's the description of umami in a book titled Sensory Processes published in 2002 (before the taste receptors were identified):

Umami originated from a glutamate derived from seaweed. The chemical substance is commonly known as MSG, monosodium glutamate, and, by itself, has no odor and an unusual taste that is approximated, so they say, by appropriate combinations of the four primary taste qualities. Whether umami is a result of the unique combination of the four tastes or an independent classification of is own is open to debate (176).

Oh, they and the things they say.

Umami's been gaining traction—Kikkkoman's current advertising campaign is "discover umami"(.com)—but it hasn't quite arrived. This past Sunday on Iron Chef America, one of the judges said he detected some "umami" in a coconut-based soup, and then he had to define it for the other judges (and perhaps the audience?). His first stab was to call it an "illusory" taste, although he did follow that up by ranking it with "sweet, salty and sour," so perhaps he actually meant something more like "ineffable." Either way it shows how dominant the classical four tastes still are.

Except "classical" isn't quite right word, because it turns out the idea that we only experience four distinct tastes is actually a pretty recent invention—more recent than Ikeda's "discovery" of umami, actually. Traditional Chinese medicine named five tastes: sour, bitter, sweet, pungent, and salty, each one corresponding with one of the five elements or movements that are omnipresent in early Chinese thought. Aristotle claimed there were only two, which doesn't come as that much of a surprise given his characteristic love of dualities. Just as he divided visual perception into the "fundamental colors" black and white, which contain all the elements of all the other colors we perceive, Aristotle thought the whole range of gustatory sensations derived from the "fundamental tastes" of sweetness and bitterness. He also proposed a second-order classification of seven "primary flavors" that corresponded with his rainbow of seven "primary colors": sweet (which included fatty or oily), bitter, salty, harsh, pungent, astringent, and acidic or sour. Hard to say now what exactly the difference was between harsh, pungent, and astringent—I suppose the latter might be something like the tannins in tea and red wine while "pungent" instantly evokes blue cheese although it often just acts as a modifier rather than a descriptor—a pungent smell is strong, not necessarily strongly any particular thing. It's hard to even think of those things as taste categories on the same level as "sweet" or "sour."

But one question that raises is whether or not it's hard to think of them that way because there's some objective difference between sweetness and astringency or because it's just unfamiliar to think of "astringent" as a primary taste category. Certainly tannins cause a particular reaction on people's tongues—is that less of a distinct taste experience than the reaction caused by sugars?

Colors are a useful parallel, again. A linguistics professor I had at NYU told us about this experiment that my casual googling is not coming up with, but here's the gist: if you give children a set of colored tiles and tell them sort them into as many piles as they want, by color, there are predictable, reliable differences between the number of piles they make that correspond to the number of primary colors in their primary language. So, for example, English-speaking kids generally put all hues of blue in one pile while Russian-speaking kids usually separate lighter blues from darker blues because they have two "primary color" words for those shades. It's one of the classic examples of how language can shape how we perceive the world rather than just reflecting it. Also a reason why translation is always imperfect. 

Henning taste tetrahedronGetting back to the four taste orthodoxy, that was something a German psychologist named Hans Henning  came up with in 1916. He devised a ""taste tetrahedron" with each of the four tastes he thought were primary at the four vertexes. The idea was that flavors could be conceptually mapped onto geometric plane based on which of the primary flavors they were comprised of—a flavor relying on two of the primary tastes would be located on the edge between those two vertexes. Flavors that used three would be on the surface between the relevant three points. And the tetrahedron was hollow, according to Henning, because no substance could produce all four taste sensations. So while taste itself was three-dimensional, tastes were two-dimensional at best. Read more